Hepatic Encephalopathy

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Hepatic Encephalopathy

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Full Text Available ... friend, spouse, life partner, parent, sibling or other family member. What is HE? Hepatic Encephalopathy, sometimes referred ... disease is. It’s important for you and your family to become familiar with the signs of Hepatic ...

Rifaximin in the treatment of hepatic encephalopathy

Directory of Open Access Journals (Sweden)

Iadevaia MD

2011-12-01

Full Text Available Maddalena Diana Iadevaia, Anna Del Prete, Claudia Cesaro, Laura Gaeta, Claudio Zulli, Carmelina LoguercioDepartment of Internistica Clinica e Sperimentale, F Magrassi e A Lanzara, Hepatogastroenterology Unit, Second University of Naples, Naples, ItalyAbstract: Hepatic encephalopathy is a challenging complication in patients with advanced liver disease. It can be defined as a neuropsychiatric syndrome caused by portosystemic venous shunting, ranging from minimal to overt hepatic encephalopathy or coma. Its pathophysiology is still unclear, although increased levels of ammonia play a key role. Diagnosis of hepatic encephalopathy is currently based on specific tests evaluating the neuropsychiatric state of patients and their quality of life; the severity of hepatic encephalopathy is measured by the West Haven criteria. Treatment of hepatic encephalopathy consists of pharmacological and corrective measures, as well as nutritional interventions. Rifaximin received approval for the treatment of hepatic encephalopathy in 2010 because of its few side effects and pharmacological benefits. The aim of this work is to review the use and efficacy of rifaximin both in acute and long-term management of hepatic encephalopathy. Treatment of overt hepatic encephalopathy involves management of the acute episode as well as maintenance of remission in those patients who have previously experienced an episode, in order to improve their quality of life. The positive effect of rifaximin in reducing health care costs is also discussed.Keywords: acute hepatic encephalopathy, recurrent hepatic encephalopathy, rifaximin, lactulose, cost, health-related quality of life

Branched-chain amino acids for hepatic encephalopathy

DEFF Research Database (Denmark)

Als-Nielsen, B; Koretz, R L; Kjaergard, L L

2003-01-01

Hepatic encephalopathy may be caused by a decreased plasma ratio of branched-chain amino acids (BCAA) to aromatic amino acids. Treatment with BCAA may therefore have a beneficial effect on patients with hepatic encephalopathy.......Hepatic encephalopathy may be caused by a decreased plasma ratio of branched-chain amino acids (BCAA) to aromatic amino acids. Treatment with BCAA may therefore have a beneficial effect on patients with hepatic encephalopathy....

Dopamine agents for hepatic encephalopathy

DEFF Research Database (Denmark)

Junker, Anders Ellekær; Als-Nielsen, Bodil; Gluud, Christian

2014-01-01

BACKGROUND: Patients with hepatic encephalopathy may present with extrapyramidal symptoms and changes in basal ganglia. These changes are similar to those seen in patients with Parkinson's disease. Dopamine agents (such as bromocriptine and levodopa, used for patients with Parkinson's disease) have...... therefore been assessed as a potential treatment for patients with hepatic encephalopathy. OBJECTIVES: To evaluate the beneficial and harmful effects of dopamine agents versus placebo or no intervention for patients with hepatic encephalopathy. SEARCH METHODS: Trials were identified through the Cochrane...... hepatic encephalopathy that were published during 1979 to 1982 were included. Three trials assessed levodopa, and two trials assessed bromocriptine. The mean daily dose was 4 grams for levodopa and 15 grams for bromocriptine. The median duration of treatment was 14 days (range seven to 56 days). None...

Screening of subclinical hepatic encephalopathy

NARCIS (Netherlands)

Groeneweg, M; Moerland, W; Quero, J C; Hop, W C; Krabbe, P F; Schalm, S W

BACKGROUND/AIMS: Subclinical hepatic encephalopathy adversely affects daily functioning. The aim of this study was to determine which elements of daily life have predictive value for subclinical hepatic encephalopathy. METHODS: The study was performed in 179 outpatients with liver cirrhosis.

Hepatic Encephalopathy due to Congenital Multiple Intrahepatic Portosystemic Venous Shunts Successfully Treated by Percutaneous Transhepatic Obliteration

Directory of Open Access Journals (Sweden)

Shinsuke Takenaga

2016-11-01

Full Text Available Hepatic encephalopathy due to intrahepatic portosystemic venous shunts (IPSVS in a non-cirrhotic condition is rare. Here we report a rare case of a patient with congenital multiple IPSVS successfully treated by percutaneous transhepatic obliteration. The patient was a 67-year-old woman who presented to our hospital with progressive episodes of consciousness disorder and vomiting. Laboratory tests revealed hyperammonemia (192.0 μg/dL, and computed tomography revealed multiple IPSVS in both lobes. There was no evidence of underlying liver disease or hepatic trauma. Transcatheter embolization for IPSVS was performed because conservative therapy was not sufficiently effective. After endovascular shunt closure, hepatic encephalopathy improved. The serum ammonia level normalized during the 5-year follow-up period. Thus, transcatheter embolization may be an effective therapy for patients with symptomatic and refractory IPSVS. Careful follow-up is necessary for portal hypertension-related complications after transcatheter embolization for IPSVS.

Hepatic Encephalopathy

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Hepatic Encephalopathy

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Association between Helicobacter pylori seropositivity and Hepatic Encephalopathy

International Nuclear Information System (INIS)

Behroozian, R.; Faramarzpur, M.; Rahimi, E.

2010-01-01

Objective: The knowledge on Helicobacter pylori (H. pylori) contribution in the pathology of the liver and biliary tract diseases in human is very limited. The aim of this study was to assess the probable association between H. pylori seropositivity and hepatic encephalopathy. Methodology: This is a case control study conducted through three groups, cirrhotics with hepatic encephalopathy (HE), cirrhotics without HE and healthy controls. All subjects were examined serologically for determination of IgG class antibodies to H. pylori based on ELISA technique. Results: H. pylori seropositivity was present in 88% cirrhotic patients with hepatic encephalopathy, 86% cirrhotics without hepatic encephalopathy and 66% healthy controls. Conclusion: According to our results, H. pylori seropositivity rate in cirrhotic patients with or without hepatic encephalopathy was higher than healthy controls. But H. pylori seropositivity rate was not significantly different among cirrhotics with hepatic encephalopathy and those without it.

Hepatic Encephalopathy

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Hepatic Encephalopathy

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Hepatic Encephalopathy

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Full Text Available ... your body when your liver isn’t working well, it may affect your brain and cause HE. ... it apparent that the liver is not doing well. These could be the symptoms of Hepatic Encephalopathy ( ...

Hepatic Encephalopathy

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Full Text Available ... build-up and painful swelling of the legs (edema) and abdomen (ascites) or hepatic encephalopathy. For more ... build up and painful swelling of the legs (edema) and abdomen (ascites) Bruising and bleeding easily Enlarged ...

Hepatic Encephalopathy

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Hepatic Encephalopathy

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Full Text Available ... Patient Advisory Council Media Center Careers How You Can Help OVERVIEW Donate Now Join an Event Volunteer ... Hepatic Encephalopathy is a short-term problem that can be corrected . It may also occur as part ...

Hepatic Encephalopathy

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Full Text Available ... important for you and your family to become familiar with the signs of Hepatic Encephalopathy so you ... team evaluates the person’s overall physical and mental health, plan to pay for transplant related medical expenses, ...

Hepatic Encephalopathy

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Full Text Available ... become familiar with the signs of Hepatic Encephalopathy so you can tell your doctor right away if ... with continuous treatment, HE can usually be controlled. So it’s important to tell your doctor about any ...

Hepatic Encephalopathy

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Hepatic Encephalopathy

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Hepatic Encephalopathy

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Hepatic Encephalopathy

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Full Text Available ... bad. It sends the good things – such as vitamins and nutrients – into your bloodstream for your body ... for Wife Joyce O. Caregiver for Mother Lynette K. Hepatic Encephalopathy Samantha W. Caregiver for Husband Stan ...

Qualifying and quantifying minimal hepatic encephalopathy

DEFF Research Database (Denmark)

Morgan, Marsha Y; Amodio, Piero; Cook, Nicola A

2016-01-01

Minimal hepatic encephalopathy is the term applied to the neuropsychiatric status of patients with cirrhosis who are unimpaired on clinical examination but show alterations in neuropsychological tests exploring psychomotor speed/executive function and/or in neurophysiological variables. There is ......Minimal hepatic encephalopathy is the term applied to the neuropsychiatric status of patients with cirrhosis who are unimpaired on clinical examination but show alterations in neuropsychological tests exploring psychomotor speed/executive function and/or in neurophysiological variables...... analytical techniques may provide better diagnostic information while the advent of portable wireless headsets may facilitate more widespread use. A large number of other diagnostic tools have been validated for the diagnosis of minimal hepatic encephalopathy including Critical Flicker Frequency......, the Inhibitory Control Test, the Stroop test, the Scan package and the Continuous Reaction Time; each has its pros and cons; strengths and weaknesses; protagonists and detractors. Recent AASLD/EASL Practice Guidelines suggest that the diagnosis of minimal hepatic encephalopathy should be based on the PHES test...

No oxygen delivery limitation in hepatic encephalopathy

DEFF Research Database (Denmark)

Gjedde, Albert; Keiding, Susanne; Vilstrup, Hendrik

2010-01-01

to choose between cause and effect in three groups of volunteers, including healthy control subjects (HC), patients with cirrhosis of the liver without hepatic encephalopathy (CL), and patients with cirrhosis with acute hepatic encephalopathy. Compared to HC subjects, blood flow and energy metabolism had......Hepatic encephalopathy is a condition of reduced brain functioning in which both blood flow and brain energy metabolism declined. It is not known whether blood flow or metabolism is the primary limiting factor of brain function in this condition. We used calculations of mitochondrial oxygen tension...

Reversible cortical blindness in a case of hepatic encephalopathy

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Amlan Kanti Biswas

2016-01-01

Full Text Available Hepatic encephalopathy is a frequent and often fatal manifestation of chronic liver disease. The pathogenesis of hepatic encephalopathy is believed to be multifactorial including impaired blood-brain barrier function, imbalance between the excitatory and inhibitory neurotransmitters in cortex, accumulation of various toxic and false neurotransmitters, and lack of nutrients like oxygen and glucose. Signs and symptoms of hepatic encephalopathy varies and commonly ranges from personality changes, disturbed consciousness, sleep pattern alternation, intellectual deterioration, speech disturbances, asterixis to frank coma and even death. Reversible or transient cortical blindness is rare manifestation of hepatic encephalopathy. It may even precede the phase of altered consciousness in such patients. Very few similar cases have been reported worldwide. Hence, we would like to report a case of transient cortical blindness in a patient of hepatic encephalopathy.

The thalamus in cirrhotic patients with and without hepatic encephalopathy: A volumetric MRI study

International Nuclear Information System (INIS)

Tao, Ran; Zhang, Jiuquan; You, Zhonglan; Wei, Luqing; Fan, Yi; Cui, Jinguo; Wang, Jian

2013-01-01

Background and aims: The thalamus is a major relay and filter station in the central neural system. Some previous studies have suggested that the thalamus maybe implicated in the pathogenesis of hepatic encephalopathy. The aim of our study was to investigate changing thalamic volumes in cirrhotic patients with and without hepatic encephalopathy. Methods: Neuropsychological tests and structural MR scanning were performed on 24 cirrhotic patients, 23 cirrhotic patients with minimal hepatic encephalopathy, 24 cirrhotic patients during their first episode of overt hepatic encephalopathy, and 33 healthy controls. Voxel-based morphometry analysis was performed to detect gray matter morphological changes. The thalamus and whole brain volume were extrapolated. A receiver operating characteristic curve analysis of thalamic volumes was used to discriminate patients with minimal hepatic encephalopathy from those with hepatic cirrhosis. Results: Thalamic volume increased in a stepwise manner in patients with progressively worse stages of hepatic encephalopathy compared to healthy subjects. Additionally, a comparison of gray matter morphometry between patients with Child–Pugh grades A, B, or C and controls revealed a progression in thalamic volumes in parallel with the degree of liver failure. Moreover, thalamic volume was significantly correlated with the number connection test A time and digit-symbol test score in cirrhotic patients with minimal hepatic encephalopathy (r = 0.659, P = 0.001; r = −0.577, P = 0.004; respectively). The area under the receiver operating characteristic curve was 0.827 (P = 0.001). Conclusions: A significantly increased thalamic volume may be provide an objective imaging measure for predicting seizures due to minimal hepatic encephalopathy in cirrhotic patients

The thalamus in cirrhotic patients with and without hepatic encephalopathy: A volumetric MRI study

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Tao, Ran, E-mail: taoran1648@yahoo.cn [Department of Radiology, Southwest Hospital, Third Military Medical University, Chongqing 400038 (China); Department of Radiology, Bethune International Peace Hospital of People' s Liberty Army, Shijiazhuang 050082, Hebei Province (China); Zhang, Jiuquan, E-mail: jiuquanzhang@yahoo.com [Department of Radiology, Southwest Hospital, Third Military Medical University, Chongqing 400038 (China); You, Zhonglan, E-mail: you_zhonglan@163.com [Department of Infectious Diseases, Southwest Hospital, Third Military Medical University, Chongqing 400038 (China); Wei, Luqing, E-mail: weiluqing@foxmail.com [Department of Radiology, Southwest Hospital, Third Military Medical University, Chongqing 400038 (China); Fan, Yi, E-mail: fanyi1978@yahoo.cn [Department of Infectious Diseases, Southwest Hospital, Third Military Medical University, Chongqing 400038 (China); Cui, Jinguo, E-mail: cuijinguo2005@163.com [Department of Radiology, Bethune International Peace Hospital of People' s Liberty Army, Shijiazhuang 050082, Hebei Province (China); Wang, Jian, E-mail: wangjian_811@yahoo.com [Department of Radiology, Southwest Hospital, Third Military Medical University, Chongqing 400038 (China)

2013-11-01

Background and aims: The thalamus is a major relay and filter station in the central neural system. Some previous studies have suggested that the thalamus maybe implicated in the pathogenesis of hepatic encephalopathy. The aim of our study was to investigate changing thalamic volumes in cirrhotic patients with and without hepatic encephalopathy. Methods: Neuropsychological tests and structural MR scanning were performed on 24 cirrhotic patients, 23 cirrhotic patients with minimal hepatic encephalopathy, 24 cirrhotic patients during their first episode of overt hepatic encephalopathy, and 33 healthy controls. Voxel-based morphometry analysis was performed to detect gray matter morphological changes. The thalamus and whole brain volume were extrapolated. A receiver operating characteristic curve analysis of thalamic volumes was used to discriminate patients with minimal hepatic encephalopathy from those with hepatic cirrhosis. Results: Thalamic volume increased in a stepwise manner in patients with progressively worse stages of hepatic encephalopathy compared to healthy subjects. Additionally, a comparison of gray matter morphometry between patients with Child–Pugh grades A, B, or C and controls revealed a progression in thalamic volumes in parallel with the degree of liver failure. Moreover, thalamic volume was significantly correlated with the number connection test A time and digit-symbol test score in cirrhotic patients with minimal hepatic encephalopathy (r = 0.659, P = 0.001; r = −0.577, P = 0.004; respectively). The area under the receiver operating characteristic curve was 0.827 (P = 0.001). Conclusions: A significantly increased thalamic volume may be provide an objective imaging measure for predicting seizures due to minimal hepatic encephalopathy in cirrhotic patients.

Hepatic Encephalopathy

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Full Text Available ... of brain function in people with advanced liver disease. When your liver is damaged it can no longer remove toxic substances from your blood. These toxins build up and can travel through your body until they reach your brain, causing mental and physical symptoms of HE. Hepatic Encephalopathy often ...

Evaluation and Management of Hepatic Encephalopathy: Current Status and Future Directions

OpenAIRE

Suraweera, Duminda; Sundaram, Vinay; Saab, Sammy

2016-01-01

Hepatic encephalopathy is a spectrum of neurocognitive manifestations often seen in patients with liver injury or rarely in patients with portosystemic shunting without liver injury. It can be divided into minimal (covert) hepatic encephalopathy and overt hepatic encephalopathy, depending on the severity. Patients with hepatic encephalopathy have compromised clinical outcomes, decreased quality of life, and increased healthcare utilization, often resulting in a heavy financial and personal bu...

Evaluation and Management of Hepatic Encephalopathy: Current Status and Future Directions

Science.gov (United States)

Suraweera, Duminda; Sundaram, Vinay; Saab, Sammy

2016-01-01

Hepatic encephalopathy is a spectrum of neurocognitive manifestations often seen in patients with liver injury or rarely in patients with portosystemic shunting without liver injury. It can be divided into minimal (covert) hepatic encephalopathy and overt hepatic encephalopathy, depending on the severity. Patients with hepatic encephalopathy have compromised clinical outcomes, decreased quality of life, and increased healthcare utilization, often resulting in a heavy financial and personal burden on caregivers. The diagnosis remains largely clinical, with the exclusion of possible other causes for the altered mental status. Current treatment strategies include nonabsorbable disaccharides and antibiotics. This review will focus on the diagnosis, management and clinical impact of hepatic encephalopathy. PMID:27377741

Research progress of BOLD-fMRI in minimal hepatic encephalopathy

International Nuclear Information System (INIS)

Zhou Zhiming; Zhao Jiannong

2013-01-01

The minimal hepatic encephalopathy is the early stage of hepatic encephalopathy. It has few apparent clinical symptoms and specific manifestations, and is difficult to diagnose. In the recent years, BOLD-fMRI has been used to study hepatic encephalopathy gradually. Through detection of the brain neuron activities in different states, it can not only locate the abnormal activity of brain functional areas, but also can find the changes of brain functional connectivity. BOLD- fMRI combining with other MR technologies can explore the pathology and pathogenesis of minimal hepatic encephalopathy from micro to macro and from structure to function. (authors)

Hepatic encephalopathy associated with hepatic lipidosis in llamas (Lama glama).

Science.gov (United States)

Pillitteri, C A; Craig, L E

2013-01-01

Hepatic encephalopathy has been listed as a differential for llamas displaying neurologic signs, but it has not been histopathologically described. This report details the neurologic histopathologic findings associated with 3 cases of hepatic lipidosis with concurrent neurologic signs and compares them to 3 cases of hepatic lipidosis in the absence of neurologic signs and 3 cases without hepatic lipidosis. Brain from all 3 llamas displaying neurologic signs contained Alzheimer type II cells, which were not detected in either subset of llamas without neurologic signs. Astrocytic immunohistochemical staining intensity for glial fibrillary acid protein was decreased in llamas with neurologic signs as compared to 2 of 3 llamas with hepatic lipidosis and without neurologic signs and to 2 of 3 llamas without hepatic lipidosis. Immunohistochemical staining for S100 did not vary between groups. These findings suggest that hepatic encephalopathy may be associated with hepatic lipidosis in llamas.

Recent advances in hepatic encephalopathy [version 1; referees: 4 approved

Directory of Open Access Journals (Sweden)

Victoria Liere

2017-09-01

Full Text Available Hepatic encephalopathy describes the array of neurological alterations that occur during acute liver failure or chronic liver injury. While key players in the pathogenesis of hepatic encephalopathy, such as increases in brain ammonia, alterations in neurosteroid levels, and neuroinflammation, have been identified, there is still a paucity in our knowledge of the precise pathogenic mechanism. This review gives a brief overview of our understanding of the pathogenesis of hepatic encephalopathy and then summarizes the significant recent advances made in clinical and basic research contributing to our understanding, diagnosis, and possible treatment of hepatic encephalopathy. A literature search using the PubMed database was conducted in May 2017 using “hepatic encephalopathy” as a keyword, and selected manuscripts were limited to those research articles published since May 2014. While the authors acknowledge that many significant advances have been made in the understanding of hepatic encephalopathy prior to May 2014, we have limited the scope of this review to the previous three years only.

Acute hepatic encephalopathy with diffuse cortical lesions

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Arnold, S.M.; Spreer, J.; Schumacher, M. [Section of Neuroradiology, Univ. of Freiburg (Germany); Els, T. [Dept. of Neurology, University of Freiburg (Germany)

2001-07-01

Acute hepatic encephalopathy is a poorly defined syndrome of heterogeneous aetiology. We report a 49-year-old woman with alcoholic cirrhosis and hereditary haemorrhagic telangiectasia who developed acute hepatic coma induced by severe gastrointestinal bleeding. Laboratory analysis revealed excessively elevated blood ammonia. MRI showed lesions compatible with chronic hepatic encephalopathy and widespread cortical signal change sparing the perirolandic and occipital cortex. The cortical lesions resembled those of hypoxic brain damage and were interpreted as acute toxic cortical laminar necrosis. (orig.)

Acute hepatic encephalopathy with diffuse cortical lesions

International Nuclear Information System (INIS)

Arnold, S.M.; Spreer, J.; Schumacher, M.; Els, T.

2001-01-01

Acute hepatic encephalopathy is a poorly defined syndrome of heterogeneous aetiology. We report a 49-year-old woman with alcoholic cirrhosis and hereditary haemorrhagic telangiectasia who developed acute hepatic coma induced by severe gastrointestinal bleeding. Laboratory analysis revealed excessively elevated blood ammonia. MRI showed lesions compatible with chronic hepatic encephalopathy and widespread cortical signal change sparing the perirolandic and occipital cortex. The cortical lesions resembled those of hypoxic brain damage and were interpreted as acute toxic cortical laminar necrosis. (orig.)

Normalization of the psychometric hepatic encephalopathy score for ...

African Journals Online (AJOL)

Aim: To construct normal values for the tests of the psychometric hepatic encephalopathy score (PHES) and evaluate the prevalence of minimal hepatic encephalopathy (MHE) among Turkish patients with liver cirrhosis. Materials and Methods: One hundred and eighty-five healthy subjects and sixty patients with liver ...

Safety, efficacy, and patient acceptability of rifaximin for hepatic encephalopathy

DEFF Research Database (Denmark)

Kimer, Nina; Krag, Aleksander; Gluud, Lise L

2014-01-01

Hepatic encephalopathy is a complex disease entity ranging from mild cognitive dysfunction to deep coma. Traditionally, treatment has focused on a reduction of ammonia through a reduced production, absorption, or clearance. Rifaximin is a nonabsorbable antibiotic, which reduces the production of ...... and safety of long-term treatment with rifaximin and evaluate effects of combination therapy with lactulose and branched-chain amino acids for patients with liver cirrhosis and hepatic encephalopathy.......Hepatic encephalopathy is a complex disease entity ranging from mild cognitive dysfunction to deep coma. Traditionally, treatment has focused on a reduction of ammonia through a reduced production, absorption, or clearance. Rifaximin is a nonabsorbable antibiotic, which reduces the production...... of ammonia by gut bacteria and, to some extent, other toxic derivatives from the gut. Clinical trials show that these effects improve episodes of hepatic encephalopathy. A large randomized trial found that rifaximin prevents recurrent episodes of hepatic encephalopathy. Most patients were treated...

Branched-chain amino acids for people with hepatic encephalopathy

DEFF Research Database (Denmark)

Gluud, Lise Lotte; Dam, Gitte; Les, Iñigo

2015-01-01

-chain amino acids (BCAA) versus control interventions has evaluated if BCAA may benefit people with hepatic encephalopathy. OBJECTIVES: To evaluate the beneficial and harmful effects of BCAA versus any control intervention for people with hepatic encephalopathy. SEARCH METHODS: We identified trials through...

Branched-chain amino acids for people with hepatic encephalopathy

DEFF Research Database (Denmark)

Gluud, Lise Lotte; Dam, Gitte; Les, Iñigo

2017-01-01

-chain amino acids (BCAA) versus control interventions has evaluated if BCAA may benefit people with hepatic encephalopathy. Objectives: To evaluate the beneficial and harmful effects of BCAA versus any control intervention for people with hepatic encephalopathy. Search methods: We identified trials through...

Flumazenil versus placebo or no intervention for people with cirrhosis and hepatic encephalopathy

DEFF Research Database (Denmark)

Goh, Ee Teng; Andersen, Mette L.; Morgan, Marsha Y.

2017-01-01

Background: Hepatic encephalopathy is a common complication of cirrhosis which results in poor brain functioning. The spectrum of changes associated with hepatic encephalopathy ranges from the clinically 'indiscernible' or minimal hepatic encephalopathy to the clinically 'obvious' or overt hepatic...... encephalopathy. Flumazenil is a synthetic benzodiazepine antagonist with high affinity for the central benzodiazepine recognition site. Flumazenil may benefit people with hepatic encephalopathy through an indirect negative allosteric modulatory effect on gamma-aminobutyric acid receptor function. The previous...... version of this review, which included 13 randomised clinical trials, found no effect of flumazenil on all-cause mortality, based on an analysis of 10 randomised clinical trials, but found a beneficial effect on hepatic encephalopathy, based on an analysis of eight randomised clinical trials. Objectives...

Research progress of BOLD-functional MRI of hepatic encephalopathy

International Nuclear Information System (INIS)

Ni Ling; Zhang Longjiang; Lu Guangming

2013-01-01

Hepatic encephalopathy (HE), characterized by a wide spectrum of clinical manifestations, ranging from behavior abnormality, conscious disorder and even coma, is a consequence of liver dysfunction in both acute and chronic hepatic diseases. Minimal hepatic encephalopathy (MHE) refers to a subgroup of cirrhotic patients without clinical overt hepatic encephalopathy symptoms hut with abnormalities in neuro -cognitive functions. HE/MHE can have a far-reaching impact on quality of life and prognosis. The exact neuropathology mechanism was still unclear. Recently, functional MRI (fMRI) has been increasingly applied for investigating the neuro-pathophysiological mechanism of HE. This paper will review the fMRI research applied on uncovering the neuropathology mechanism of HE. (authors)

Current state of knowledge of hepatic encephalopathy (part IV): Management of Hepatic Encephalopathy by liver support systems.

Science.gov (United States)

Hassanein, Tarek

2017-04-01

Hepatic Encephalopathy is a devastating complication of End-Stage Liver Disease. In its severe grades it requires extra intervention beyond the standard medical approaches. In this article were view the role of liver support systems in managing hepatic encephalopthy.

Probiotics for people with hepatic encephalopathy.

Science.gov (United States)

Dalal, Rohan; McGee, Richard G; Riordan, Stephen M; Webster, Angela C

2017-02-23

Hepatic encephalopathy is a disorder of brain function as a result of liver failure or portosystemic shunt or both. Both hepatic encephalopathy (clinically overt) and minimal hepatic encephalopathy (not clinically overt) significantly impair patient's quality of life and daily functioning, and represent a significant burden on healthcare resources. Probiotics are live micro-organisms, which when administered in adequate amounts, may confer a health benefit on the host. To determine the beneficial and harmful effects of probiotics in any dosage, compared with placebo or no intervention, or with any other treatment for people with any grade of acute or chronic hepatic encephalopathy. This review did not consider the primary prophylaxis of hepatic encephalopathy. We searched The Cochrane Hepato-Biliary Group Controlled Trials Register, CENTRAL, MEDLINE, Embase, Science Citation Index Expanded, conference proceedings, reference lists of included trials, and the World Health Organization International Clinical Trials Registry Platform until June 2016. We included randomised clinical trials that compared probiotics in any dosage with placebo or no intervention, or with any other treatment in people with hepatic encephalopathy. We used standard methodological procedures expected by The Cochrane Collaboration. We conducted random-effects model meta-analysis due to obvious heterogeneity of participants and interventions. We defined a P value of 0.05 or less as significant. We expressed dichotomous outcomes as risk ratio (RR) and continuous outcomes as mean difference (MD) with 95% confidence intervals (CI). We included 21 trials with 1420 participants, of these, 14 were new trials. Fourteen trials compared a probiotic with placebo or no treatment, and seven trials compared a probiotic with lactulose. The trials used a variety of probiotics; the most commonly used group of probiotic was VSL#3, a proprietary name for a group of eight probiotics. Duration of administration

Metformin inhibits glutaminase activity and protects against hepatic encephalopathy.

Directory of Open Access Journals (Sweden)

Javier Ampuero

Full Text Available AIM: To investigate the influence of metformin use on liver dysfunction and hepatic encephalopathy in a retrospective cohort of diabetic cirrhotic patients. To analyze the impact of metformin on glutaminase activity and ammonia production in vitro. METHODS: Eighty-two cirrhotic patients with type 2 diabetes were included. Forty-one patients were classified as insulin sensitizers experienced (metformin and 41 as controls (cirrhotic patients with type 2 diabetes mellitus without metformin treatment. Baseline analysis included: insulin, glucose, glucagon, leptin, adiponectin, TNFr2, AST, ALT. HOMA-IR was calculated. Baseline HE risk was calculated according to minimal hepatic encephalopathy, oral glutamine challenge and mutations in glutaminase gene. We performed an experimental study in vitro including an enzymatic activity assay where glutaminase inhibition was measured according to different metformin concentrations. In Caco2 cells, glutaminase activity inhibition was evaluated by ammonia production at 24, 48 and 72 hours after metformina treatment. RESULTS: Hepatic encephalopathy was diagnosed during follow-up in 23.2% (19/82: 4.9% (2/41 in patients receiving metformin and 41.5% (17/41 in patients without metformin treatment (logRank 9.81; p=0.002. In multivariate analysis, metformin use [H.R.11.4 (95% CI: 1.2-108.8; p=0.034], age at diagnosis [H.R.1.12 (95% CI: 1.04-1.2; p=0.002], female sex [H.R.10.4 (95% CI: 1.5-71.6; p=0.017] and HE risk [H.R.21.3 (95% CI: 2.8-163.4; p=0.003] were found independently associated with hepatic encephalopathy. In the enzymatic assay, glutaminase activity inhibition reached 68% with metformin 100 mM. In Caco2 cells, metformin (20 mM decreased glutaminase activity up to 24% at 72 hours post-treatment (p<0.05. CONCLUSIONS: Metformin was found independently related to overt hepatic encephalopathy in patients with type 2 diabetes mellitus and high risk of hepatic encephalopathy. Metformin inhibits glutaminase

Radiographical findings in patients with liver cirrhosis and hepatic encephalopathy.

Science.gov (United States)

Elwir, Saleh; Hal, Hassan; Veith, Joshua; Schreibman, Ian; Kadry, Zakiyah; Riley, Thomas

2016-08-01

Hepatic encephalopathy is a common complication encountered in patients with liver cirrhosis. Hepatic encephalopathy is not reflected in the current liver transplant allocation system. Correlation was sought between hepatic encephalopathy with findings detected on radiographic imaging studies and the patient's clinical profile. A retrospective analysis was conducted of patients with cirrhosis, who presented for liver transplant evaluation in 2009 and 2010. Patients with hepatocellular carcinoma, ejection fraction less than 60% and who had a TIPS (transjugular intrahepatic portosystemic shunting) procedure or who did not complete the evaluation were excluded. Statistical analysis was performed and variables found to be significant on univariate analysis (P encephalopathy group (n = 58) and a control group (n = 59). Univariate analysis found that a smaller portal vein diameter, smaller liver antero-posterior diameter, liver nodularity and use of diuretics or centrally acting medications showed significant correlation with hepatic encephalopathy. This association was confirmed for smaller portal vein, use of diuretics and centrally acting medications in the multivariate analysis. A decrease in portal vein diameter was associated with increased risk of encephalopathy. Identifying patients with smaller portal vein diameter may warrant screening for encephalopathy by more advanced psychometric testing, and more aggressive control of constipation and other factors that may precipitate encephalopathy. © The Author(s) 2015. Published by Oxford University Press and the Digestive Science Publishing Co. Limited.

Current concepts in the assessment and treatment of hepatic encephalopathy.

LENUS (Irish Health Repository)

Cash, W J

2012-02-01

Hepatic encephalopathy (HE) is defined as a metabolically induced, potentially reversible, functional disturbance of the brain that may occur in acute or chronic liver disease. Standardized nomenclature has been proposed but a standardized approach to the treatment, particularly of persistent, episodic and recurrent encephalopathy associated with liver cirrhosis has not been proposed. This review focuses on the pathogenesis and treatment of HE in patients with cirrhosis. The pathogenesis and treatment of hepatic encephalopathy in fulminant hepatic failure is quite different and is reviewed elsewhere.

Benzodiazepine receptor antagonists for acute and chronic hepatic encephalopathy

DEFF Research Database (Denmark)

Als-Nielsen, B; Kjaergard, L L; Gluud, C

2001-01-01

The pathogenesis of hepatic encephalopathy is unknown. It has been suggested that liver failure leads to the accumulation of substances that bind to a receptor-complex in the brain resulting in neural inhibition which may progress to coma. Several trials have assessed benzodiazepine receptor...... antagonists for hepatic encephalopathy, but the results are conflicting....

RECENT THEORIES OF PATHOGENESIS OF HEPATIC ENCEPHALOPATHY IN HEPATITIS C VIRAL INFECTION

Directory of Open Access Journals (Sweden)

Lidija Popović Dragonjić

2013-01-01

Full Text Available Hepatic encephalopathy is potentially reversible, or progressive neuropsychiatric syndrome characterized by changes in cognitive function, behavior and personality changes, and transient neurologic symptoms and characteristic electroencephalographic patterns associated with acute and chronic liver failure. For some time, there has been controversy regarding the origin of toxins responsible for the change of mental state. It was found that the occurrence of hepatic encephalopathy is responsible for multiple organ peripheral changes (intestinal changes, abnormalities of portal-systemic circulation, liver failure, loss of muscle tissue, changes in brain intracellular communication (osmotic changes, astrocytes and axonal abnormalities in communication, changes in cerebral perfusion and ammonia, endogenous benzodiazepines, gamma amino butyric acid, derivatives of methionine and false neurotransmitters. The aforementioned metabolic factors that contribute to the development of hepatic encephalopathy are not mutually exclusive and multiple factors may be present at the same time.

Case of hepatic encephalopathy induced by thortrast

Energy Technology Data Exchange (ETDEWEB)

Shirato, H.; Kudo, N.; Takita, K. (Nakatori Hospital, Akita (Japan))

1980-09-01

A case of hepatic encephalopathy induced by thorotrast injected as a contrast 40 years before was reported. The patient was a 64-year-old man with severe liver dysfunction, and had psychic and neurological symptoms, and hyperammonemia. There was a relationship between ammonium concentration in blood and psychic and neurological symptoms. Electroencephalogram showed three phases waves peculiar to hepatic coma intermittently. Thorotrast in the liver was detected by radiological methods and in vivo measurement of the radioactivity. From the above-mentioned result, this disease was diagnosed as hepatic encephalopathy induced by long-term sedimentation of thorotrast without complication of malignant tumors. Because of the concurrent presence of cerebral infarction, the diagnosis was difficult to make.

Is lactulose plus rifaximin better than lactulose alone in the management of hepatic encephalopathy?

International Nuclear Information System (INIS)

Butt, N.I.; Siddiqui, A.M.; Butt, U.I.

2018-01-01

To compare the efficacy of lactulose plus rifaximin with efficacy of lactulose alone in the treatment of hepatic encephalopathy. Study Design:A randomized controlled trial. Place and Duration of study:Department of Medicine, Jinnah Hospital, Lahore, from December 2014 to June 2015. Methodology:All patients who presented with hepatic encephalopathy due to decompensated chronic liver disease were randomly divided into two groups of 65 patients each. One group was given 30 ml thrice daily lactulose alone and the other lactulose plus rifaximin 550 mg twice daily for 10 days. Informed consents were taken from the participants' attendants. Grades II-IV hepatic encephalopathy was noted according to West-Haven Classification. All subjects were followed until 10 days after admission. Results:The mean age of patients was 56.06 +11.2 years, among which 46.9% were females and 53.1% were males. After ten days of follow-up, reversal was seen in 58.46% in lactulose alone group and 67.69% in lactulose plus rifaximin group (Chi-square p=0.276). Conclusion:There was no difference in effectiveness of lactulose plus rifaximin and lactulose alone in treatment of hepatic encephalopathy. (author)

Hepatic Encephalopathy: Early Diagnosis in Pediatric Patients With Cirrhosis

Science.gov (United States)

DARA, Naghi; SAYYARI, Ali-Akbar; IMANZADEH, Farid

2014-01-01

Objective As acute liver failure (ALF) and chronic liver disease (cirrhosis) continue to increase in prevalence, we will see more cases of hepatic encephalopathy. Primary care physician are often the first to suspect it, since they are familiar with the patient’s usual physical and mental status. This serious complication typically occurs in patients with severe comorbidities and needs multidisciplinary evaluation and care. Hepatic encephalopathy should be considered in any patient with acute liver failure and cirrhosis who presents with neuropsychiatric manifestations, decrease level of consciousness (coma), change of personality, intellectual and behavioral deterioration, speech and motor dysfunction. Every cirrhotic patient may be at risk; potential precipitating factors should be addressed in regular clinic visits. The encephalopathy of liver disease may be prominent, or can be present in subtle forms, such as decline of school performance, emotional outbursts, or depression. “Subtle form” of hepatic encephalopathy may not be obvious on clinical examination, but can be detected by neurophysiologic and neuropsychiatric testing. PMID:24665321

Post-TIPS Hepatic Encephalopathy Treated by Occlusion Balloon-Assisted Retrograde Embolization of a Coexisting Spontaneous Splenorenal Shunt

International Nuclear Information System (INIS)

Shioyama, Yasukazu; Matsueda, Kiyoshi; Horihata, Koushi; Kimura, Masashi; Nishida, Norifumi; Kishi, Kazushi; Terada, Masaki; Sato, Morio; Yamada, Ryusaku

1996-01-01

A 51-year-old man with posthepatitis cirrhosis underwent a transjugular intrahepatic portosystemic shunt (TIPS) for bleeding of recurrent esophageal varices. The patient had a coexisting, spontaneous, splenorenal shunt. He subsequently developed hepatic encephalopathy, presumably due to excessive portosystemic shunting. Since medical management resulted in no significant improvement, the splenorenal shunt was embolized from the jugular vein approach via renal vein access during temporary balloon occlusion. Within a few days, the patient's hepatic encephalopathy resolved. Twelve months later the patient showed no recurrence of encephalopathy and had maintained a patent TIPS

Nonconvulsive Status Epilepticus in Hepatic Encephalopathy

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Hyung Kim

2011-05-01

Full Text Available We discuss a case of a 64-year-old male with a history of liver failure presenting with altered mental status, initially diagnosed with hepatic encephalopathy but ultimately diagnosed with nonconvulsive status epilepticus (NCSE by electroencephalogram (EEG. NCSE is a difficult diagnosis to make, given no clear consensus on diagnostic criteria. Especially in the intensive care unit setting of persistent altered mental status with no clear etiology, NCSE must be considered in the differential diagnosis, as the consequences of delayed diagnosis and treatment can be substantial. EEG can be useful in the evaluation of patients with hepatic encephalopathy who have persistently altered levels of consciousness despite optimal medical management. [West J Emerg Med. 2011;12(4:372–374.

Effect of antibiotics, prebiotics and probiotics in treatment for hepatic encephalopathy.

NARCIS (Netherlands)

Bongaerts, G.P.A.; Severijnen, R.S.V.M.; Timmerman, H.

2005-01-01

In order to reduce ammonia production by urease-positive bacteria Solga recently hypothesised (S.F. Solga, Probiotics can treat hepatic encephalopathy, Medical Hypotheses 2003; 61: 307-13), that probiotics are new therapeutics for hepatic encephalopathy (HE), and that they may replace antibiotics

Increased brain uptake of gamma-aminobutyric acid in a rabbit model of hepatic encephalopathy

International Nuclear Information System (INIS)

Bassett, M.L.; Mullen, K.D.; Scholz, B.; Fenstermacher, J.D.; Jones, E.A.

1990-01-01

Transfer of the inhibitory neurotransmitter gamma-aminobutyric acid across the normal blood-brain barrier is minimal. One prerequisite for gamma-aminobutyric acid in plasma contributing to the neural inhibition of hepatic encephalopathy would be that increased transfer of gamma-aminobutyric acid across the blood-brain barrier occurs in liver failure. The aim of the present study was to determine if brain gamma-aminobutyric acid uptake is increased in rabbits with stage II-III (precoma) hepatic encephalopathy due to galactosamine-induced fulminant hepatic failure. A modification of the Oldendorf intracarotid artery-injection technique was applied. [3H] gamma-aminobutyric acid, [14C] butanol, and 113mIn-labeled serum protein (transferrin) were injected simultaneously 4 s before decapitation. The ipsilateral brain uptake index of gamma-aminobutyric acid was determined from measurements of the 3 isotopes in 5 brain regions. Uncorrected or simple brain uptake indices of [3H] gamma-aminobutyric acid and [113mIn] transferrin were calculated using [14C] butanol as the highly extracted reference compound. The [113mIn] transferrin data were also used to correct the brain uptake index of [3H] gamma-aminobutyric acid for intravascular retention of [3H] gamma-aminobutyric acid. The methodology adopted minimized problems attributable to rapid [3H] gamma-aminobutyric acid metabolism, and slow brain washout and recirculation of the radiolabeled tracers. Both the uncorrected and corrected brain uptake indices of gamma-aminobutyric acid as well as the simple brain uptake index of transferrin were significantly increased in both stage II and III hepatic encephalopathy in all brain regions studied. Moreover, these brain uptake indices were significantly greater in stage III hepatic encephalopathy than in stage II hepatic encephalopathy

Branched-chain amino acids for people with hepatic encephalopathy.

Science.gov (United States)

Gluud, Lise Lotte; Dam, Gitte; Les, Iñigo; Marchesini, Giulio; Borre, Mette; Aagaard, Niels Kristian; Vilstrup, Hendrik

2017-05-18

BCAA. The control groups received placebo/no intervention (two trials), diets (10 trials), lactulose (two trials), or neomycin (two trials). In 15 trials, all participants had cirrhosis. We classed seven trials as low risk of bias and nine trials as high risk of bias (mainly due to lack of blinding or for-profit funding). In a random-effects meta-analysis of mortality, we found no difference between BCAA and controls (risk ratio (RR) 0.88, 95% confidence interval (CI) 0.69 to 1.11; 760 participants; 15 trials; moderate quality of evidence). We found no evidence of small-study effects. Sensitivity analyses of trials with a low risk of bias found no beneficial or detrimental effect of BCAA on mortality. Trial sequential analysis showed that the required information size was not reached, suggesting that additional evidence was needed. BCAA had a beneficial effect on hepatic encephalopathy (RR 0.73, 95% CI 0.61 to 0.88; 827 participants; 16 trials; high quality of evidence). We found no small-study effects and confirmed the beneficial effect of BCAA in a sensitivity analysis that only included trials with a low risk of bias (RR 0.71, 95% CI 0.52 to 0.96). The trial sequential analysis showed that firm evidence was reached. In a fixed-effect meta-analysis, we found that BCAA increased the risk of nausea and vomiting (RR 5.56; 2.93 to 10.55; moderate quality of evidence). We found no beneficial or detrimental effects of BCAA on nausea or vomiting in a random-effects meta-analysis or on quality of life or nutritional parameters. We did not identify predictors of the intervention effect in the subgroup, sensitivity, or meta-regression analyses. In sensitivity analyses that excluded trials with a lactulose or neomycin control, BCAA had a beneficial effect on hepatic encephalopathy (RR 0.76, 95% CI 0.63 to 0.92). Additional sensitivity analyses found no difference between BCAA and lactulose or neomycin (RR 0.66, 95% CI 0.34 to 1.30). In this updated review, we included five

Hepatic encephalopathy in acute-on-chronic liver failure.

Science.gov (United States)

Lee, Guan-Huei

2015-10-01

The presence of hepatic encephalopathy (HE) within 4 weeks is part of the criteria for defining acute-on-chronic liver failure (ACLF). The pathophysiology of HE is complex, and hyperammonemia and cerebral hemodynamic dysfunction appear to be central in the pathogenesis of encephalopathy. Recent data also suggest that inflammatory mediators may have a significant role in modulating the cerebral effect of ammonia. Multiple prospective and retrospective studies have shown that hepatic encephalopathy in ACLF patients is associated with higher mortality, especially in those with grade III-IV encephalopathy, similar to that of acute liver failure (ALF). Although significant cerebral edema detected by CT in ACLF patients appeared to be less common, specialized MRI imaging was able to detect cerebral edema even in low grade HE. Ammonia-focused therapy constitutes the basis of current therapy, as in the treatment of ALF. Emerging treatment strategies focusing on modulating the gut-liver-circulation-brain axis are discussed.

A case of hepatic encephalopathy induced by trotrast

International Nuclear Information System (INIS)

Shirato, Hideo; Kudo, Norishige; Takita, Kyoji

1980-01-01

A case of hepatic encephalopathy induced by thorotrast injected as a contrast 40 years before was reported. The patient was a 64-year-old man with severe liver dysfunction, and had psychic and neurological symptoms, and hyperammonemia. There was a relationship between ammonium concentration in blood and psychic and neurological symptoms. Electroencephalogram showed three phases waves peculiar to hepatic coma intermittently. Throtrast in the liver was detected by radiological methods and in vivo measurement of the radioactivity. From the above-mentioned result, this disease was diagnosed as hepatic encephalopathy induced by long-term sedimentation of thorotrast without complication of malignant tumors. Because of the concurrent presence of cerebral infarction, the diagnosis was difficult to make. (Tsunoda, M.)

Management of Hepatic Encephalopathy

Directory of Open Access Journals (Sweden)

G. Wright

2011-01-01

Full Text Available Hepatic encephalopathy (HE, the neuropsychiatric presentation of liver disease, is associated with high morbidity and mortality. Reduction of plasma ammonia remains the central therapeutic strategy, but there is a need for newer novel therapies. We discuss current evidence supporting the use of interventions for both the general management of chronic HE and that necessary for more acute and advanced disease.

The relationship between plasma free fatty acids and experimentally induced hepatic encephalopathy in the rat

NARCIS (Netherlands)

Smit, J. J.; Bosman, D. K.; Jörning, G. G.; de Haan, J. G.; Maas, M. A.; Chamuleau, R. A.

1991-01-01

Two experimental models of hepatic encephalopathy in the rat have been investigated in order to study the postulated relationship between plasma free fatty acids concentration (C6 - C22:0) and the degree of hepatic encephalopathy. As a model of chronic hepatic encephalopathy, porta caval shunted

Type and etiology of liver cirrhosis are not related to the presence of hepatic encephalopathy or health-related quality of life: a cross-sectional study

Directory of Open Access Journals (Sweden)

Björnsson Einar

2008-10-01

Full Text Available Abstract Background Hepatic encephalopathy has a negative impact on health-related quality of life (QoL in liver cirrhosis. There are scarce and conflicting data on whether type or etiology of liver cirrhosis could be related to hepatic encephalopathy in patients with cirrhosis. We aimed to determine the impact of cirrhosis etiology on hepatic encephalopathy and whether hepatic encephalopathy affects health-related QoL among patients with cirrhosis of different etiologies. Methods A total of 156 cirrhotic patients were prospectively evaluated for the presence of hepatic encephalopathy according to the West-Haven criteria as well as by means of two psychometric tests. Patients with cryptogenic cirrhosis or cirrhosis due to mixed hepatocellular/cholestatic etiologies were excluded. Fasting plasma glucose levels were also measured. QoL was evaluated by means of a validated questionnaire (SF-36. Results Diabetes mellitus was more common in patients with hepatocellular cirrhosis compared to those with cholestatic cirrhosis but the two groups did not differ in cirrhosis severity or the prevalence of hepatic encephalopathy (p > 0.05. The groups of patients with cirrhosis due to alcohol, hepatitis C, or cholestatic liver disease did not differ in severity of liver cirrhosis or the prevalence of hepatic encephalopathy (p > 0.05. Patients with cirrhosis of different etiologies did not differ in any SF-36 domain (p > 0.05. In multivariate analysis, performance at neuropsychological testing was independently related only to age, diabetes mellitus, and the Child-Pugh score whereas the SF-36 physical component summary only to the Child-Pugh score and hepatic encephalopathy. Conclusion Cirrhosis etiology does not seem to be related to hepatic encephalopathy or health-related QoL. Cognitive impairment is associated mainly with age, liver disease severity and diabetes mellitus.

MRI and CT appearances in metabolic encephalopathies due to systemic diseases in adults

International Nuclear Information System (INIS)

Bathla, G.; Hegde, A.N.

2013-01-01

The term encephalopathy refers to a clinical scenario of diffuse brain dysfunction, commonly due to a systemic, metabolic, or toxic derangement. Often the clinical evaluation is unsatisfactory in this scenario and imaging plays an important role in the diagnosis, assessment of treatment response, and prognostication of the disorder. Hence, it is important for radiologists to be familiar with the imaging features of some relatively frequently acquired metabolic encephalopathies encountered in the hospital setting. This study reviews the computed tomography (CT) and magnetic resonance imaging (MRI) features of a number of metabolic encephalopathies that occur as part of systemic diseases in adults. The following conditions are covered in this review: hypoglycaemic encephalopathy, hypoxic ischaemic encephalopathy, non-ketotic hyperglycaemia, hepatic encephalopathy, uraemic encephalopathy, hyperammonaemic encephalopathy, and posterior reversible encephalopathy syndrome. MRI is the imaging method of choice in evaluating these conditions. Due to their high metabolic activity, bilateral basal ganglia changes are evident in the majority of cases. Concurrent imaging abnormalities in other parts of the central nervous system often provide useful diagnostic information about the likely underlying cause of the encephalopathy. Besides this, abnormal signal intensity and diffusion restriction patterns on MRI and MR spectroscopy features may provide important clues as to the diagnosis and guide further management. Frequently, the diagnosis is not straightforward and typical imaging features require correlation with clinical and laboratory data for accurate assessment

Memantine, a noncompetitive NMDA receptor antagonist improves hyperammonemia-induced encephalopathy and acute hepatic encephalopathy in rats

NARCIS (Netherlands)

Vogels, B. A.; Maas, M. A.; Daalhuisen, J.; Quack, G.; Chamuleau, R. A.

1997-01-01

The aim of this study was to investigate the possible role of N-methyl-D-aspartate (NMDA)-receptor overactivity in two different experimental rat models of encephalopathy: subacute encephalopathy caused by severe hyperammonemia in portacaval-shunted rats (AI-PCS rats) and acute hepatic

Hepatic Encephalopathy: Early Diagnosis in Pediatric Patients With Cirrhosis

OpenAIRE

DARA, Naghi; SAYYARI, Ali-Akbar; IMANZADEH, Farid

2014-01-01

How to Cite This Article: Dara N, Sayyari AA, Imanzadeh F. Hepatic Encephalopathy: Early Diagnosis in Pediatric Patients With Cirrhosis. Iran J Child Neurol. 2014 Winter; 8(1):1-11.ObjectiveAs acute liver failure (ALF) and chronic liver disease (cirrhosis) continue to increase in prevalence, we will see more cases of hepatic encephalopathy.Primary care physician are often the first to suspect it, since they are familiar with the patient’s usual physical and mental status. This serious complic...

Hepatic encephalopathy: clinical and experimental studies

NARCIS (Netherlands)

C.C.D. van der Rijt (Carin)

1991-01-01

textabstractThe pathogenesis of hepatic encephalopathy is still unsolved. Therapy, therefore, is often insufficient. For the development of effective, new therapies insight into the disease-inducing substrates and the mechanisms of its toxic actions in the central nervous system ·are required. For

Neuronal CCL2 is upregulated during hepatic encephalopathy and contributes to microglia activation and neurological decline.

Science.gov (United States)

McMillin, Matthew; Frampton, Gabriel; Thompson, Michelle; Galindo, Cheryl; Standeford, Holly; Whittington, Eric; Alpini, Gianfranco; DeMorrow, Sharon

2014-07-10

microglia activation and neurological decline associated with hepatic encephalopathy. Methods used to modulate CCL2 levels and/or reduce CCR2/CCR4 activity may be potential therapeutic targets for the management of hepatic encephalopathy due to acute liver injury.

Brain MRI findings in acute hepatic encephalopathy in liver transplant recipients.

Science.gov (United States)

Guo, Ruo-Mi; Li, Qing-Ling; Zhong, Li-Ru; Guo, Yu; Jiao, Ju; Chen, Shao-Qiong; Wang, Jin; Zhang, Yong

2018-06-01

Acute hepatic encephalopathy has significant morbidity and mortality in liver transplant recipients unless it is promptly treated. We evaluated the brain magnetic resonance (MR) imaging findings associated with acute hepatic encephalopathy in transplant recipients. We retrospectively reviewed the clinical and imaging data and outcomes of twenty-five liver transplant patients (16 male; mean age, 49.3 years) with clinically diagnosed acute hepatic encephalopathy and forty liver transplant patients (20 males; mean age, 45.5 years) without neurological symptoms suggestive of hepatic encephalopathy at our institution. Bilateral symmetric hyperintensities of the insular cortex and cingulate gyrus were observed in twenty-one patients (84.00%), bilateral symmetric extensive increased cortical signal intensity (involving two or more regions) was observed in 72.00% of the patients, leptomeningeal enhancement in 73.68%, and visualization of prominent venules in 52.00%. The most common symptom at diagnosis was rigidity (n = 14), and the plasma ammonia levels ranged from 68.63 to 192.16 μmol/L. After active treatment, 17 patients gradually recovered, four patients suffered from mild or moderate neurologic deficits, and four patients with widespread brain edema died. The specific brain MR imaging features were bilateral symmetric increased cortical signal intensity, especially in the insular cortex and cingulate gyrus, leptomeningeal enhancement, visualization of the prominent venules, and widespread brain edema. These features may indicate poor prognosis and should alert radiologists to the possibility of acute hepatic encephalopathy in liver transplant recipients and encourage clinicians to prepare appropriate treatment in advance.

L-ornithine-L-aspartate infusion efficacy in hepatic encephalopathy

International Nuclear Information System (INIS)

Ahmad, I.

2008-01-01

To determine the efficacy of L-ornithine-L-aspartate in treatment of hepatic encephalopathy. Cirrhotic patients with hyperammonemia and overt hepatic encephalopathy were enrolled. Eighty patients were randomized to two treatment groups, L-ornithine-L-aspartate (20g/d) or placebo, both dissolved in 250mL of 5% dextrose water and infused intravenously for four hours a day for five consecutive days with 0.5 g/kg dietary protein intake at the end of daily treatment period. Outcome variables were postprandial blood ammonia and mental state grade. Adverse reactions and mortality were also determined. Both treatment groups were comparable regarding age, gender, etiology of cirrhosis, Child-Pugh class, mental state grade and blood ammonia at baseline. Although, improvement occurred in both groups, there was a greater improvement in L-ornithine-L-aspartate group with regard to both variables. Four patients in the placebo group and 2 in L-ornithine-L-aspartate group died. L-ornithine-L-aspartate infusions were found to be effective in cirrhotic patients with hepatic encephalopathy. (author)

Hepatic encephalopathy: Ever closer to its big bang.

Science.gov (United States)

Souto, Pablo A; Marcotegui, Ariel R; Orbea, Lisandro; Skerl, Juan; Perazzo, Juan Carlos

2016-11-14

Hepatic encephalopathy (HE) is a neuropsychiatric disorder that commonly complicates the course of patients with liver disease. Despite the fact that the syndrome was probably first recognized hundreds of years ago, the exact pathogenesis still remains unclear. Minimal hepatic encephalopathy (MHE) is the earliest form of HE and is estimated to affect more that 75% of patients with liver cirrhosis. It is characterized by cognitive impairment predominantly attention, reactiveness and integrative function with very subtle clinical manifestations. The development of MHE is associated with worsen in driving skills, daily activities and the increase of overall mortality. Skeletal muscle has the ability to shift from ammonia producer to ammonia detoxifying organ. Due to its large size, becomes the main ammonia detoxifying organ in case of chronic liver failure and muscular glutamine-synthase becomes important due to the failing liver and brain metabolic activity. Gut is the major glutamine consumer and ammonia producer organ in the body. Hepatocellular dysfunction due to liver disease, results in an impaired clearance of ammonium and in its inter-organ trafficking. Intestinal bacteria, can also represent an extra source of ammonia production and in cirrhosis, small intestinal bacterial overgrowth and symbiosis can be observed. In the study of HE, to get close to MHE is to get closer to its big bang; and from here, to travel less transited roads such as skeletal muscle and intestine, is to go even closer. The aim of this editorial is to expose this road for further and deeper work.

The effects of benzodiazepine-receptor antagonists and partial inverse agonists on acute hepatic encephalopathy in the rat

NARCIS (Netherlands)

Bosman, D. K.; van den Buijs, C. A.; de Haan, J. G.; Maas, M. A.; Chamuleau, R. A.

1991-01-01

Two benzodiazepine-receptor partial inverse agonists (Ro 15-4513, Ro 15-3505) and one benzodiazepine-receptor antagonist (flumazenil) were administered to rats with hepatic encephalopathy due to acute liver ischemia. Significant improvement (P less than 0.002) of both the clinical grade of hepatic

Performance of the hepatic encephalopathy scoring algorithm in a clinical trial of patients with cirrhosis and severe hepatic encephalopathy

DEFF Research Database (Denmark)

Hassanein, T.; Blei, A.T.; Perry, W.

2009-01-01

OBJECTIVES: The grading of hepatic encephalopathy (HE) is based on a combination of indicators that reflect the state of consciousness, intellectual function, changes in behavior, and neuromuscular alterations seen in patients with liver failure. METHODS: We modified the traditional West Haven...... criteria (WHC) to provide an objective assessment of the cognitive parameters to complement the subjective clinical ratings for the performance of extracorporeal albumin dialysis (ECAD) using a molecular adsorption recirculating system in patients with cirrhosis and severe (grade III / IV) encephalopathy...

Brain concentrations of benzodiazepines are elevated in an animal model of hepatic encephalopathy

International Nuclear Information System (INIS)

Basile, A.S.; Pannell, L.; Jaouni, T.; Gammal, S.H.; Fales, H.M.; Jones, E.A.; Skolnick, P.

1990-01-01

Brain extracts from rats with hepatic encephalopathy due to thioacetamide-induced fulminant hepatic failure contained 4- to 6-fold higher concentrations of substances that inhibit radioligand binding to benzodiazepine receptors than corresponding control rat extracts. Both isocratic and gradient-elution HPLC indicated that this inhibitory activity was localized in 3-8 peaks with retention times corresponding to deschlorodiazepam, deschlorolorazepam, lorazepam, oxazepam, diazepam, and N-desmethyldiazepam. The presence of diazepam and N-desmethyldiazepam was confirmed by mass spectroscopy. Both mass spectroscopic and radiometric techniques indicated that the concentrations of N-desmethyldiazepam and diazepam in brain extracts from encephalopathic rats were 2-9 and 5-7 times higher, respectively, than in control brain extracts. While benzodiazepines have been identified previously in mammalian and plant tissues, this report demonstrates that concentrations of these substances are increased in a pathophysiological condition. These findings provide a rational basis for the use of benzodiazepine receptor antagonists in the management of hepatic encephalopathy in humans

Efficacy of Rifaximin in Prevention of Recurrence of Hepatic Encephalopathy in Patients with Cirrhosis of Liver

International Nuclear Information System (INIS)

Ali, B.; Zaidi, Y. A.; Alam, A.; Anjum, H. S.

2014-01-01

Objective: To determine the efficacy of Rifaximin in prevention of repeated episodes of hepatic encephalopathy in patients with liver cirrhosis as compared to placebo. Study Design: Triple-blind, randomized placebo-controlled trial. Place and Duration of Study: Department of Gastroenterology-Hepatology, Shaikh Zayed Hospital, Lahore, from October 2012 to April 2013. Methodology: Patients in remission from recurrent hepatic encephalopathy resulting from cirrhosis were randomly assigned to receive either Rifaximin, at a dose of 550 mg twice daily (63 patients), or placebo (63 patients.) Patients were requested to take the drug orally twice daily for 6 months or until they developed a breakthrough episode of hepatic encephalopathy. Results: Mean age of patients in treatment and control group was 40.21 A +- 2.33 years and 42.87 A +- 4.54 years respectively. The most common etiology of cirrhosis was hepatitis C followed by hepatitis B. Patients who remained free of hepatic encephalopathy during study period were 40 out of 63 patients in control group and 35 patients out of 63 patients (p = 0.56). Most of the patients who developed breakthrough hepatic encephalopathy had a MELD score range of 21-25 in both groups. The number of deaths and adverse events was similar in both groups. Conclusion: Over a 6-month period, treatment with Rifaximin failed to maintain remission from hepatic encephalopathy more effectively than placebo in the studied group. (author)

Effects of raloxifene on portal hypertension and hepatic encephalopathy in cirrhotic rats.

Science.gov (United States)

Chang, Ching-Chih; Lee, Wen-Shin; Chuang, Chiao-Lin; Hsin, I-Fang; Hsu, Shao-Jung; Chang, Ting; Huang, Hui-Chun; Lee, Fa-Yauh; Lee, Shou-Dong

2017-05-05

Raloxifene, a selective estrogen receptor modulator, has been used extensively for osteoporosis. In addition to the effect of osteoporosis treatment, emerging evidences show that raloxifene affects the vascular function in different tissues. Cirrhosis is characterized with portal hypertension and complicated with hepatic encephalopathy. Portal hypertension affects portal-systemic shunt which leads to hepatic encephalopathy that the vascular modulation might influence severity of hepatic encephalopathy. Herein, we evaluated the impact of raloxifene on bile duct ligation (BDL)-induced cirrhotic rats. The female Sprague-Dawley rats received BDL plus ovariectomy or sham-operation. Four weeks later, rats were divided into 2 subgroups respectively to receive of raloxifene (10mg/kg/day) or saline (vehicle) for 14 days. On the 43th day, motor activities and hemodynamic parameters were measured. Hepatic and vascular mRNA and protein expressions were determined. The histopathological change of liver was examined. We found that the liver biochemistry, ammonia level and motor activity were similar between cirrhotic rats with or without raloxifene administration. The hemodynamic parameters were not significantly different except that raloxifene reduced portal venous inflow. Raloxifene exacerbated hepatic fibrosis and up-regulated hepatic endothelin-1 and cyclooxygenase 2 protein expressions. In addition, raloxifene modulated the mRNA expressions of endothelial nitric oxide synthase, cyclooxygenase and endothelin-1 in the superior mesenteric artery and collateral vessel. In conclusion, raloxifene aggravates hepatic fibrosis and decreases portal venous inflow in cirrhotic rats without adversely affecting portal hypertension and hepatic encephalopathy. The modulation of hepatic and vascular endothelin-1, endothelial nitric oxide synthase and cyclooxygenase expressions may play a role in the mechanism. Copyright © 2017 Elsevier B.V. All rights reserved.

Expression of glutamine transporter isoforms in cerebral cortex of rats with chronic hepatic encephalopathy

DEFF Research Database (Denmark)

Leke, Renata; Escobar, Thayssa D.C.; Rama Rao, Kakulavarapu V.

2015-01-01

Hepatic encephalopathy (HE) is a neuropsychiatric disorder that occurs due to acute and chronic liver diseases, the hallmark of which is the increased levels of ammonia and subsequent alterations in glutamine synthesis, i.e. conditions associated with the pathophysiology of HE. Under physiological...

How to diagnose and manage hepatic encephalopathy: a consensus statement on roles and responsibilities beyond the liver specialist.

Science.gov (United States)

Shawcross, Debbie L; Dunk, Arthur A; Jalan, Rajiv; Kircheis, Gerald; de Knegt, Robert J; Laleman, Wim; Ramage, John K; Wedemeyer, Heiner; Morgan, Ian E J

2016-02-01

Hepatic encephalopathy is defined as brain dysfunction caused by liver insufficiency and/or portosystemic shunting. Symptoms include nonspecific cognitive impairment, personality changes and changes in consciousness. Overt (symptomatic) hepatic encephalopathy is a common complication of cirrhosis that is associated with a poor prognosis. Patients with hepatic encephalopathy may present to healthcare providers who do not have primary responsibility for management of patients with cirrhosis. Therefore, we developed a series of 'consensus points' to provide some guidance on management. Using a modified 'Delphi' process, consensus statements were developed that summarize our recommendations for the diagnosis and management of patients with hepatic encephalopathy. Points on which full consensus could not be reached are also discussed. Our recommendations emphasize the role of all healthcare providers in the identification of cognitive impairment in patients with cirrhosis and provide guidance on steps that might be considered to make a diagnosis of overt hepatic encephalopathy. In addition, treatment recommendations are summarized. Minimal hepatic encephalopathy can have a significant impact on patients; however, in most circumstances identification and management of minimal hepatic encephalopathy remains the responsibility of specialists in liver diseases. Our opinion statements aim to define the roles and responsibilities of all healthcare providers who at times care for patients with cirrhosis and hepatic encephalopathy. We suggest that these recommendations be considered further by colleagues in other disciplines and hope that future guidelines consider the management of patients with cirrhosis and with a 'suspicion' of cognitive impairment through to a formal diagnosis of hepatic encephalopathy.

Hepatic encephalopathy: experimental studies on the pathogenesis

NARCIS (Netherlands)

R.J. de Knegt (Robert)

1993-01-01

textabstractAims of this thesis: 1. To study, in rabbits, the suitability of experimental acute liver failure and acute hyperammonemia simulating acute liver failure for the study of hepatic encephalopathy and ammonia toxicity. 2. To study glutamate neurotransmission in rabbits with acute liver

Clinical and experimental aspects of hepatic encephalopathy

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M. Groeneweg (Michael)

1998-01-01

textabstractHepatic encephalopathy (HE) is a neuropsychiatnc syndrome associated with severe liver disease. Clinical symptoms range from minimal changes in mental state and neuromuscular defects to unresponsive coma. 1-' The syndrome of HE can be divided into three major groups: HE associated with

Ammonia levels and the severity of hepatic encephalopathy

International Nuclear Information System (INIS)

Qureshi, M.O.; Khokhar, N.; Shafqat, F.

2014-01-01

Objective: To evaluate the correlation between ammonia levels with the severity of HE in patients coming to the tertiary care hospital with liver cirrhosis and hepatic encephalopathy (HE). Study Design: Descriptive, analytical study. Place and Duration of Study: Shifa International Hospital, Islamabad, from January 2011 to February 2012. Methodology: A total of 135 patients with liver cirrhosis and HE had serum ammonia levels measured on admission. The diagnosis of HE was based on clinical criteria, and its severity was graded according to the West Haven Criteria for grading of mental status. Ammonia levels were correlated with the severity of HE using Spearman rank correlation. Results: Out of 20 patients with normal ammonia levels, 13 (65%) were in HE I-II, 6 (30%) were in grade-III, while 1 (5%) patient was in grade-IV HE. Out of 45 patients with mild hyperammonemia, 27 (60%) were in grade I-II, 12 (26%) were in grade-III and 6 (13%) were in grade-IV HE. Out of 34 patients with moderate hyperammonemia, 9 (26%) were in grade I-II, 18 (53%) were in grade-III, and 7 (20%) were in grade-IV HE. Out of 36 patients with severe hyperammonemia, 31 (86%) patients were in grade-IV HE (p < 0.001). Conclusion: Ammonia levels correlated with the severity of hepatic encephalopathy. Greater the ammonia level, severe is the grade of hepatic encephalopathy. (author)

Hepatic encephalopathy: current challenges and future prospects

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Swaminathan M

2018-03-01

Full Text Available Mirashini Swaminathan,1 Mark Alexander Ellul,2 Timothy JS Cross1 1Department of Gastroenterology, Royal Liverpool University Hospital, 2Faculty of Health and Life Sciences, Institute of Infection and Global Health, University of Liverpool, Liverpool, UK Abstract: Hepatic encephalopathy (HE is a common complication of liver dysfunction, including acute liver failure and liver cirrhosis. HE presents as a spectrum of neuropsychiatric symptoms ranging from subtle fluctuating cognitive impairment to coma. It is a significant contributor of morbidity in patients with liver disease. HE is observed in acute liver failure, liver bypass procedures, for example, shunt surgery and transjugular intrahepatic portosystemic shunt, and cirrhosis. These are classified as Type A, B and C HE, respectively. HE can also be classified according to whether its presence is overt or covert. The pathogenesis is linked with ammonia and glutamine production, and treatment is based on mechanisms to reduce the formation and/or removal of these compounds. There is no specific diagnostic test for HE, and diagnosis is based on clinical suspicion, excluding other causes and use of clinical tests that may support its diagnosis. Many tests are used in trials and experimentally, but have not yet gained universal acceptance. This review focuses on the definitions, pathogenesis and treatment of HE. Consideration will be given to existing treatment, including avoidance of precipitating factors and novel therapies such as prebiotics, probiotics, antibiotics, laxatives, branched-chain amino acids, shunt embolization and the importance of considering liver transplant in appropriate cases. Keywords: hepatic encephalopathy, pathogenesis, treatment, lactulose, rifaximin, probiotics, covert hepatic encephalopathy

Systematic review and meta-analysis of randomized trials on probiotics for hepatic encephalopathy

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Holte, Kathrine; Krag, Aleksander; Gluud, Lise Lotte

2012-01-01

Aim:  The objective of this systematic review and meta-analysis was to assess the efficacy of probiotics and synbiotics in patients with hepatic encephalopathy. Methods:  Eligible trials were identified by searching electronic databases including MEDLINE, the Cochrane Library, Science Citation...... Index and Embase, abstract proceedings, reference lists and ongoing trial registers until 13 October 2010. We included randomized controlled trials comparing probiotics and synbiotics with no intervention, placebo or lactulose in patients with hepatic encephalopathy. The primary outcome measure...... was improvement in hepatic encephalopathy. Results were expressed as risk rates (RR) with confidence intervals (CI) and intertrial heterogeneity as I(2) . Results:  Seven trials with a total of 393 patients were analyzed. Compared to placebo or lactulose, treatment with probiotics or synbiotics significantly...

Hepatic encephalopathy: cause and possible management with botanicals.

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Tripathi, Suyash; Tripathi, Yamini B

2014-01-01

Hepatic encephalopathy is a brain functional disorder, characterized by neuropsychiatric abnormalities with liver failure. High blood ammonia, causing glutamate neurotoxicity is the basic cause, finally leading to low-grade cerebral edema. Its manifestation is more likely in patients of sepsis, oxidative stress, generalized inflammation, gut mal-functioning, amoebiaesis, viral hepatitis, nervous imbalance, etc. Thus, the therapeutic goals primarily include the maintenance of proper blood supply and prevention of hypoxic condition in liver, along with management of factors responsible for high blood ammonia, oxidative stress, inflammation, and high GI- serotonin. The drugs in clinical practice include lactulose, sodium benzoate, flumazenil and rifaximin, supplementation of zinc, branched chain amino acids (BCAA), l-ornithine-l aspartate, antioxidants and iNOS inhibitors. However, herbal formulations would be of great importance as it shows multi-targeted action because it possesses a natural cocktail of secondary metabolites. It can collectively act as an antioxidant, anti-inflammatory, prebiotic, hepatoprotective and neuron-protective agents. We have briefly outlined some of these plants and also recent patents useful in the management of hepatic encephalopathy.

Correlation of hyponatremia with hepatic encephalopathy and severity of liver disease.

Science.gov (United States)

Qureshi, Muhammad Omar; Khokhar, Nasir; Saleem, Atif; Niazi, Tariq Khan

2014-02-01

To assess the frequency of low serum sodium levels and to correlate it with the severity of liver disease and hepatic encephalopathy (HE) in patients coming to the tertiary care hospital. Observational study. Shifa International Hospital, Islamabad, from January 2011 to January 2012. A total of 202 patients with hepatic encephalopathy and chronic liver disease had serum sodium measured. The HE was graded according to the West Haven classification (4 grades). Relationship of hyponatremia was correlated with severity grade of encephalopathy using Spearman rank correlation test. Out of 202 patients, 62 (30.7%) patients had serum sodium less than 130 meq/l. Out of 202, HE was present in 69 (34.15%) patients and out of these, 38 had grade III-IV HE and 31 had grade I - II HE. Out of 69 patients with HE 57 had sodium less than 135 (p liver disease. The existence of serum sodium concentration encephalopathy compared with patients with serum sodium concentration > 135 mmol/L.

Current trends in the treatment of hepatic encephalopathy

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Mohamad Rasm Al Sibae

2009-07-01

Full Text Available Mohamad Rasm Al Sibae, Brendan M McGuireDepartment of Medicine, Division of Gastroenterology and Hepatology, University of Alabama at Birmingham, Birmingham, AL, USAAbstract: Hepatic encephalopathy (HE is a common reversible neuropsychiatric syndrome associated with chronic and acute liver dysfunction and significant morbidity and mortality. Although a clear pathogenesis is yet to be determined, elevated ammonia in the serum and central nervous system are the mainstay for pathogenesis and treatment. Management includes early diagnosis and prompt treatment of precipitating factors (infection, gastrointestinal bleeding, electrolyte disturbances, hepatocellular carcinoma, dehydration, hypotension, and use of benzodiazepines, psychoactive drugs, and/or alcohol. Clinical trials have established the efficacy of lactulose and lactitol enemas in the treatment of acute hepatic encephalopathy. Extensive clinical experience has demonstrated the efficacy of oral lactulose and lactitol with the goal of two to three soft bowel movements a day for the treatment of chronic HE. However, lactulose and lactitol have significant gastrointestinal side effects. For patients unable to tolerate lactulose or lactitol or who still have persistent chronic HE with lactulose or lactitol, neomycin, metronidazole and rifaximin are second-line agents. More recent data supports the benefits of rifaximin used solely and as an additional agent with fewer side effects than neomycin or metronidazole. Newer therapies being investigated in humans with clinical promise include nitazoxanide, the molecular adsorbent recirculating system (MARS, L-ornithine phenylacetate, sodium benzoate, and/or sodium phenylacetate and Kremezin® (AST-120.Keywords: hepatic encephalopathy, liver dysfunction, lactulose, lactitol

Hyperammonemia Is Associated with Increasing Severity of Both Liver Cirrhosis and Hepatic Encephalopathy

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Abidullah Khan

2016-01-01

Full Text Available Background. Hyperammonemia resulting from chronic liver disease (CLD can potentially challenge and damage any organ system of the body, particularly the brain. However, there is still some controversy regarding the diagnostic or prognostic values of serum ammonia in patients with over hepatic encephalopathy, especially in the setting of acute-on-chronic or chronic liver failure. Moreover, the association of serum ammonia with worsening Child-Pugh grade of liver cirrhosis has not been studied. Objective. This study was conducted to solve the controversy regarding the association between hyperammonemia and cirrhosis, especially hepatic encephalopathy in chronically failed liver. Material and Methods. In this study, 171 cirrhotic patients had their serum ammonia measured and analyzed by SPSS version 16. Chi-squared test and one-way ANOVA were applied. Results. The study had 110 male and 61 female participants. The mean age of all the participants in years was 42.33±7.60. The mean duration (years of CLD was 10.15±3.53 while the mean Child-Pugh (CP score was 8.84±3.30. Chronic viral hepatitis alone was responsible for 71.3% of the cases. Moreover, 86.5% of participants had hepatic encephalopathy (HE. The frequency of hyperammonemia was 67.3%, more frequent in males (N=81, z-score = 2.4, and P<0.05 than in females (N=34, z-score = 2.4, and P<0.05, and had a statistically significant relationship with increasing CP grade of cirrhosis (χ2(2 = 27.46, P<0.001, Phi = 0.40, and P<0.001. Furthermore, serum ammonia level was higher in patients with hepatic encephalopathy than in those without it; P<0.001. Conclusion. Hyperammonemia is associated with both increasing Child-Pugh grade of liver cirrhosis and hepatic encephalopathy.

Hepatic encephalopathy in a liver transplant recipient with stable liver function.

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Arab, Juan Pablo; Meneses, Luis; Pérez, Rosa M; Arrese, Marco; Benítez, Carlos

2013-04-01

Postshunt hepatic encephalopathy after liver transplantation (LT) is an infrequent condition and is commonly associated with portal occlusion or stenosis and the presence of a patent portosystemic shunt. Portal vein stenosis (PVS) or thrombosis (PVT) are uncommon complications after LT. The overall frequency of both complications is reported to be less than 3%. When PVS or PVT develop early after LT, the occlusion of the portal vein can have catastrophic consequences to the graft including acute liver failure and graft loss. Late PVT/PVS are asymptomatic in approximately 50% of the cases and mainly diagnosed by a routine ultrasound. Symptomatic postshunt hepatic encephalopathy (HE) is a very infrequent condition after LT that has been scarcely reported in the literature. We present here the case of a liver recipient with normal graft function who presented with hepatic encephalopathy 3 months after LT with stable liver function but a severe portal stenosis and the presence of a spontaneous portosystemic shunt whose successful endovascular treatment was followed by the complete resolution of the HE.

Update on the Therapeutic Management of Hepatic Encephalopathy

DEFF Research Database (Denmark)

Kornerup, Linda Skibsted; Gluud, Lise Lotte; Vilstrup, Hendrik

2018-01-01

PURPOSE OF REVIEW: Hepatic encephalopathy (HE) is a common and devastating complication to chronic liver disease. In this paper, we summarize the latest research and evidence of both conventional and up-coming treatments. RECENT FINDINGS: Meta-analyses report beneficial effects of lactulose...

Incisional hernia as an unusual cause of hepatic encephalopathy in a 62-year-old man with cirrhosis: a case report

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Ustaoglu Muge

2009-09-01

Full Text Available Abstract Introduction Hepatic encephalopathy may be initiated by many factors such as gastrointestinal bleeding, infections, fluid and electrolyte disturbances. Hypokalemia is one of the most commonly encountered electrolyte abnormalities causing hepatic encephalopathy in patients with cirrhosis. Case presentation We present the case of a 62-year-old Caucasian man with decompensated liver cirrhosis having multiple episodes of hepatic encephalopathy precipitated by vomiting. He had an incisional hernia at the right lumbar region. A barium contrast study of the small intestine and magnetic resonance imaging showed that the hernial sac included gastric antrum and bowel. We observed that hepatic encephalopathy coincided with hypokalemia as a result of a large volume of vomiting triggered by the collapsed hernial sac. Hepatic encephalopathy was resolved by administration of intravenous potassium. Conclusion This case illustrates that a hernia causing a large volume of vomiting may be a precipitant factor in the development of hepatic encephalopathy.

Preliminary report of the Hepatic Encephalopathy Assessment Driving Simulator (HEADS) score.

Science.gov (United States)

Baskin-Bey, Edwina S; Stewart, Charmaine A; Mitchell, Mary M; Bida, John P; Rosenthal, Theodore J; Nyberg, Scott L

2008-01-01

Audiovisual simulations of real-life driving (ie, driving simulators) have been used to assess neurologic dysfunction in a variety of medical applications. However, the use of simulated driving to assess neurologic impairment in the setting of liver disease (ie, hepatic encephalopathy) is limited. The aim of this analysis was to develop a scoring system based on simulated driving performance to assess mild cognitive impairment in cirrhotic patients with hepatic encephalopathy. This preliminary analysis was conducted as part of the Hepatic Encephalopathy Assessment Driving Simulator (HEADS) pilot study. Cirrhotic volunteers initially underwent a battery of neuropsychological tests to identify those cirrhotic patients with mild cognitive impairment. Performance during an audiovisually simulated course of on-road driving was then compared between mildly impaired cirrhotic patients and healthy volunteers. A scoring system was developed to quantify the likelihood of cognitive impairment on the basis of data from the simulated on-road driving. Mildly impaired cirrhotic patients performed below the level of healthy volunteers on the driving simulator. Univariate logistic regression and correlation models indicated that several driving simulator variables were significant predictors of cognitive impairment. Five variables (run time, total map performance, number of collisions, visual divided attention response, and average lane position) were incorporated into a quantitative model, the HEADS scoring system. The HEADS score (0-9 points) showed a strong correlation with cognitive impairment as measured by area under the receiver-operator curve (.89). The HEADS system appears to be a promising new tool for the assessment of mild hepatic encephalopathy.

Hepatic Encephalopathy Secondary to Intrahepatic Portosystemic Venous Shunt: Balloon-Occluded Retrograde Transvenous Embolization with n-Butyl Cyanoacrylate and Microcoils

International Nuclear Information System (INIS)

Yamagami, Takuji; Nakamura, Toshiyuki; Iida, Shigeharu; Kato, Takeharu; Tanaka, Osamu; Matsushima, Shigenori; Ito, Hirotoshi; Okuyama, Chio; Ushijima, Yo; Shiga, Kensuke; Nishimura, Tsunehiko

2002-01-01

We report a 70-year-old woman with hepatic encephalopathy due to an intrahepatic portosystemic venous shunt that was successfully occluded by percutaneous transcatheter embolization with n-butyl cyanoacrylate and microcoils

Capsaicin affects brain function in a model of hepatic encephalopathy associated with fulminant hepatic failure in mice

Science.gov (United States)

Avraham, Y; Grigoriadis, NC; Magen, I; Poutahidis, T; Vorobiav, L; Zolotarev, O; Ilan, Y; Mechoulam, R; Berry, EM

2009-01-01

Background and purpose: Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver failure. In view of the effects of cannabinoids in a thioacetamide-induced model of hepatic encephalopathy and liver disease and the beneficial effect of capsaicin (a TRPV1 agonist) in liver disease, we assumed that capsaicin may also affect hepatic encephalopathy. Experimental approach: Fulminant hepatic failure was induced in mice by thioacetamide and 24 h later, the animals were injected with one of the following compound(s): 2-arachidonoylglycerol (CB1, CB2 and TRPV1 receptor agonist); HU308 (CB2 receptor agonist), SR141716A (CB1 receptor antagonist); SR141716A+2-arachidonoylglycerol; SR144528 (CB2 receptor antagonist); capsaicin; and capsazepine (TRPV1 receptor agonist and antagonist respectively). Their neurological effects were evaluated on the basis of activity in the open field, cognitive function in an eight-arm maze and a neurological severity score. The mice were killed 3 or 14 days after thioacetamide administration. 2-arachidonoylglycerol and 5-hydroxytryptamine (5-HT) levels were determined by gas chromatography-mass spectrometry and high-performance liquid chromatography with electrochemical detection, respectively. Results: Capsaicin had a neuroprotective effect in this animal model as shown by the neurological score, activity and cognitive function. The effect of capsaicin was blocked by capsazepine. Thioacetamide induced astrogliosis in the hippocampus and the cerebellum and raised brain 5-hydroxytryptamine levels, which were decreased by capsaicin, SR141716A and HU-308. Thioacetamide lowered brain 2-arachidonoylglycerol levels, an effect reversed by capsaicin. Conclusions: Capsaicin improved both liver and brain dysfunction caused by thioacetamide, suggesting that both the endocannabinoid and the vanilloid systems play important roles in hepatic encephalopathy. Modulation of these systems may have therapeutic value. PMID:19764982

Assessment of minimal hepatic encephalopathy (with emphasis on computerized psychometric tests).

Science.gov (United States)

Kappus, Matthew R; Bajaj, Jasmohan S

2012-02-01

Minimal hepatic encephalopathy (MHE) is associated with a high risk of development of overt hepatic encephalopathy, impaired quality of life, and driving accidents. The detection of MHE requires specialized testing because it cannot, by definition, be diagnosed on standard clinical examination. Psychometric and neurophysiologic techniques are often used to test for MHE. Paper-pencil psychometric batteries and computerized tests have proved useful in diagnosing MHE and predicting its outcomes. Neurophysiologic tests also provide useful information. The diagnosis of MHE is an important issue for clinicians and patients alike. Testing strategies depend on the normative data available, patient comfort, and local expertise. Copyright © 2012 Elsevier Inc. All rights reserved.

Tranilast reduces serum IL-6 and IL-13 and protects against thioacetamide-induced acute liver injury and hepatic encephalopathy.

Science.gov (United States)

Abdelaziz, Rania R; Elkashef, Wagdi F; Said, Eman

2015-07-01

Hepatic encephalopathy is a serious neuropsychiatric disorder usually affecting either acute or chronic hepatic failure patients. Hepatic encephalopathy was replicated in a validated rat model to assess the potential protective efficacy of tranilast against experimentally induced hepatic encephalopathy. Thioacetamide injection significantly impaired hepatic synthetic, metabolic and excretory functions with significant increase in serum NO, IL-6 and IL-13 levels and negative shift in the oxidant/antioxidant balance. Most importantly, there was a significant increase in serum ammonia levels with significant astrocytes' swelling and vacuolization; hallmarks of hepatic encephalopathy. Tranilast administration (300 mg/kg, orally) for 15 days significantly improved hepatic functions, restored oxidant/antioxidant balance, reduced serum NO, IL-6 and IL-13 levels. Meanwhile, serum ammonia significantly declined with significant reduction in astrocytes' swelling and vacuolization. Several mechanisms can be implicated in the observed hepato- and neuroprotective potentials of tranilast, such as its anti-inflammatory potential, its antioxidant potential as well as its immunomodulatory properties. Copyright © 2015 Elsevier B.V. All rights reserved.

Minimal hepatic encephalopathy characterized by parallel use of the continuous reaction time and portosystemic encephalopathy tests

DEFF Research Database (Denmark)

Lauridsen, M M; Schaffalitzky de Muckadell, O B; Vilstrup, H

2015-01-01

Minimal hepatic encephalopathy (MHE) is a frequent complication to liver cirrhosis that causes poor quality of life, a great burden to caregivers, and can be treated. For diagnosis and grading the international guidelines recommend the use of psychometric tests of different modalities (computer...... based vs. paper and pencil). To compare results of the Continuous Reaction time (CRT) and the Portosystemic Encephalopathy (PSE) tests in a large unselected cohort of cirrhosis patients without clinically detectable brain impairment and to clinically characterize the patients according to their test...

How to diagnose and manage hepatic encephalopathy: A consensus statement on roles and responsibilities beyond the liver specialist

NARCIS (Netherlands)

Shawcross, D.L. (Debbie L.); Dunk, A.A. (Arthur A.); Jalan, R. (Rajiv); Kircheis, G. (Gerald); R.J. de Knegt (Robert); W. Laleman (Wim); Ramage, J.K. (John K.); H. Wedemeyer (Heiner); Morgan, I.E.J. (Ian E.J.)

2016-01-01

textabstractIntroduction Hepatic encephalopathy is defined as brain dysfunction caused by liver insufficiency and/or portosystemic shunting. Symptoms include nonspecific cognitive impairment, personality changes and changes in consciousness. Overt (symptomatic) hepatic encephalopathy is a common

Correlation of Hyponatremia with Hepatic Encephalopathy and Severity of Liver Disease

International Nuclear Information System (INIS)

Qureshi, M. O.; Khokhar, N.; Saleem, A.; Niazi, T. K.

2014-01-01

Objective: To assess the frequency of low serum sodium levels and to correlate it with the severity of liver disease and hepatic encephalopathy (HE) in patients coming to the tertiary care hospital. Study Design: Observational study. Place and Duration of Study: Shifa International Hospital, Islamabad, from January 2011 to January 2012. Methodology: A total of 202 patients with hepatic encephalopathy and chronic liver disease had serum sodium measured. The HE was graded according to the West Haven classification (4 grades). Relationship of hyponatremia was correlated with severity grade of encephalopathy using Spearman rank correlation test. Results: Out of 202 patients, 62 (30.7%) patients had serum sodium less than 130 meq/l. Out of 202, HE was present in 69 (34.15%) patients and out of these, 38 had grade III-IV HE and 31 had grade I - II HE. Out of 69 patients with HE 57 had sodium less than 135 (p 135 mmol/L. (author)

Advances in ammonia metabolism and hepatic encephalopathy

International Nuclear Information System (INIS)

Soeters, P.B.; Wilson, J.H.P.; Meijer, A.J.; Holm, E.

1988-01-01

There are four main 'parts' within the book: the first is devoted to peripheral and hepatic ammonia metabolism, the urea cycle, acid base status and its regulation; part two addresses animal models in liver failure, GABA-ergic neurotransmission and its relevance in hepatic failure; a third part concerns neurochemistry including brain ammonia metabolism, serotonin metabolism and energy status, in vivo evaluated with modern techniques like infusion of compounds labeled with stable or radioactive isotopes and with NMR, while the last section provides a description of the determination of ammonia and the treatment of encephalopathy with established but also with experimental techniques. refs.; figs.; tabs

Structural and functional cerebral impairments in cirrhotic patients with a history of overt hepatic encephalopathy

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Chen, Hua-Jun [Jiangsu Key Laboratory of Molecular Imaging and Functional Imaging, Department of Radiology, Zhongda Hospital, Medical School of Southeast University, Nanjing 210009 (China); Zhu, Xi-Qi [Jiangsu Key Laboratory of Molecular Imaging and Functional Imaging, Department of Radiology, Zhongda Hospital, Medical School of Southeast University, Nanjing 210009 (China); Department of Radiology, The Second Hospital of Nanjing, Medical School of Southeast University, Nanjing 210002 (China); Shu, Hao [Department of Neurology, Zhongda Hospital, Medical School of Southeast University, Nanjing 210009 (China); Yang, Ming; Zhang, Yi; Ding, Jie; Wang, Yu [Jiangsu Key Laboratory of Molecular Imaging and Functional Imaging, Department of Radiology, Zhongda Hospital, Medical School of Southeast University, Nanjing 210009 (China); Teng, Gao-Jun, E-mail: gjteng@vip.sina.com [Jiangsu Key Laboratory of Molecular Imaging and Functional Imaging, Department of Radiology, Zhongda Hospital, Medical School of Southeast University, Nanjing 210009 (China)

2012-10-15

Objective: Diffuse brain atrophy has been observed in cirrhotic patients and recent reports have revealed the persistence of cognitive impairment after clinical resolution of overt hepatic encephalopathy. We sought to explore the continued influence of overt hepatic encephalopathy on neurological function by measuring brain resting-state inherent connectivity, based on an investigation of structural abnormalities. Methods: Neuropsychological tests and structural and functional magnetic resonance scanning were conducted in 20 healthy controls and 21 cirrhotic patients with a history of overt hepatic encephalopathy. The analysis of voxel-based morphometry and functional connectivity were performed to detect the alterations in brain structure and function, respectively. Results: Patients showed significantly worse performance in neuropsychological tests as compared with controls, despite apparently normal mental status. Analysis of voxel-based morphometry revealed a decrease in gray matter volume primarily in the midline regions, bilateral insular cortex and caudates, left parahippocampal gyrus, and right cerebellum posterior lobe, while the volume of the bilateral thalamus showed an increase. Of these regions, the posterior cingulate cortex with peak atrophy was selected as the origin for the analysis of functional connectivity. Typical patterns of a default mode network were identified in both groups. Decreased functional connectivity was found in the medial prefrontal gyrus, left inferior parietal lobule, and left middle temporal gyrus in the patients. Conclusions: Both functional and structural impairments were evident after apparent recovery from overt hepatic encephalopathy, demonstrating that brain dysfunction induced by hepatic encephalopathy persisted after clinical resolution and provided a basis for further evolution of the disease.

Structural and functional cerebral impairments in cirrhotic patients with a history of overt hepatic encephalopathy

International Nuclear Information System (INIS)

Chen, Hua-Jun; Zhu, Xi-Qi; Shu, Hao; Yang, Ming; Zhang, Yi; Ding, Jie; Wang, Yu; Teng, Gao-Jun

2012-01-01

Objective: Diffuse brain atrophy has been observed in cirrhotic patients and recent reports have revealed the persistence of cognitive impairment after clinical resolution of overt hepatic encephalopathy. We sought to explore the continued influence of overt hepatic encephalopathy on neurological function by measuring brain resting-state inherent connectivity, based on an investigation of structural abnormalities. Methods: Neuropsychological tests and structural and functional magnetic resonance scanning were conducted in 20 healthy controls and 21 cirrhotic patients with a history of overt hepatic encephalopathy. The analysis of voxel-based morphometry and functional connectivity were performed to detect the alterations in brain structure and function, respectively. Results: Patients showed significantly worse performance in neuropsychological tests as compared with controls, despite apparently normal mental status. Analysis of voxel-based morphometry revealed a decrease in gray matter volume primarily in the midline regions, bilateral insular cortex and caudates, left parahippocampal gyrus, and right cerebellum posterior lobe, while the volume of the bilateral thalamus showed an increase. Of these regions, the posterior cingulate cortex with peak atrophy was selected as the origin for the analysis of functional connectivity. Typical patterns of a default mode network were identified in both groups. Decreased functional connectivity was found in the medial prefrontal gyrus, left inferior parietal lobule, and left middle temporal gyrus in the patients. Conclusions: Both functional and structural impairments were evident after apparent recovery from overt hepatic encephalopathy, demonstrating that brain dysfunction induced by hepatic encephalopathy persisted after clinical resolution and provided a basis for further evolution of the disease

Probiotics in management of hepatic encephalopathy.

Science.gov (United States)

Sharma, Barjesh Chander; Singh, Jatinderpal

2016-12-01

Gut microflora leads to production of ammonia and endotoxins which play important role in the pathogenesis of hepatic encephalopathy (HE). There is relationship between HE and absorption of nitrogenous substances from the intestines. Probiotics play a role in treatment of HE by causing alterations in gut flora by decreasing the counts of pathogen bacteria, intestinal mucosal acidification, decrease in production and absorption of ammonia, alterations in permeability of gut, decreased endotoxin levels and changes in production of short chain fatty acids. Role of gut microbiota using prebiotics, probiotics and synbiotics have been evaluated in the management of minimal hepatic encephalopathy (MHE), overt HE and prevention of HE. Many studies have shown efficacy of probiotics in reduction of blood ammonia levels, treatment of MHE and prevention of HE. However these trials have problems like inclusion of small number of patients, short treatment durations, variability in HE/MHE related outcomes utilized and high bias risk, errors of systematic and random types. Systematic reviews also have shown different results with one systematic review showing clinical benefits whereas another concluded that probiotics do not have any role in treatment of MHE or HE. Also practical questions on optimal dose, ideal combination of organisms, and duration of treatment and persistence of benefits on long term follow-up are still to be clarified. At present, there are no recommendations for use of probiotics in patients with HE.

Acute hyperammonemic encephalopathy with features on diffusion-weighted images: Report of two cases

International Nuclear Information System (INIS)

Kim, Ja Young; Yu, In Kyu

2015-01-01

Acute hyperammonemic encephalopathy is a rare toxic encephalopathy caused by accumulated plasma ammonia. A few literatures are reported about MRI findings of acute hyperammonemic encephalopathy. It is different from the well-known chronic hepatic encephalopathy. The clinical symptom and MRI findings of acute hyperammonemic encephalopathy can be reversible with proper treatment. Acute hepatic encephalopathy involves the cingulate cortex, diffuse cerebral cortices, insula, bilateral thalami on diffusion-weighted imaging (DWI), and fluid-attenuated inversion-recovery. Acute hepatic encephalopathy might mimic hypoxic-ischemic encephalopathy because of their similar predominant involving sites. We experienced 2 cases of acute hyperammonemic encephalopathy consecutively. They showed restricted diffusion at the cingulate cortex, cerebral cortices, insula, and bilateral dorsomedial thalami on DWI. One patient underwent acute fulminant hepatitis A, the other patient with underlying chronic liver disease had acute liver failure due to hepatotoxicity of tuberculosis medication. In this report, we presented the characteristic features of DWI in acute hyperammonemic encephalopathy. In addition, we reviewed articles on MRI findings of acute hyperammonemic encephalopathy.

Acute hyperammonemic encephalopathy with features on diffusion-weighted images: Report of two cases

Energy Technology Data Exchange (ETDEWEB)

Kim, Ja Young; Yu, In Kyu [Dept. of Radiology, Eulji University Hospital, Daejeon (Korea, Republic of)

2015-02-15

Acute hyperammonemic encephalopathy is a rare toxic encephalopathy caused by accumulated plasma ammonia. A few literatures are reported about MRI findings of acute hyperammonemic encephalopathy. It is different from the well-known chronic hepatic encephalopathy. The clinical symptom and MRI findings of acute hyperammonemic encephalopathy can be reversible with proper treatment. Acute hepatic encephalopathy involves the cingulate cortex, diffuse cerebral cortices, insula, bilateral thalami on diffusion-weighted imaging (DWI), and fluid-attenuated inversion-recovery. Acute hepatic encephalopathy might mimic hypoxic-ischemic encephalopathy because of their similar predominant involving sites. We experienced 2 cases of acute hyperammonemic encephalopathy consecutively. They showed restricted diffusion at the cingulate cortex, cerebral cortices, insula, and bilateral dorsomedial thalami on DWI. One patient underwent acute fulminant hepatitis A, the other patient with underlying chronic liver disease had acute liver failure due to hepatotoxicity of tuberculosis medication. In this report, we presented the characteristic features of DWI in acute hyperammonemic encephalopathy. In addition, we reviewed articles on MRI findings of acute hyperammonemic encephalopathy.

Benzodiazepine receptor antagonists for acute and chronic hepatic encephalopathy

DEFF Research Database (Denmark)

Als-Nielsen, B; Kjaergard, L L; Gluud, C

2001-01-01

The pathogenesis of hepatic encephalopathy is unknown. It has been suggested that liver failure leads to the accumulation of substances that bind to a receptor-complex in the brain resulting in neural inhibition which may progress to coma. Several trials have assessed benzodiazepine receptor...

The relation of plasma octopamine to hepatic encephalopathy studied with stable isotope dilution technique

International Nuclear Information System (INIS)

Zhang Jianhua

1992-01-01

In order to investigate the relationship between octopamine and hepatic encephalopathy, plasma octopamine content of normal adults and hepatic patients (compensated or de-compensated cirrhotic, patients with encephalopathy) were determined with isotope dilution and GCMS technique, 200 ng of [1, 1-D]-octopamine was added to each sample as internal standard. After the de-proteinized plasma was subjected to cation exchange chromatography, the amine fraction was derivatized with PFP and analyzed with GCMS using the selected ion monitoring technique. The result showed that the level of plasma octopamine was significantly elevated in patients with encephalopathy. Since this method is sensitive and specific, it is readily applicable to the analysis of a few nano grams of octopamine

Cerebral blood flow and liver function in patients with encephalopathy due to acute and chronic liver diseases

DEFF Research Database (Denmark)

Almdal, T; Schroeder, T; Ranek, L

1989-01-01

The purpose of the present investigation was to study changes in cerebral blood flow (CBF) in hepatic encephalopathy, to ascertain whether this was related to the changes in liver function and whether these changes gave any prognostic information. CBF, determined by the intravenous xenon-133 method......, and liver functions, assessed by the prothrombin index, bilirubin concentration, and the galactose elimination capacity, were studied in patients with acute fulminant liver failure and in patients with encephalopathy due to chronic liver diseases--that is, cirrhosis of various etiologies. The CBF range...

Alcoholic liver disease patients’ perspective on coping and physical activity-oriented rehabilitation intervention after hepatic encephalopathy

DEFF Research Database (Denmark)

Mikkelsen, Maria Rudkjær; Hendriksen, Carsten; Schiødt, Frank

2016-01-01

Aim and objective: To identify and describe the impact of a coping and physical activity-oriented rehabilitation intervention on alcoholic liver disease patients after hepatic encephalopathy in terms of their interaction with professionals and relatives. Background: Patients who have experienced...... were conducted with 10 alcoholic liver disease patients who were diagnosed with hepatic encephalopathy and participated in a coping and physical activity-oriented rehabilitation intervention. Richard S. Lazarus's theory of stress and coping inspired the interview guide. Results: The significance...... of a coping and physical activity-oriented rehabilitation intervention on alcoholic liver disease patients’ ability to cope with problems after surviving alcohol-induced hepatic encephalopathy in terms of their interaction with professionals and relatives was characterised by the core category ‘regain control...

Pattern approach to MR imaging in patients with end-stage hepatic failure: a proposal for a new disease entity ''hepatic encephalopathy continuum''

International Nuclear Information System (INIS)

Kim, Ho Kyun; Lee, Hui Joong; Lee, Wonho; Kim, Yong Sun; Jang, Han Won; Byun, Kyung Hwan

2008-01-01

The purpose of this study was to evaluate the clinical features and the characteristics of MR images of patients with end-stage hepatic failure. We reviewed the MR findings and clinical features of 31 consecutive patients (20 men, 11 women=31, mean age 58.7 years) who had been diagnosed with clinical hepatic encephalopathy. Associations between the lesion locations on each MR sequence were analyzed using a binominal test. The clinical and MR findings were compared in relation to the etiology and clinical status. The most frequently involved site, seen as high signal intensity on T2-W images, was the corpus callosum (20 patients), followed by the dentate nucleus (16 patients) and the globus pallidus (13 patients). Significant associations were seen between the pallidus and the crus cerebri, between the crus cerebri and the red nucleus, between the crus cerebri and the dentate nucleus, and between the red nucleus and the dentate nucleus on the T2-W and DW images (P<0.004). The crus cerebri, red nucleus, and dentate nucleus were involved concurrently with the corpus callosum more frequently in hepatic encephalopathy grades 3 and 4. Concurrent involvement of the globus pallidus-crus cerebri-red nucleus-dentate nucleus axis was the main MR pattern in end-stage hepatic encephalopathy, which connected with various areas of the brain. We hypothesize that these overlapping MR features could be regarded as an entity denoted as the ''hepatic encephalopathy continuum''. (orig.)

(/sup 14/C)-L-valine binding to membranes of the frontal cortex in hepatic encephalopathy

Energy Technology Data Exchange (ETDEWEB)

Kienzl, E.; Riederer, P.; Jellinger, K. (Krankenhaus der Stadt Wien-Lainz (Austria). Ludwig Boltzmann Inst. fuer Neurobiologie); Kleinberger, G. (Vienna Univ. (Austria). 1. Medizinische Klinik)

1982-01-01

Serotonin (5-HT) receptors are modulated by L-valine (VAL). For further characterization of this effect a binding assay of (/sup 14/C)-L-VAL has been developed. A brief description of the experimental conditions is given. Moreover, measurement of VAL-binding has been applied to human brain tissue either from controls or hepatic failure. A marked increase of VAL-binding sites with no change in affinity was noted in hepatic coma, while in patients treated with parenteral nutrition plus VAL no such change could be measured. It is concluded that the beneficial therapeutic effects of VAL in hepatic encephalopathy are, at least in part, due to its modulating action on postsynaptic receptor membranes.

An availability of brain magnetic resonance imaging (MRI) in the early diagnosis of latent hepatic encephalopathy

International Nuclear Information System (INIS)

Kuwahara, Noaki; Tanabe, Masako; Fujiwara, Akiko; Minato, Takeshi; Sasaki, Hiromasa; Higashi, Toshihiro; Tsuji, Takao.

1996-01-01

Brain MRI was carried out in patients with chronic liver diseases. No abnormal findings were recognized in patients with chronic viral hepatitis, while 59.2% of cirrhotics showed a symmetrically strong signal in basal ganglia on T1 weighted image in MRI. This finding significantly related with lowered Fischer's ratio of serum amino acid, increased levels of serum phenylalanine, tyrosine and hyaluronic acid, prolonged prothrombin time and decreased platelet counts in the peripheral blood. Overt hepatic encephalopathy was observed in 6 of 34 patients with the strong signal in MRI during follow-up period, while none of patients without that finding developed hepatic encephalopathy. These results have indicated that the strong signal in basal ganglia on MRI appears in cirrhotic patients with severe liver dysfunction, and it is an useful index in the early diagnosis of latent hepatic encephalopathy. An improvement of this MRI finding was not observed by long-term oral administration of branched-chain amino acid. (author)

An availability of brain magnetic resonance imaging (MRI) in the early diagnosis of latent hepatic encephalopathy

Energy Technology Data Exchange (ETDEWEB)

Kuwahara, Noaki; Tanabe, Masako; Fujiwara, Akiko; Minato, Takeshi; Sasaki, Hiromasa [Hiroshima Posts and Telecommunications Hospital (Japan); Higashi, Toshihiro; Tsuji, Takao

1996-03-01

Brain MRI was carried out in patients with chronic liver diseases. No abnormal findings were recognized in patients with chronic viral hepatitis, while 59.2% of cirrhotics showed a symmetrically strong signal in basal ganglia on T1 weighted image in MRI. This finding significantly related with lowered Fischer`s ratio of serum amino acid, increased levels of serum phenylalanine, tyrosine and hyaluronic acid, prolonged prothrombin time and decreased platelet counts in the peripheral blood. Overt hepatic encephalopathy was observed in 6 of 34 patients with the strong signal in MRI during follow-up period, while none of patients without that finding developed hepatic encephalopathy. These results have indicated that the strong signal in basal ganglia on MRI appears in cirrhotic patients with severe liver dysfunction, and it is an useful index in the early diagnosis of latent hepatic encephalopathy. An improvement of this MRI finding was not observed by long-term oral administration of branched-chain amino acid. (author).

Reversal of Transjugular Intrahepatic Portosystemic Shunt (TIPS)-Induced Hepatic Encephalopathy Using a Strictured Self-Expanding Covered Stent

International Nuclear Information System (INIS)

Cox, Mitchell W.; Soltes, George D.; Lin, Peter H.; Bush, Ruth L.; Lumsden, Alan B.

2003-01-01

Hepatic encephalopathy is a known complication following percutaneous transjugular intrahepatic portosystemic shunt (TIPS) placement. We describe herein a simple and effective strategy of TIPS revision by creating an intraluminal stricture within a self-expanding covered stent, which is deployed in the portosystemic shunt to reduce the TIPS blood flow. This technique was successful in reversing a TIPS-induced hepatic encephalopathy in our patient

In vitro adsorption of possible aetiological factors of hepatic encephalopathy

NARCIS (Netherlands)

Chamuleau, R. A.; Schoemaker, L. P.; Smit, E. M.

1979-01-01

Four different adsorbents (activated charcoal, XAD-4, a strong base anion and a strong acid cation-exchange resin) were tested in vitro for their capacity to remove substances that may be important in the development of hepatic encephalopathy. Separate columns packed with one of these adsorbents

Pathophysiological aspects of acute hepatic encephalopathy in the rat

International Nuclear Information System (INIS)

Deutz, N.E.P.

1988-01-01

The aim of the present thesis is to elucidate the pathogenesis of acute hepatic encephalopathy (HE). In order to study acute HE, plasma and brain concentrations were measured of ammonia, aminoacids, lactate and polyamines as well as brain energy rich phosphates. In addition new techniques of brain research were developed and applied. 277 refs.; 29 figs.; 18 tabs

Pattern approach to MR imaging in patients with end-stage hepatic failure: a proposal for a new disease entity 'hepatic encephalopathy continuum'

Energy Technology Data Exchange (ETDEWEB)

Kim, Ho Kyun [Catholic University of Daegu, Department of Radiology, School of Medicine, Daegu (Korea); Lee, Hui Joong; Lee, Wonho; Kim, Yong Sun [Kyungpook National University Hospital, Department of Radiology, Daegu (Korea); Jang, Han Won [Yeungnam University College of Medicine, Department of Radiology, Daegu (Korea); Byun, Kyung Hwan [Pochon CHA University, Department of Radiology, School of Medicine, Kumi CHA Hospital, Kumi (Korea)

2008-08-15

The purpose of this study was to evaluate the clinical features and the characteristics of MR images of patients with end-stage hepatic failure. We reviewed the MR findings and clinical features of 31 consecutive patients (20 men, 11 women=31, mean age 58.7 years) who had been diagnosed with clinical hepatic encephalopathy. Associations between the lesion locations on each MR sequence were analyzed using a binominal test. The clinical and MR findings were compared in relation to the etiology and clinical status. The most frequently involved site, seen as high signal intensity on T2-W images, was the corpus callosum (20 patients), followed by the dentate nucleus (16 patients) and the globus pallidus (13 patients). Significant associations were seen between the pallidus and the crus cerebri, between the crus cerebri and the red nucleus, between the crus cerebri and the dentate nucleus, and between the red nucleus and the dentate nucleus on the T2-W and DW images (P<0.004). The crus cerebri, red nucleus, and dentate nucleus were involved concurrently with the corpus callosum more frequently in hepatic encephalopathy grades 3 and 4. Concurrent involvement of the globus pallidus-crus cerebri-red nucleus-dentate nucleus axis was the main MR pattern in end-stage hepatic encephalopathy, which connected with various areas of the brain. We hypothesize that these overlapping MR features could be regarded as an entity denoted as the 'hepatic encephalopathy continuum'. (orig.)

Detection of carboxyhemoglobin in patients with hepatic encephalopathy due to hepatitis B virus-related cirrhosis.

Science.gov (United States)

Sun, Xiao-yu; Duan, Zhi-jun; Li, Yan-lian; Chang, Qing-shan

2012-11-01

The heme oxygenase/carbon monoxide (HO/CO) system plays an important role in the development of hepatic fibrosis. The level of the HO/CO can be directly obtained by determining the carboxyhemoglobin (COHb) level. The aims of this study were to reveal the significance of COHb in patients with hepatitis B virus-related cirrhosis (HBC) complicated by hepatic encephalopathy (HE), and to further investigate the influence of the HO/CO pathway on the end-stage cirrhosis, hoping to find a reliable indicator to evaluate the course of HBC. According to the diagnostic criteria, 63 HBC inpatients with HE were enrolled in group H. Patients regaining awareness with current therapies were categorized into group P-H. Comparisons were made with a control group (group N) consisting of 20 health volunteers. The levels of COHb, partial pressure of oxygen (PaO2) and oxygen saturation (SaO2) were determined by arterial blood gas analysis method. The incidences of hepatorenal syndrome (HRS), upper gastrointestinal bleeding, esophagogastric varices and spontaneous bacterial peritonitis (SBP) in group H were recorded. COHb levels in different groups were compared, and the correlations of COHb levels with HE grades (I, II, III, and IV), PaO2, SaO2 and hypoxemia were analyzed. The COHb level in group P-H ((1.672 ± 0.761)%) was significantly higher than that in group N ((0.983 ± 0.231)%) (P 0.05) or the occurrence of SBP ((2.960 ± 0.561)% vs. (2.030 ± 1.021)%, P > 0.05). Compared with HE patients with HRS, the level of COHb was significantly higher in HE patients without HRS ((2.502 ± 1.073)% vs. (1.981 ± 1.020)%, P = 0.029). The COHb level had a negative correlation with PaO2 (r = -0.335, P = 0.007) while no statistically significant relationship was found with SaO2 (r = -0.071, P > 0.05). However, when the above two parameters met the diagnostic criteria of hypoxemia, the COHb concentration increased ((2.621 ± 0.880)% vs. (1.910 ± 0.931)%, P = 0.011). COHb is a potential candidate

The why and wherefore of hepatic encephalopathy

Directory of Open Access Journals (Sweden)

Grover VPB

2015-12-01

Full Text Available Vijay PB Grover, Joshua M Tognarelli, Nicolas Massie, Mary ME Crossey, Nicola A Cook, Simon D Taylor-Robinson Liver Unit, Division of Diabetes, Endocrinology and Metabolism, Department of Medicine, Imperial College London, London, UK Abstract: Hepatic encephalopathy is a common neuropsychiatric abnormality, which complicates the course of patients with liver disease. It was probably first described by Hippocrates over 2000 years ago, who said that "those whose madness arises from phlegm are quiet and neither shout nor make a disturbance, while those whose madness arises from bile shout, play tricks and will not keep still, but are always up to some mischief". He was presumably describing the differences between patients with pneumonia and acute liver failure. Despite the fact that the syndrome was probably first recognized thousands of years ago, the exact pathogenesis still remains unclear. Furthermore, a precise definition of the syndrome is lacking, as are definitive methods of diagnosing this condition. It is important as both patients with cirrhosis and the general population with whom they interact may be affected as a consequence. At a minimum, the individual may be affected by impaired quality of life, impaired ability to work, and slowed reaction times, which are relevant to the population at large if affected individuals operate heavy machinery or drive a car. Pathogenic mechanisms, diagnostic tools, and treatment options are discussed. Keywords: hepatic encephalopathy, cirrhosis, ammonia, pathology, treatment, rifaximin, lactulose

Flumazenil does not improve hepatic encephalopathy associated with acute ischemic liver failure in the rabbit

NARCIS (Netherlands)

C.C.D. van der Rijt (Carin); R.J. de Knegt (Robert); S.W. Schalm (Solko); O.T. Terpstra (Onno); K. Mechelse (Karel)

1990-01-01

textabstractThe effect of flumazenil, a benzodiazepine antagonist, on hepatic encephalopathy was studied in rabbits with acute hepatic failure induced by a two-stage liver devascularization procedure. The rabbits were randomized for treatment with 5 mg/kg of flumazenil or the placebo. The drug was

Benzodiazepines and risk for hepatic encephalopathy in patients with cirrhosis and ascites

DEFF Research Database (Denmark)

Grønbæk, Lisbet; Watson, Hugh; Vilstrup, Hendrik

2018-01-01

Background: There is limited evidence to support the belief that benzodiazepines increase cirrhosis patients’ risk of hepatic encephalopathy (HE). Objective: We aimed to examine the association between benzodiazepine use and HE development in cirrhosis patients. Methods: We used data on 865...

Conservative management of severe serotonin syndrome with coma, myoclonus, and crossed-extensor reflex complicated by hepatic encephalopathy.

Science.gov (United States)

Ramachandran, Vignesh; Ding, Belicia; George, Rollin; Novakovic, Matthew

2018-01-01

Serotonin syndrome (SS) is an underrecognized and potentially fatal disorder that occurs secondary to combinational use or overdose of a single serotonergic medication. The presentation may be complicated by hepatic encephalopathy in cirrhotic patients, which may also affect metabolism of these serotonergic agents. The authors report a rare case of severe SS complicated by hepatic encephalopathy secondary to cirrhosis in a 52-year-old woman after an increase in her home dosage of fluoxetine and addition of other psychiatric medications.

The Effects of Probiotics and Symbiotics on Risk Factors for Hepatic Encephalopathy: A Systematic Review.

Science.gov (United States)

Viramontes Hörner, Daniela; Avery, Amanda; Stow, Ruth

2017-04-01

Alterations in the levels of intestinal microbiota, endotoxemia, and inflammation are novel areas of interest in the pathogenesis of hepatic encephalopathy (HE). Probiotics and symbiotics are a promising treatment option for HE due to possible beneficial effects in modulating gut microflora and might be better tolerated and more cost-effective than the traditional treatment with lactulose, rifaximin or L-ornithine-L-aspartate. A systematic search of the electronic databases PubMed, ISI Web of Science, EMBASE, and Cochrane Library was conducted for randomized controlled clinical trials in adult patients with cirrhosis, evaluating the effect of probiotics and symbiotics in changes on intestinal microflora, reduction of endotoxemia, inflammation, and ammonia, reversal of minimal hepatic encephalopathy (MHE), prevention of overt hepatic encephalopathy (OHE), and improvement of quality of life. Nineteen trials met the inclusion criteria. Probiotics and symbiotics increased beneficial microflora and decreased pathogenic bacteria and endotoxemia compared with placebo/no treatment, but no effect was observed on inflammation. Probiotics significantly reversed MHE [risk ratio, 1.53; 95% confidence interval (CI): 1.14, 2.05; P=0.005] and reduced OHE development (risk ratio, 0.62; 95% CI: 0.48, 0.80; P=0.0002) compared with placebo/no treatment. Symbiotics significantly decreased ammonia levels compared with placebo (15.24; 95% CI: -26.01, -4.47; P=0.006). Probiotics did not show any additional benefit on reversal of MHE and prevention of OHE development when compared with lactulose, rifaximin, and L-ornithine-L-aspartate. Only 5 trials considered tolerance with minimal side effects reported. Although further research is warranted, probiotics and symbiotics should be considered as an alternative therapy for the treatment and management of HE given the results reported in this systematic review.

Minimal hepatic encephalopathy in patients with cirrhosis by measuring liver stiffness and hepatic venous pressure gradient.

Science.gov (United States)

Sharma, Praveen; Kumar, Ashish

2012-01-01

Transient elastography (TE) of liver and hepatic venous pressure gradient (HVPG) allows accurate prediction of cirrhosis and its complications in patients with chronic liver disease. There is no study on prediction of minimal hepatic encephalopathy (MHE) using TE and HVPG in patients with cirrhosis. Consecutive cirrhotic patients who never had an episode of hepatic encephalopathy (HE) were enrolled. All patients were assessed by psychometry (number connection test (NCT-A and B), digit symbol test (DST), serial dot test (SDT), line tracing test (LTT)), critical flicker frequency test (CFF), TE by FibroScan and HVPG. MHE was diagnosed if there were two or more abnormal psychometry tests (± 2 SD controls). 150 patients with cirrhosis who underwent HVPG were screened; 91 patients (61%, age 44.0 ± 11.4 years, M:F:75:16, Child's A:B:C 18:54:19) met the inclusion criteria. Fifty three (58%) patients had MHE (Child A (7/18, 39%), Child B (32/54, 59%) and Child C (14/19, 74%)). There was no significant difference between alanine aminotranferease (ALT), aspartate aminotransferase (AST) and total bilirubin level in patients with MHE versus non MHE. Patients with MHE had significantly lower CFF than non MHE patients (38.4 ± 3.0 vs. 40.2 ± 2.2 Hz, P = 0.002). TE and HVPG in patients with MHE did not significantly differ from patients with no MHE (30.9 ± 17.2 vs. 29.8 ± 18.2 KPas, P = 0.78; and 13.6 ± 2.7 vs. 13.6 ± 3.2 mmHg, P = 0.90, respectively).There was significant correlation of TE with Child's score (0.25, P = 0.01), MELD (0.40, P = 0.001) and HVPG (0.72, P = 0.001) while no correlation with psychometric tests, CFF and MHE. TE by FibroScan and HVPG cannot predict minimal hepatic encephalopathy in patients with cirrhosis.

Effects of probiotic therapy on hepatic encephalopathy in patients with liver cirrhosis: an updated meta-analysis of six randomized controlled trials.

Science.gov (United States)

Xu, Jun; Ma, Rui; Chen, Li-Feng; Zhao, Li-Jun; Chen, Kan; Zhang, Ren-Bing

2014-08-01

Liver cirrhotic patients with hepatic encephalopathy have poor prognosis. Probiotics alter the intestinal microbiota and reduce the production of ammonia. We conducted a meta-analysis about the role of probiotics on liver cirrhotic patients with hepatic encephalopathy. We collected the relevant literatures up to February 21, 2014 from databases of PubMed, EMBASE and the Cochrane Central Register of Controlled Trials. A statistical analysis was conducted by RevMan 5.2 and STATA 12.0 software. Six randomized controlled trials involving 496 liver cirrhotic patients were included. The results showed that probiotic therapy significantly reduced the development of overt hepatic encephalopathy (OR [95% CI]: 0.42 [0.26, 0.70], P=0.0007). However, probiotics did not affect mortality, levels of serum ammonia and constipation (mortality: OR [95% CI]: 0.73 [0.38, 1.41], P=0.35; serum ammonia: WMD [95% CI]: -3.67 [-15.71, 8.37], P=0.55; constipation: OR [95% CI]: 0.67 [0.29, 1.56], P=0.35). Probiotics decrease overt hepatic encephalopathy in patients with liver cirrhosis.

Hepatic encephalopathy before and neurological complications after liver transplantation have no impact on the employment status 1 year after transplantation

OpenAIRE

Pflugrad, Henning; Tryc, Anita B; Goldbecker, Annemarie; Strassburg, Christian P; Barg-Hock, Hannelore; Klempnauer, J?rgen; Weissenborn, Karin

2017-01-01

AIM To investigate the impact of hepatic encephalopathy before orthotopic liver transplantation (OLT) and neurological complications after OLT on employment after OLT. METHODS One hundred and fourteen patients with chronic liver disease aged 18-60 years underwent neurological examination to identify neurological complications, neuropsychological tests comprising the PSE-Syndrome-Test yielding the psychometric hepatic encephalopathy score, the critical flicker frequency and the Repeatable Batt...

A Current Review of the Diagnostic and Treatment Strategies of Hepatic Encephalopathy

Directory of Open Access Journals (Sweden)

Z. Poh

2012-01-01

Full Text Available Hepatic encephalopathy (HE is a serious and potentially fatal complication in patients with cirrhotic liver disease. It is a spectrum ranging from minimal hepatic encephalopathy (MHE without recognizable clinical symptoms or signs, to overt HE with risk of cerebral edema and death. HE results in diminished quality of life and survival. The broad range of neuropsychiatric manifestations reflects the range of pathophysiological mechanisms and impairment in neurotransmission that are purported to cause HE including hyperammonemia, astrocyte swelling, intra-astrocytic glutamine, upregulation of 18-kDa translocator protein (TSPO (formerly known as peripheral benzodiazepine receptor or PBTR, and manganese. There is a myriad of diagnostic tools including simple bedside clinical assessment, and more complex neuropsychological batteries and neurophysiological tests available today. Current treatment strategies are directed at reducing ammonia, with newer agents showing some early promise. This paper describes the pathophysiology of the disease and summarises current diagnostic and treatment therapies available.

Nonabsorbable disaccharides for hepatic encephalopathy

DEFF Research Database (Denmark)

Gluud, Lise Lotte; Vilstrup, Hendrik; Morgan, Marsha Y

2016-01-01

UNLABELLED: Nonabsorbable disaccharides (NADs) have been used to treat hepatic encephalopathy (HE) since 1966. However, a Cochrane Review, published in 2004, found insufficient evidence to recommend their use in this context. This updated systematic review evaluates the effects of the NADs...... primary/secondary prevention. Random-effects meta-analyses showed that, compared to placebo/no intervention, NADs had a beneficial effect on HE (relative risk [RR] = 0.63, 95% confidence interval [CI] 0.53-0.74, number needed to treat [NNT] = 4) and serious liver-related adverse events such as liver...... with minimal HE. Meta-analyses of the prevention randomized controlled trials showed that NADs prevented the development of HE (RR = 0.47, 95% CI 0.33-0.68, NNT = 6), the risk of developing serious liver-related adverse events (RR = 0.48, 95% CI 0.33-0.70, NNT = 6), and reduced mortality (RR = 0.63, 95% CI 0...

Prognostic Assessment in Patients with Hepatic Encephalopathy

Directory of Open Access Journals (Sweden)

Rita García-Martínez

2011-01-01

Full Text Available Hepatic encephalopathy (HE is a common complication of liver failure that is associated with poor prognosis. However, the prognosis is not uniform and depends on the underlying liver disease. Acute liver failure is an uncommon cause of HE that carries bad prognosis but is potentially reversible. There are several prognostic systems that have been specifically developed for selecting patients for liver transplantation. In patients with cirrhosis the prognosis of the episode of HE is usually dictated by the underlying precipitating factor. Acute-on-chronic liver failure is the most severe form of decompensation of cirrhosis, the prognosis depends on the number of associated organ failures. Patients with cirrhosis that have experienced an episode of HE should be considered candidates for liver transplant. The selection depends on the underlying liver function assessed by the Model for End-stage Liver Disease (MELD index. There is a subgroup that exhibits low MELD and recurrent HE, usually due to the coexistence of large portosystemic shunts. The recurrence of HE is more common in patients that develop progressive deterioration of liver function and hyponatremia. The bouts of HE may cause sequels that have been shown to persist after liver transplant.

NUTRITIVE THERAPY OF HEPATIC ENCEPHALOPATHY AS A COMPLICATION OF LIVER CIRRHOSIS

Directory of Open Access Journals (Sweden)

Bojana Marković-Živković

2012-06-01

Full Text Available Hepatic encephalopathy is a complication of liver cirrhosis and is defined as a neuropsychiatric disease, with a reversibile character. Besides classical ways of therapy, an increasing importance is attached to nutritional therapy that is an effective prevention of the onset and leads to an ease of symptoms in hepathic encephalopathy that already exists. After the patient's nutritional status evaluation, the prescription of diet that includes adequate protein, calories and vitamins is assessed. The greatest importance is attached to the zinc intake as well as branched chain amino acids (BCAA therapy supplementation. It is believed that further development of science in terms of nutrigenomics and nutrigenetics will give detailed guidance on further developments since the possibility of clinical investigation in these patients is limited.

The burden of minimal hepatic encephalopathy: from diagnosis to therapeutic strategies

Science.gov (United States)

Ridola, Lorenzo; Cardinale, Vincenzo; Riggio, Oliviero

2018-01-01

Minimal hepatic encephalopathy (MHE) is the mildest form of hepatic encephalopathy (HE). It affects the performance of psychometric tests focused on attention, working memory, psychomotor speed, and visuospatial ability, as well as electrophysiological and other functional brain measures. MHE is a frequent complication of liver disease, affecting up to 80% of tested patients. By being related to falls, an impairment in fitness to drive and the development of overt HE, MHE severely affects the lives of patients and caregivers by altering their quality of life and their socioeconomic status. MHE is detected in clinically asymptomatic patients using appropriate psychometric tests and neurophysiological methods that highlight neuropsychological alterations, such as video-spatial orientation deficits, attention disorders, memory, reaction times, electroencephalogram slowing, prolongation of latency-evoked cognitive potentials, and reduction in the critical flicker frequency. Several treatments have been proposed for MHE treatment, including non-absorbable disaccharides, poorly absorbable antibiotics such as rifaximin, probiotics and branched-chain amino acids. However, because of the multiple diagnosis methods, the various endpoints of treatment trials and the variety of agents used in trials, the treatment of MHE is not currently recommended as routine, but only on a case-by-case basis. PMID:29507462

Probiotics are helpful in hepatic encephalopathy: a meta-analysis of randomized trials.

Science.gov (United States)

Saab, Sammy; Suraweera, Duminda; Au, Jennifer; Saab, Elena G; Alper, Tori S; Tong, Myron J

2016-07-01

Hepatic encephalopathy (HE) is a major complication of cirrhosis and is associated with decreased survival and increased health care utilization. The aim of this study was to evaluate the efficacy of probiotics in the management minimal hepatic encephalopathy HE (MHE) and overt HE (OHE) in comparison to no treatment/placebo and lactulose. The main outcomes measured were mortality, improvement in MHE, progression to OHE in patients with MHE and hospitalization. We calculated odds ratios (OR) with 95% confidence intervals (CI). Study heterogeneity was assessed using the I(2) statistic. Fourteen studies totalling 1152 patients were included in the analysis. The use of probiotics had no impact on the overall mortality when compared to either lactulose (OR: 1.07, 95% CI: 0.47-2.44, P = 0.88) or no treatment/placebo (OR: 0.69, 95% CI: 0.42-1.14, P = 0.15). When probiotics was compared to no treatment/placebo, it was associated with a significant improvement in MHE (OR: 3.91, 95% CI: 2.25-6.80, P probiotics did not show a significant difference in improvement of MHE (OR: 0.81, 95% CI: 0.52-1.27, P = 0.35), hospitalization rates (OR: 1.02, 95% CI: 0.52-1.99, P = 0.96) or progression to overt hepatic encephalopathy (OR: 1.24, 95% CI 0.73-2.10, P = 0.42). Overall the use of probiotics was more effective in decreasing hospitalization rates, improving MHE and preventing progression to OHE in patients with underlying MHE than placebo, but similar to that seen with lactulose. The use of probiotics did not affect mortality rates. © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Interplay between glutamatergic and GABAergic neurotransmission alterations in cognitive and motor impairment in minimal hepatic encephalopathy.

Science.gov (United States)

Llansola, Marta; Montoliu, Carmina; Agusti, Ana; Hernandez-Rabaza, Vicente; Cabrera-Pastor, Andrea; Gomez-Gimenez, Belen; Malaguarnera, Michele; Dadsetan, Sherry; Belghiti, Majedeline; Garcia-Garcia, Raquel; Balzano, Tiziano; Taoro, Lucas; Felipo, Vicente

2015-09-01

The cognitive and motor alterations in hepatic encephalopathy (HE) are the final result of altered neurotransmission and communication between neurons in neuronal networks and circuits. Different neurotransmitter systems cooperate to modulate cognitive and motor function, with a main role for glutamatergic and GABAergic neurotransmission in different brain areas and neuronal circuits. There is an interplay between glutamatergic and GABAergic neurotransmission alterations in cognitive and motor impairment in HE. This interplay may occur: (a) in different brain areas involved in specific neuronal circuits; (b) in the same brain area through cross-modulation of glutamatergic and GABAergic neurotransmission. We will summarize some examples of the (1) interplay between glutamatergic and GABAergic neurotransmission alterations in different areas in the basal ganglia-thalamus-cortex circuit in the motor alterations in minimal hepatic encephalopathy (MHE); (2) interplay between glutamatergic and GABAergic neurotransmission alterations in cerebellum in the impairment of cognitive function in MHE through altered function of the glutamate-nitric oxide-cGMP pathway. We will also comment the therapeutic implications of the above studies and the utility of modulators of glutamate and GABA receptors to restore cognitive and motor function in rats with hyperammonemia and hepatic encephalopathy. Copyright © 2014 Elsevier Ltd. All rights reserved.

Cannabidiol improves brain and liver function in a fulminant hepatic failure-induced model of hepatic encephalopathy in mice.

Science.gov (United States)

Avraham, Y; Grigoriadis, Nc; Poutahidis, T; Vorobiev, L; Magen, I; Ilan, Y; Mechoulam, R; Berry, Em

2011-04-01

Hepatic encephalopathy is a neuropsychiatric disorder of complex pathogenesis caused by acute or chronic liver failure. We investigated the effects of cannabidiol, a non-psychoactive constituent of Cannabis sativa with anti-inflammatory properties that activates the 5-hydroxytryptamine receptor 5-HT(1A) , on brain and liver functions in a model of hepatic encephalopathy associated with fulminant hepatic failure induced in mice by thioacetamide. Female Sabra mice were injected with either saline or thioacetamide and were treated with either vehicle or cannabidiol. Neurological and motor functions were evaluated 2 and 3 days, respectively, after induction of hepatic failure, after which brains and livers were removed for histopathological analysis and blood was drawn for analysis of plasma liver enzymes. In a separate group of animals, cognitive function was tested after 8 days and brain 5-HT levels were measured 12 days after induction of hepatic failure. Neurological and cognitive functions were severely impaired in thioacetamide-treated mice and were restored by cannabidiol. Similarly, decreased motor activity in thioacetamide-treated mice was partially restored by cannabidiol. Increased plasma levels of ammonia, bilirubin and liver enzymes, as well as enhanced 5-HT levels in thioacetamide-treated mice were normalized following cannabidiol administration. Likewise, astrogliosis in the brains of thioacetamide-treated mice was moderated after cannabidiol treatment. Cannabidiol restores liver function, normalizes 5-HT levels and improves brain pathology in accordance with normalization of brain function. Therefore, the effects of cannabidiol may result from a combination of its actions in the liver and brain. © 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.

Endovascular Management of Refractory Hepatic Encephalopathy Complication of Transjugular Intrahepatic Portosystemic Shunt (TIPS): Comprehensive Review and Clinical Practice Algorithm

International Nuclear Information System (INIS)

Pereira, Keith; Carrion, Andres F.; Salsamendi, Jason; Doshi, Mehul; Baker, Reginald; Kably, Issam

2016-01-01

Transjugular intrahepatic portosystemic shunt (TIPS) has evolved as an effective intervention for treatment of complications of portal hypertension. The use of polytetrafluoroethylene-covered stents have improved the patency of the shunts and diminished the incidence of TIPS dysfunction. However, TIPS-related refractory hepatic encephalopathy (rHE) poses a significant challenge. Approximately 3–7 % of patients with TIPS develop rHE. Refractory hepatic encephalopathy is defined as a recurrent or persistent encephalopathy despite appropriate medical treatment. Hepatic encephalopathy can be an extremely debilitating complication that profoundly affects quality of life. The approach to management of patients with rHE is complex and typically requires collaboration between different specialties. Liver transplantation is the ultimate treatment for rHE; however, the ongoing shortage of organ donation markedly limits this treatment option. Alternative therapies such as shunt occlusion or reduction can control symptoms and serve as a ‘bridge’ therapy to liver transplantation. Therefore, interventional radiologists play a key role in the management of these patients by offering a variety of endovascular techniques. The purpose of this review is to highlight some of these endovascular techniques and to develop a therapeutic algorithm that can be applied in clinical practice for the management of rHE

Endovascular Management of Refractory Hepatic Encephalopathy Complication of Transjugular Intrahepatic Portosystemic Shunt (TIPS): Comprehensive Review and Clinical Practice Algorithm

Energy Technology Data Exchange (ETDEWEB)

Pereira, Keith, E-mail: keithjppereira@gmail.com [Jackson Memorial Hospital/University of Miami Hospital, Department of Interventional Radiology (United States); Carrion, Andres F., E-mail: andres.carrionmonsa@jhsmiami.org [Jackson Memorial Hospital/University of Miami Hospital, Department of Hepatology (United States); Salsamendi, Jason, E-mail: JSalsamendi@med.miami.edu; Doshi, Mehul, E-mail: MDoshi@med.miami.edu; Baker, Reginald, E-mail: RBaker@med.miami.edu; Kably, Issam, E-mail: ikably@med.miami.edu [Jackson Memorial Hospital/University of Miami Hospital, Department of Interventional Radiology (United States)

2016-02-15

Transjugular intrahepatic portosystemic shunt (TIPS) has evolved as an effective intervention for treatment of complications of portal hypertension. The use of polytetrafluoroethylene-covered stents have improved the patency of the shunts and diminished the incidence of TIPS dysfunction. However, TIPS-related refractory hepatic encephalopathy (rHE) poses a significant challenge. Approximately 3–7 % of patients with TIPS develop rHE. Refractory hepatic encephalopathy is defined as a recurrent or persistent encephalopathy despite appropriate medical treatment. Hepatic encephalopathy can be an extremely debilitating complication that profoundly affects quality of life. The approach to management of patients with rHE is complex and typically requires collaboration between different specialties. Liver transplantation is the ultimate treatment for rHE; however, the ongoing shortage of organ donation markedly limits this treatment option. Alternative therapies such as shunt occlusion or reduction can control symptoms and serve as a ‘bridge’ therapy to liver transplantation. Therefore, interventional radiologists play a key role in the management of these patients by offering a variety of endovascular techniques. The purpose of this review is to highlight some of these endovascular techniques and to develop a therapeutic algorithm that can be applied in clinical practice for the management of rHE.

Non-absorbable disaccharides versus placebo/no intervention and lactulose versus lactitol for the prevention and treatment of hepatic encephalopathy in people with cirrhosis

DEFF Research Database (Denmark)

Gluud, Lise Lotte; Vilstrup, Hendrik; Morgan, Marsha Y

2016-01-01

BACKGROUND: Non-absorbable disaccharides (lactulose and lactitol) are recommended as first-line treatment for hepatic encephalopathy. The previous (second) version of this review included 10 randomised clinical trials (RCTs) evaluating non-absorbable disaccharides versus placebo/no intervention...... and eight RCTs evaluating lactulose versus lactitol for people with cirrhosis and hepatic encephalopathy. The review found no evidence to either support or refute the use of the non-absorbable disaccharides and no differences between lactulose versus lactitol. OBJECTIVES: To assess the beneficial...... and harmful effects of i) non-absorbable disaccharides versus placebo/no intervention and ii) lactulose versus lactitol in people with cirrhosis and hepatic encephalopathy. SEARCH METHODS: We carried out electronic searches of the Cochrane Hepato-Biliary Group Controlled Trials Register, the Cochrane Central...

Diagnosis of hepatic encephalopathy with magentic resonance imaging

International Nuclear Information System (INIS)

Inoue, Etsuo; Narumi, Yoshifumi; Kadota, Tsuyoshi; Fujita, Makoto; Kuriyama, Keiko; Kuroda, Chikazumi

1993-01-01

Cranial magnetic resonance (MR) images were examined in 16 patients with liver cirrhosis. The findings of MR imaging were correlated with portal-systemic collateral vessel shown on angiograms. In 9 of 16 patients, basal ganglia was hyperintense compared with white matter on T1-weighted images. These 9 patients had portal-systemic collateral vessel 10 mm or more in diameter that was suppied by superior mesenteric vein (SMV), and 4 of the 9 patients had portal-systemic encephalopathy on angiograms. In the remaining 7 patients, no hyperintense lesions were seen in basal ganglia relative to white matter on T1-weighted images; angiography revealed that 2 patients had portal-systemic collateral vessel that was supplied by SMV but was 5 mm or less in diameter, 3 had bood supplies from splenic vein, and 2 had no collateral vessel. There was no change in signal intensity on T2-weighted images. In conclusion, a large portal-systemic collateral vessel supplied by SMV may be shown as a high intensity lesion in basal ganglia, thus making it possible to diagnose hepatic encephalopathy even if there was no psychoneurologic symptoms or signs. (N.K.)

Being an informal caregiver for a relative with liver cirrhosis and overt hepatic encephalopathy: a phenomenological study.

Science.gov (United States)

Künzler-Heule, Patrizia; Beckmann, Sonja; Mahrer-Imhof, Romy; Semela, David; Händler-Schuster, Daniela

2016-09-01

To explore the experiences of being an informal caregiver for a relative with liver cirrhosis and overt hepatic encephalopathy. Overt hepatic encephalopathy is a common complication in patients with liver cirrhosis. It is associated with decreased quality of life for patients, and presents a major burden for caregivers. The involvement of informal caregivers in medical care is recommended, but it has not been clearly described. An understanding of the experience of caregivers is needed to improve the support provided to them by healthcare professionals. A qualitative, interpretative, phenomenological approach was used. Twelve informal caregivers participated in qualitative interviews. The analysis followed the six steps of the interpretative phenomenological approach. Caregivers' experiences were described using five themes: (1) feeling overwhelmed by their loved one having unexplainable symptoms and behaviours; (2) learning that this and previous experiences were complications of liver disease; (3) becoming aware of the symptoms of hepatic encephalopathy; (4) having feelings of being tied down and (5) experiencing and overcoming obstacles in working with healthcare professionals. This study provides insight into caregivers' experiences and the consequences for their lives. The first occurrence of symptoms was a shock, but receiving the diagnosis was seen as an important step in understanding and learning. Caregivers provide daily assessments of their relatives' conditions, and they feel responsible for medication management. Over time, the caregivers impressively showed how they were able to incorporate their personal experiences into caregiving and to accept more accountability in managing the disease. Nurses should acknowledge caregivers as experts in caring for their loved ones. Nurses can assist caregivers in managing an episode of hepatic encephalopathy and can provide individualised interventions to ease the future burden. © 2016 John Wiley & Sons Ltd.

Hepatic Encephalopathy

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Full Text Available ... A Hepatitis B Hepatitis C Intrahepatic Cholestasis of Pregnancy (ICP) Jaundice In Newborns Diseases of the Liver ... A Hepatitis B Hepatitis C Intrahepatic Cholestasis of Pregnancy (ICP) Jaundice In Newborns Diseases of the Liver ...

Encephalopathy and liver transplantation.

Science.gov (United States)

Chavarria, Laia; Cordoba, Juan

2013-06-01

Liver transplantation (LT) candidates experience frequently episodic or persistent hepatic encephalopathy. In addition, these patients can exhibit neurological comorbidities that contribute to cognitive impairment in the pre-transplant period. Assessment of the respective contribution of hepatic encephalopathy or comorbidities in the cognitive manifestations is critical to estimate the neurological benefits of restoring liver function. Magnetic resonance imaging and spectroscopy are useful to assess the impact of liver failure or comorbidities. This assessment is critical to decide liver transplant in difficult cases. In the early postoperative period, LT is commonly complicated by a confusional syndrome. The possible role of persisting hepatic encephalopathy in its development has not been clearly established. The origin is usually considered multifactorial and relates to complications following LT, such as infections, rejection, primary liver dysfunction, immunosuppressors, etc.… The diagnosis and treatment is based in the recognition of comorbidities and optimal care of metabolic disturbances. Several studies have demonstrated recovery of cognitive function after LT in patients that have exhibited hepatic encephalopathy. However, some deficits may persist specifically among patients with persistent HE. Other factors present before LT that contribute to a worse neuropsychological outcome after LT are diabetes mellitus and alcohol consumption. Long-term after LT, cognitive function may worsen in relation to vascular risk factors.

Effects of common chronic medical conditions on psychometric tests used to diagnose minimal hepatic encephalopathy

DEFF Research Database (Denmark)

Lauridsen, M M; Poulsen, L; Rasmussen, C K

2016-01-01

Many chronic medical conditions are accompanied by cognitive disturbances but these have only to a very limited extent been psychometrically quantified. An exception is liver cirrhosis where hepatic encephalopathy is an inherent risk and mild forms are diagnosed by psychometric tests. The preferred...... diagnostic test battery in cirrhosis is often the Continuous Reaction Time (CRT) and the Portosystemic Encephalopathy (PSE) tests but the effect on these of other medical conditions is not known. We aimed to examine the effects of common chronic (non-cirrhosis) medical conditions on the CRT and PSE tests. We...

Approach to Clinical Syndrome of Jaundice and Encephalopathy in Tropics

Science.gov (United States)

Anand, Anil C.; Garg, Hitendra K.

2015-01-01

A large number of patients present with jaundice and encephalopathy in tropical country like India and acute liver failure is the usual cause. Clinical presentation like ALF is also a complication of many tropical infections, and these conditions may mimic ALF but may have subtle differences from ALF. Moreover, what hepatologists see as acute liver failure in tropics is different from what is commonly described in Western Textbooks. Paracetamol overdose, which is possibly the commonest cause of ALF in UK and USA, is hardly ever seen in India. Most common etiology here is viral hepatitis (hepatitis E > hepatitis B> hepatitis A). Apart from ALF, one may also come across subacute hepatic failure (SAHF) as well as acute-on-chronic liver failure (ACLF) due to viral hepatitis. Interestingly, a host of other conditions can mimic ALF because clinical presentation in these conditions can be dominated by jaundice and encephalopathy. Malarial hepatopathy is possibly the best-known condition out of these and is not an uncommon manifestation of severe malaria. A similar presentation can also be seen in other common infections in tropics such as dengue fever, typhoid fever, leptospirosis, scrub typhus, amoebic liver abscesses, tuberculosis and other bacterial and fungal infections with or without human immunodeficiency virus (HIV) related disease. In many of these conditions, liver failure may not be underlying pathophysiology. Some pregnancy related liver diseases could also present with jaundice and encephalopathy. This review summarizes the commonly seen presentations in tropical country like India, where jaundice and encephalopathy dominate the clinical picture. PMID:26041951

Rare and unusual ... or are they? Less commonly diagnosed encephalopathies associated with systemic disease.

Science.gov (United States)

Weathers, Allison L; Lewis, Steven L

2009-04-01

Encephalopathy due to hepatic or renal failure, electrolyte disturbances, or the administration of benzodiazepines and narcotics is commonly encountered, well reviewed in the literature, and, therefore, not usually missed. This article focuses on encephalopathies that were previously well described but may be overlooked by modern clinicians, as well as those that are still taught in the classroom but seldom thought of in practice. Due to the presumed relative rarity of these cases and emphasis on the well-memorized "classic" clinical presentations, these often treatable, and perhaps not so rare, encephalopathies due to systemic medical illness may go undiagnosed and untreated. Pancreatic encephalopathy, Wernicke's encephalopathy, and pellagra encephalopathy are reviewed in detail; cefepime and ifosfamide encephalopathies are discussed as examples of specific medication-induced encephalopathies. Septic encephalopathy, central pontine myelinolysis, and fat embolism syndrome are briefly reviewed. The encephalopathies reviewed have the potential for devastating neurological consequences if recognition and, therefore, treatment are delayed. Clinical improvement for many of these syndromes depends on prompt intervention. This article highlights some representative examples of less-commonly diagnosed metabolic and toxic encephalopathies.

Leucine metabolism in patients with Hepatic Encephalopathy

International Nuclear Information System (INIS)

McGhee, A.S.; Kassouny, M.E.; Matthews, D.E.; Millikan, W.

1986-01-01

A primed continuous infusion of [ 15 N, 1- 13 C]leucine was used to determine whether increased oxidation and/or protein synthesis of leucine occurs in patients with cirrhosis. Five controls and patients were equilibrated on a metabolic balance diet [0.6 g protein per kg ideal body weight (IBW)]. An additional four patients were equilibrated in the same manner with the same type of diet with a protein level of 0.75 g per kg IBW. Plasma leucine and breath CO 2 enrichments were measured by mass spectrometry. Protein synthesis and leucine metabolism were identical in controls and patients when both were fed a diet with 0.6 g protein/kg IBW. Results indicate that systemic derangements of leucine metabolism are not the cause of Hepatic Encephalopathy

Effects of a branched-chain amino acid-enriched diet on chronic hepatic encephalopathy in dogs

NARCIS (Netherlands)

Meyer, H. P.; Chamuleau, R. A.; Legemate, D. A.; Mol, J. A.; Rothuizen, J.

1999-01-01

A decreased ratio of branched-chain amino acids (BCAA) to aromatic amino acids (AAA) is considered an important pathogenetic factor in hepatic encephalopathy (HE). A relationship between the deranged BCAA/AAA ratio and dopaminergic dysfunction through the formation of "false" neurotransmitters has

Diagnosis of hepatic encephalopathy with magentic resonance imaging; With special reference to portal system encephalopathy

Energy Technology Data Exchange (ETDEWEB)

Inoue, Etsuo; Narumi, Yoshifumi; Kadota, Tsuyoshi; Fujita, Makoto; Kuriyama, Keiko; Kuroda, Chikazumi (Osaka Prefectural Center for Adult Diseases (Japan))

1993-01-01

Cranial magnetic resonance (MR) images were examined in 16 patients with liver cirrhosis. The findings of MR imaging were correlated with portal-systemic collateral vessel shown on angiograms. In 9 of 16 patients, basal ganglia was hyperintense compared with white matter on T1-weighted images. These 9 patients had portal-systemic collateral vessel 10 mm or more in diameter that was suppied by superior mesenteric vein (SMV), and 4 of the 9 patients had portal-systemic encephalopathy on angiograms. In the remaining 7 patients, no hyperintense lesions were seen in basal ganglia relative to white matter on T1-weighted images; angiography revealed that 2 patients had portal-systemic collateral vessel that was supplied by SMV but was 5 mm or less in diameter, 3 had bood supplies from splenic vein, and 2 had no collateral vessel. There was no change in signal intensity on T2-weighted images. In conclusion, a large portal-systemic collateral vessel supplied by SMV may be shown as a high intensity lesion in basal ganglia, thus making it possible to diagnose hepatic encephalopathy even if there was no psychoneurologic symptoms or signs. (N.K.).

Frequency of helicobacter pylori antibodies in porto-systemic encephalopathy,

International Nuclear Information System (INIS)

Sethar, G.H.; Ahmed, R.; Afsar, S.; Zuberi, B.F.

2004-01-01

Objective: To study the frequency of Helicobacter pylori antibodies in patients presenting with porto-systemic encephalopathy due to liver disease. Patients and Methods: During the study period, seventy-six patients of porto-systemic encephalopathy due to liver diseases was selected. These subjects were evaluated for hepatic encephalopathy grade, modified Child-Pugh classification and were managed according to the standard practices. These patients were evaluated for Helicobacter (H. pylori) antibody status by ELlSA (Abbott Laboratories) method. Results: Out of 76 patients studied and tested for H. pylori antibodies, 48(63.2%) were males and 28(36.8%) were females with age ranging between 17 and 85 years. Out of 76 patients who presented with porto-systemic encephalopathy, 59(77.6%) had a positive H. pylori antibody test. Thirty-five of these were males and 24 were females. A significant number of patients who presented with higher grade of encephalopathy were H. pylori antibody positive (p<0.001). Conclusion: In this study, frequency of H. pylori antibodies was significantly high in patients of porto-systematic encephalopathy. (author)

Oxidative metabolism of astrocytes is not reduced in hepatic encephalopathy

DEFF Research Database (Denmark)

Iversen, Peter; Mouridsen, Kim; Hansen, Mikkel B

2014-01-01

In patients with impaired liver function and hepatic encephalopathy (HE), consistent elevations of blood ammonia concentration suggest a crucial role in the pathogenesis of HE. Ammonia and acetate are metabolized in brain both primarily in astrocytes. Here, we used dynamic [(11)C]acetate PET...... of the brain to measure the contribution of astrocytes to the previously observed reduction of brain oxidative metabolism in patients with liver cirrhosis and HE, compared to patients with cirrhosis without HE, and to healthy subjects. We used a new kinetic model to estimate uptake from blood to astrocytes...

Bacterial infections and hepatic encephalopathy in liver cirrhosis-prophylaxis and treatment.

Science.gov (United States)

Piotrowski, Damian; Boroń-Kaczmarska, Anna

2017-09-01

Infections are common among patients with liver cirrhosis. They occur more often in cirrhotic patient groups than in the general population and result in higher mortality. One reason for this phenomenon is bacterial translocation from the intestinal lumen that occurs as a consequence of intestinal bacterial overgrowth, increased permeability and decreased motility. The most common infections in cirrhotic patients are spontaneous bacterial peritonitis and urinary tract infections, followed by pneumonia, skin and soft tissue infections. Intestinal bacterial overgrowth is also responsible for hyperammonemia, which leads to hepatic encephalopathy. All of these complications make this group of patients at high risk for mortality. The role of antibiotics in liver cirrhosis is to treat and in some cases to prevent the development of infectious complications. Based on our current knowledge, antibiotic prophylaxis should be administered to patients with gastrointestinal hemorrhage, low ascitic fluid protein concentration combined with liver or renal failure, and spontaneous bacterial peritonitis as a secondary prophylaxis, as well as after hepatic encephalopathy episodes (also as a secondary prophylaxis). In some cases, the use of non-antibiotic prophylaxis can also be considered. Current knowledge of the treatment of infections allows the choice of a preferred antibiotic for empiric therapy depending on the infection location and whether the source of the disease is nosocomial or community-acquired. Copyright © 2017 Medical University of Bialystok. Published by Elsevier B.V. All rights reserved.

Alcoholic liver disease patients' perspective of a coping and physical activity-oriented rehabilitation intervention after hepatic encephalopathy.

Science.gov (United States)

Mikkelsen, Maria Rudkjaer; Hendriksen, Carsten; Schiødt, Frank Vinholt; Rydahl-Hansen, Susan

2016-09-01

To identify and describe the impact of a coping and physical activity-oriented rehabilitation intervention on alcoholic liver disease patients after hepatic encephalopathy in terms of their interaction with professionals and relatives. Patients who have experienced alcohol-induced hepatic encephalopathy have reduced quality of life, multiple complications, and social problems, and rehabilitation opportunities for these patients are limited. A grounded theory study and an evaluation study of a controlled intervention study. Semi-structured interviews were conducted with 10 alcoholic liver disease patients who were diagnosed with hepatic encephalopathy and participated in a coping and physical activity-oriented rehabilitation intervention. Richard S. Lazarus's theory of stress and coping inspired the interview guide. The significance of a coping and physical activity-oriented rehabilitation intervention on alcoholic liver disease patients' ability to cope with problems after surviving alcohol-induced hepatic encephalopathy in terms of their interaction with professionals and relatives was characterised by the core category 'regain control over the diseased body'. This is subdivided into three separate categories: 'the experience of being physically strong', 'togetherness' and 'self-control', and they impact each other and are mutually interdependent. Alcoholic liver disease patients described the strength of the rehabilitation as regaining control over the diseased body. Professionals and relatives of patients with alcoholic liver disease may need to focus on strengthening and preserving patients' control of their diseased body by facilitating the experience of togetherness, self-control and physical strength when interacting with and supporting patients with alcoholic liver disease. A coping and physical activity-oriented rehabilitation intervention may help alcoholic liver disease patients to regain control over their diseased body and give patients the experience

Metabolic and improved organ scan studies. III. 13N-ammonia metabolic studies in hepatic encephalopathy

International Nuclear Information System (INIS)

Anon.

1976-01-01

Results are reported from an investigation into the nature of hepatic encephalopathy, through study of the uptake and metabolism of 13 N-labeled ammonia by the brain in relation to liver function, in order to develop improved methods for the management of patients with this condition

Nonconvulsive status epilepticus disguising as hepatic encephalopathy.

Science.gov (United States)

Jo, Yong Min; Lee, Sung Wook; Han, Sang Young; Baek, Yang Hyun; Ahn, Ji Hye; Choi, Won Jong; Lee, Ji Young; Kim, Sang Ho; Yoon, Byeol A

2015-04-28

Nonconvulsive status epilepticus has become an important issue in modern neurology and epileptology. This is based on difficulty in definitively elucidating the condition and its various clinical phenomena and on our inadequate insight into the intrinsic pathophysiological processes. Despite nonconvulsive status epilepticus being a situation that requires immediate treatment, this disorder may not be appreciated as the cause of mental status impairment. Although the pathophysiology of nonconvulsive status epilepticus remains unknown, this disorder is thought to lead to neuronal damage, so its identification and treatment are important. Nonconvulsive status epilepticus should be considered in the differential diagnosis of patients with liver cirrhosis presenting an altered mental status. We report a case of a 52-year-old male with liver cirrhosis presenting an altered mental status. He was initially diagnosed with hepatic encephalopathy but ultimately diagnosed with nonconvulsive status epilepticus by electroencephalogram.

Quantitative evaluation of hyperintensity on T1-weighted MRI in liver cirrhosis : correlation with child-pugh classification and hepatic encephalopathy

International Nuclear Information System (INIS)

Eun, Hyo Won; Choi, Hye Young; Lee, Sun Wha; Yi, Sun Young

1999-01-01

To investigate the differences in signal changes in the globus pallidus and white matter, as seen on T1-weighted MR brain images, and to determine whether these differences can be used as an indicator of subclinical hepatic encephalopathy. A total of 25 cases of liver cirrhosis were evaluated and as a control group, 20 subjects were also studied. Using a 1.5T MRI scannet, brain MR images were obtained, and the differences in signal intensity in both the globus pallidus and thalamus and in both white and gray matter were then quantified using the contrast to noise ratio(CNR). On the basis of the Child-Pugh classification, 25patients with liver cirrhosis were divided into three groups, with eight in group A, eight in B, and nine in C. Using clinical criteria, hepatic encephalopathy was diagnosed in seven of the 25 patients. There after, CNRs(CNR1 and CNR2) were conpared between the control and cirrhotic groups and between cirrhotic groups with or without hepatic encephalopathy. In the control group, mean values were 3.2±5.9 for CNR1 and 8.4±8.0 for CNR2. In the cirrhotic group, these values were 10.6±9.0 for CNR1 and 9.8±6.4 for CNR2. A statistically significant difference was noted between normal and cirrhotic groups only for CNR1(p<0.05). CNR values in patients with liver cirrhosis were 8.5±11.5 for CNR1 and 11.7±8.7 for CNR2 in the Child A group, 10.4±5.1 for CNR1 and 9.3±3.2 for CNR2 in the B group, and 12.8±9.7 for CNR1 and 8.7±6.5 for CNR2 in the C group. There was no significant difference in mean CNRI values between patients with or without hepatic encephalopathy. Differences in signal intensities in the globus pallidus and white matter, as seen on T1-weighted MR brain images, cannot be used as an indicator of hepatic encephalopathy in patients with liver cirrhosis

Quantitative evaluation of hyperintensity on T1-weighted MRI in liver cirrhosis : correlation with child-pugh classification and hepatic encephalopathy

Energy Technology Data Exchange (ETDEWEB)

Eun, Hyo Won; Choi, Hye Young; Lee, Sun Wha; Yi, Sun Young [Ewha Womans Univ. College of Medicine, Seoul (Korea, Republic of)

1999-11-01

To investigate the differences in signal changes in the globus pallidus and white matter, as seen on T1-weighted MR brain images, and to determine whether these differences can be used as an indicator of subclinical hepatic encephalopathy. A total of 25 cases of liver cirrhosis were evaluated and as a control group, 20 subjects were also studied. Using a 1.5T MRI scannet, brain MR images were obtained, and the differences in signal intensity in both the globus pallidus and thalamus and in both white and gray matter were then quantified using the contrast to noise ratio(CNR). On the basis of the Child-Pugh classification, 25patients with liver cirrhosis were divided into three groups, with eight in group A, eight in B, and nine in C. Using clinical criteria, hepatic encephalopathy was diagnosed in seven of the 25 patients. There after, CNRs(CNR1 and CNR2) were conpared between the control and cirrhotic groups and between cirrhotic groups with or without hepatic encephalopathy. In the control group, mean values were 3.2{+-}5.9 for CNR1 and 8.4{+-}8.0 for CNR2. In the cirrhotic group, these values were 10.6{+-}9.0 for CNR1 and 9.8{+-}6.4 for CNR2. A statistically significant difference was noted between normal and cirrhotic groups only for CNR1(p<0.05). CNR values in patients with liver cirrhosis were 8.5{+-}11.5 for CNR1 and 11.7{+-}8.7 for CNR2 in the Child A group, 10.4{+-}5.1 for CNR1 and 9.3{+-}3.2 for CNR2 in the B group, and 12.8{+-}9.7 for CNR1 and 8.7{+-}6.5 for CNR2 in the C group. There was no significant difference in mean CNRI values between patients with or without hepatic encephalopathy. Differences in signal intensities in the globus pallidus and white matter, as seen on T1-weighted MR brain images, cannot be used as an indicator of hepatic encephalopathy in patients with liver cirrhosis.

Non invasive blood flow measurement in cerebellum detects minimal hepatic encephalopathy earlier than psychometric tests.

Science.gov (United States)

Felipo, Vicente; Urios, Amparo; Giménez-Garzó, Carla; Cauli, Omar; Andrés-Costa, Maria-Jesús; González, Olga; Serra, Miguel A; Sánchez-González, Javier; Aliaga, Roberto; Giner-Durán, Remedios; Belloch, Vicente; Montoliu, Carmina

2014-09-07

To assess whether non invasive blood flow measurement by arterial spin labeling in several brain regions detects minimal hepatic encephalopathy. Blood flow (BF) was analyzed by arterial spin labeling (ASL) in different brain areas of 14 controls, 24 cirrhotic patients without and 16 cirrhotic patients with minimal hepatic encephalopathy (MHE). Images were collected using a 3 Tesla MR scanner (Achieva 3T-TX, Philips, Netherlands). Pulsed ASL was performed. Patients showing MHE were detected using the battery Psychometric Hepatic Encephalopathy Score (PHES) consisting of five tests. Different cognitive and motor functions were also assessed: alterations in selective attention were evaluated using the Stroop test. Patients and controls also performed visuo-motor and bimanual coordination tests. Several biochemical parameters were measured: serum pro-inflammatory interleukins (IL-6 and IL-18), 3-nitrotyrosine, cGMP and nitrates+nitrites in plasma, and blood ammonia. Bivariate correlations were evaluated. In patients with MHE, BF was increased in cerebellar hemisphere (P = 0.03) and vermis (P = 0.012) and reduced in occipital lobe (P = 0.017). BF in cerebellar hemisphere was also increased in patients without MHE (P = 0.02). Bimanual coordination was impaired in patients without MHE (P = 0.05) and much more in patients with MHE (P battery and with CFF. BF in cerebellar hemisphere correlates with plasma cGMP and nitric oxide (NO) metabolites. BF in vermis cerebellar also correlates with NO metabolites and with 3-nitrotyrosine. IL-18 in plasma correlates with BF in thalamus and occipital lobe. Non invasive BF determination in cerebellum using ASL may detect MHE earlier than the PHES. Altered NO-cGMP pathway seems to be associated to altered BF in cerebellum.

Reduction of cerebral blood flow in subclinical hepatic encephalopathy and its correlation with plasma-free tryptophan

International Nuclear Information System (INIS)

Rodriguez, G.; Testa, R.; Celle, G.; Gris, A.; Marenco, S.; Nobili, F.; Novellone, G.; Rosadini, G.

1987-01-01

Cerebral blood flow (CBF), measured by the noninvasive xenon-133 inhalation method, EEG, and plasma levels of ammonia (NH 3 ) and free tryptophan were determined in 18 hospitalized cirrhotic patients affected with subclinical hepatic encephalopathy, as diagnosed by the Kurtz test. CBF results were significantly lower (p less than 0.001) in the patients' group as compared with a sex- and age-matched normal control population, although seven patients had values in the normal range. NH 3 was increased only in six, while free tryptophan was increased in all but two patients. A significant negative correlation (p = 0.02) between CBF and free tryptophan was found, even though it appears to be difficult to interpret. We suggest that CBF impairment in some cirrhotic patients with subclinical hepatic encephalopathy may be related to the systemic metabolic derangement caused by the liver disease; free tryptophan could have some implication in producing CBF reduction

Continuous intravenous flumazenil infusion in a patient with chlordiazepoxide toxicity and hepatic encephalopathy

Directory of Open Access Journals (Sweden)

Moh′d Al-Halawani

2015-01-01

Full Text Available Flumazenil, a benzodiazepine receptor antagonist, is the drug of choice for the diagnosis and treatment of benzodiazepine overdose. We are presenting a patient with chronic alcoholism and alcoholic liver disease, who came with alcohol withdrawal symptoms and treated chlordiazepoxide. Subsequently he developed a prolonged change in mental status that required treatment for benzodiazepine overdose and hepatic encephalopathy with flumazenil infusion for 28 days.

Lactulose vs Polyethylene Glycol 3350-Electrolyte Solution for Treatment of Overt Hepatic Encephalopathy

Science.gov (United States)

Rahimi, Robert S.; Singal, Amit G.; Cuthbert, Jennifer A.; Rockey, Don C.

2017-01-01

IMPORTANCE Hepatic encephalopathy (HE) is a common cause of hospitalization in patients with cirrhosis. Pharmacologic treatment for acute (overt) HE has remained the same for decades. OBJECTIVE To compare polyethylene glycol 3350–electrolyte solution (PEG) and lactulose treatments in patients with cirrhosis admitted to the hospital for HE. We hypothesized that rapid catharsis of the gut using PEG may resolve HE more effectively than lactulose. DESIGN, SETTING, AND PARTICIPANTS The HELP (Hepatic Encephalopathy: Lactulose vs Polyethylene Glycol 3350-Electrolyte Solution) study is a randomized clinical trial in an academic tertiary hospital of 50 patients with cirrhosis (of 186 screened) admitted for HE. INTERVENTIONS Participants were block randomized to receive treatment with PEG, 4-L dose (n = 25), or standard-of-care lactulose (n = 25) during hospitalization. MAIN OUTCOMES AND MEASURES The primary end point was an improvement of 1 or more in HE grade at 24 hours, determined using the hepatic encephalopathy scoring algorithm (HESA), ranging from 0 (normal clinical and neuropsychological assessments) to 4 (coma). Secondary outcomes included time to HE resolution and overall length of stay. RESULTS A total of 25 patients were randomized to each treatment arm. Baseline clinical features at admission were similar in the groups. Thirteen of 25 patients in the standard therapy arm (52%) had an improvement of 1 or more in HESA score, thus meeting the primary outcome measure, compared with 21 of 23 evaluated patients receiving PEG (91%) (P PEG-treated groups (P = .002). The median time for HE resolution was 2 days for standard therapy and 1 day for PEG (P = .01). Adverse events were uncommon, and none was definitely study related. CONCLUSIONS AND RELEVANCE PEG led to more rapid HE resolution than standard therapy, suggesting that PEG may be superior to standard lactulose therapy in patients with cirrhosis hospitalized for acute HE. TRIAL REGISTRATION clinicaltrials

[Changes in serotonin and noradrenaline in hepatic encephalopathy as a result of liver failure in rat].

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Song, Min-ning; Song, Yu-na; Chen, Fu; Luo, Mei-lan

2007-01-01

To investigate the changes in serotonin (5-HT) and noradrenaline (NA) in hepatic encephalopathy as a result of acute and chronic liver failure in rat. One hundred and ten Sprague-Dawley (SD) rats were randomly divided into groups of normal control (n=20), experimental group of acute liver failure (ALF) encephalopathy (n=45), and experimental group of chronic liver failure (CLF) encephalopathy (n=45). Two dosages of thioacetamide (TAA) of 500 mg/kg were gavaged with an interval of 24 hours to reproduce ALF model. To reproduce CLF model rats were fed with 0.03% TAA in drinking water for 10 weeks, and 50% of TAA dosage was added or withheld according to the change in weekly body weight measurement. Animals were sacrificed and venous blood specimens were obtained after successful replication of model, and 5-HT, NA, ammonia, parameters of liver function were determined, and liver and brain were studied pathologically. The experiment showed that the liver functions of rats in groups ALF encephalopathy and CLF encephalopathy deteriorated seriously, changes in alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL), albumen (ALB), ALB/globulin (A/G), and blood ammonia were observed(Pliver and brain pathologies were identical to those of ALF and CLF encephalopathy. The values of 5-HT were increased in groups ALF encephalopathy and CLF encephalopathy [(16.06+/-1.08) micromol/L and (15.32+/-1.48) micromol/L] compared with the normal group [(2.75+/-0.26) micromol/L, both Pencephalopathy [(94.0+/-2.13) pmol/L vs.(121.2+/-14.8) pmol/L,Pencephalopathy and CLF encephalopathy. The content of NA decreases remarkably in CLF encephalopathy.

Brainstem evoked response audiometry: an investigatory tool in detecting hepatic encephalopathy in decompensated chronic liver disease.

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Kabali, Balasubramanian; Velayutham, Gowri; Kapali, Suresh Chander

2014-01-01

It is estimated that globally there is a marked increase in liver disease with reports of rising morbidity and mortality, particularly in younger age groups. Brainstem auditory evoked potential (BAEP) was recorded in 60 decompensated chronic liver disease (DCLD) subjects who fulfilled the selection criteria and compared to 60 age and gender matched healthy subjects with normal liver functions. DCLD subjects were divided into two inter groups based on presence or absence of hepatic encephalopathy (HE). Group 1 comprises of 30 subjects of grade- I HE and Group 2 included 30 subjects without hepatic encephalopathy (NHE). Absolute and interpeak wave latencies were measured. Results were analysed by student independent t- test using SPSS software 11 version. Statistical significance was tested using P value. From the present study it can be concluded that the central nervous system is involved in liver cirrhosis evidenced by an abnormal BAEP latencies parameters. This shows that there may be progressive demyelination occurring along with axonal loss or dysfunction in liver cirrhosis HE. This study suggests that periodic evaluation of cirrhotic individuals to such test will help in monitoring the progress of encephalopathy. The prime goal of this study is early diagnosis and initiation of treatment before the onset of coma can reduce the fatality rate.

A CLINICAL STUDY OF HEPATIC ENCEPHALOPATHY IN CHRONIC LIVER DISEASE WITH REFERENCE TO SERUM AMMONIA IN A TERTIARY CARE HOSPITAL OF NORTH EAST INDIA

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Tribeni Sharma

2016-07-01

Full Text Available INTRODUCTION Hepatic encephalopathy is the term used to describe the complex, sometimes irreversible, and variable changes in neuropsychiatric status that can complicate both acute and chronic liver disease. A spectrum of neuropsychiatric abnormalities exists ranging from clinically indiscernible changes in cognition to clinically obvious changes in intellect behaviour, motor function, and consciousness. METHODS We conducted a hospital-based observational descriptive study comprising of 80 patients of chronic liver disease from June 2014-May 2015 who had been diagnosed on the basis of a thorough history, physical examination, including mini-mental status examination, Glasgow Coma Score, biochemical tests including arterial ammonia, radiological findings, EEG and CFF (critical flicker frequency Tests after excluding other causes of neurological impairment. The patients were admitted in Gauhati Medical College and Hospital, Guwahati, Assam (India and fulfilled the inclusion and exclusion criteria of the study. Statistical analysis was performed using one way ANOVA method of analysis. RESULTS In our study, 61 patients were male and 19 patients were female. 30% patients were in the third decade of life followed by 26.25% in the fourth decade and 18.75% in the fifth decade. Most of the patients were in Child-Pugh Class C (72.5% followed by Class A (16.25% and Class B (11.25%. The patients were assigned grades of hepatic encephalopathy according to the West-Haven classification. Majority of patients were in grade I hepatic encephalopathy (30% followed by grade III (28.75% and grade IV (21.25%. The lowest mean arterial ammonia level was found in grade 0 and grade I hepatic encephalopathy - 39.2±7.4 mg/dL and 58.7±9.8 mg/dL (mean±standard deviation respectively and the highest values were found in the highest grades of hepatic encephalopathy - grade III and IV (98.4±10.7 mg/dL and 145.0±17.0 mg/dL respectively. CONCLUSION The arterial ammonia

Reversible splenial lesion on the corpus callosum in nonfulminant hepatitis A presenting as encephalopathy

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Soon Young Ko

2014-12-01

Full Text Available Reversible focal lesions on the splenium of the corpus callosum (SCC have been reported in patients with mild encephalitis/encephalopathy caused by various infectious agents, such as influenza, mumps, adenovirus, Varicella zoster, Escherichia coli, Legionella pneumophila, and Staphylococcus aureus. We report a case of a reversible SCC lesion causing reversible encephalopathy in nonfulminant hepatitis A. A 30-year-old healthy male with dysarthria and fever was admitted to our hospital. After admission his mental status became confused, and so we performed electroencephalography (EEG and magnetic resonance imaging (MRI of the brain, which revealed an intensified signal on diffusion-weighted imaging (DWI at the SCC. His mental status improved 5 days after admission, and the SCC lesion had completely disappeared 15 days after admission.

Embolization of portal-systemic shunts in cirrhotic patients with chronic recurrent hepatic encephalopathy

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Sakurabayashi, Shin; Sezai, Shuichi; Yamamoto, Yoshihiro; Hirano, Masanori; Oka, Hiroshi

1997-01-01

Purpose. To evaluate the efficacy of embolization of portal-systemic shunts in cirrhotic patients with chronic recurrent hepatic encephalopathy (CRHE). Methods. Seven cirrhotic patients with CRHE refractory to medical treatment (3 men and 4 women, mean age 66 years) were studied. Five patients had splenorenal shunts, 1 had a gastrorenal shunt, and 1 had an intrahepatic portal vein-hepatic vein shunt. Shunt embolization was performed using stainless steel coils, with a percutaneous transhepatic portal vein approach in 4 patients and a transrenal vein approach in 3 patients. Results. After embolization, the shunt disappeared in 4 patients on either ultrasound pulsed Doppler monitoring or portography. Complications observed in the 7 patients were fever, transient pleural effusion, ascites, and mild esophageal varices. For 3-6 months after embolization, the 4 patients whose shunts disappeared showed minimal or no reappearance of a shunt, and had no recurrence of encephalopathy. The serum ammonia levels decreased and electroencephalograms also improved. One of the 4 patients, who developed mild esophageal varices, required no treatment. Treatment was effective in 3 of the 4 patients (75%) who underwent embolization via a transhepatic portal vein. Conclusion. Transvascular embolization of shunts improved the outcome in 4 of 7 patients. The most effective embolization was achieved via the percutaneous transhepatic portal vein approach

Intracortical inhibitory and excitatory circuits in subjects with minimal hepatic encephalopathy: a TMS study.

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Nardone, Raffaele; De Blasi, Pierpaolo; Höller, Yvonne; Brigo, Francesco; Golaszewski, Stefan; Frey, Vanessa N; Orioli, Andrea; Trinka, Eugen

2016-10-01

Minimal hepatic encephalopathy (MHE) is the earliest form of hepatic encephalopathy (HE) and affects up to 80 % of patients with liver cirrhosis. By definition, MHE is characterized by psychomotor slowing and subtle cognitive deficits,  but obvious clinical manifestations are lacking. Given its covert nature, MHE is often underdiagnosed. This study was aimed at detecting neurophysiological changes, as assessed by means of transcranial magnetic stimulation (TMS), involved in the early pathogenesis of the HE. We investigated motor cortex excitability in 15 patients with MHE and in 15 age-matched age-matched cirrhotic patients without MHE; the resting motor threshold, the short-interval intracortical inhibition (SICI) and the intracortical facilitation (ICF) were examined. Paired-pulse TMS revealed significant increased SICI and reduced ICF in the patients with MHE. These findings may reflect abnormalities in intrinsic brain activity and altered organization of functional connectivity networks. In particular, the results suggest a shift in the balance between intracortical inhibitory and excitatory mechanisms towards a net increase of inhibitory neurotransmission. Together with other neurophysiological (in particular EEG) and neuroimaging techniques, TMS may thus provide early markers of cerebral dysfunction in cirrhotic patients with MHE.

Ameliorative effects of rutin on hepatic encephalopathy-induced by thioacetamide or gamma irradiation.

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Mansour, Somaya Z; El-Marakby, Seham M; Moawed, Fatma S M

2017-07-01

Hepatic encephalopathy (HE) is a syndrome resulting from acute or chronic liver failure. This study was designed to evaluate the effect of rutin on thioacetamide (TAA) or γ-radiation-induced HE model. Animals were received with TAA (200mg/kg, i.p.) twice weekly for four weeks or exposed to 6Gy of γ-radiation to induce HE then groups orally treated with rutin (50mg/kg b.wt.) for four weeks. At the end of experiment, blood, liver and brain samples were collected to assess biochemical and biophysical markers as well histopathological investigations. TAA or γ-radiation exposed rats experienced increases in serum activities of ALT, AST, ALP and ammonia level. Also an alteration in relative permeability and conductivity of erythrocytes was observed. Furthermore, cytokines levels and AChE activity were induced whereas the activities of HO-1 and neurotransmitters contents were depleted. TAA or γ-radiation caused distortion of hepatic and brain architecture as shown by histopathological examination. Treatment with rutin resulted in improvement in liver function by the decline in serum AST and ALT activities and reduction in serum ammonia level. In addition, the administration of rutin significantly modulated the alteration in cytokines levels and neurotransmitters content. Histopathological examinations of liver and brain tissues showed that administration of rutin has attenuate TAA or radiation-induced damage and improve tissue architecture. Consequently, rutin has been a powerful hepatoprotective effect to combat hepatic encephalopathy associated hyperammonemia and its consequential damage in liver and brain. Copyright © 2017 Elsevier B.V. All rights reserved.

Alcoholic Hepatitis

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... yellow color. Confusion, drowsiness and slurred speech (hepatic encephalopathy). A damaged liver has trouble removing toxins from your body. The ... of toxins can damage your brain. Severe hepatic encephalopathy can result in ... of the liver frequently leads to liver failure. Kidney failure. A ...

Metronidazole-induced encephalopathy in a patient with liver cirrhosis.

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Cheong, Hyeong Cheol; Jeong, Taek Geun; Cho, Young Bum; Yang, Bong Joon; Kim, Tae Hyeon; Kim, Haak Cheoul; Cho, Eun-Young

2011-06-01

Encephalopathy is a disorder characterized by altered brain function, which can be attributed to various causes. Encephalopathy associated with metronidazole administration occurs rarely and depends on the cumulative metronidazole dose, and most patients with this condition recover rapidly after discontinuation of therapy. Because metronidazole is metabolized in the liver and can be transported by the cerebrospinal fluid and cross the blood-brain barrier, it may induce encephalopathy even at a low cumulative dose in patients with hepatic dysfunction. We experienced a patient who showed ataxic gait and dysarthric speech after receiving metronidazole for the treatment of hepatic encephalopathy that was not controlled by the administration of lactulose. The patient was diagnosed as metronidazole-induced encephalopathy, and stopping drug administration resulted in a complete recovery from encephalopathy. This case shows that caution should be exercised when administering metronidazole because even a low dose can induce encephalopathy in patients with liver cirrhosis.

An unusual cause of anemia and encephalopathy

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Sanjeev Kumar Sharma

2015-04-01

Full Text Available The authors present here an interesting case of recent onset anemia that was associated with an encephalopathy of the unusual cause.Although severe anemia can theoretically result in anemic hypoxia and can then lead to hypoxic encephalopathy, it is not a primary cause of encephalopathy. More frequently anemia can contribute together with other multiple causes of encephalopathy, such as infections, metabolic abnormalities, trauma, hepatic dysfunction, hypertension, toxins.

Critical flicker frequency and continuous reaction times for the diagnosis of minimal hepatic encephalopathy

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Lauridsen, Mette Enok Munk; Jepsen, Peter; Vilstrup, Hendrik

2011-01-01

Abstract Minimal hepatic encephalopathy (MHE) is intermittently present in up to 2/3 of patients with chronic liver disease. It impairs their daily living and can be treated. However, there is no consensus on diagnostic criteria except that psychometric methods are required. We compared two easy...... appropriately to a sensory stimulus. The choice of test depends on the information needed in the clinical and scientific care and study of the patients....

Ammonia Levels and Hepatic Encephalopathy in Patients with Known Chronic Liver Disease.

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Ninan, Jacob; Feldman, Leonard

2017-08-01

Ammonia is predominantly generated in the gut by intestinal bacteria and enzymes and detoxified primarily in the liver. Since the 1930s, ammonia has been identified as the principal culprit in hepatic encephalopathy (HE). Many physicians utilize serum ammonia to diagnose, assess severity, and determine the resolution of HE in patients with chronic liver disease (CLD) despite research showing that ammonia levels are unhelpful in all of these clinical circumstances. HE in patients with CLD is a clinical diagnosis of exclusion that should not be based on ammonia levels. © 2017 Society of Hospital Medicine.

Detecção da encefalopatia hepática subclínica por espectroscopia cerebral Detection of subclinical hepatic encephalopathy by magnetic resonance spectroscopy

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Gustavo Justo Schulz

2007-06-01

Full Text Available RACIONAL: A encefalopatia hepática é anormalidade neuropsiquiátrica comum em cirróticos e está associada com alterações típicas de determinados metabólitos cerebrais, como o decréscimo de mio-inositol e colina e o aumento de glutamina-glutamato, observadas na espectroscopia cerebral por ressonância magnética. OBJETIVO: Determinar os níveis dos metabólitos cerebrais em pacientes cirróticos para diagnóstico da encefalopatia hepática em estágios iniciais. MÉTODOS Foram estudados 25 pacientes com cirrose hepática, do Serviço de Transplante Hepático da Universidade Federal do Paraná, através de avaliação clínica (exame neurológico e testes neuropsicométricos e espectroscopia por ressonância magnética cerebral. A área espectral estudada por ressonância magnética envolveu a região occipital (substância branca e cinzenta. Trinta voluntários sadios formaram o grupo controle. RESULTADOS: A encefalopatia hepática subclínica foi diagnosticada em 12 pacientes (48%. Reduções significativas nos índices de MI/Cr foram observadas nos pacientes com encefalopatia quando comparados aos controles (0,49±0,10 vs. 0,83±0,13; P BACKGROUND: Hepatic encephalopathy is a common neuro-psychiatric abnormality in liver cirrhosis associated with typical changes of cerebral metabolite pattern, such as a decrease of myo-inositol and cholina and increase of glutamine-glutamate, observed by magnetic resonance spectroscopy. AIM: To determine cerebral metabolite ratios in liver cirrhosis patients with early stages of hepatic encephalopathy. METHODS: Twenty-five patients with chronic hepatic failure from Liver Transplantation Unit of the Federal University of Paraná were studied with clinical evaluation and magnetic resonance spectroscopy. Localized magnetic resonance spectra were acquired in the occipital gray/white matter regions. Thirty healthy volunteers were also subjected to the same evaluations, making up the control group. RESULTS

Metronidazole-Induced Encephalopathy in Alcoholic Liver Disease: A Diagnostic and Therapeutic Challenge.

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Sonthalia, Nikhil; Pawar, Sunil V; Mohite, Ashok R; Jain, Samit S; Surude, Ravindra G; Rathi, Pravin M; Contractor, Qais

2016-10-01

Acute encephalopathy in a patient with alcoholic liver disease (ALD) is a commonly encountered emergency situation occurring most frequently due to liver failure precipitated by varying etiologies. Acute reversible cerebellar ataxia with confusion secondary to prolonged metronidazole use has been reported rarely as a cause of encephalopathy in patients with ALD. We describe a decompensated ALD patient with recurrent pyogenic cholangitis associated with hepatolithiasis who presented to the emergency department with sudden-onset cerebellar ataxia with dysarthria and mental confusion after prolonged use of metronidazole. Magnetic resonance imaging (MRI) of the brain was suggestive of bilateral dentate nuclei hyper intensities on T2 and fluid-attenuated inversion recovery sections seen classically in metronidazole-induced encephalopathy (MIE). Decompensated liver cirrhosis resulted in decreased hepatic clearance and increased cerebrospinal fluid concentration of metronidazole leading to toxicity at a relatively low total cumulative dose of 22 g. Both the clinical symptoms and MRI brain changes were reversed at 7 days and 6 weeks, respectively, after discontinuation of metronidazole. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: A patient with ALD presenting with encephalopathy creates a diagnostic dilemma for the emergency physician regarding whether to continue metronidazole and treat for hepatic encephalopathy or to suspect for MIE and withhold the drug. Failure to timely discontinue metronidazole may worsen the associated hepatic encephalopathy in these patients. Liver cirrhosis patients have higher mean concentration of metronidazole and its metabolite in the blood, making it necessary to keep the cumulative dose of metronidazole to < 20 g in them. Copyright © 2016 Elsevier Inc. All rights reserved.

The continuous reaction time test for minimal hepatic encephalopathy validated by a randomized controlled multi-modal intervention-A pilot study

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Lauridsen, M M; Mikkelsen, S; Svensson, T

2017-01-01

Background: Minimal hepatic encephalopathy (MHE) is clinically undetectable and the diagnosis requires psychometric tests. However, a lack of clarity exists as to whether the tests are in fact able to detect changes in cognition. Aim: To examine if the continuous reaction time test (CRT) can detect...... changes in cognition with anti-HE intervention in patients with cirrhosis and without clinically manifest hepatic encephalopathy (HE). Methods: Firstly, we conducted a reproducibility analysis and secondly measured change in CRT induced by anti-HE treatment in a randomized controlled pilot study: We...... stratified 44 patients with liver cirrhosis and without clinically manifest HE according to a normal (n = 22) or abnormal (n = 22) CRT. Each stratum was then block randomized to receive multimodal anti-HE intervention (lactulose+branched-chain amino acids+rifaximin) or triple placebos for 3 months...

Refractory hepatic encephalopathy in a patient with hypothyroidism: Another element in ammonia metabolism.

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Díaz-Fontenla, Fernando; Castillo-Pradillo, Marta; Díaz-Gómez, Arantxa; Ibañez-Samaniego, Luis; Gancedo, Pilar; Guzmán-de-Villoria, Juan Adan; Fernández-García, Pilar; Bañares-Cañizares, Rafael; García-Martínez, Rita

2017-07-28

Hepatic encephalopathy (HE) remains a diagnosis of exclusion due to the lack of specific signs and symptoms. Refractory HE is an uncommon but serious condition that requires the search of hidden precipitating events ( i.e ., portosystemic shunt) and alternative diagnosis. Hypothyroidism shares clinical manifestations with HE and is usually considered within the differential diagnosis of HE. Here, we describe a patient with refractory HE who presented a large portosystemic shunt and post-ablative hypothyroidism. Her cognitive impairment, hyperammonaemia, electroencephalograph alterations, impaired neuropsychological performance, and magnetic resonance imaging and spectroscopy disturbances were highly suggestive of HE, paralleled the course of hypothyroidism and normalized after thyroid hormone replacement. There was no need for intervention over the portosystemic shunt. The case findings support that hypothyroidism may precipitate HE in cirrhotic patients by inducing hyperammonaemia and/or enhancing ammonia brain toxicity. This case led us to consider hypothyroidism not only in the differential diagnosis but also as a precipitating factor of HE.

Spectral electroencephalogram in liver cirrhosis with minimal hepatic encephalopathy before and after lactulose therapy.

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Singh, Jatinderpal; Sharma, Barjesh Chander; Maharshi, Sudhir; Puri, Vinod; Srivastava, Siddharth

2016-06-01

Minimal hepatic encephalopathy (MHE) represents the mildest form of hepatic encephalopathy. Spectral electroencephalogram (sEEG) analysis improves the recognition of MHE by decreasing inter-operator variability and providing quantitative parameters of brain dysfunction. We compared sEEG in patients with cirrhosis with and without MHE and the effects of lactulose on sEEG in patients with MHE. One hundred patients with cirrhosis (50 with and 50 without MHE) were enrolled. Diagnosis of MHE was based on psychometric hepatic encephalopathy score (PHES) of ≤ -5. Critical flicker frequency, model of end-stage liver disease score, and sEEG were performed at baseline in all patients. The spectral variables considered were the mean dominant frequency (MDF) and relative power in beta, alpha, theta, and delta bands. Patients with MHE were given 3 months of lactulose, and all parameters were repeated. Spectral electroencephalogram analysis showed lower MDF (7.8 ± 1.7 vs 8.7 ± 1.3 Hz, P < 0.05) and higher theta relative power (34.29 ± 4.8 vs 24 ± 6.7%, P = 001) while lower alpha relative power (28.6 ± 4.0 vs 33.5 ± 5.3%, P = .001) in patients with MHE than in patients without MHE. With theta relative power, sensitivity 96%, specificity 84%, and accuracy of 90% were obtained for diagnosis of MHE. After lactulose treatment, MHE improved in 21 patients, and significant changes were seen in MDF (7.8 ± 0.5 vs 8.5 ± 0.6), theta (34.2 ± 4.8 vs 23.3 ± 4.1%), alpha (28.6 ± 4.0 vs 35.5 ± 4.5%), and delta relative power (13.7 ± 3.5 vs 17.0 ± 3.3%) after treatment (P ≤ 0.05). Spectral EEG is a useful objective and quantitative tool for diagnosis and to assess the response to treatment in patients with cirrhosis with MHE. © 2015 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd.

Coping and rehabilitation in alcoholic liver disease patients after hepatic encephalopathy--in interaction with professionals and relatives.

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Mikkelsen, Maria Rudkjær; Hendriksen, Carsten; Schiødt, Frank Vinholt; Rydahl-Hansen, Susan

2015-12-01

To identify and describe conditions that limit or support patients, with alcoholic liver disease after surviving alcohol-induced hepatic encephalopathy, ability to cope with current and potential physical and psychosocial problems--in interaction with professionals and relatives--and to recommend appropriate interventions. Alcoholic liver disease patients surviving alcohol-induced hepatic encephalopathy have significantly impaired quality of life. Internationally, there is a lack of knowledge about the conditions that affect alcoholic liver disease patients' coping and rehabilitation. A grounded theory study. Semi-structured interviews, conducted with 11 alcoholic liver disease patients who were diagnosed with hepatic encephalopathy. The interview guide was inspired by Richard S. Lazarus's theory of stress and coping. The elements that support or limit alcoholic liver disease patients' ability to cope with physical and psychosocial problems in interaction with professionals and relatives were represented by the core category 'Struggle for preservation of identity as a significant individual'. It was characterised by three categories, which are interrelated and impact upon each other: 'Acknowledgement', 'Struggle to maintain control' and 'Achieving a sense of security'. Alcoholic liver disease patients experience a struggle to preserve their identity as a significant individual. It can be assumed that professionals and relatives in their interaction with, and support of, patients should focus on strengthening and preserving patients' identity in the form of acknowledgement, helping alcoholic liver disease patients maintain self-control and providing a safety net so patients feel a sense of security. It can be assumed that professionals should support alcoholic liver disease patients' appraisal of, and coping with, physical and psychosocial problems based on acknowledgment, understanding and a sympathetic attitude. Professionals should proactively approach patients

Neuroinflammation in hepatic encephalopathy: mechanistic aspects.

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Jayakumar, Arumugam R; Rama Rao, Kakulavarapu V; Norenberg, Michael D

2015-03-01

Hepatic encephalopathy (HE) is a major neurological complication of severe liver disease that presents in acute and chronic forms. While elevated brain ammonia level is known to be a major etiological factor in this disorder, recent studies have shown a significant role of neuroinflammation in the pathogenesis of both acute and chronic HE. This review summarizes the involvement of ammonia in the activation of microglia, as well as the means by which ammonia triggers inflammatory responses in these cells. Additionally, the role of ammonia in stimulating inflammatory events in brain endothelial cells (ECs), likely through the activation of the toll-like receptor-4 and the associated production of cytokines, as well as the stimulation of various inflammatory factors in ECs and in astrocytes, are discussed. This review also summarizes the inflammatory mechanisms by which activation of ECs and microglia impact on astrocytes leading to their dysfunction, ultimately contributing to astrocyte swelling/brain edema in acute HE. The role of microglial activation and its contribution to the progression of neurobehavioral abnormalities in chronic HE are also briefly presented. We posit that a better understanding of the inflammatory events associated with acute and chronic HE will uncover novel therapeutic targets useful in the treatment of patients afflicted with HE.

Efficacy of l-ornithine-l-aspartate as an adjuvant therapy in cirrhotic patients with hepatic encephalopathy

International Nuclear Information System (INIS)

Abid, S.; Jafri, W.; Mumtaz, K.; Islam, M.; Abbas, Z.

2011-01-01

To evaluate the efficacy of L-ornithine-L-aspartate (LOLA) as an adjuvant therapy in cirrhotic patients with hepatic encephalopathy (HE). Study Design: Randomized placebo controlled study. Place and Duration of Study: The Aga Khan University Hospital, Karachi in the year 2003-2004. Methodology: Patients with HE were randomized to receive LOLA or placebo medicine as an adjuvant to treatment of HE. Number connection test-A (NCT-A), ammonia level, clinical grade of HE and duration of hospitalization were assessed. Results: Out of 120 patients, there were 62 males with mean age of 57 +- 11 years. Improvement in HE was higher (n=40, 66.7%) in LOLA group as compared to the placebo group (n=28, 46.7%, p=0.027). In patients with grade I or less encephalopathy, improvement was seen in 6 (35.3%) and 3 (20%) patients in LOLA and placebo groups respectively (p=0.667). Patients with HE grade II and above showed improvement in 34 (79.1%) and 25 (55.6%) cases in LOLA and placebo group respectively (p=0.019). On multivariate analysis patients with HE of grade II and above showed prothrombin time, creatinine level and use of LOLA influencing the outcome. Duration of hospitalization was 93.6 +- 25.7 hours and 135.2 +- 103.5 hours in LOLA and placebo groups respectively (p=0.025). No side effects were observed in either groups. Conclusion: In cirrhotic patients with advanced hepatic encephalopathy treatment with LOLA was safe and associated with relatively rapid improvement and shorter hospital stay. (author)

Hyperammonemic encephalopathy due to suture line breakdown after bladder operation.

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Boogerd, W; Zoetmulder, F A; Moffie, D

1990-01-01

A patient is described with a severe encephalopathy and hyperammonemia in absence of liver dysfunction, attributed to urine absorption into the systemic circulation due to suture line breakdown after bladder dome resection. At autopsy characteristic Alzheimer type II astrocytes were found in the basal ganglia.

Clinical features and predictors of outcome in acute hepatitis A and hepatitis E virus hepatitis on cirrhosis.

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Radha Krishna, Yellapu; Saraswat, Vivek Anand; Das, Khaunish; Himanshu, Goel; Yachha, Surender Kumar; Aggarwal, Rakesh; Choudhuri, Gour

2009-03-01

Acute hepatitis A and E are recognized triggers of hepatic decompensation in patients with cirrhosis, particularly from the Indian subcontinent. However, the resulting acute-on-chronic liver failure (ACLF) has not been well characterized and no large studies are available. Our study aimed to evaluate the clinical profile and predictors of 3-month mortality in patients with this distinctive form of liver failure. ACLF was diagnosed in patients with acute hepatitis A or E [abrupt rise in serum bilirubin and/or alanine aminotransferase with positive immunoglobulin M anti-hepatitis A virus (HAV)/anti-hepatitis E virus (HEV)] presenting with clinical evidence of liver failure (significant ascites and/or hepatic encephalopathy) and clinical, biochemical, endoscopic (oesophageal varices at least grade II in size), ultrasonographical (presence of nodular irregular liver with porto-systemic collaterals) or histological evidence of cirrhosis. Clinical and laboratory profile were evaluated, predictors of 3-month mortality were determined using univariate and multivariate logistic regression and a prognostic model was constructed. Receiver-operating curves were plotted to measure performance of the present prognostic model, model for end-stage liver disease (MELD) score and Child-Turcotte-Pugh (CTP) score. ACLF occurred in 121 (3.75%) of 3220 patients (mean age 36.3+/-18.0 years; M:F 85:36) with liver cirrhosis admitted from January 2000 to June 2006. It was due to HEV in 80 (61.1%), HAV in 33 (27.2%) and both in 8 (6.1%). The underlying liver cirrhosis was due to HBV (37), alcohol (17), Wilson's disease (8), HCV (5), autoimmune (6), Budd-Chiari syndrome (2), haemochromatosis (2) and was cryptogenic in the rest (42). Common presentations were jaundice (100%), ascites (78%) and hepatic encephalopathy (55%). Mean (SD) CTP score was 11.4+/-1.6 and mean MELD score was 28.6+/-9.06. Three-month mortality was 54 (44.6%). Complications seen were sepsis in 42 (31.8%), renal failure in

Wernicke encephalopathy in a patient with liver failure

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Zhao, Pan; Zhao, Yanling; Wei, Zhenman; Chen, Jing; Yan, Lilong

2016-01-01

Abstract Early recognition and diagnosis of Wernicke encephalopathy is pivotal for the prognosis of this medical emergency, especially in patients with liver failure which predisposes individuals to develop hepatic encephalopathy. For these patients, distinguishing between hepatic encephalopathy and Wernicke encephalopathy is a challenge in real-world clinical practice. A male patient with 21-year medical history of liver cirrhosis presented diarrhea and ascites. One month before this visit, he was noted to have poor appetite and progressive fatigue. After admission, although several major symptoms, including diarrhea, ascites, hyponatremia, and hypoproteinemia, were greatly improved through appropriate treatments, his laboratory indicators were not changed much. His appetite was not reversed at discharge. On the 5th day after discharge, the patient suddenly became reluctant to speak and did not remember the recent happenings. Simultaneously, unsteady gait and strabismus occurred. On the basis of clinical manifestations and brain magnetic resonance imaging scan results, the patient was diagnosed as Wernicke encephalopathy and these relative symptoms were resolved after intravenous vitamin B1. To our knowledge, this is the second case report of Wernicke encephalopathy developing in a critically ill cirrhotic patient without hepatocellular carcinoma or operative intervention. Wernicke encephalopathy may be underdiagnosed in these patients and this case raises physicians’ awareness of its possible onset. PMID:27399058

Lactulose vs polyethylene glycol 3350--electrolyte solution for treatment of overt hepatic encephalopathy: the HELP randomized clinical trial.

Science.gov (United States)

Rahimi, Robert S; Singal, Amit G; Cuthbert, Jennifer A; Rockey, Don C

2014-11-01

Hepatic encephalopathy (HE) is a common cause of hospitalization in patients with cirrhosis. Pharmacologic treatment for acute (overt) HE has remained the same for decades. To compare polyethylene glycol 3350-electrolyte solution (PEG) and lactulose treatments in patients with cirrhosis admitted to the hospital for HE. We hypothesized that rapid catharsis of the gut using PEG may resolve HE more effectively than lactulose. The HELP (Hepatic Encephalopathy: Lactulose vs Polyethylene Glycol 3350-Electrolyte Solution) study is a randomized clinical trial in an academic tertiary hospital of 50 patients with cirrhosis (of 186 screened) admitted for HE. Participants were block randomized to receive treatment with PEG, 4-L dose (n = 25), or standard-of-care lactulose (n = 25) during hospitalization. The primary end point was an improvement of 1 or more in HE grade at 24 hours, determined using the hepatic encephalopathy scoring algorithm (HESA), ranging from 0 (normal clinical and neuropsychological assessments) to 4 (coma). Secondary outcomes included time to HE resolution and overall length of stay. A total of 25 patients were randomized to each treatment arm. Baseline clinical features at admission were similar in the groups. Thirteen of 25 patients in the standard therapy arm (52%) had an improvement of 1 or more in HESA score, thus meeting the primary outcome measure, compared with 21 of 23 evaluated patients receiving PEG (91%) (P PEG-treated groups (P = .002). The median time for HE resolution was 2 days for standard therapy and 1 day for PEG (P = .01). Adverse events were uncommon, and none was definitely study related. PEG led to more rapid HE resolution than standard therapy, suggesting that PEG may be superior to standard lactulose therapy in patients with cirrhosis hospitalized for acute HE. clinicaltrials.gov Identifier: NCT01283152.

Hepatic encephalopathy is associated with decreased cerebral oxygen metabolism and blood flow, not increased ammonia uptake

DEFF Research Database (Denmark)

Dam, Gitte; Keiding, Susanne; Munk, Ole Lajord

2013-01-01

Studies have shown decreased cerebral oxygen metabolism (CMRO(2)) and blood flow (CBF) in patients with cirrhosis with hepatic encephalopathy (HE). It remains unclear, however, whether these disturbances are associated with HE or with cirrhosis itself and how they may relate to arterial blood...... associated with HE rather than the liver disease as such. The changes in CMRO(2) and CBF could not be linked to blood ammonia concentration or CMRA....

Impaired brain glymphatic flow in a rodent model of chronic liver disease and minimal hepatic encephalopathy

OpenAIRE

Lythgoe, Mark; Hosford, Patrick; Arias, Natalia; Gallego-Duran, Rocio; Hadjihambi, Anna; Jalan, Rajiv; Gourine, Alexander; Habtesion, Abeba; Davies, Nathan; Harrison, Ian

2017-01-01

Neuronal function is exquisitely sensitive to alterations in extracellular environment. In patients with hepatic encephalopathy (HE), accumulation of metabolic waste products and noxious substances in the interstitial fluid of the brain may contribute to neuronal dysfunction and cognitive impairment. In a rat model of chronic liver disease, we used an emerging dynamic contrast-enhanced MRI technique to assess the efficacy of the glymphatic system, which facilitates clearance of solutes from t...

Sepsis and meningoencephalitis due to Listeria monocytogenes in patients with liver cirrhosis: a case of nonhepatic encephalopathy?

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Federico Lari

2012-10-01

Full Text Available Introduction The appearance of neurological disorders in a patient with liver cirrhosis initially suggests hepatic encephalopathy, but other causes should be considered, including bacterial infections.Materials and methods An 80-year-old woman suffering from HCV-related cirrhosis was admitted for fever, confusion, and stupor. No improvement was seen after treatment with cephalosporins, lactulose, and fluids.Results Listeria monocytogenes was isolated from blood cultures and subsequently from a cerebrospinal fluid specimen as well. On the basis of the antibiogram, the antibiotic therapy was modified to include ampicillin, but shock and multiorgan failure developed and the patient died one week later.Discussion Bacterial infections are more common and more aggressive in patients with liver cirrhosis, probably because of the immune dysfunction associated with this disorder. The presence of neurological disorders in a patient with liver cirrhosis may be a sign of hepatic encephalopathy, but it is important to recall that there are other potential causes as well, including bacterial infections. In this case, it is possible that the patient's symptoms were the result of the CNS infection with L. monocytogenes, which was particularly aggressive as a result of her cirrhosis.

Hepatic encephalopathy in patients with non-cirrhotic portal hypertension: Description, prevalence and risk factors.

Science.gov (United States)

Nicoletti, Valeria; Gioia, Stefania; Lucatelli, Pierleone; Nardelli, Silvia; Pasquale, Chiara; Nogas Sobrinho, Stefano; Pentassuglio, Ilaria; Greco, Francesca; De Santis, Adriano; Merli, Manuela; Riggio, Oliviero

2016-09-01

Hepatic encephalopathy (HE) is a common complication of cirrhosis but it is less studied in patients with non-cirrhotic portal hypertension (NCPH). To describe the prevalence of cognitive impairment (overt and covert HE) in NCPH patients and to identify the risk factors for its development. 51 patients with NCPH, 35 with chronic portal vein thrombosis (PVT) and 16 with idiopathic non-cirrhotic portal hypertension (INCPH), were evaluated for the presence of previous or present overt HE (OHE). The psychometric hepatic encephalopathy score and the SCAN battery were used to detect the presence of covert HE (CHE). 34 compensated cirrhotic patients were used as control. In NCPH patients, abdominal scans were performed to detect the presence of shunts. None of the patients experienced OHE at evaluation while 5.7% of PVT and 12.5% of INCPH patients referred at least one documented episode of previous OHE, similarly to patients with cirrhosis (14.7%). Even if lower than in patients with cirrhosis (64.7%), a considerable proportion of patients with chronic PVT (34.3%) and INCPH (25%) had CHE (p=0.008). The presence of a large portal-systemic shunt was the only factor significantly correlated to cognitive impairment in NCPH patients. HE is a tangible complication of NCPH and is mainly related to the presence of portal-systemic shunts. Copyright © 2016 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.

Disrupted topological organization of brain structural network associated with prior overt hepatic encephalopathy in cirrhotic patients

Energy Technology Data Exchange (ETDEWEB)

Chen, Hua-Jun [Fujian Medical University Union Hospital, Department of Radiology, Fuzhou (China); The First Affiliated Hospital of Nanjing Medical University, Department of Radiology, Nanjing (China); Shi, Hai-Bin [The First Affiliated Hospital of Nanjing Medical University, Department of Radiology, Nanjing (China); Jiang, Long-Feng [The First Affiliated Hospital of Nanjing Medical University, Department of Infectious Diseases, Nanjing (China); Li, Lan [Fujian Medical University Union Hospital, Department of Radiology, Fuzhou (China); Chen, Rong [University of Maryland School of Medicine, Department of Diagnostic Radiology and Nuclear Medicine, Baltimore, MD (United States); Beijing Institute of Technology, Advanced Innovation Center for Intelligent Robots and Systems, Beijing (China)

2018-01-15

To investigate structural brain connectome alterations in cirrhotic patients with prior overt hepatic encephalopathy (OHE). Seventeen cirrhotic patients with prior OHE (prior-OHE), 18 cirrhotic patients without prior OHE (non-prior-OHE) and 18 healthy controls (HC) underwent diffusion tensor imaging. Neurocognitive functioning was assessed with Psychometric Hepatic Encephalopathy Score (PHES). Using a probabilistic fibre tracking approach, we depicted the whole-brain structural network as a connectivity matrix of 90 regions (derived from the Automated Anatomic Labeling atlas). Graph theory-based analyses were performed to analyse topological properties of the brain network. The analysis of variance showed significant group effects on several topological properties, including network strength, global efficiency and local efficiency. A progressive decrease trend for these metrics was found from non-prior-OHE to prior-OHE, compared with HC. Among the three groups, the regions with altered nodal efficiency were mainly distributed in the frontal and occipital cortices, paralimbic system and subcortical regions. The topological metrics, such as network strength and global efficiency, were correlated with PHES among cirrhotic patients. The cirrhotic patients developed structural brain connectome alterations; this is aggravated by prior OHE episode. Disrupted topological organization of the brain structural network may account for cognitive impairments related to prior OHE. (orig.)

Disrupted topological organization of brain structural network associated with prior overt hepatic encephalopathy in cirrhotic patients

International Nuclear Information System (INIS)

Chen, Hua-Jun; Shi, Hai-Bin; Jiang, Long-Feng; Li, Lan; Chen, Rong

2018-01-01

To investigate structural brain connectome alterations in cirrhotic patients with prior overt hepatic encephalopathy (OHE). Seventeen cirrhotic patients with prior OHE (prior-OHE), 18 cirrhotic patients without prior OHE (non-prior-OHE) and 18 healthy controls (HC) underwent diffusion tensor imaging. Neurocognitive functioning was assessed with Psychometric Hepatic Encephalopathy Score (PHES). Using a probabilistic fibre tracking approach, we depicted the whole-brain structural network as a connectivity matrix of 90 regions (derived from the Automated Anatomic Labeling atlas). Graph theory-based analyses were performed to analyse topological properties of the brain network. The analysis of variance showed significant group effects on several topological properties, including network strength, global efficiency and local efficiency. A progressive decrease trend for these metrics was found from non-prior-OHE to prior-OHE, compared with HC. Among the three groups, the regions with altered nodal efficiency were mainly distributed in the frontal and occipital cortices, paralimbic system and subcortical regions. The topological metrics, such as network strength and global efficiency, were correlated with PHES among cirrhotic patients. The cirrhotic patients developed structural brain connectome alterations; this is aggravated by prior OHE episode. Disrupted topological organization of the brain structural network may account for cognitive impairments related to prior OHE. (orig.)

The Levels Of Cytokines And S 100β Which Associated With The Pathogenesis Of Hepatic Encephalopathy In Rats: Role Of Lactulose And N-Acetylcysteine In Its Treatment

International Nuclear Information System (INIS)

Heibashy, M.I.A.; Mazen, G.M.A.; Ibrahim, M.A.

2012-01-01

Hepatic encephalopathy (HE) is a reversible syndrome of impaired brain function occurring in patients with advanced liver failure. Recently, it has been reported that pro inflammatory cytokines are involved in the pathogenesis of brain oedema during HE. This study was conducted to elucidate the changes of plasma and brain pro inflammatory cytokines in encephalopathy rats and to evaluate the hepato-protective activity of lactulose or N-acetylcysteine against thioacetamide (TAA) induced hepatopathy in rats. Acute hepatic encephalopathy (HE) in rats was induced by intraperitoneal injection of thioacetamide in 24 hours intervals for two consecutive days. The obtained results revealed significant increase (P<0.05) in liver function tests (ALT, AST, ALP, bilirubin), ammonia, nitric oxide and total oxidant capacity (TOC) in TAA rats than those in control ones. Brain water content was significantly elevated in TAA rats as compared with the control. In addition, the levels of pro inflammatory cytokines (IL-1Β, IL-6, TNF-α) in both serum and brain were significantly increased associated with a remarkable elevation in the level of serum S 100β in TAA rats. On the other hand, induction of hepatic encephalopathy caused significant decrease (P<0.05) in total antioxidant capacity (TAC) levels. When HE rats group was treated with lactulose or N-acetylcysteine, considerable amelioration effects in all previous studied parameters were pronounced dependent on certain mechanisms

Branched chain enriched amino acid versus glucose treatment of hepatic encephalopathy. A double-blind study of 65 patients with cirrhosis

DEFF Research Database (Denmark)

Vilstrup, Hendrik; Gluud, C; Hardt, F

1990-01-01

We studied the effects of infusion of a branched chain enriched amino acid mixture versus glucose on acute hepatic encephalopathy in patients with cirrhosis. Sixty-five patients were randomly treated with 1 g/kg per day of an amino acid mixture with 40% branched chain contents (32 patients...

Treatment of hepatic encephalopathy by on-line hemodiafiltration: a case series study

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Sugiyama Mitsugi

2010-05-01

Full Text Available Abstract Background It is thought that a good survival rate of patients with acute liver failure can be achieved by establishing an artificial liver support system that reliably compensates liver function until the liver regenerates or a patient undergoes transplantation. We introduced a new artificial liver support system, on-line hemodiafiltration, in patients with acute liver failure. Methods This case series study was conducted from May 2001 to October 2008 at the medical intensive care unit of a tertiary care academic medical center. Seventeen consecutive patients who admitted to our hospital presenting with acute liver failure were treated with artificial liver support including daily on-line hemodiafiltration and plasma exchange. Results After 4.9 ± 0.7 (mean ± SD on-line hemodiafiltration sessions, 16 of 17 (94.1% patients completely recovered from hepatic encephalopathy and maintained consciousness for 16.4 ± 3.4 (7-55 days until discontinuation of artificial liver support (a total of 14.4 ± 2.6 [6-47] on-line hemodiafiltration sessions. Significant correlation was observed between the degree of encephalopathy and number of sessions of on-line HDF required for recovery of consciousness. Of the 16 patients who recovered consciousness, 7 fully recovered and returned to society with no cognitive sequelae, 3 died of complications of acute liver failure except brain edema, and the remaining 6 were candidates for liver transplantation; 2 of them received living-related liver transplantation but 4 died without transplantation after discontinuation of therapy. Conclusions On-line hemodiafiltration was effective in patients with acute liver failure, and consciousness was maintained for the duration of artificial liver support, even in those in whom it was considered that hepatic function was completely abolished.

Association between road accidents and low-grade hepatic encephalopathy among Sri Lankan drivers with cirrhosis: a prospective case control study.

Science.gov (United States)

Subasinghe, S K C E; Nandamuni, Y; Ranasinghe, S; Niriella, M A; Miththinda, J K N D; Dassanayake, A; de Silva, A P; de Silva, H J

2016-06-13

Low-grade hepatic encephalopathy (LGHE) comprises minimal hepatic encephalopathy (MHE) and grade 1 hepatic encephalopathy. LGHE has no or minimal recognizable symptoms but has mild cognitive and psychomotor deficits. Studies in Western countries have demonstrated increased road accidents (RA) among patients with MHE. Our objective was to investigate the association between Sri Lankan LGHE phenotype and RA. A prospective, case-control study was conducted in the University Medical Unit, North Colombo Teaching Hospital, Ragama Sri Lanka. Patients with cirrhosis of any aetiology, without OHE, who had been driving during previous 1 month were included. A similar number of age matched, healthy control drivers were also enrolled. Both groups were subjected to five pencil-paper based psychometric tests used to detect LGHE in cirrhotics. Self-reported RA during the previous 1 month were recorded: categorized as 'major' when resulted in hospitalization of the involved, 'minor' when there were injuries, but not serious enough for hospitalization of the involved and 'other' when limited to damages to vehicle or environment without injuries. Among 55 drivers with cirrhosis and LGHE [males, median age 53 years (range 30-60)], 7 (12.7 %) reported RA compared to 6 (10.9 %) among 55 controls [males; median age 51 years (range 30-60)]. There were no 'major' accidents in either group. 2/55 (3.6 %) cases and 2/55 (3.6 %) controls reported 'minor' accidents. There was no increased frequency of RA among Sri Lankan drivers with LGHE compared to healthy controls. This is with the limitation of the study based only on self reported RA.

Central nervous system immunoreactive somatostatin, substance P and met-enkephalin concentrations in experimental hepatic encephalopathy in the rat

Energy Technology Data Exchange (ETDEWEB)

Miller, J.L.; Millar, R.P.; Kirsch, R. (Cape Town Univ. (South Africa))

1982-06-12

Immunoreactive somatostatin, substance P and met-enkephalin concentrations were measured in various regions of the rat brain 65 hours after portacaval shunt and compared with concentrations in sham-operated animals. No significant difference was detected in any of the three peptides in the regions studied, suggesting that these peptides do not play a role in the pathogenesis of hepatic encephalopathy.

Resveratrol in Patients with Minimal Hepatic Encephalopathy

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Giulia Malaguarnera

2018-03-01

Full Text Available Background: Minimal Hepatic Encephalopathy (MHE is characterized by an impairment of social interaction, emotional behavior, sleep disorders, physical and mental symptoms, and diminished Quality of Life (QoL. The aim of our study is evaluating the potential liver health promoting a perspective of Resveratrol (RV activities and evaluate whether RV treatment may improve health related quality of life (HRQL and reduce depression and anxiety in patients with MHE. Methods: We evaluated depression using the Beck Depression Inventory test, anxiety with State-trait anxiety inventory test, quality of life through SF-36 test, and ammonia serum levels in 70 MHE patients that were randomized into two groups. Results: In the comparison between RV group and placebo group we observed a decrease in Back Depression Inventory (BDI (p < 0.001, in State-trait anxiety inventory (STAI (p < 0.001, and improve in physical function (p < 0.001, in role physical (p < 0.05, in body pain (p < 0.05, in general health (p < 0.001, in vitality (p < 0.05, and in social function (p < 0.001. Conclusions: Resveratrol showed efficacy in the treatment of depression, anxiety, and ammonia serum levels, and improved the quality of life Of MHE patients.

9 CFR 96.2 - Prohibition of casings due to African swine fever and bovine spongiform encephalopathy.

Science.gov (United States)

2010-01-01

... 9 Animals and Animal Products 1 2010-01-01 2010-01-01 false Prohibition of casings due to African swine fever and bovine spongiform encephalopathy. 96.2 Section 96.2 Animals and Animal Products ANIMAL... spongiform encephalopathy. (a) Swine casings. The importation of swine casings that originated in or were...

Hepatic Encephalopathy

Medline Plus

Full Text Available ... Disease (NAFLD) & Non-alcoholic Steatohepatitis (NASH) Autoimmune Hepatitis Bile duct disease such as Primary Biliary Cirrhosis (PBC) ... spleen (splenomegaly) Stone-like particles in gallbladder and bile duct (gallstones) Liver cancer (hepatocellular carcinoma) Chronic liver ...

Hepatic Encephalopathy

Medline Plus

Full Text Available ... is a condition that causes temporary worsening of brain function in people with advanced liver disease. When ... travel through your body until they reach your brain, causing mental and physical symptoms of HE. Hepatic ...

The continuous reaction times method for diagnosing, grading, and monitoring minimal/covert hepatic encephalopathy

DEFF Research Database (Denmark)

Lauridsen, Mette Enok Munk; Thiele, Maja; Kimer, N

2013-01-01

Abstract Existing tests for minimal/covert hepatic encephalopathy (m/cHE) are time- and expertise consuming and primarily useable for research purposes. An easy-to-use, fast and reliable diagnostic and grading tool is needed. We here report on the background, experience, and ongoing research......-10) percentile) as a parameter of reaction time variability. The index is a measure of alertness stability and is used to assess attention and cognition deficits. The CRTindex identifies half of patients in a Danish cohort with chronic liver disease, as having m/cHE, a normal value safely precludes HE, it has...

Hepatic Encephalopathy

Medline Plus

Full Text Available ... Lipase Deficiency Liver Cancer Liver Cysts Non-Alcoholic Fatty Liver Disease Primary Biliary Cholangitis Primary Sclerosing Cholangitis What ... B & C Alcohol-related Liver Disease Non-alcoholic Fatty Liver Disease (NAFLD) & Non-alcoholic Steatohepatitis (NASH) Autoimmune Hepatitis ...

Hepatic Encephalopathy

Medline Plus

Full Text Available ... damages your liver over many years – such as long-term alcohol abuse or chronic hepatitis – can cause ... treated. It’s important to continue treatment for as long as necessary to keep HE from coming back. ...

Modification in CSF specific gravity in acutely decompensated cirrhosis and acute on chronic liver failure independent of encephalopathy, evidences for an early blood-CSF barrier dysfunction in cirrhosis.

Science.gov (United States)

Weiss, Nicolas; Rosselli, Matteo; Mouri, Sarah; Galanaud, Damien; Puybasset, Louis; Agarwal, Banwari; Thabut, Dominique; Jalan, Rajiv

2017-04-01

Although hepatic encephalopathy (HE) on the background of acute on chronic liver failure (ACLF) is associated with high mortality rates, it is unknown whether this is due to increased blood-brain barrier permeability. Specific gravity of cerebrospinal fluid measured by CT is able to estimate blood-cerebrospinal fluid-barrier permeability. This study aimed to assess cerebrospinal fluid specific gravity in acutely decompensated cirrhosis and to compare it in patients with or without ACLF and with or without hepatic encephalopathy. We identified all the patients admitted for acute decompensation of cirrhosis who underwent a brain CT-scan. Those patients could present acute decompensation with or without ACLF. The presence of hepatic encephalopathy was noted. They were compared to a group of stable cirrhotic patients and healthy controls. Quantitative brain CT analysis used the Brainview software that gives the weight, the volume and the specific gravity of each determined brain regions. Results are given as median and interquartile ranges and as relative variation compared to the control/baseline group. 36 patients presented an acute decompensation of cirrhosis. Among them, 25 presented with ACLF and 11 without ACLF; 20 presented with hepatic encephalopathy grade ≥ 2. They were compared to 31 stable cirrhosis patients and 61 healthy controls. Cirrhotic patients had increased cerebrospinal fluid specific gravity (CSF-SG) compared to healthy controls (+0.4 %, p encephalopathy did not modify CSF-SG (-0.09 %, p = 0.1757). Specific gravity did not differ between different brain regions according to the presence or absence of either ACLF or HE. In patients with acute decompensation of cirrhosis, and those with ACLF, CSF specific gravity is modified compared to both stable cirrhotic patients and healthy controls. This pattern is observed even in the absence of hepatic encephalopathy suggesting that blood-CSF barrier impairment is manifest even in absence of overt

Efficacy of liver assisting in patients with hepatic encephalopathy with special focus on plasma exchange

DEFF Research Database (Denmark)

Stenbøg, Poul; Busk, Troels; Larsen, Fin Stolze

2013-01-01

Severe liver injury result in development of hepatic encephalopathy (HE) and often also in brain edema that is a potentially fatal complication. HE and brain edema are correlated to the level and persistence of hyperammonemia and the presence of systemic inflammation. Treatment of HE and brain...... edema is based on restoring and keeping normal physiological variables including tonicity, blood gasses, lactate, temperature and vascular resistance by a wide variety of interventions. In addition liver support devices improve the stage of HE, cerebral metabolic rate for oxygen and glucose......, and are used either as a bridge to liver transplantation or liver recovery in patients with fulminant hepatic failure and in patients with acute-on-chronic liver failure. This short review will mainly focus on the management and efficacy of doing plasma exchange on HE in patients with acute HE....

Surgical disconnection of patent paraumbilical vein in refractory hepatic encephalopathy.

Science.gov (United States)

Ishikawa, Yoshinori; Yoshida, Hiroshi; Mamada, Yasuhiro; Taniai, Nobuhiko; Bando, Koichi; Mizuguchi, Yoshiaki; Kakinuma, Daisuke; Kanda, Tomohiro; Akimaru, Koho; Tajiri, Takashi

2008-06-01

Refractory hepatic encephalopathy (HE) frequently develops in patients with cirrhosis and portal-systemic shunt. Recently, patients with refractory HE associated with portal-systemic shunt have been treated with interventional radiology. We describe a promising new treatment for portal-systemic shunt, ligation of the patent paraumbilical vein (PUV) after partial splenic embolization, in patients with refractory HE. Four patients with cirrhosis (3 women and 1 man; mean age, 56 years) and refractory HE due to a patent PUV were studied. Patency of the PUV had recurred in 1 patient after primary occlusion by interventional radiological procedures. The Child-Pugh class was B in 2 patients and C in 2. Before the present treatment, all patients had been hospitalized at least 3 times because of recurrent HE. Partial splenic embolization was performed in all patients to decrease portal venous pressure before surgery. Surgical ligation of the patent PUV was performed under epidural anesthesia. The patent PUV was carefully skeletonized and doubly ligated. Esophageal varices were evaluated with upper gastrointestinal endoscopy before and after surgery. The mean follow-up duration was 15.8 months. After ligation, there were no clinically significant complications. Esophageal varices were unchanged. The serum ammonia level was higher before surgery (162.3 +/- 56.4 mug/dL, mean +/- SD) than after surgery (41.8 +/- 20.2 mug/dL; p=0.0299). No patient had symptoms of HE. Ligation of the patent PUV is an effective treatment for patients with refractory HE.

The role of neurosteroids in the pathogenesis of hepatic encephalopathy

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Mladenović Dušan

2016-01-01

Full Text Available Hepatic Encephalopathy (HE represents a neuropsychiatric syndrome caused by acute or chronic liver failure. Hyperammonemia plays a pivotal role in the development of HE through modulation of neurotransmission, oxidative stress, neuroinflammation, mitochondrial dysfunction, and energy deficit. Neurosteroids contribute significantly to increased GABAergic tone in HE. Ammonia, in combination with manganese and proinflammatory cytokines, stimulate neurosteroid synthesis by up-regulation of translocator protein, a component of multiprotein complex that stimulate cholesterol transport into astrocytic mitochondria. Cholesterol serves as a substrate for the synthesis of neurosteroids allopregnanolone and tetrahydro-deoxycorticosterone. After release from astrocytes, allopregnanolone and tetrahydro-deoxycorticosterone potentiate GABAergic transmission by positive allosteric modulation of GABAA receptor, thus contributing to cognitive deficit and alterations in sleep-wake cycle. Additional potential mechanisms of neurosteroid action in HE include modulation of serotoninergic, cholinergic, glutamatergic, glycinergic, and opioid receptor activities, as well as modulation of gene expression. This review aimed to summarize current knowledge of the role of neurosteroids in the pathogenesis of HE.

Wernicke encephalopathy in a patient with liver failure: Clinical case report.

Science.gov (United States)

Zhao, Pan; Zhao, Yanling; Wei, Zhenman; Chen, Jing; Yan, Lilong

2016-07-01

Early recognition and diagnosis of Wernicke encephalopathy is pivotal for the prognosis of this medical emergency, especially in patients with liver failure which predisposes individuals to develop hepatic encephalopathy. For these patients, distinguishing between hepatic encephalopathy and Wernicke encephalopathy is a challenge in real-world clinical practice.A male patient with 21-year medical history of liver cirrhosis presented diarrhea and ascites. One month before this visit, he was noted to have poor appetite and progressive fatigue. After admission, although several major symptoms, including diarrhea, ascites, hyponatremia, and hypoproteinemia, were greatly improved through appropriate treatments, his laboratory indicators were not changed much. His appetite was not reversed at discharge. On the 5th day after discharge, the patient suddenly became reluctant to speak and did not remember the recent happenings. Simultaneously, unsteady gait and strabismus occurred. On the basis of clinical manifestations and brain magnetic resonance imaging scan results, the patient was diagnosed as Wernicke encephalopathy and these relative symptoms were resolved after intravenous vitamin B1.To our knowledge, this is the second case report of Wernicke encephalopathy developing in a critically ill cirrhotic patient without hepatocellular carcinoma or operative intervention. Wernicke encephalopathy may be underdiagnosed in these patients and this case raises physicians' awareness of its possible onset.

Espectroscopia cerebral em candidatos a transplante hepático Cerebral magnetic resonance spectroscopy in patients with hepatic encephalopathy: analysis before and after liver transplantation

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Gustavo Justo Schulz

2009-01-01

Full Text Available OBJETIVOS: Determinar os níveis dos metabólitos (mio-inositol [MI], colina [Cho], glutamina [Glx], creatina [Cr] e N-acetilaspartato [NAA] por meio da espectroscopia por ressonância magnética em portadores de hepatopatia crônica, antes e após o transplante hepático, correlacionando com a avaliação clínica. MÉTODOS: Foram estudados prospectivamente 25 pacientes portadores de hepatopatia crônica do Serviço de Transplante Hepático da Universidade Federal do Paraná por meio de avaliação clínica e espectroscópica. Trinta voluntários sadios formaram o grupo controle, sendo submetidos às mesmas avaliações. Dezesseis dos 25 pacientes também foram avaliados após o transplante. RESULTADOS: Antes do transplante hepático reduções significativas nos índices de MI/Cr e Cho/Cr e aumento significativo no índice de Glx/Cr foram observadas nos pacientes portadores de encefalopatia hepática comparados ao grupo controle. Os critérios quantitativos de Ross para diagnóstico espectroscópico da encefalopatia hepática (MI/Cr e Cho/Cr OBJECTIVES: To determine the metabolite levels (myo-inositol [MI], choline [Cho], glutamate [Glx], creatine [Cr] and N-acetylaspartate [NAA] visible on magnetic resonance spectroscopy in patients with chronic hepatic failure, before and after liver transplantation and to correlate these data with results of neuropsychiatric tests and clinical findings. METHODS: Twenty five patients with chronic hepatic failure from the Liver Transplantation Unit of the Federal University of Parana were prospectively studied. Patients were submitted to clinical evaluation and magnetic resonance spectroscopy. Thirty healthy volunteers also submitted to the same evaluations. Sixteen of the 25 patients were evaluated after liver transplantation. RESULTS: Before liver transplantation, significant reductions in MI/Cr and Cho/Cr and a significant increase in Glx/Cr were observed in patients with hepatic encephalopathy compared

Psychopathology and Hepatic Encephalopathy

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João Gama Marques

2013-12-01

Full Text Available Since Hippocrates that neuropsychiatric illness secondary to liver disease fascinates physicians, but only in the XIX century Marcel Nencki and Ivan Pavlov suggested the relation between high concentrations of ammonia and Hepatic Encephalopathy (HE. The reaction of ammonia and glutamate (origins glutamine, “the Trojan Horse of neurotoxicity of ammonia continues to be the main responsible for the neurologic lesions, recently confirmed by neurochemistry and neuroimagiology studies. Glutamine starts the inflammatory reaction at the central nervous sys- tem but other important actors seem to be manganese and the neurotransmitters systems of GABA and endocanabinoids. Nowadays there are three different etiologic big groups for HE: type A associated with acute liver failure; type B associated with portosystemic bypass; and type C associated with cirrhosis of the liver. The staging of HE is still based on classic West Haven system, but a latent Grade 0 was introduced (the so called minimal HE; remaining the aggra- vating HE from Grade 1 (subtle changes at clinical examination to Grade 4 (coma. In this work a bibliographic review was made on 30 of the most pertinent and recent papers, focusing in psychopathology, physiopathology, etiology and staging of this clinical entity transversal to Psychiatry and Gastroenterology. Alterations are described in vigility and conscience like temporal, spatial and personal disorientation. Attention, concentration and memory are impaired very early, on latent phase and can be accessed through neuropsychological tests. Mood oscillates between euphoric and depressive. Personality changes begin obviously and abruptly or in a subtle and insidious way. There can be changes in perception like visual hallucinations or even of acoustic-verbal. The thought disorders can be of delusional type, paranoid, systematized or not, but also monothematic ala Capgras Syndrome. Speech can be accelerated, slowed down or completely in

Diabetes as a risk factor for hepatic encephalopathy in cirrhosis patients

DEFF Research Database (Denmark)

Jepsen, Peter; Watson, Hugh; Andersen, Per Kragh

2015-01-01

BACKGROUND & AIMS: It remains unclear whether diabetes increases the risk for hepatic encephalopathy (HE) in cirrhotic patients. We examined this question using data from three randomized trials of satavaptan, a vasopressin receptor antagonist that does not affect HE risk, in cirrhotic patients...... with ascites. METHODS: The trials included 1198 patients, and we excluded those with HE before or at randomization and followed the remaining patients for the one year duration of the trials. They were examined for HE regularly, and we compared rates of first-time overt HE between diabetics and non-diabetic......Com comorbidity score. RESULTS: We included 862 patients of whom 193 (22%) had diabetes. In total, they experienced 115 first-time episodes of overt HE during the follow-up. Fewer diabetics than non-diabetic patients were in Child-Pugh class C at baseline (13% vs. 23%), yet they had higher cumulative risk...

Clinical relevance of magnetic resonance imaging and magnetic resonance spectroscopy for the cirrhotic without overt hepatic encephalopathy

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Fujishima, Yukou; Kato, Akinobu; Suzuki, Kazuyuki [Iwate Medical Univ., Morioka (Japan). School of Medicine

1999-04-01

To clarify the changes of pallidal high intensity on T1-weighted magnetic resonance imaging (MRI) and brain metabolites on magnetic resonance spectroscopy (MRS) as related to the severity of hepatic functions, the concentrations of blood ammonia (B-NH{sub 3}) and the levels of trace elements (Mn, Cu and Zn), 30 patients with liver cirrhosis without hepatic encephalopathy (HE) and 5 age-matched healthy control subjects underwent MRI and proton MRS. Pallidal high intensity (Pl index) and glutamine are higher in cirrhosis, and myo-inositol is lower than that of control statistically. In cirrhosis, there were statistically negative correlation between B-NH{sub 3} and myo-inositol and positive correlation between B-NH{sub 3} and glutamine. There was a statistically lower myo-inositol and higher Pl index, glutamine as the severity of hepatic functions increased. Furthermore there was a statistically positive correlation between Pl index and Mn. These data suggest that the changes of MRI and MRS findings already detected in cirrhosis without HE and these abnormalities may be reflect the B-NH{sub 3} and Mn metabolism and the severity of the hepatic functions. (author)

Clinical relevance of magnetic resonance imaging and magnetic resonance spectroscopy for the cirrhotic without overt hepatic encephalopathy

International Nuclear Information System (INIS)

Fujishima, Yukou; Kato, Akinobu; Suzuki, Kazuyuki

1999-01-01

To clarify the changes of pallidal high intensity on T1-weighted magnetic resonance imaging (MRI) and brain metabolites on magnetic resonance spectroscopy (MRS) as related to the severity of hepatic functions, the concentrations of blood ammonia (B-NH 3 ) and the levels of trace elements (Mn, Cu and Zn), 30 patients with liver cirrhosis without hepatic encephalopathy (HE) and 5 age-matched healthy control subjects underwent MRI and proton MRS. Pallidal high intensity (Pl index) and glutamine are higher in cirrhosis, and myo-inositol is lower than that of control statistically. In cirrhosis, there were statistically negative correlation between B-NH 3 and myo-inositol and positive correlation between B-NH 3 and glutamine. There was a statistically lower myo-inositol and higher Pl index, glutamine as the severity of hepatic functions increased. Furthermore there was a statistically positive correlation between Pl index and Mn. These data suggest that the changes of MRI and MRS findings already detected in cirrhosis without HE and these abnormalities may be reflect the B-NH 3 and Mn metabolism and the severity of the hepatic functions. (author)

Increase in hepatic arterial blood flow after transjugular intrahepatic portosystemic shunt creation and its potential predictive value of postprocedural encephalopathy and mortality.

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Patel, N H; Sasadeusz, K J; Seshadri, R; Chalasani, N; Shah, H; Johnson, M S; Namyslowski, J; Moresco, K P; Trerotola, S O

2001-11-01

To determine (i) whether there is a significant increase in hepatic artery blood flow (HABF) after transjugular intrahepatic portosystemic shunt (TIPS) creation and (ii) whether the extent of incremental increase in HABF is predictive of clinical outcome after TIPS creation. Prospective, nonrandomized, nonblinded duplex Doppler ultrasound (US) examinations were performed on 24 consecutive patients (19 men; Child Class A/B/C: 4/12/8, respectively) with a mean age of 52.8 years who were referred for TIPS creation for variceal bleeding. Peak hepatic artery velocity and vessel dimensions were used to calculate the hepatic arterial blood flow (HABF) before and after TIPS creation. Patients were clinically followed in the gastrohepatology clinic and TIPS US surveillance was performed at 1 and 3 months to assess shunt function. The extent of incremental increase in HABF was analyzed as a predictor of post-TIPS encephalopathy and/or death. The technical success rate of TIPS creation was 100%. The shunt diameters were either 10 mm (n = 11) or 12 mm (n = 13). TIPS resulted in a significant reduction in the portosystemic gradient from 24.3 mm Hg +/- 5.7 to 9.3 mm Hg +/- 2.9 (P creation, from 60.8 cm/sec +/- 26.7 to 121 cm/sec +/- 51.5 (P creation, new or worsened encephalopathy developed in five patients at 30 days and in an additional three at 90 days. They were all successfully managed medically. Three patients (12.5%) died within 30 days of the TIPS procedure. The extent of incremental increase in HABF after TIPS was variable and did not correlate with the development of 30-day and 90-day encephalopathy (P =.41 and P =.83, respectively) or 30-day mortality (P =.2). HABF increases significantly after TIPS but is not predictive of clinical outcome. The significance of the incremental increase is yet to be determined.

Colectomy for porto-systemic encephalopathy: is it still topical?

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Rym Ennaifer

2013-06-01

Full Text Available Hepatic encephalopathy (HE is a common long term complication of porto-systemic shunt. We report herein the case of a 59-year-old man with Child-Pugh A cirrhosis treated successfully 9 years earlier with distal splenorenal shunt for uncontrolled variceal bleeding. In the last year, he developed a severe and persistent hepatic encephalopathy secondary to the shunt, which was resistant to medical therapy. As liver transplantation was not available and obliteration of the shunt was hazardous, we performed subtotal colectomy in order to reduce ammonia production. This therapeutic option proved successful, as the grade of encephalopathy decreased and the patient improved. Our experience indicates that colonic exclusion should be considered as an option in the management of HE refractory to medical treatment in highly selected patients when liver transplantation is not available or even as a bridge given the long waiting time on lists.

Hemorrhagic shock and encephalopathy syndrome: a case report

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Yoon, Sook Ja; Choi, Yun Sun; Shin, Chung Ho; Cho, Sung Bum; Cho, Jae Min; Kim, Hyun Sook; Han, Tae Il; Yoon, Yong Kyu

2001-01-01

Hemorrhagic shock and encephalopathy syndrome (HSES) is a sudden-onset symptom complex that involves multisystem failure and includes encephalopathy, shock, coma, convulsions, prerenal azotemia, hepatic dysfunction, and bleeding coagulopathy and progressive thrombocytopenia in previously healthy infants and children. Its radiologic findings have rarely been reported, and it has not been described in Korea. We present a case of clinically diagnosed HSES, and include the CT and MRI findings

Lipopolysaccharide precipitates hepatic encephalopathy and increases blood-brain barrier permeability in mice with acute liver failure.

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Chastre, Anne; Bélanger, Mireille; Nguyen, Bich N; Butterworth, Roger F

2014-03-01

Acute liver failure (ALF) is frequently complicated by infection leading to precipitation of central nervous system complications such as hepatic encephalopathy (HE) and increased mortality. There is evidence to suggest that when infection occurs in ALF patients, the resulting pro-inflammatory mechanisms may be amplified that could, in turn, have a major impact on blood-brain barrier (BBB) function. The aim of this study was to investigate the role of endotoxemia on the progression of encephalopathy in relation to BBB permeability during ALF. Adult male C57-BL6 mice with ALF resulting from azoxymethane-induced toxic liver injury were administered trace amounts of the endotoxin component lipopolysaccharide (LPS). Effects on the magnitude of the systemic inflammatory response, liver pathology and BBB integrity were measured as a function of progression of HE, defined as time to loss of corneal reflex (coma). Lipopolysaccharide caused additional two- to seven-fold (P liver pathology and associated increases of circulating transaminases as well as increased hyperammonaemia consistent with a further loss of viable hepatocytes. LPS treatment of ALF mice led to a rapid precipitation of hepatic coma and the BBB became permeable to the 25-kDa protein immunoglobulin G (IgG). This extravasation of IgG was accompanied by ignificant up-regulation of matrix metalloproteinase-9 (MMP-9), an endopeptidase known to modulate opening of the BBB in a wide range of neurological disorders. These findings represent the first direct evidence of inflammation-related BBB permeability changes in ALF. © 2013 John Wiley & Sons A/S. Publishing by John Wiley & Sons Ltd.

Hepatic Complications of Anorexia Nervosa.

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Rosen, Elissa; Bakshi, Neeru; Watters, Ashlie; Rosen, Hugo R; Mehler, Philip S

2017-11-01

Anorexia nervosa (AN) has the highest mortality rate of all psychiatric illnesses due to the widespread organ dysfunction caused by the underlying severe malnutrition. Starvation causes hepatocyte injury and death leading to a rise in aminotransferases. Malnutrition-induced hepatitis is common among individuals with AN especially as body mass index decreases. Acute liver failure associated with coagulopathy and encephalopathy can rarely occur. Liver enzymes may also less commonly increase as part of the refeeding process due to hepatic steatosis and can be distinguished from starvation hepatitis by the finding of a fatty liver on ultrasonography. Individuals with AN and starvation-induced hepatitis are at increased risk of hypoglycemia due to depleted glycogen stores and impaired gluconeogenesis. Gastroenterology and hepatology consultations are often requested when patients with AN and signs of hepatitis are hospitalized. It should be noted that additional laboratory testing, imaging, or liver biopsy all have low diagnostic yield, are costly, and potentially invasive, therefore, not generally recommended for diagnostic purposes. While the hepatitis of AN can reach severe levels, a supervised increase in caloric intake and a return to a healthy body weight often quickly lead to normalization of elevated aminotransferases caused by starvation.

Hyperammonemic coma after craniotomy: Hepatic encephalopathy from upper gastrointestinal hemorrhage or valproate side effect?: Case report and literature review.

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Guo, Xiaopeng; Wei, Junji; Gao, Lu; Xing, Bing; Xu, Zhiqin

2017-04-01

Postoperative coma is not uncommon in patients after craniotomy. It generally presents as mental state changes and is usually caused by intracranial hematoma, brain edema, or swelling. Hyperammonemia can also result in postoperative coma; however, it is rarely recognized as a potential cause in coma patients. Hyperammonemic coma is determined through a complicated differential diagnosis, and although it can also be induced as a side effect of valproate (VPA), this cause is frequently unrecognized or confused with upper gastrointestinal hemorrhage (UGH)-induced hepatic encephalopathy. We herein present a case of valproate-induced hyperammonemic encephalopathy (VHE) to illustrate the rarity of such cases and emphasize the importance of correct diagnosis and proper treatment. A 61-year-old woman with meningioma was admitted into our hospital. Radical resection of the tumor was performed, and the patient recovered well as expected. After administration of valproate for 7 days, the patient was suddenly found in a deep coma, and her mental state deteriorated rapidly. The diagnoses of hepatic encephalopathy was confirmed. However, whether it origins from upper gastrointestinal hemorrhage or valproate side effect is uncertain. The patient's condition fluctuated without improvement during the subsequent 3 days under the treatment of reducing ammonia. With the discontinuation of valproate treatment, the patient regained complete consciousness within 48 hours, and her blood ammonia decreased to the normal range within 4 days. VHE is a rare but serious complication in patients after craniotomy and is diagnosed by mental state changes and elevated blood ammonia. Thus, the regular perioperative administration of VPA, which is frequently neglected as a cause of VHE, should be emphasized. In addition, excluding UGH prior to providing a diagnosis and immediately discontinuing VPA administration are recommended.

[Expression of aquaporin-4 during brain edema in rats with thioacetamide-induced acute encephalopathy].

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Wang, Li-Qing; Zhu, Sheng-Mei; Zhou, Heng-Jun; Pan, Cai-Fei

2011-09-27

To investigate the expression of aquaporin-4 (AQP4) during brain edema in rats with thioacetamide-induced acute liver failure and encephalopathy. The rat model of acute hepatic failure and encephalopathy was induced by intraperitoneal injection of thioacetamide (TAA) at a 24-hour interval for 2 consecutive days. Thirty-two SD rats were randomly divided into the model group (n = 24) and the control group (normal saline, n = 8). And then the model group was further divided into 3 subgroups by the timepoint of decapitation: 24 h (n = 8), 48 h (n = 8) and 60 h (n = 8). Then we observed their clinical symptoms and stages of HE, indices of liver function and ammonia, liver histology and brain water content. The expression of AQP4 protein in brain tissues was measured with Western blot and the expression of AQP4mRNA with RT-PCR (reverse transcription-polymerase chain reaction). Typical clinical manifestations of hepatic encephalopathy occurred in all TAA-administrated rats. The model rats showed the higher indices of ALT (alanine aminotransferase), AST (aspartate aminotransferase), TBIL (total bilirubin) and ammonia than the control rats (P liver failure and encephalopathy plays a significant role during brain edema. AQP4 is one of the molecular mechanisms for the occurrence of brain edema in hepatic encephalopathy.

Assessing inter- and intra-individual cognitive variability in patients at risk for cognitive impairment: the case of minimal hepatic encephalopathy.

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Bisiacchi, Patrizia; Cona, Giorgia; Tarantino, Vincenza; Schiff, Sami; Montagnese, Sara; Amodio, Piero; Capizzi, Giovanna

2014-12-01

Recent evidence reveals that inter- and intra-individual variability significantly affects cognitive performance in a number of neuropsychological pathologies. We applied a flexible family of statistical models to elucidate the contribution of inter- and intra-individual variables on cognitive functioning in healthy volunteers and patients at risk for hepatic encephalopathy (HE). Sixty-five volunteers (32 patients with cirrhosis and 33 healthy volunteers) were assessed by means of the Inhibitory Control Task (ICT). A Generalized Additive Model for Location, Scale and Shape (GAMLSS) was fitted for jointly modeling the mean and the intra-variability of Reaction Times (RTs) as a function of socio-demographic and task related covariates. Furthermore, a Generalized Linear Mixed Model (GLMM) was fitted for modeling accuracy. When controlling for the covariates, patients without minimal hepatic encephalopathy (MHE) did not differ from patients with MHE in the low-demanding condition, both in terms of RTs and accuracy. Moreover, they showed a significant decline in accuracy compared to the control group. Compared to patients with MHE, patients without MHE showed faster RTs and higher accuracy only in the high-demanding condition. The results revealed that the application of GAMLSS and GLMM models are able to capture subtle cognitive alterations, previously not detected, in patients' subclinical pathologies.

Machine Learning Classification of Cirrhotic Patients with and without Minimal Hepatic Encephalopathy Based on Regional Homogeneity of Intrinsic Brain Activity.

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Chen, Qiu-Feng; Chen, Hua-Jun; Liu, Jun; Sun, Tao; Shen, Qun-Tai

2016-01-01

Machine learning-based approaches play an important role in examining functional magnetic resonance imaging (fMRI) data in a multivariate manner and extracting features predictive of group membership. This study was performed to assess the potential for measuring brain intrinsic activity to identify minimal hepatic encephalopathy (MHE) in cirrhotic patients, using the support vector machine (SVM) method. Resting-state fMRI data were acquired in 16 cirrhotic patients with MHE and 19 cirrhotic patients without MHE. The regional homogeneity (ReHo) method was used to investigate the local synchrony of intrinsic brain activity. Psychometric Hepatic Encephalopathy Score (PHES) was used to define MHE condition. SVM-classifier was then applied using leave-one-out cross-validation, to determine the discriminative ReHo-map for MHE. The discrimination map highlights a set of regions, including the prefrontal cortex, anterior cingulate cortex, anterior insular cortex, inferior parietal lobule, precentral and postcentral gyri, superior and medial temporal cortices, and middle and inferior occipital gyri. The optimized discriminative model showed total accuracy of 82.9% and sensitivity of 81.3%. Our results suggested that a combination of the SVM approach and brain intrinsic activity measurement could be helpful for detection of MHE in cirrhotic patients.

MRI findings in acute hyperammonemic encephalopathy resulting from decompensated chronic liver disease.

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Sureka, Jyoti; Jakkani, Ravi Kanth; Panwar, Sanuj

2012-06-01

Hyperammonemic encephalopathy is a type of metabolic encephalopathy with diversified etiology. Hyperammonemia is the end result of several metabolic disorders such as congenital deficiencies of urea cycle enzymes, hepatic encephalopathy, Reye's syndrome and other toxic encephalopathies. Non-specific clinical presentation poses a great challenge in early diagnosis of this entity. Irrespective of the underlying etiology, hyperammonemia causes a distinctive pattern of brain parenchymal injury. The cingulate gyrus and insular cortex are more vulnerable to this type of toxic insult. Characteristic magnetic resonance imaging findings in combination with laboratory parameters can help to differentiate this entity from other metabolic encephalopathy and thus aiding in early diagnosis and treatment.

Disrupted small world networks in patients without overt hepatic encephalopathy: A resting state fMRI study

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Zhang, Long Jiang, E-mail: kevinzhlj@163.com [Department of Medical Imaging, Jinling Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210002 (China); Zheng, Gang [Department of Medical Imaging, Jinling Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210002 (China); College of Civil Aviation, Nanjing University of Aeronautics and Astronautics, Nanjing, Jiangsu 210016 (China); Zhang, Liping [College of Natural Science, Nanjing University of Aeronautics and Astronautics, Nanjing, Jiangsu 210016 (China); Zhong, Jianhui [Department of Biomedical Engineering, Zhejiang University, Hangzhou, Zhejiang 310027 (China); Li, Qiang [College of Natural Science, Nanjing University of Aeronautics and Astronautics, Nanjing, Jiangsu 210016 (China); Zhao, Tie Zhu [Department of Medical Imaging, Jinling Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210002 (China); College of Civil Aviation, Nanjing University of Aeronautics and Astronautics, Nanjing, Jiangsu 210016 (China); Lu, Guang Ming, E-mail: cjr.luguangming@vip.163.com [Department of Medical Imaging, Jinling Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210002 (China)

2014-10-15

Purpose: To explore changes in functional connectivity and topological organization of brain functional networks in cirrhotic patients with minimal hepatic encephalopathy (MHE) and non hepatic encephalopathy (nonHE) and their relationship with clinical markers. Materials and methods: Resting-state functional MR imaging was acquired in 22 MHE, 29 nonHE patients and 33 healthy controls. Functional connectivity networks were obtained by computing temporal correlations between any pairs of 90 cortical and subcortical regions. Graph analysis measures were quantitatively assessed for each subject. One-way analysis of covariance was applied to identify statistical differences of functional connectivity and network parameters among three groups. Correlations between clinical markers, such as Child–Pugh scores, venous blood ammonia level, and number connection test type A (NCT-A)/digit symbol test (DST) scores, and connectivity/graph metrics were calculated. Results: Thirty functional connectivities represented by edges were found to be abnormal (P < 0.05, FDR corrected) in cirrhotic patients, in which 16 edges (53.3%) were related with sub-cortical regions. MHE patients showed abnormal small-world attributes in the functional connectivity networks. Cirrhotic patients had significantly reduced nodal degree in 8 cortical regions and increased nodal centrality in 3 cortical regions. Twenty edges were correlated with either NCT-A or DST scores, in which 13 edges were related with sub-cortical regions. No correlation was found between Child–Pugh scores and graph theoretical measures in cirrhotic patients. Conclusion: Disturbances of brain functional connectivity and small world property loss are associated with neurocognitive impairment of cirrhotic patients. Reorganization of brain network occurred during disease progression from nonHE to MHE.

Disrupted small world networks in patients without overt hepatic encephalopathy: A resting state fMRI study

International Nuclear Information System (INIS)

Zhang, Long Jiang; Zheng, Gang; Zhang, Liping; Zhong, Jianhui; Li, Qiang; Zhao, Tie Zhu; Lu, Guang Ming

2014-01-01

Purpose: To explore changes in functional connectivity and topological organization of brain functional networks in cirrhotic patients with minimal hepatic encephalopathy (MHE) and non hepatic encephalopathy (nonHE) and their relationship with clinical markers. Materials and methods: Resting-state functional MR imaging was acquired in 22 MHE, 29 nonHE patients and 33 healthy controls. Functional connectivity networks were obtained by computing temporal correlations between any pairs of 90 cortical and subcortical regions. Graph analysis measures were quantitatively assessed for each subject. One-way analysis of covariance was applied to identify statistical differences of functional connectivity and network parameters among three groups. Correlations between clinical markers, such as Child–Pugh scores, venous blood ammonia level, and number connection test type A (NCT-A)/digit symbol test (DST) scores, and connectivity/graph metrics were calculated. Results: Thirty functional connectivities represented by edges were found to be abnormal (P < 0.05, FDR corrected) in cirrhotic patients, in which 16 edges (53.3%) were related with sub-cortical regions. MHE patients showed abnormal small-world attributes in the functional connectivity networks. Cirrhotic patients had significantly reduced nodal degree in 8 cortical regions and increased nodal centrality in 3 cortical regions. Twenty edges were correlated with either NCT-A or DST scores, in which 13 edges were related with sub-cortical regions. No correlation was found between Child–Pugh scores and graph theoretical measures in cirrhotic patients. Conclusion: Disturbances of brain functional connectivity and small world property loss are associated with neurocognitive impairment of cirrhotic patients. Reorganization of brain network occurred during disease progression from nonHE to MHE

Feasibility of adjunct therapeutic hypothermia treatment for hyperammonemia and encephalopathy due to urea cycle disorders and organic acidemias.

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Lichter-Konecki, Uta; Nadkarni, Vinay; Moudgil, Asha; Cook, Noah; Poeschl, Johannes; Meyer, Michael T; Dimmock, David; Baumgart, Stephen

2013-08-01

Children with urea cycle disorders (UCDs) or organic acidemias (OAs) and acute hyperammonemia and encephalopathy are at great risk for neurological injury, developmental delay, intellectual disability, and death. Nutritional support, intravenous alternative pathway therapy, and dialysis are used to treat severe hyperammonemia associated with UCDs and nutritional support and dialysis are used to treat severe hyperammonemia in OAs. Brain protective treatment while therapy is initiated may improve neurological and cognitive function for the lifetime of the child. Animal experiments and small clinical trials in hepatic encephalopathy caused by acute liver failure suggest that therapeutic hypothermia provides neuroprotection in hyperammonemia associated encephalopathy. We report results of an ongoing pilot study that assesses if whole body cooling during rescue treatment of neonates with acute hyperammonemia and encephalopathy is feasible and can be conducted safely. Adjunct whole body therapeutic hypothermia was conducted in addition to standard treatment in acutely encephalopathic, hyperammonemic neonates with UCDs and OAs requiring dialysis. Therapeutic hypothermia was initiated using cooling blankets as preparations for dialysis were underway. Similar to standard therapeutic hypothermia treatment for neonatal hypoxic ischemic encephalopathy, patients were maintained at 33.5°C±1°C for 72h, they were then slowly rewarmed by 0.5°C every 3h over 18h. In addition data of age-matched historic controls were collected for comparison. Seven patients were cooled using the pilot study protocol and data of seven historic controls were reviewed. All seven patients survived the initial rescue and cooling treatment, 6 patients were discharged home 2-4weeks after hospitalization, five of them feeding orally. The main complication observed in a majority of patients was hypotension. Adjunct therapeutic hypothermia for neonates with UCDs and OAs receiving standard treatment was

Multi-Sensory Integration Impairment in Patients with Minimal Hepatic Encephalopathy.

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Seo, Kyoungwon; Jun, Dae Won; Kim, Jae-Kwan; Ryu, Hokyoung

2017-11-02

Paper-and-pencil-based psychometric tests are the gold standard for diagnosis of cognitive dysfunction in liver disease. However, they take time, can be affected by demographic factors, and lack ecological validity. This study explored multi-sensory integration ability to discriminate cognitive dysfunction in cirrhosis. Thirty-two healthy controls and 30 cirrhotic patients were recruited. The sensory integration test presents stimuli from two different modalities (e.g., image/sound) with a short time lag, and subjects judge which stimuli appeared first. Repetitive tests reveal the sensory integration capability. Performance in the sensory integration test, psychometric tests, and functional near-infrared spectroscopy for patients was compared to controls. Sensory integration capability, the perceptual threshold to discriminate the time gap between an image and sound stimulus, was significantly impaired in cirrhotic patients with minimal hepatic encephalopathy (MHE) compared to controls (p integration test showed good correlation with psychometric tests (NCT-A, r = 0.383, p = 0.002; NCT-B, r = 0.450, p integration test was not affected. The sensory integration test, where a cut-off value for the perceptual threshold was 133.3ms, recognized MHE patients at 90% sensitivity and 86.5% specificity.

Economic impact of the use of rifaximin 550 mg twice daily for the treatment of overt hepatic encephalopathy in Italy

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Roggeri DP

2017-09-01

, results in a reduction in total health care costs charged to INHS due to a reduction in hospitalizations for HE recurrences. Keywords: overt hepatic encephalopathy recurrences, health care expenditure, costs, hospitalizations, budget impact

Comparison of once a day rifaximin to twice a day dosage in the prevention of recurrence of hepatic encephalopathy in patients with chronic liver disease.

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Khokhar, Nasir; Qureshi, Muhammad Omar; Ahmad, Shafiq; Ahmad, Aiza; Khan, Hamza Hassan; Shafqat, Farzana; Salih, Muhammad

2015-09-01

Rifaximin has been used for prevention of recurrence of hepatic encephalopathy in twice a day dosage. The drug is expensive and lower dising may be possible. To determine the efficacy of rifaximin once a day dose in the prevention of hepatic encephalopathy (HE) in patients with liver cirrhosis as compared with twice daily dose of rifaximin. This Randomized control trial was carried out at the Department of Gastroenterology and Hepatology, Shifa International Hospital, Islamabad, Pakistan from November 2012 to February 2014. Patients with known chronic liver disease with at least one episode of HE in the past were randomized to group A (rifaximin 550 mg OD) and group B (rifaximin 550 mg BD), after fulfilling the inclusion criteria. Each patient was followed for 6 months for any episode of HE. Patients in each group were identified for any breakthrough episode of encephalopathy during this period. Data were analyzed using SPSS version 16. Chi-squared test and t-test were applied where required to determine the significant difference between the two groups. There were a total of 306 patients: 128 patients in Group A while 178 in group B. Majority of patients (75.81%) had hepatitis C virus with mean age of 52.30 ± 9.92, MELD score 13.58 ± 8.3, and 55.22% were in Child-Pugh B. Eighty-one patients had an episode of HE during the study period. There were 27 patients in group A and 54 patients in group B with breakthrough episode of HE (P = 0.088). This study suggests that there is no significant difference in rifaximin once a day or twice daily dose in preventing HE. © 2015 Journal of Gastroenterology and Hepatology Foundation and Wiley Publishing Asia Pty Ltd.

Synthesis of neurotransmitter GABA via the neuronal tricarboxylic acid cycle is elevated in rats with liver cirrhosis consistent with a high GABAergic tone in chronic hepatic encephalopathy

DEFF Research Database (Denmark)

Leke, Renata; Bak, Lasse Kristoffer; Iversen, Peter

2011-01-01

J. Neurochem. (2011) 117, 824-832. ABSTRACT: Hepatic encephalopathy (HE) is a neuropsychiatric complication to liver disease. It is known that ammonia plays a role in the pathogenesis of HE and disturbances in the GABAergic system have been related to HE. Synthesis of GABA occurs by decarboxylation...

Acquired hepatocerebral degeneration and hepatic encephalopathy: correlations and variety of clinical presentations in overt and subclinical liver disease

Directory of Open Access Journals (Sweden)

Fernando G. Romeiro

2011-06-01

Full Text Available Acquired hepatocerebral degeneration (AHD and hepatolenticular degeneration can have similar clinical presentations, but when a chronic liver disease and atypical motor findings coexist, the distinction between AHD and hepatic encephalopathy (HE can be even more complicated. We describe three cases of AHD (two having HE with different neuroimaging findings, distinct hepatic diseases and similar motor presentations, all presenting chronic arterial hypertension and weight loss before the disease manifestations. The diagnosis and physiopathology are commented upon and compared with previous reports. In conclusion, there are many correlations among HE, hepatolenticular degeneration and AHD, but the overlapping of AHD and HE could be more common depending on the clinical knowledge and diagnostic criteria adopted for each condition. Since AHD is not considered a priority that affects the liver transplant list, the prognosis in AHD patients remains poor, and flow interruption in portosystemic shunts must always be taken into account.

A New Look at Precipitants of Overt Hepatic Encephalopathy in Cirrhosis.

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Pantham, Ganesh; Post, Anthony; Venkat, Deepak; Einstadter, Douglas; Mullen, Kevin D

2017-08-01

Overt hepatic encephalopathy (HE) is a major cause of significant morbidity and mortality in patients with liver cirrhosis. We examined the frequency and profile of the precipitating factors resulting in hospitalizations for overt HE. We conducted both retrospective and prospective studies to identify clinical precipitants of overt HE in patients with cirrhosis. The retrospective study patients were hospitalized at a large urban safety-net hospital, and the prospective study included the patients admitted at a liver transplant center. There were a total of 149 patients with cirrhosis and overt HE (91 males, mean age 55.3 ± 8.6 years) in the retrospective group and 45 patients (27 males, mean age 58.3 ± 8.2 years) in the prospective group of the study. The average MELD score was 16 ± 6.8 in the retrospective group and 22.7 ± 7.2 in the prospective group. Dehydration (46-76%), acute kidney injury (32-76%), lactulose nonadherence (about 50%), constipation (about 40%), and infections (20-42%) were the most frequently identified precipitants for hospitalization in retrospective and prospective groups. Multiple precipitants were identified in 60 (40.3%) patients in the retrospective group and 34 (76%) patients in the prospective group. Multiple concurrent precipitating factors were identified in the majority of patients with overt HE requiring hospitalization. Dehydration due to various causes was the most common precipitant of overt HE, followed by acute kidney injury (AKI), constipation, and infections. Prevention of dehydration, AKI, and constipation by close outpatient monitoring may be an effective measure to prevent hospitalization for overt HE in patients with cirrhosis.

Presumptive Iatrogenic Microcystin-Associated Liver Failure and Encephalopathy in a Holsteiner Gelding.

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Mittelman, N S; Engiles, J B; Murphy, L; Vudathala, D; Johnson, A L

2016-09-01

An 8-year-old Holsteiner gelding was presented for evaluation of anorexia, obtundation, icterus, and mild colic signs of 48 hours duration. History, physical examination, and initial diagnostics were suggestive of hepatic disease and encephalopathy. Microcystin toxicosis was suspected based on historical administration of a cyanobacteria supplement, associated serum biochemistry abnormalities, and characteristic histopathological changes. Microcystin contamination was confirmed in both supplement containers fed to the horse. Fulminant hepatic failure and encephalopathy progressed resulting in euthanasia. Necropsy findings were consistent with microcystin induced liver failure. Copyright © 2016 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine.

Increased toll-like receptor 4 in cerebral endothelial cells contributes to the astrocyte swelling and brain edema in acute hepatic encephalopathy.

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Jayakumar, Arumugam R; Tong, Xiao Y; Curtis, Kevin M; Ruiz-Cordero, Roberto; Abreu, Maria T; Norenberg, Michael D

2014-03-01

Astrocyte swelling and the subsequent increase in intracranial pressure and brain herniation are major clinical consequences in patients with acute hepatic encephalopathy. We recently reported that conditioned media from brain endothelial cells (ECs) exposed to ammonia, a mixture of cytokines (CKs) or lipopolysaccharide (LPS), when added to astrocytes caused cell swelling. In this study, we investigated the possibility that ammonia and inflammatory agents activate the toll-like receptor 4 (TLR4) in ECs, resulting in the release of factors that ultimately cause astrocyte swelling. We found a significant increase in TLR4 protein expression when ECs were exposed to ammonia, CKs or LPS alone, while exposure of ECs to a combination of these agents potentiate such effects. In addition, astrocytes exposed to conditioned media from TLR4-silenced ECs that were treated with ammonia, CKs or LPS, resulted in a significant reduction in astrocyte swelling. TLR4 protein up-regulation was also detected in rat brain ECs after treatment with the liver toxin thioacetamide, and that thioacetamide-treated TLR4 knock-out mice exhibited a reduction in brain edema. These studies strongly suggest that ECs significantly contribute to the astrocyte swelling/brain edema in acute hepatic encephalopathy, likely as a consequence of increased TLR4 protein expression by blood-borne noxious agents. © 2013 International Society for Neurochemistry.

Modern view on hepatic encephalopathy: basic terms and concepts of pathogenesis

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T. V. Shulyatnikova

2017-12-01

Full Text Available Background. The problem of acute and chronic forms of hepatic encephalopathy (HE is not clearly identified among modern problems of hepatology and neuroscience in Ukraine. Despite the significant contribution to the development of lethal complications in patients with liver pathology and long history of the study of this issue, there is still no unified opinion on the links of HE pathogenesis. The aim of this review is to conduct a comprehensive analysis of current data on the spreading and mechanisms of development of HE. HE is a complex of potentially reversible neurocognitive disorders in patients with chronic or acute hepatic failure (ALF. HE is more often a complication of liver cirrhosis and is the second most frequent cause of hospitalization of such patients after ascites. When decompensating liver failure in acute or chronic hepatic pathology in patients severe forms of HE develop, accompanied by a progressive increase in intracranial pressure and the development of coma, which often ends lethal due to poor corrigibility of intracranial hypertension while maintaining hepatogenic neurointoxication. HE is considered as the end result of the accumulation of a number of neurotoxic substances in the brain, among which are ammonia, mercaptans, short chain fatty acids, false neurotransmitters, gamma-aminobutyric acid, manganese. The most popular among the reasons for the development of HE is the neurotoxic theory of ammonia. Ammonia is subjected to detoxification in the liver, turning into urea, a smaller fraction with the participation of glutamine synthetase is used in the synthesis of glutamine in muscles, liver and astrocytes of brain. In case of hepatic dysfunction and/or portosystemic shunting, the concentration of ammonia in blood increases up to 10 times and the main load for its detoxification is shifted to myocytes and astroglia. In ALF glutamine overload of astrocytes occurs with a change in intracellular osmolarity and subsequent

Bile Acid-Mediated Sphingosine-1-Phosphate Receptor 2 Signaling Promotes Neuroinflammation during Hepatic Encephalopathy in Mice

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Matthew McMillin

2017-07-01

Full Text Available Hepatic encephalopathy (HE is a neuropsychiatric complication that occurs due to deteriorating hepatic function and this syndrome influences patient quality of life, clinical management strategies and survival. During acute liver failure, circulating bile acids increase due to a disruption of the enterohepatic circulation. We previously identified that bile acid-mediated signaling occurs in the brain during HE and contributes to cognitive impairment. However, the influences of bile acids and their downstream signaling pathways on HE-induced neuroinflammation have not been assessed. Conjugated bile acids, such as taurocholic acid (TCA, can activate sphingosine-1-phosphate receptor 2 (S1PR2, which has been shown to promote immune cell infiltration and inflammation in other models. The current study aimed to assess the role of bile-acid mediated S1PR2 signaling in neuroinflammation and disease progression during azoxymethane (AOM-induced HE in mice. Our findings demonstrate a temporal increase of bile acids in the cortex during AOM-induced HE and identified that cortical bile acids were elevated as an early event in this model. In order to classify the specific bile acids that were elevated during HE, a metabolic screen was performed and this assay identified that TCA was increased in the serum and cortex during AOM-induced HE. To reduce bile acid concentrations in the brain, mice were fed a diet supplemented with cholestyramine, which alleviated neuroinflammation by reducing proinflammatory cytokine expression in the cortex compared to the control diet-fed AOM-treated mice. S1PR2 was expressed primarily in neurons and TCA treatment increased chemokine ligand 2 mRNA expression in these cells. The infusion of JTE-013, a S1PR2 antagonist, into the lateral ventricle prior to AOM injection protected against neurological decline and reduced neuroinflammation compared to DMSO-infused AOM-treated mice. Together, this identifies that reducing bile acid

Limonene in exhaled breath is elevated in hepatic encephalopathy

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O’Hara, M E; Fernández del Río, R; Holt, A; Pemberton, P; Shah, T; Whitehouse, T; Mayhew, C A

2016-01-01

Abstract Breath samples were taken from 31 patients with liver disease and 30 controls in a clinical setting and proton transfer reaction quadrupole mass spectrometry (PTR-Quad-MS) used to measure the concentration of volatile organic compounds (VOCs). All patients had cirrhosis of various etiologies, with some also suffering from hepatocellular cancer (HCC) and/or hepatic encephalopathy (HE). Breath limonene was higher in patients with No-HCC than with HCC, median (lower/upper quartile) 14.2 (7.2/60.1) versus 3.6 (2.0/13.7) and 1.5 (1.1/2.3) nmol mol−1 in controls. This may reflect disease severity, as those with No-HCC had significantly higher UKELD (United Kingdom model for End stage Liver Disease) scores. Patients with HE were categorized as having HE symptoms presently, having a history but no current symptoms and having neither history nor current symptoms. Breath limonene in these groups was median (lower/upper quartile) 46.0 (14.0/103), 4.2 (2.6/6.4) and 7.2 (2.0/19.1) nmol mol−1, respectively. The higher concentration of limonene in those with current symptoms of HE than with a history but no current symptoms cannot be explained by disease severity as their UKELD scores were not significantly different. Longitudinal data from two patients admitted to hospital with HE show a large intra-subject variation in breath limonene, median (range) 18 (10–44) and 42 (32–58) nmol mol−1. PMID:27869108

Pathological Predictors of Shunt Stenosis and Hepatic Encephalopathy after Transjugular Intrahepatic Portosystemic Shunt

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Fuliang He

2016-01-01

Full Text Available Background. Transjugular intrahepatic portosystemic shunt (TIPS is an artificial channel from the portal vein to the hepatic vein or vena cava for controlling portal vein hypertension. The major drawbacks of TIPS are shunt stenosis and hepatic encephalopathy (HE; previous studies showed that post-TIPS shunt stenosis and HE might be correlated with the pathological features of the liver tissues. Therefore, we analyzed the pathological predictors for clinical outcome, to determine the risk factors for shunt stenosis and HE after TIPS. Methods. We recruited 361 patients who suffered from portal hypertension symptoms and were treated with TIPS from January 2009 to December 2012. Results. Multivariate logistic regression analysis showed that the risk of shunt stenosis was increased with more severe inflammation in the liver tissue (OR, 2.864; 95% CI: 1.466–5.592; P=0.002, HE comorbidity (OR, 6.266; 95% CI, 3.141–12.501; P<0.001, or higher MELD score (95% CI, 1.298–1.731; P<0.001. Higher risk of HE was associated with shunt stenosis comorbidity (OR, 6.266; 95% CI, 3.141–12.501; P<0.001, higher stage of the liver fibrosis (OR, 2.431; 95% CI, 1.355–4.359; P=0.003, and higher MELD score (95% CI, 1.711–2.406; P<0.001. Conclusion. The pathological features can predict individual susceptibility to shunt stenosis and HE.

Special focus on cerebral myo-inositol in patients with hepatic encephalopathy : proton MR spectroscopic evaluation

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Choi, Choong Gon; Lee, Ho Kyu; Suh, Dae Chul; Lim, Tae Whan; Auh, Yong Ho; Lee Young Sang [Ulsan Univ. College of Medicine , Seoul (Korea, Republic of); Lee, Jung Hee [Asan Institute for Life Sciences, Seoul (Korea, Republic of)

1996-08-01

To determine whether or not cerebral myo-inositol/creatine-phos-phocreatine (MI/Cr) level can be used as a criterion of hepatic encephalopathy (HE). Single voxel stimulated echo sequence with short echo time (30ms) was applied to parietal white matter of 14 healthy control subjects, 11 patients with chronic viral hepatitis, 29 cirrhotic patients without HE, and 33 cirrhotic patients with HE. The metabolite ratios of N-acetylaspartate (NAA), choline containing compounds (Cho), and myo-Inositol (MI) were calculated using creatine/phosphocreatine (Cr) as an internal reference. Clinical data including modified Child-Pugh score, estimated serum osmolarity, and grade of HE, were obtained at the day of MR spectroscopy. MI/Cr was 34% lower in cirrhotic patients with HE than in control subjects. It was reduced below two standard deviation from normal in 17 of 33 cirrhotic patients with HE (52%). MI/Cr did not correlate with grade of HE (r=-0.55, p=0.00). In the analysis of Child class C patients, there was no significant difference of MI/Cr between cirrhotic patients with HE and those without HE (0.83 {+-} 0.11, n= 29 vs. 0.39 {+-} 0.11, n= 15, p= 0.59, respectively). A reduction of cerebral MI/Cr cannot be used as a diagnostic criterion of HE.

A critical analysis of studies assessing L-ornithine-L-aspartate (LOLA in hepatic encephalopathy treatment Uma análise crítica dos estudos de avaliação do L-ornitina-L-aspartato (LOLA no tratamento da encefalopatia hepática

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Patrícia Coelho de Soárez

2009-09-01

Full Text Available CONTEXT: Experimental and clinical studies suggest that LOLA may have a favorable influence on hepatic encephalopathy due to the effect on the reduction of ammonia, and improvement of the symptoms and laboratory findings. OBJECTIVES: To evaluate and to critically analyze the efficacy and/or effectiveness results of the use of LOLA when compared to placebo in the treatment of hepatic encephalopathy. DATA SOURCES: LILACS, SciELO, MEDLINE, PubMed database and Cochrane Collaboration Register of Controlled Trials were searched from 1966 to September of 2006. The review has included all the randomized controlled double-blind clinical trials performed in humans in English language. RESULTS: Four studies published between 1993 and 2000 were selected and reviewed. LOLA was showed as being able to reduce hyperammonemia in patients with hepatic encephalopathy, when compared to patients in the placebo group. CONCLUSIONS: Although the trials have shown efficacy of LOLA in reducing hyperammonemia of hepatic encephalopathy, sufficient evidence of a significant beneficial effect of LOLA on patients with hepatic encephalopathy was not found. The studies performed in this area were small, with short follow-up periods and half of them showed low methodological quality.CONTEXTO: Estudos experimentais e clínicos sugerem que a L-ornitina-L-aspartato pode ter uma influência favorável na encefalopatia hepática em virtude do seu efeito na redução da amônia, e melhora dos sintomas e achados laboratoriais. OBJETIVOS: Avaliar e analisar criticamente os estudos de eficácia e/ou efetividade do uso de L-ornitina-L-aspartato quando comparado com placebo no tratamento da encefalopatia hepática. FONTES DE INFORMAÇÃO: Foram pesquisadas as bases de dados LILACS, SciELO, MEDLINE, PubMed e o Registro de Ensaios Controlados da Colaboração Cochrane no período de 1966 até setembro de 2006. A revisão incluiu todos os ensaios clínicos controlados randomizados, duplo

Adult onset urea cycle disorder in a patient with presumed hepatic encephalopathy.

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Atiq, Muslim; Holt, Andrew F; Safdar, Kamran; Weber, Frederick; Ravinuthala, Ravi; Jonas, Mark E; Neff, Guy W

2008-02-01

Deficiency of any of the 5 enzymes in the urea cycle results in the accumulation of ammonia, leading to encephalopathy; which if untreated, can be lethal and produce devastating neurologic sequelae in long-term survivors. We hereby present an interesting case that presented with hyperammonemia and encephalopathy; later found to have an urea cycle defect.

Cerebral blood flow measured by arterial-spin labeling MRI: A useful biomarker for characterization of minimal hepatic encephalopathy in patients with cirrhosis

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Zheng, Gang; Zhang, Long Jiang; Zhong, Jianhui; Wang, Ze; Qi, Rongfeng; Shi, Donghong; Lu, Guang Ming

2013-01-01

Purpose: To investigate the role of arterial-spin labeling (ASL) MRI to non-invasively characterize the patterns of cerebral blood flow (CBF) changes in cirrhotic patients and to assess the potential of ASL MRI to characterize minimal hepatic encephalopathy (MHE). Materials and methods: This study was approved by the local ethics committee, and written informed consent was obtained from all participants. Thirty six cirrhosis patients without overt hepatic encephalopathy (16 MHE patients and 20 non hepatic encephalopathy (non-HE) patients) and 25 controls underwent ASL MRI, and CBF was measured for each subject. One-way ANOCOVA test with age and gender as covariences was used to compare CBF difference among three groups, and post hoc analysis was performed between each two groups. Region-based correlation analysis was applied between Child–Pugh score, venous blood ammonia level, neuropsychological tests and CBF values in cirrhosis patients. Receiver operator characteristic (ROC) analysis was used for assessing CBF measurements in ASL MRI to differentiate MHE from non-HE patients. Results: The gray matter CBF of MHE patients (71.09 ± 11.88 mL min −1 100 g −1 ) was significantly higher than that of non-HE patients (55.28 ± 12.30 mL min −1 100 g −1 , P < 0.01) and controls (52.09 ± 9.27 mL min −1 100 g −1 , P < 0.001). Voxel-wise ANOCOVA results showed that CBFs were significantly different among three groups in multiple gray matter areas (P < 0.05, Bonferroni corrected). Post hoc comparisons showed that CBF of these brain regions was increased in MHE patients compared with controls and non-HE patients (P < 0.05, Bonferroni corrected). CBF of the right putamen was of the highest sensitivity (93.8%) and moderate specificity (75.0%) for characterization of MHE when using the cutoff value of 50.57 mL min −1 100 g −1 . CBFs in the bilateral median cingulate gyri, left supramarginal gyrus, right angular gyrus, right heschl gyrus and right superior

Cerebral blood flow measured by arterial-spin labeling MRI: A useful biomarker for characterization of minimal hepatic encephalopathy in patients with cirrhosis

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Zheng, Gang [Department of Medical Imaging, Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing, Jiangsu, 210002 (China); College of Civil Aviation, Nanjing University of Aeronautics and Astronautics, Nanjing, Jiangsu, 210016 (China); Zhang, Long Jiang, E-mail: kevinzhlj@163.com [Department of Medical Imaging, Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing, Jiangsu, 210002 (China); Zhong, Jianhui [Department of Imaging Sciences, University of Rochester School of Medicine and Dentistry, Box648, 601 Elmwood Avenue, Rochester, NY 14642-8648 (United States); Wang, Ze [Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, 3900 Chestnut St., Philadelphia, PA 19104 (United States); Qi, Rongfeng; Shi, Donghong [Department of Medical Imaging, Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing, Jiangsu, 210002 (China); Lu, Guang Ming, E-mail: cjr.luguangming@vip.163.com [Department of Medical Imaging, Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing, Jiangsu, 210002 (China)

2013-11-01

Purpose: To investigate the role of arterial-spin labeling (ASL) MRI to non-invasively characterize the patterns of cerebral blood flow (CBF) changes in cirrhotic patients and to assess the potential of ASL MRI to characterize minimal hepatic encephalopathy (MHE). Materials and methods: This study was approved by the local ethics committee, and written informed consent was obtained from all participants. Thirty six cirrhosis patients without overt hepatic encephalopathy (16 MHE patients and 20 non hepatic encephalopathy (non-HE) patients) and 25 controls underwent ASL MRI, and CBF was measured for each subject. One-way ANOCOVA test with age and gender as covariences was used to compare CBF difference among three groups, and post hoc analysis was performed between each two groups. Region-based correlation analysis was applied between Child–Pugh score, venous blood ammonia level, neuropsychological tests and CBF values in cirrhosis patients. Receiver operator characteristic (ROC) analysis was used for assessing CBF measurements in ASL MRI to differentiate MHE from non-HE patients. Results: The gray matter CBF of MHE patients (71.09 ± 11.88 mL min{sup −1} 100 g{sup −1}) was significantly higher than that of non-HE patients (55.28 ± 12.30 mL min{sup −1} 100 g{sup −1}, P < 0.01) and controls (52.09 ± 9.27 mL min{sup −1} 100 g{sup −1}, P < 0.001). Voxel-wise ANOCOVA results showed that CBFs were significantly different among three groups in multiple gray matter areas (P < 0.05, Bonferroni corrected). Post hoc comparisons showed that CBF of these brain regions was increased in MHE patients compared with controls and non-HE patients (P < 0.05, Bonferroni corrected). CBF of the right putamen was of the highest sensitivity (93.8%) and moderate specificity (75.0%) for characterization of MHE when using the cutoff value of 50.57 mL min{sup −1} 100 g{sup −1}. CBFs in the bilateral median cingulate gyri, left supramarginal gyrus, right angular gyrus, right

A study of proton MR spectroscopy in patients with minimal hepatic encephalopathy

International Nuclear Information System (INIS)

Li Mei; Wu Lizhong; Ding Xiaolong; Hu Xing; Xu Jie; Dai Qiang; Bao Zhijun

2009-01-01

Objective: To evaluate changes of regional cerebral metabolism by proton MR spectroscopy ( 1 H-MRS) in patients with minimal hepatic encephalopathy (MHE) and to correlate these changes with the neuropsychological test. Methods: Fifty-four patients with cirrhosis including nine patients with hepatic encephalopathy (HE), 23 patients with MHE, 22 patients without HE and 13 controls underwent neuropsychological tests and 1 H-MRS scanning. The volumes of interest included occipital gray matter and left parietal white matter regions. Ratio of spectral peak areas of N-acetylaspartate (NAA), choline (Cho), myo-inositol (mI), and glutamine/glutamate (Glx) relative to creatine (Cr) were acquired. Statistical analysis was conducted using independent t test and one-way analysis of variance. The results of different groups were compared by using the nonparametric Mann-Whitney U test with Bonferroni correction. Correlations among the 1 H-MRS ratios, the grade of HE, neuropsychological test and ammonia data were calculated with Spearman correlation test. Results: The ratios of NAA/Cr, Cho/Cr, mI/Cr, Glx/Cr of the occipital gray matter and left parietal white matter regions in patients with cirrhosis are 1.55± 0.12, 0.48±0.10, 0.42±0.14, 2.52±0.48 and 1.73±0.17, 0.75±0.16, 0.42±0.16, 2.75±0.59 respectively, and they are 1.53±0.10, 0.48±0.09, 0.51±0.11, 2.20±0.39 and 1.69±0.15, 0.82± 0.14, 0.53±0.12, 2.40±0.40 in patients without HE, 1.58±0.13, 0.48±0.08, 0.38±0.13, 2.62± 0.39 and 1.78±0.18, 0.74±0.14, 0.38±0.15, 2.84±0.58 in patients with MHE, 1.54±0.12, 0.50±0.13, 0.29±0.07, 3.04±0.31 and 1.70±0.19, 0.62±0.16, 0.29±0.07, 3.37±0.38 in patients with HE. Compared with controls, decreased mI/Cr and Cho/Cr ratios and elevated Glx/Cr ratios were found in patients with cirrhosis (t=3.196, 9.394, -6.527, P 1 H-MRS study shows cerebral metabolic alterations of gray and white matter in patients with cirrhosis, especially the reduction in mI/Cr ratio and

Baseline MELD score predicts hepatic decompensation during antiviral therapy in patients with chronic hepatitis C and advanced cirrhosis.

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Georg Dultz

Full Text Available In patients with advanced liver cirrhosis due to chronic hepatitis C virus (HCV infection antiviral therapy with peginterferon and ribavirin is feasible in selected cases only due to potentially life-threatening side effects. However, predictive factors associated with hepatic decompensation during antiviral therapy are poorly defined.In a retrospective cohort study, 68 patients with HCV-associated liver cirrhosis (mean MELD score 9.18 ± 2.72 were treated with peginterferon and ribavirin. Clinical events indicating hepatic decompensation (onset of ascites, hepatic encephalopathy, upper gastrointestinal bleeding, hospitalization as well as laboratory data were recorded at baseline and during a follow up period of 72 weeks after initiation of antiviral therapy. To monitor long term sequelae of end stage liver disease an extended follow up for HCC development, transplantation and death was applied (240 weeks, ± SD 136 weeks.Eighteen patients (26.5% achieved a sustained virologic response. During the observational period a hepatic decompensation was observed in 36.8%. Patients with hepatic decompensation had higher MELD scores (10.84 vs. 8.23, p14, respectively. Baseline MELD score was significantly associated with the risk for transplantation/death (p<0.001.Our data suggest that the baseline MELD score predicts the risk of hepatic decompensation during antiviral therapy and thus contributes to decision making when antiviral therapy is discussed in HCV patients with advanced liver cirrhosis.

Hepatic Scintigraphic Findings of Budd-Chiari Syndrome due to Inferior Vena Caval Obstruction

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Kim, Sung Hoon; Chung, Soo Kyo; Byun, Jae Young; Lee, Sung Yong; Shinn, Kyung Sub; Kim, Choon Yul; Bahk, Yong Whee [Catholic University College of Medicine, Seoul (Korea, Republic of)

1988-03-15

Budd-Chiari syndrome (BCS) is a rare clinical entity characterized by post-sinusoidal portal hypertension caused by the obstruction to the hepatic vein outflow. The diagnosis is suggested by hepatic scintigraphy and is usually confirmed by hepatic venography, inferior vena cavography and biopsy. The scintigraphic finding of BCS caused by the obstruction of main hepatic vein has been reported to consist typically of hypertrophy of the caudate lobe with increased radionuclide accumulation. Such a typical finding has been accounted for by the fact that the venous outflow from the caudate lobe is preserved when the main hepatic vein is obstructed. But usually, the hepatic venous outflow from the caudate lobe is also obstructed in BCS due to inferior vena caval obstruction. So hepatic scintigraphic findings of BCS due to inferior vena caval obstruction show different findings as compared with the BCS due to hepatic vein obstruction. We evaluate the hepatic scintigrams of the 13 cases of BCS due to inferior vena caval obstruction and review the literatures. The results are as follows: 1) We cannot observe the caudate lobe hypertrophy with increased uptake, which is known as a classic finding in BCS due to hepatic vein obstruction. 2) The most prominent hepatic scintigraphic findings of BCS are nonhomogenous uptake in the liver with extrahepatic uptake in the all cases. 3) We can see cold areas at the superior aspect of right hepatic lobe in 7 cases (54%). This is a useful finding suggesting BCS due to inferior vena caval obstruction.

Hepatic Scintigraphic Findings of Budd-Chiari Syndrome due to Inferior Vena Caval Obstruction

International Nuclear Information System (INIS)

Kim, Sung Hoon; Chung, Soo Kyo; Byun, Jae Young; Lee, Sung Yong; Shinn, Kyung Sub; Kim, Choon Yul; Bahk, Yong Whee

1988-01-01

Budd-Chiari syndrome (BCS) is a rare clinical entity characterized by post-sinusoidal portal hypertension caused by the obstruction to the hepatic vein outflow. The diagnosis is suggested by hepatic scintigraphy and is usually confirmed by hepatic venography, inferior vena cavography and biopsy. The scintigraphic finding of BCS caused by the obstruction of main hepatic vein has been reported to consist typically of hypertrophy of the caudate lobe with increased radionuclide accumulation. Such a typical finding has been accounted for by the fact that the venous outflow from the caudate lobe is preserved when the main hepatic vein is obstructed. But usually, the hepatic venous outflow from the caudate lobe is also obstructed in BCS due to inferior vena caval obstruction. So hepatic scintigraphic findings of BCS due to inferior vena caval obstruction show different findings as compared with the BCS due to hepatic vein obstruction. We evaluate the hepatic scintigrams of the 13 cases of BCS due to inferior vena caval obstruction and review the literatures. The results are as follows: 1) We cannot observe the caudate lobe hypertrophy with increased uptake, which is known as a classic finding in BCS due to hepatic vein obstruction. 2) The most prominent hepatic scintigraphic findings of BCS are nonhomogenous uptake in the liver with extrahepatic uptake in the all cases. 3) We can see cold areas at the superior aspect of right hepatic lobe in 7 cases (54%). This is a useful finding suggesting BCS due to inferior vena caval obstruction.

Spectral Electroencephalogram Analysis for the Evaluation of Encephalopathy Grade in Children With Acute Liver Failure.

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Press, Craig A; Morgan, Lindsey; Mills, Michele; Stack, Cynthia V; Goldstein, Joshua L; Alonso, Estella M; Wainwright, Mark S

2017-01-01

Spectral electroencephalogram analysis is a method for automated analysis of electroencephalogram patterns, which can be performed at the bedside. We sought to determine the utility of spectral electroencephalogram for grading hepatic encephalopathy in children with acute liver failure. Retrospective cohort study. Tertiary care pediatric hospital. Patients between 0 and 18 years old who presented with acute liver failure and were admitted to the PICU. None. Electroencephalograms were analyzed by spectral analysis including total power, relative δ, relative θ, relative α, relative β, θ-to-Δ ratio, and α-to-Δ ratio. Normal values and ranges were first derived using normal electroencephalograms from 70 children of 0-18 years old. Age had a significant effect on each variable measured (p liver failure were available for spectral analysis. The median age was 4.3 years, 14 of 33 were male, and the majority had an indeterminate etiology of acute liver failure. Neuroimaging was performed in 26 cases and was normal in 20 cases (77%). The majority (64%) survived, and 82% had a good outcome with a score of 1-3 on the Pediatric Glasgow Outcome Scale-Extended at the time of discharge. Hepatic encephalopathy grade correlated with the qualitative visual electroencephalogram scores assigned by blinded neurophysiologists (rs = 0.493; p encephalopathy was correlated with a total power of less than or equal to 50% of normal for children 0-3 years old, and with a relative θ of less than or equal to 50% normal for children more than 3 years old (p > 0.05). Spectral electroencephalogram classification correlated with outcome (p encephalopathy and correlates with outcome. Spectral electroencephalogram may allow improved quantitative and reproducible assessment of hepatic encephalopathy grade in children with acute liver failure.

Syncytial giant-cell hepatitis due to autoimmune hepatitis type II (LKM1+) presenting as subfulminant hepatitis.

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Ben-Ari, Z; Broida, E; Monselise, Y; Kazatsker, A; Baruch, J; Pappo, O; Skappa, E; Tur-Kaspa, R

2000-03-01

Giant cell hepatitis (GCH) in adults is a rare event. The diagnosis of GCH is based on findings of syncytial giant hepatocytes. It is commonly associated with either viral infection or autoimmune hepatitis type I. A patient with GCH due to autoimmune hepatitis type II (LKM1+) is described, a combination that has not been previously reported. Corticosteroid therapy was effective in decreasing serum liver enzymes; however, the patient deteriorated rapidly and developed subfulminant hepatic failure. Although an emergency orthotopic liver transplantation was performed, the patient died because of reperfusion injury. Interestingly, only a few giant hepatocytes were noted in the explanted liver. This case stresses the association of GCH with autoimmune disorders, the possible immune mechanism involved in the formation of giant cell hepatocytes, and illustrates the rapidly progressive course and unfavorable prognosis that these patients can develop.

Sleep disturbances in patients of liver cirrhosis with minimal hepatic encephalopathy before and after lactulose therapy.

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Singh, Jatinderpal; Sharma, Barjesh Chander; Puri, Vinod; Sachdeva, Sanjeev; Srivastava, Siddharth

2017-04-01

Sleep disturbances are common in patients of cirrhosis with minimal hepatic encephalopathy (MHE) and affect health related quality of life (HRQOL). No study has evaluated effect of lactulose on sleep disturbances and correlation with HRQOL in patients with MHE. We assessed sleep disturbances in cirrhosis with MHE and effect of lactulose on sleep disturbances and HRQOL. One hundred patients of cirrhosis [MHE; (n = 50, age 45.3 ± 11.2 years, 45 males) no-MHE (n = 50, age 46.3 ± 10.4 years, 44 males)] were included. MHE was diagnosed with psychometric hepatic encephalopathy score (PHES) ≤ -5. All patients underwent laboratory parameters including arterial ammonia and critical flicker frequency (CFF) Sleep disturbances were measured with Pittsburgh Sleep Quality Index (PSQI), Epworth Sleepiness Scale (ESS) and polysomnography. HRQOL was measured with SF-36(v2) questionnaire. Patients with MHE were given lactulose therapy for 3 months and all the parameters were repeated. Poor quality of sleep and excessive day time sleepiness were more common in patients with MHE, compared to without MHE. With lactulose therapy there was improvement in MHE in 21 patients and arterial ammonia levels (93.74 ± 14.8 vs. 71.44 ± 18.8 μmol/L: p < 0.001), CFF (34.83 ± 3.54 vs. 39.44 ± 4.95 Hz: p < 0.001), PHES (-7.64 ± 2.1 vs. -5.58 ± 2.09: p < 0.001), PSQI (8.6 ± 3.3 vs. 5.2 ± 1.5: p < 0.001), ESS (12.52 ± 3.01 vs. 9.24 ± 2.27: p < 0.001) and HRQOL (p = 0.01). Excessive day time sleepiness and impaired sleep quality are common in patients with MHE and correlate with neuropsychiatric impairment. Improvement in MHE with lactulose also leads to improvement in sleep disturbances and HRQOL.

Inflammation: A novel target of current therapies for hepatic encephalopathy in liver cirrhosis.

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Luo, Ming; Guo, Jian-Yang; Cao, Wu-Kui

2015-11-07

Hepatic encephalopathy (HE) is a severe neuropsychiatric syndrome that most commonly occurs in decompensated liver cirrhosis and incorporates a spectrum of manifestations that ranges from mild cognitive impairment to coma. Although the etiology of HE is not completely understood, it is believed that multiple underlying mechanisms are involved in the pathogenesis of HE, and one of the main factors is thought to be ammonia; however, the ammonia hypothesis in the pathogenesis of HE is incomplete. Recently, it has been increasingly demonstrated that inflammation, including systemic inflammation, neuroinflammation and endotoxemia, acts in concert with ammonia in the pathogenesis of HE in cirrhotic patients. Meanwhile, a good number of studies have found that current therapies for HE, such as lactulose, rifaximin, probiotics and the molecular adsorbent recirculating system, could inhibit different types of inflammation, thereby improving the neuropsychiatric manifestations and preventing the progression of HE in cirrhotic patients. The anti-inflammatory effects of these current therapies provide a novel therapeutic approach for cirrhotic patients with HE. The purpose of this review is to describe the inflammatory mechanisms behind the etiology of HE in cirrhosis and discuss the current therapies that target the inflammatory pathogenesis of HE.

Activation of neuronal nitric oxide synthase in cerebellum of chronic hepatic encephalopathy rats is associated with up-regulation of NADPH-producing pathway.

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Singh, Santosh; Trigun, Surendra K

2010-09-01

Cerebellum-associated functions get affected during mild hepatic encephalopathy (MHE) in patients with chronic liver failure (CLF). Involvement of nitrosative and antioxidant factors in the pathogenesis of chronic hepatic encephalopathy is an evolving concept and needs to be defined in a true CLF animal model. This article describes profiles of NADPH-dependent neuronal nitric oxide synthase (nNOS) and those of glutathione peroxidase and glutathione reductase (GR) vis-a-vis regulation of NADPH-producing pathway in the cerebellum of CLF rats induced by administration of thioacetamide (100 mg kg⁻¹ b.w., i.p.) up to 10 days and confirming MHE on Morris water maze tests. Significant increases in the expression of nNOS protein and nitric oxide (NOx) level coincided with a similar increment in NADPH-diaphorase activity in the cerebellum of CLF rats. Glutathione peroxidase and GR utilize NADPH to regenerate reduced glutathione (GSH) in the cells. Both these enzymes and GSH level were found to be static and thus suggested efficient turnover of GSH in the cerebellum of MHE rats. Relative levels of glucose-6-phosphate dehydrogenase (G6PD) vs. phosphofructokinase 2 (PFK2) determine the rate of pentose phosphate pathway (PPP) responsible to synthesize NADPH. The cerebellum of CLF rats showed overactivation of G6PD with a significant decline in the expression of PFK2 and thus suggested activation of PPP in the cerebellum during MHE. It is concluded that concordant activations of PPP and nNOS in cerebellum of MHE rats could be associated with the implication of NOx in the pathogenesis of MHE.

Long term results of balloon-occluded retrograde transvenous obliteration for portosystemic shunt encephalopathy in patients with liver cirrhosis and portal hypertension.

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Inoue, Hiroto; Emori, Keigo; Toyonaga, Atsushi; Oho, Kazuhiko; Kumamoto, Masafumi; Haruta, Tsuyoshi; Mitsuyama, Keiichi; Tsuruta, Osamu; Sata, Michio

2014-01-01

This study examined 19 patients with portosystemic shunt encephalopathy caused by a splenorenal shunt (SRS), which was treated with balloon-occluded retrograde transvenous obliteration (B-RTO). Long-term treatment outcomes were evaluated based on hepatic functional reserve and vital prognosis. Encephalopathy improved in all patients after shunt embolization and closure. Albumin, serum ammonia, and the Child-Pugh score, a measure of liver function, were significantly improved 3 years after B-RTO, and exacerbation of damage to liver function was avoided (pliver failure and two patients from hepatocellular carcinoma. Patients had a poor prognosis if their albumin levels were less than 2.8 mg / dL before B-RTO (pEncephalopathy patients had complete response to B-RTO, but long-term prognosis was affected by hepatic functional reserve before B-RTO and by concurrent hepatocellular carcinoma. The results of this study suggest that in patients with SRS, it is important to perform B-RTO at an early stage when the hepatic functional reserve is still satisfactory.

Covert hepatic encephalopathy: not as minimal as you might think.

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Kappus, Matthew R; Bajaj, Jasmohan S

2012-11-01

Hepatic encephalopathy (HE) is a serious neuropsychiatric and neurocognitive complication of acute and chronic liver disease. Symptoms are often overt (confusion, disorientation, ataxia, or coma) but can also be subtle (difficulty with cognitive abilities such as executive decision-making and psychomotor speed). There is consensus that HE is characterized as a spectrum of neuropsychiatric symptoms in the absence of brain disease, ranging from overt HE (OHE) to minimal HE (MHE). The West Haven Criteria are most often used to grade HE, with scores ranging from 0-4 (4 being coma). However, it is a challenge to diagnose patients with MHE or grade 1 HE; it might be practical to combine these entities and name them covert HE for clinical use. The severity of HE is associated with the stage of liver disease. Although the pathologic mechanisms of HE are not well understood, they are believed to involve increased levels of ammonia and inflammation, which lead to low-grade cerebral edema. A diagnosis of MHE requires dedicated psychometric tests and neurophysiological techniques rather than a simple clinical assessment. Although these tests can be difficult to perform in practice, they are cost effective and important; the disorder affects patients' quality of life, socioeconomic status, and driving ability and increases their risk for falls and the development of OHE. Patients with MHE are first managed by excluding other causes of neurocognitive dysfunction. Therapy with gut-specific agents might be effective. We review management strategies and important areas of research for MHE and covert HE. Copyright © 2012 AGA Institute. Published by Elsevier Inc. All rights reserved.

About pathognomonic images: an infrequent case of acute encephalopathy

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Alessandro Grasso

2013-05-01

Full Text Available BACKGROUND The occurrence of acute encephalopathy is a dramatic clinical dilemma when usual diagnostic techniques (blood tests, cerebral CT and cerebrospinal fluid analysis show no abnormalities. CLINICAL CASE We describe a case of a 73 years old man admitted in our Internal Medicine Unit for acute diarrhoea with vomiting and fever who developed a prolonged gastrointestinal dysmotility syndrome with poor nutritional intake. Although a parenteral support was provided, he developed acute encephalopathy followed by hypotension and lactic acidosis without evidence of renal and hepatic disease or glycemic alterations. Likewise, no cerebral CT and cerebrospinal fluid alterations were found. Conversely, cerebral MRI showed marked and diffuse DP-2 and FLAIR hyperintensity of the mesencephalic tectal plate, of the periaqueductal area, and of the periventricular region of the third ventricle including the median thalamic area. These MRI descriptions were considered pathognomonic of Wernicke encephalopathy. Thus, the immediate use of ev thiamine was followed by a prompt and complete recovery of neurological, hemodinamic and metabolic conditions. CONCLUSIONS Non-alcoholic Wernicke encephalopathy is a rare and dramatic clinical event with high mortality. In this context, brain MRI is the best diagnostic tool providing a typical picture.

Brain Training with Video Games in Covert Hepatic Encephalopathy.

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Bajaj, Jasmohan S; Ahluwalia, Vishwadeep; Thacker, Leroy R; Fagan, Andrew; Gavis, Edith A; Lennon, Michael; Heuman, Douglas M; Fuchs, Michael; Wade, James B

2017-02-01

Despite the associated adverse outcomes, pharmacologic intervention for covert hepatic encephalopathy (CHE) is not the standard of care. We hypothesized that a video game-based rehabilitation program would improve white matter integrity and brain connectivity in the visuospatial network on brain magnetic resonance imaging (MRI), resulting in improved cognitive function in CHE subjects on measures consistent with the cognitive skill set emphasized by the two video games (e.g., IQ Boost-visual working memory, and Aim and Fire Challenge-psychomotor speed), but also generalize to thinking skills beyond the focus of the cognitive training (Hopkins verbal learning test (HVLT)-verbal learning/memory) and improve their health-related quality of life (HRQOL). The trial included three phases over 8 weeks; during the learning phase (cognitive tests administered twice over 2 weeks without intervening intervention), training phase (daily video game training for 4 weeks), and post-training phase (testing 2 weeks after the video game training ended). Thirty CHE patients completed all visits with significant daily achievement on the video games. In a subset of 13 subjects that underwent brain MRI, there was a significant decrease in fractional anisotropy, and increased radial diffusivity (suggesting axonal sprouting or increased cross-fiber formation) involving similar brain regions (i.e., corpus callosum, internal capsule, and sections of the corticospinal tract) and improvement in the visuospatial resting-state connectivity corresponding to the video game training domains. No significant corresponding improvement in HRQOL or HVLT performance was noted, but cognitive performance did transiently improve on cognitive tests similar to the video games during training. Although multimodal brain imaging changes suggest reductions in tract edema and improved neural network connectivity, this trial of video game brain training did not improve the HRQOL or produce lasting improvement in

Acetylcholinesterase inhibitor treatment alleviated cognitive impairment caused by delayed encephalopathy due to carbon monoxide poisoning: Two case reports and a review of the literature.

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Yanagiha, Kumi; Ishii, Kazuhiro; Tamaoka, Akira

2017-02-01

Delayed encephalopathy due to carbon monoxide (CO) poisoning can even occur in patients with mild symptoms of acute CO poisoning. Some cases taking conventional hyperbaric oxygen (HBO) therapy or steroid-pulse therapy may be insufficient, and AchEI may be effective. We report two cases of delayed encephalopathy after acute CO poisoning involving two women aged 69 (Case 1) and 60 years (Case 2) whose cognitive function improved with acetylcholinesterase inhibitor (AchEI) treatment. Delayed encephalopathy occurred 25 and 35 days after acute CO poisoning in Case 1 and Case 2, respectively. Both patients demonstrated cognitive impairment, apathy, and hypokinesia on admission. Although hyperbaric oxygen therapy did not yield any significant improvements, cognitive dysfunction improved substantially. This was evidenced by an improved Mini-Mental State Examination score ffom 9 to 28 points in Case 1 and an improved Hasegawa's dementia rating scale score from 4 to 25 points in Case 2 after administration of an AchEI. In Case 1, we administered galantamine hydrobromide, which was related with improved white matter lesions initially detected on brain magnetic resonance imaging. However, in Case 2 white matter lesions persisted despite AchEI treatment. AchEI treatment may result in improved cognitive and frontal lobe function by increasing low acetylcholine concentrations in the hippocampus and frontal lobe caused by decreased nicotinic acetylcholine receptor levels in delayed encephalopathy after CO poisoning. Physicians should consider AchEIs for patients demonstrating delayed encephalopathy due to CO poisoning.

Disrupted functional connectivity of the anterior cingulate cortex in cirrhotic patients without overt hepatic encephalopathy: a resting state fMRI study.

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Long Jiang Zhang

Full Text Available BACKGROUND: To evaluate the changes of functional connectivity of the anterior cingulate cortex (ACC in patients with cirrhosis without overt hepatic encephalopathy (HE using resting state functional MRI. METHODOLOGY/PRINCIPAL FINDINGS: Participants included 67 cirrhotic patients (27 minimal hepatic encephalopathy (MHE and 40 cirrhotic patients without MHE (non-HE, and 40 age- and gender- matched healthy controls. rsfMRI were performed on 3 Telsa scanners. The pregenual ACC resting-state networks (RSNs were characterized by using a standard seed-based whole-brain correlation method and compared between cirrhotic patients and healthy controls. Pearson correlation analysis was performed between the ACC RSNs and venous blood ammonia levels, neuropsychological tests (number connection test type A [NCT-A] and digit symbol test [DST] scores in cirrhotic patients. All thresholds were set at P<0.05, with false discovery rate corrected. Compared with controls, non-HE and MHE patients showed significantly decreased functional connectivity in the bilateral ACC, bilateral middle frontal cortex (MFC, bilateral middle cingulate cortex (MCC, bilateral superior temporal gyri (STG/middle temporal gyri (MTG, bilateral thalami, bilateral putamen and bilateral insula, and increased functional connectivity of bilateral precuneus and left temporo-occipital lobe and bilateral lingual gyri. Compared with non-HE patients, MHE showed the decreased functional connectivity of right MCC, bilateral STG/MTG and right putamen. This indicates decreased ACC functional connectivity predominated with the increasing severity of HE. NCT-A scores negatively correlated with ACC functional connectivity in the bilateral MCC, right temporal lobe, and DST scores positively correlated with functional connectivity in the bilateral ACC and the right putamen. No correlation was found between venous blood ammonia levels and functional connectivity in ACC in cirrhotic patients. CONCLUSIONS

Posterior encephalopathy with vasospasm: MRI and angiography

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Weidauer, S.; Gaa, J.; Lanfermann, H.; Zanella, F.E.; Sitzer, M.; Hefner, R.

2003-01-01

Posterior encephalopathy is characterised by headache, impairment of consciousness, seizures and progressive visual loss. MRI shows bilateral, predominantly posterior, cortical and subcortical lesions with a distribution. Our aim was to analyse the MRI lesion pattern and angiographic findings because the pathophysiology of posterior encephalopathy is incompletely understood. We report three patients with clinical and imaging findings consistent with posterior encephalopathy who underwent serial MRI including diffusion-weighted imaging (DWI) and construction of apparent diffusion coefficient (ADC) maps, and four-vessel digital subtraction angiography (DSA). DWI revealed symmetrical subcortical and cortical parieto-occipital high signal. High and also low ADCs indicated probable vasogenic and cytotoxic oedema. On follow-up there was focal cortical laminar necrosis, while the white-matter lesions resolved almost completely, except in the arterial border zones. DSA revealed diffuse arterial narrowing, slightly more marked in the posterior circulation. These findings suggest that posterior encephalopathy may in some cases be due to diffuse, severe vasospasm affecting especially in the parieto-occipital grey matter, with its higher vulnerability to ischemia. Cerebral vasospasm due to digitoxin intoxication, resulting in posterior encephalopathy, has not yet been described previously. (orig.)

Clues for minimal hepatic encephalopathy in children with noncirrhotic portal hypertension.

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D'Antiga, Lorenzo; Dacchille, Patrizia; Boniver, Clementina; Poledri, Sara; Schiff, Sami; Zancan, Lucia; Amodio, Piero

2014-12-01

In children with noncirrhotic extrahepatic portal vein obstruction (EHPVO), minimal hepatic encephalopathy (MHE) was reported in a few series, but neither is it routinely investigated nor does consensus about its diagnosis exist. In this prospective observational study we aimed at detecting the prevalence of MHE in children with EHPVO and providing a practical diagnostic protocol. A consecutive sample of 13 noncirrhotic children (age range 4-18 years) with EHPVO underwent a screening for MHE based on level of fasting ammonia, quantified electroencephalogram (EEG) evaluation, and a wide battery of 26 psychometric tests exploring learning ability, abstract reasoning, phonemic and semantic fluency, selective attention, executive functions, short-term verbal and visual memory, long-term verbal memory, and visuopractic ability. Five children had at least 2 altered psychometric tests. Selective attention, executive function, and short-term visual memory were the domains more frequently altered, and 4 tests were enough to detect 80% of these children. Fasting ammonia plasma level was increased in 6 children. EEG mean dominant frequency adjusted for age was associated with serum ammonia concentration (β = -0.44 ± 0.19, P children with EHPVO showed trends for lower α (median 41% vs 49%) and higher θ power than controls (median 41% vs 49% and 29% vs 20%, respectively). MHE affects approximately 50% of children with EHPVO and, therefore, is worthwhile to be investigated. Three simple tools, serum ammonia, quantified EEG, and neuropsychological examination, focused on selective attention, executive function, and short-term visual memory can be used effectively in the evaluation of MHE in this setting.

Development of methods for quantitative in vivo NMR and their application to the study of hepatic encephalopathy in the brain

International Nuclear Information System (INIS)

Graaf, A.A. de.

1989-01-01

The aim of the work presented in this thesis was to develop reliable methods for quantitative MRS that are medically relevant for the study of Hepatic Encephalopathy (HE) in rats. The required modifications of the initiation and control software of the 7 Tesla spectrometer system of the Spin Imaging group at the Technical University Delft (Netherlands), are described. Experimental methods for localized, water suppressed 1 H MRS with a surface coil, including Spectroscopic Imaging, were developed in order to solve the problems of irreproducibility and spectral overlap caused by water and lipid signals. A method for correction of line-shape distortions as a consequence of static magnetic field imperfections was developed and evaluated both theoretically and experimentally. An approach to solve the problems in the quantification of the 1 H MRS spectra, caused especially by spectral overlap, frequency dependent intensity distortions and intensity modulations in coupled spin systems, was developed and evaluated. The brain energy state during HE was investigated using 31 P MRS. The developed methods for quantitative 1 H MRS were applied to monitor the concentrations of severeal important brain amino acids and other metabolic compounds during the development of acute HE, and during the development of ammonia induced encephalopathy in two different animal models. (author). 201 refs.; 32 figs.; 28 schemes.; 11 tabs

A look at the hepatic encephalopathy in cirrhosis

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Giacomo Zaccherini

2013-01-01

Full Text Available Hepatic encephalopathy (HE is a neuropsychiatric syndrome complicating acute and chronic liver failure and characterized by a wide range of manifestations, in absence of other brain disease. HE is very frequent in course of cirrhosis and even mild forms involve a great additional burden on patients, their families and health-care resources. Its onset affects subsequent survival of patients. Historically, pathophysiology of HE was connected to several substances (mostly ammonia produced in the gut and normally metabolized by the liver, but more recently other factors such as inflammation, bacterial translocation and oxidative stress have shown a crucial role. Symptoms are often overt (confusion, asterixis, disorientation, ataxia or coma but can also be subtle (sleep disturbances, cognitive impairment, mood alterations, impairment of executive decision-making, and psychomotor speed – Minimal HE; the West Haven Criteria are most often used to grade Overt HE (OHE, with grade ranging from 0 to 4 (4 corresponding to coma. Since both Minimal HE and grade 1 HE cannot be diagnosed by clinical examination and need for specific tests, it results practical to combine these entities and name them "Covert" HE (CHE to aid clinical use. Diagnosis is based on evidence of neurological impairment in presence of liver cirrhosis, only after the exclusion of other brain diseases. Measurement of serum ammonia and electroencephalography are little specific, while brain magnetic resonance and search for portosystemic shunts are important in complex cases. Diagnosis of OHE is often just clinical, while that of CHE requires dedicated psychometric and neurophysiological tests. Although these tests are difficult to be performed in the clinical practice, detection and treatment of CHE are cost-effective and important; indeed, CHE affects patients’ quality of life, socioeconomic status and driving skills, and increases the risk for falls, car accidents, development of OHE

Selective impairments of resting-state networks in minimal hepatic encephalopathy.

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Rongfeng Qi

Full Text Available BACKGROUND: Minimal hepatic encephalopathy (MHE is a neuro-cognitive dysfunction characterized by impairment in attention, vigilance and integrative functions, while the sensorimotor function was often unaffected. Little is known, so far, about the exact neuro-pathophysiological mechanisms of aberrant cognition function in this disease. METHODOLOGY/PRINCIPAL FINDINGS: To investigate how the brain function is changed in MHE, we applied a resting-state fMRI approach with independent component analysis (ICA to assess the differences of resting-state networks (RSNs between MHE patients and healthy controls. Fourteen MHE patients and 14 age-and sex-matched healthy subjects underwent resting-state fMRI scans. ICA was used to identify six RSNs [dorsal attention network (DAN, default mode network (DMN, visual network (VN, auditory network (AN, sensorimotor network (SMN, self-referential network (SRN] in each subject. Group maps of each RSN were compared between the MHE and healthy control groups. Pearson correlation analysis was performed between the RSNs functional connectivity (FC and venous blood ammonia levels, and neuropsychological tests scores for all patients. Compared with the healthy controls, MHE patients showed significantly decreased FC in DAN, both decreased and increased FC in DMN, AN and VN. No significant differences were found in SRN and SMN between two groups. A relationship between FC and blood ammonia levels/neuropsychological tests scores were found in specific regions of RSNs, including middle and medial frontal gyrus, inferior parietal lobule, as well as anterior and posterior cingulate cortex/precuneus. CONCLUSIONS/SIGNIFICANCE: MHE patients have selective impairments of RSNs intrinsic functional connectivity, with aberrant functional connectivity in DAN, DMN, VN, AN, and spared SMN and SRN. Our fMRI study might supply a novel way to understand the neuropathophysiological mechanism of cognition function changes in MHE.

Post-partum posterior reversible encephalopathy syndrome

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B. V. Triveni; Salman Mohammed Sheikh; Deepak Shedde

2014-01-01

Posterior Reversible Encephalopathy Syndrome (PRES) is a clinicopathological syndrome associated with various clinical conditions presenting with headache, encephalopathy, seizure and cortical visual disturbances. Radiological findings in PRES are thought to be due to vasogenic edema predominantly in posterior cerebral hemispheres and are reversible with appropriate management. We present a case of post partum PRES,A 29 year old primigravida of 33 weeks 3 days period of gestation who prese...

Evaluation of model for end-stage liver disease score cut off values in patients with hepatic encephalopathy

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Khurram, M.; Qayyum, W.; Umar, M.; Abedin, Z.U.; Bushra, H.T.

2015-01-01

Model for End Stage Liver Disease (MELD) is scoring system used for prioritization of patients waiting liver transplantation. Patients with decompensated chronic liver disease (DCLD) with higher MELD score and hepatic encephalopathy (HE) have poor outcome. We planned to note association between short term mortality and various cut-off values of at admission MELD score in HCV related DCLD patients presenting with HE. Methods: In this descriptive case series, 208 Hepatitis C (HCV) related chronic liver disease (CLD) patients with HE were included. At admission serum bilirubin, creatinine and INR were sought to calculate MELD score. Patients who improved were discharged and kept under regular follow up. Outcome was categorized into alive or expired in 3 months after admission. Based on MELD score cut off values of >15, >20, >25 and >30, association with outcome was determined using Chi-square test. Results: One hundred and six (51%) patients were female. Mean patient age was 55.3±10.6 years. Outcome wise, 128 (61.5%) were alive and 80 (38.5%) expired. Mean MELD score of expired was 22.17±9.14. 55 (51%) patients with MELD score >15, 44 (65.7%) patients with >20, 30 (73.2%) patients with >25, and 21 (72.5%) patients with >30 expired. MELD score >20 had strongest association with outcome, p value less than o.01. Conclusion: At admission MELD score >20 are most significantly associated with poor outcome in DCLD patients with HE. (author)

Assessment of Patients with Chronic Liver Disease and Hepatic Encephalopathy using Serum Cytokines

International Nuclear Information System (INIS)

Rasheid, S.A.; Alkady, M.M.; Emam, W.

2012-01-01

Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome characterized by central neural depression which may develop in both acute and chronic liver diseases. Its pathogenesis is not clearly understood and its main cause(s) is not yet known. The relations between several cytokines and HE pathogenesis were evaluated in many studies. In this study, we aimed to investigate the role of TNF--α, IL-6 and IL-8 in the pathogenesis of HE . Furthermore, the relation between the severity of HE and the levels of these cytokines was assessted. Methods: fourty patients with liver cirrhosis [20 patients with clinical findings of HE (group 3) and 20 without any symptoms of HE (group 2)] and 20 healthy controls (group 1) were included in this study. Serum TNF--α, IL-6 and IL-8 levels of patients and control subjects were studied using competitive enzyme immunoassay method (EIA). Results: There were statistically significant difference between serum TNF--α. IL-6 and IL-8 levels of patients with liver cirrhosis and healthy subjects, and between patients with and without HE. There was a positive correlation between the severity of liver cirrhosis according to Child-Pugh classification and cytokine levels. The severity of HE (grade 1-4) was closely related with cytokine levels, especially TNF-α. On the other hand, there was no relation between cytokine levels and the etiological factors

Chemical shift magnetic resonance spectroscopy of cingulate grey matter in patients with minimal hepatic encephalopathy

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Mechtcheriakov, Sergei; Kugener, Andre; Mattedi, Michael; Hinterhuber, Hartmann; Marksteiner, Josef; Schocke, Michael; Graziadei, Ivo W.; Vogel, Wolfgang

2005-01-01

Minimal hepatic encephalopathy (MHE) is frequently diagnosed in patients with liver cirrhosis who do not show overt clinical cirrhosis-associated neurological deficits. This condition manifests primarily with visuo-motor and attention deficits. We studied the association between visuo-motor deficits and magnetic resonance spectroscopic parameters in cingulate grey matter and white matter of centrum semiovale in patients with liver cirrhosis. The data revealed an increase in the glutamate-glutamine/creatine ratio and a decrease in choline/creatine and inositol/creatine ratios in patients with liver cirrhosis. The analysis of the data showed that cirrhosis-associated deterioration of the visuo-motor function significantly correlates with a decrease in the choline/creatine ratio and an increase in N-acetylaspartate/choline in cingulate grey matter but not in the neighbouring white matter. Furthermore, the increase in the glutamate-glutamine/creatine ratio correlated significantly with the increase in the N-acetylaspartate/creatine ratio. These data suggest an association between altered choline, glutamate-glutamine and NAA metabolism in cingulate grey matter and symptoms of MHE, and underline the importance of differentiation between grey and white matter in magnetic resonance spectroscopic studies on patients with cirrhosis-associated brain dysfunction. (orig.)

Can the tyrosine kinase inhibitors trigger metabolic encephalopathy in cirrhotic patients?

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Brandi, Giovanni; de Rosa, Francesco; Calzà, Laura; Girolamo, Stefania Di; Tufoni, Manuel; Ricci, Carmen Serena; Cirignotta, Fabio; Caraceni, Paolo; Biasco, Guido

2013-03-01

Sorafenib is the standard treatment of advanced hepatocarcinoma (HCC) in cirrhotic patients with preserved liver function. It shares many adverse effects with other tyrosine-kinase (TK) inhibitors and antiangiogenic drugs. TK inhibitors could have a direct toxicity on CNS, both by interfering with TK-related pathways and by inhibiting angiogenesis. The aim of this study was to investigate whether sorafenib administration can be associated to metabolic encephalopathy in patients with cirrhosis. We retrospectively reviewed medical records of all cirrhotic patients treated with sorafenib for HCC afferent at our Department from January 2009 to December 2011. Among 62 patients, we identified 10 patients with clinically significant cognitive impairment. Seven of these were clearly diagnosed with overt hepatic encephalopathy (HE), one with brain metastases and two with drug-related toxic-metabolic encephalopathy. These last two cases were characterized by severe cognitive impairment, mood alteration and memory deficit. Clinical exam, blood tests and brain CT excluded organic causes of encephalopathy and precipitating factors of HE. Sorafenib discontinuation was associated with complete reversal of the syndrome, which recurred on drug re-administration in one case. Our study suggests that sorafenib may be a precipitating factor of metabolic encephalopathy in cirrhotic patients with advanced HCC. This neurological syndrome appears to be not responsive to the conventional treatment for HE, but it is fully reversible by drug discontinuation. It can be speculated that the potential direct neuronal action of sorafenib may represent a trigger for the onset of metabolic encephalopathy in a subset of cirrhotic patients. © 2012 John Wiley & Sons A/S.

CT and MRI findings of cyclosporine-related encephalopathy and hypertensive encephalopathy

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Yamamoto, Akira; Hayakawa, Katsumi; Houjyou, Makoto

2002-01-01

We present the MRI and CT findings of one child with cyclosporine-related encephalopathy, and one child with hypertensive encephalopathy following cyclosporine-related encephalopathy. The imaging findings were shown well on T2-weighted and fluid-attenuated inversion recovery (FLAIR) MR images. Cyclosporine-related encephalopathy was distributed predominantly in the posterior white matter. Hypertensive encephalopathy showed similar changes of CT attenuation, but with wider distribution. These two disorders seem to have the same pathogenesis. (orig.)

Hepatitis in pregnancy

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Ain, F.U.; Amin, A.; Yasmin, F.

2007-01-01

To determine the frequency of viral hepatitis in general, spectrum of hepatitis E in particular, and to study the maternal and fetal morbidity and mortality associated with it. In this prospective study, total number of pregnant women was 4723, sera of 35 pregnant women having clinical jaundice in pregnancy were analyzed for markers of hepatitis A , B, C and E viruses. Of the 35 pregnant women with jaundice HEV IgM were 60%,HA V IgM20%, Anti HCV 8.75%,Hbs Ag 5.71%, unexplained 5.71%. Amongst HEV 23.80% had hepatic encephalopathy DIC in 42.85%, PPH in 23.80%, renal failure in 9.52% an- maternal mortality in 4.76%. Approximately two third of pregnant women with HEV infection had preterm deliveries (76.19) % and perinatal mortality of 42.8%. Hepatitis E was the commonest etiological agent in those who had fulminant disease during pregnancy and was associated with high morbidity and mortality. (author)

Serum and ascitic fluid serotonin levels and 5-hydroxyindoleacetic acid urine excretion in the liver of cirrhotic patients with encephalopathy.

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Chojnacki, C; Walecka-Kapica, E; Stepien, A; Pawlowicz, M; Wachowska-Kelly, P; Chojnacki, J

2013-01-01

The excess and deficit of serotonin can be the cause of somatic and mental disorders. The aim of this study was to evaluate serotonin levels in blood and ascitic fluid as well as excretion of 5-hydroxyindoleacetic acid (5-HIAA) in urine in patients with hepatic encephalopathy (HE). The study included 75 alcoholic cirrhotic patients divided into 3 groups (HE1, HE2, HE3), 25 patients each, with grade 1, 2 and 3 of hepatic encephalopathy according to West-Haven classification. The control group (C) included 25 clinically healthy volunteers. Venous blood and ascitic fluid were collected in fasting. On the same day a 24-hour urine collection was performed. Immunoenzymatic method was used to determine the serotonin level in serum and ascitic fluid, and 5-HIAA in urine (IBL-RE-59121, RE-59131). In the control group, mean serum serotonin level (ng/ml) was 155.5 ± 38.1 and in the 3 study groups: HE1 - 175.2 ± 32.4 (NS), HE2 - 137.2 ± 28.6 (NS), HE3 - 108.3 ± 46.3 (pencephalopathy. In patients with severe hepatic encephalopathy serotonin concentration in blood is decreased which can affect some clinical manifestation of this disease.

Acute Changes in Mentation in a Patient with Hepatic Cirrhosis Treated with High Doses of Dexamethasone.

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Dabul, Luis; Droney, Andrew; Oms, Juan; Sanchez-Gonzalez, Marcos A

2017-09-10

Despite the anti-inflammatory benefits of steroids in the management of multiple medical conditions, they are associated with undesired metabolic and psychiatric side effects. We present a case of a 57-year-old Hispanic man with hepatic cirrhosis due to hepatitis C and no past medical history of psychiatric illnesses who became delirious after treatment with high doses of intravenous Dexamethasone. The patient presented to Larkin Community Hospital, USA with complaints of lower back pain requiring treatment with steroids for severe lumbar central canal stenosis. After three days of treatment, the patient became disoriented to time and place, grossly psychotic with auditory hallucinations and disorganized behavior, manic, aggressive, combative, restless, hard to redirect, and unable to follow commands. He met the criteria for a diagnosis of substance-induced psychotic disorder according to Diagnostic and Statistical Manual of Mental Disorders (DSM) V. Furthermore, the patient had worsening hepatic profile, a high ammonia level of 125 umol/L, and clinical findings consistent with West Haven classification grade 2 encephalopathy. Head computed tomography (CT) scan was normal. He was treated with discontinuation of steroids, lactulose, and Haloperidol returning to baseline mental status after 48 hours. The patient's hospitalization was complicated with a prolonged hospital stay after lumbar surgery. This case illustrates that treatment with high doses of Dexamethasone in a patient with hepatic cirrhosis can cause acute changes in mental status by (i) inducing delirium, and (ii) precipitating hepatic encephalopathy.

Nivolumab as salvage treatment in a patient with HIV-related relapsed/refractory Hodgkin lymphoma and liver failure with encephalopathy.

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Sandoval-Sus, Jose D; Mogollon-Duffo, Francis; Patel, Ankita; Visweshwar, Nathan; Laber, Damian A; Kim, Richard; Jagal, Michael V

2017-01-01

We report the first case to our knowledge of a patient with relapsed/refractory classical hodgkin lymphoma and liver failure with encephalopathy along with human immunodeficiency virus/acquired immunodeficiency syndrome infection, successfully treated with nivolumab without major side effects and encouraging prolonged disease control. In December 2015, at the time of the patient's progression from his Hodgkin lymphoma after fourth line treatment, he developed persistent fevers, abdominal distension, jaundice and worsening of his liver function tests. Magnetic resonance imaging of abdomen/pelvis demonstrated hepatomegaly with innumerable new liver lesions, splenomegaly with multiple splenic nodules and several new mediastinal, intraperitoneal and retroperitoneal lymphadenopathy. In accordance with the patient's wishes before admission, and after agreement with the family, nivolumab (3 mg/kg every 2 weeks) was given. Of note, antiretroviral therapy was on hold due to liver function tests, his viral load was undectable and cluster of differentiation 4 counts were 103/uL at the time of nivolumab administration. One week after the first dose of nivolumab both his hepatic encephalopathy and constitutional symptoms started to improve, and after 2 doses, (January 2016) his LFTs were almost back to normal. After 5 months of nivolumab treatment (10 doses), restaging (computerized tomography scans of neck, chest, abdomen, pelvis) done on May 2016 showed resolution of hepatosplenomegaly with two residual small hepatic lesions, heterogeneous spleen with no splenic lesions, and stable non-enlarged retroperitoneal lymph nodes without intraabdominal lymphadenopathy; consistent with partial response. We report a case of a patient with human immunodeficiency virus/acquired immunodeficiency syndrome -related relapsed/refractory classical Hodgkin lymphoma and acute liver failure with encephalopathy successfully treated with nivolumab after failing all standard therapeutic options

Regional cerebral blood flow assessed by single photon emission computed tomography (SPECT) in dogs with congenital portosystemic shunt and hepatic encephalopathy.

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Or, Matan; Peremans, Kathelijne; Martlé, Valentine; Vandermeulen, Eva; Bosmans, Tim; Devriendt, Nausikaa; de Rooster, Hilde

2017-02-01

Regional cerebral blood flow (rCBF) in eight dogs with congenital portosystemic shunt (PSS) and hepatic encephalopathy (HE) was compared with rCBF in eight healthy control dogs using single photon emission computed tomography (SPECT) with a 99m technetium-hexamethylpropylene amine oxime ( 99m Tc-HMPAO) tracer. SPECT scans were abnormal in all PSS dogs. Compared to the control group, rCBF in PSS dogs was significantly decreased in the temporal lobes and increased in the subcortical (thalamic and striatal) area. Brain perfusion imaging alterations observed in the dogs with PSS and HE are similar to those in human patients with HE. These findings suggest that dogs with HE and PSS have altered perfusion of mainly the subcortical and the temporal regions of the brain. Copyright © 2016 Elsevier Ltd. All rights reserved.

Affinities and densities of high-affinity [3H]muscimol (GABA-A) binding sites and of central benzodiazepine receptors are unchanged in autopsied brain tissue from cirrhotic patients with hepatic encephalopathy

International Nuclear Information System (INIS)

Butterworth, R.F.; Lavoie, J.; Giguere, J.F.; Pomier-Layrargues, G.

1988-01-01

The integrity of GABA-A receptors and of central benzodiazepine receptors was evaluated in membrane preparations from prefrontal cortex and caudate nuclei obtained at autopsy from nine cirrhotic patients who died in hepatic coma and an equal number of age-matched control subjects. Histopathological studies revealed Alzheimer Type II astrocytosis in all cases in the cirrhotic group; controls were free from neurological, psychiatric or hepatic diseases. Binding to GABA-A receptors was studied using [ 3 H]muscimol as radioligand. The integrity of central benzodiazepine receptors was evaluated using [ 3 H]flunitrazepam and [ 3 H]Ro15-1788. Data from saturation binding assays was analyzed by Scatchard plot. No modifications of either affinities (Kd) or densities (Bmax) of [ 3 H]muscimol of central benzodiazepine binding sites were observed. These findings do not support recent suggestions that alterations of either high-affinity GABA or benzodiazepine receptors play a significant role in the pathogenesis of hepatic encephalopathy

Valproic acid-induced hyperammonemic encephalopathy - a potentially fatal adverse drug reaction.

Science.gov (United States)

Sousa, Carla

2013-12-01

A patient with an early diagnosed epilepsy Valproic acid is one of the most widely used antiepileptic drugs. Hyperammonemic encephalopathy is a rare, but potentially fatal, adverse drug reaction to valproic acid. A patient with an early diagnosed epilepsy, treated with valproic acid, experienced an altered mental state after 10 days of treatment. Valproic acid serum levels were within limits, hepatic function tests were normal but ammonia levels were above the normal range. Valproic acid was stopped and the hyperammonemic encephalopathy was treated with lactulose 15 ml twice daily, metronidazole 250 mg four times daily and L-carnitine 1 g twice daily. Monitoring liver function and ammonia levels should be recommended in patients taking valproic acid. The constraints of the pharmaceutical market had to be taken into consideration and limited the pharmacological options for this patient's treatment. Idiosyncratic symptomatic hyperammonemic encephalopathy is completely reversible, but can induce coma and even death, if not timely detected. Clinical pharmacists can help detecting adverse drug reactions and provide evidence based information for the treatment.

Gut : liver : brain axis: the microbial challenge in the hepatic encephalopathy.

Science.gov (United States)

Mancini, Andrea; Campagna, Francesca; Amodio, Piero; Tuohy, Kieran M

2018-03-01

Hepatic encephalopathy (HE) is a debilitating neuropsychiatric condition often associated with acute liver failure or cirrhosis. Advanced liver diseases are characterized by a leaky gut and systemic inflammation. There is strong evidence that the pathogenesis of HE is linked to a dysbiotic gut microbiota and to harmful microbial by-products, such as ammonia, indoles, oxindoles and endotoxins. Increased concentrations of these toxic metabolites together with the inability of the diseased liver to clear such products is thought to play an important patho-ethiological role. Current first line clinical treatments target microbiota dysbiosis by decreasing the counts of pathogenic bacteria, blood endotoxemia and ammonia levels. This review will focus on the role of the gut microbiota and its metabolism in HE and advanced cirrhosis. It will critically assess data from different clinical trials measuring the efficacy of the prebiotic lactulose, the probiotic VSL#3 and the antibiotic rifaximin in treating HE and advanced cirrhosis, through gut microbiota modulation. Additionally data from Randomised Controlled Trials using pre-, pro- and synbiotic will be also considered by reporting meta-analysis studies. The large amount of existing data showed that HE is a clear example of how an altered gut microbiota homeostasis can influence and impact on physiological functions outside the intestine, with implication for host health at the systems level. Nevertheless, a strong effort should be made to increase the information on gut microbiota ecology and its metabolic function in liver diseases and HE.

Outcomes of Children With and Without Hepatic Encephalopathy From the Pediatric Acute Liver Failure Study Group.

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Ng, Vicky L; Li, Ruosha; Loomes, Kathleen M; Leonis, Mike A; Rudnick, David A; Belle, Steven H; Squires, Robert H

2016-09-01

Hepatic encephalopathy (HE) is challenging to identify in children with acute liver failure and was not a requirement for enrollment into the Pediatric Acute Liver Failure Study Group (PALFSG). The outcomes of PALFSG participants presenting with and without HE are presented. PALFSG participants were classified based on daily assessment of HE during the first 7 days following study enrollment: group 1-never developed HE; group 2-no HE at enrollment with subsequent HE development; and group 3-HE at study enrollment. Clinical and biochemical parameters and outcomes of death, spontaneous recovery, or liver transplantation were compared between groups. Data from 769 PALFSG (54% boys; median age 4.2 years; range 0-17.9 years) participants were analyzed, with 277 in group 1 (36%), 83 in group 2 (11%), and 409 in group 3 (53%). Mortality occurred in 11% of all participants and was highest among group 3 participants who demonstrated persistent grade III-IV HE (55%) or showed progression of HE (26%). Eleven (4%) group 1 participants died within 21 days of enrollment. Spontaneous recovery was highest in group 1 (79%) and lowest in group 2 (25%; P liver failure prognostication schema are needed.

Hepato- and neuro-protective influences of biopropolis on thioacetamide-induced acute hepatic encephalopathy in rats.

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Mostafa, Rasha E; Salama, Abeer A A; Abdel-Rahman, Rehab F; Ogaly, Hanan A

2017-05-01

Hepatic encephalopathy (HE) is a neuropsychiatric syndrome that ultimately occurs as a complication of acute or chronic liver failure; accompanied by hyperammonemia. This study aimed to evaluate the potential of biopropolis as a hepato- and neuro-protective agent using thioacetamide (TAA)-induced acute HE in rats as a model. Sixty Wistar rats were divided into 5 groups: Group 1 (normal control) received only saline and paraffin oil. Group 2 (hepatotoxic control) received TAA (300 mg/kg, once). Groups 3, 4, and 5 received TAA followed by vitamin E (100 mg/kg) and biopropolis (100 and 200 mg/kg), respectively, daily for 30 days. Evidences of HE were clearly detected in TAA-hepatotoxic group including significant elevation in the serum level of ammonia, liver functions, increased oxidative stress in liver and brain, apoptotic DNA fragmentation and overexpression of iNOS gene in brain tissue. The findings for groups administered biopropolis, highlighted its efficacy as a hepato- and neuro-protectant through improving the liver functions, oxidative status and DNA fragmentation as well as suppressing the brain expression of iNOS gene. In conclusion, biopropolis, at a dose of 200 mg/kg per day protected against TAA-induced HE through its antioxidant and antiapoptotic influence; therefore, it can be used as a protective natural product.

Covert hepatic encephalopathy: does the mini-mental state examination help?

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Corrias, Michela; Turco, Matteo; Rui, Michele D; Gatta, Angelo; Angeli, Paolo; Merkel, Carlo; Amodio, Piero; Schiff, Sami; Montagnese, Sara

2014-06-01

The Mini-Mental State Examination (MMSE) has been utilized for the diagnosis of hepatic encephalopathy (HE). However, its threshold of abnormality has not been formally tested in patients with cirrhosis and its diagnostic/prognostic validity remains unknown. The aim of this study was to assess it in a large group of well-characterized outpatients with cirrhosis and no overt HE. One-hundred-and-ninety-one patients underwent clinical assessment, MMSE, electroencephalography (EEG) and paper-and-pencil psychometry (PHES); 117 were followed up for 8 ± 5 months in relation to the occurrence of HE-related hospitalizations. On the day of study, 81 patients (42%) had abnormal EEG and 67 (35%) abnormal PHES; 103 (60%) had a history of HE. Average MMSE was 26.6 ± 3.5; 22 (19%) patients had abnormal MMSE based on the standard threshold of 24. Patients with abnormal EEG/PHES/history of HE had worse MMSE performance than their counterparts with normal tests/negative history (25.7 ± 4.2 vs. 27.3 ± 2.7; P < 0.01; 25.5 ± 3.2 vs. 27.9 ± 1.8, P < 0.0001; 26.3 ± 3.7 vs. 27.4 ± 2.6, P < 0.05, respectively). Based on the above results, MMSE thresholds of 26 and 27 were tested against abnormalities in clinical/EEG/PHES indices and significant associations were observed. An MMSE threshold of 26 was also a predictor of HE-related hospitalization (Cox-Mantel: P = 0.001); patients with MMSE <26 were significantly older than those with MMSE ≥26 but comparable in terms of liver dysfunction and ammonia levels. When MMSE items were considered separately, those which correlated most significantly with standard HE indices where spatial orientation and writing. In conclusion, an MMSE <26 identifies older patients with cirrhosis who are more prone to manifest HE signs.

Severe posterior reversible encephalopathy in pheochromocytoma: Importance of susceptibility-weighted MRI

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Serter, Asil; Alkan, Alpay; Aralasmak, Ayse; Kocakoc, Ercan [Dept. of Radiology, Bezmialem Vakif University School of Medicine, Istanbul (Turkmenistan)

2013-10-15

Pheochromocytoma is a rare cause of hypertension in children. Hypertension is one of the common reasons of posterior reversible encephalopathy. Intracerebral hemorrhage is a serious and unexpected complication of hypertensive encephalopathy due to pheochromocytoma, and very rarely seen in the childhood. Intracerebral hemorrhages should be searched if there are hypertensive reversible signal changes on the brain. Susceptibility weighted imaging (SWI) is a more sensitive method than conventional MRI when demonstrating cerebral microhemorrhagic foci. This is the first report of SWI findings on intracerebral hemorrhages in basal ganglia, brain stem and periventricular white matter due to hypertensive encephalopathy in a child with pheochromocytoma.

45CaCl2 autoradiography in brain from rabbits with encephalopathy from acute liver failure or acute hyperammonemia

NARCIS (Netherlands)

R.J. de Knegt (Robert); J.-B.P. Gramsbergen (J. B P); S.W. Schalm (Solko)

1994-01-01

textabstractIn experimental hepatic encephalopathy and hyperammonemia, extracellular levels of glutamate are increased in hippocampus and cerebral cortex. It has been suggested that overstimulation of glutamate receptors causes a pathological entry of calcium into neurons via receptor-operated

Hepatic angiography: Portal hypertension

International Nuclear Information System (INIS)

Oliver, T.W. Jr.; Sones, P.J. Jr.

1985-01-01

Portal hypertension is usually a manifestation of underlying hepatic parenchymal disease, although it may be secondary to portal or hepatic venous thrombosis and rarely to hyperdynamic portal states. Portal hypertension may present as encephalopathy, ascites, jaundice, hepatic failure, or catastrophic upper gastrointestinal hemorrhage. Radiologic investigation should include indirect or direct measurements of portal pressure, assessment of portal venous perfusion, visualization of collaterals, and demonstration of arterial and venous anatomy for potential shunt procedure. Following survival of initial variceal bleeding, the most effective procedure to prevent recurrent hemorrhage is a shunt to decompress the varices. The decision whether to intervene medically or surgically during the acute hemorrhagic episode as well as the type of shunt used to prevent future hemorrhage is the subject of continuing controversy

Direct-acting antivirals for chronic hepatitis C

DEFF Research Database (Denmark)

Jakobsen, Janus C; Nielsen, Emil Eik; Feinberg, Joshua

2017-01-01

BACKGROUND: Millions of people worldwide suffer from hepatitis C, which can lead to severe liver disease, liver cancer, and death. Direct-acting antivirals (DAAs), e.g. sofosbuvir, are relatively new and expensive interventions for chronic hepatitis C, and preliminary results suggest that DAAs may...... eradicate hepatitis C virus (HCV) from the blood (sustained virological response). Sustained virological response (SVR) is used by investigators and regulatory agencies as a surrogate outcome for morbidity and mortality, based solely on observational evidence. However, there have been no randomised trials...... hepatitis C-related morbidity, serious adverse events, and health-related quality of life. Our secondary outcomes were all-cause mortality, ascites, variceal bleeding, hepato-renal syndrome, hepatic encephalopathy, hepatocellular carcinoma, non-serious adverse events (each reported separately), and SVR. We...

Minimal hepatic encephalopathy in children with chronic liver disease: Prevalence, pathogenesis and magnetic resonance-based diagnosis.

Science.gov (United States)

Srivastava, Anshu; Chaturvedi, Saurabh; Gupta, Rakesh Kumar; Malik, Rohan; Mathias, Amrita; Jagannathan, Naranamangalam R; Jain, Sunil; Pandey, Chandra Mani; Yachha, Surender Kumar; Rathore, Ram Kishor Singh

2017-03-01

Data on minimal hepatic encephalopathy (MHE) in children is scarce. We aimed to study MHE in children with chronic liver disease (CLD) and to validate non-invasive objective tests which can assist in its diagnosis. We evaluated 67 children with CLD (38 boys; age 13 [7-18] years) and 37 healthy children to determine the prevalence of MHE. We also assessed the correlation of MHE with changes in brain metabolites by magnetic resonance spectroscopy ( 1 HMRS), diffusion tensor imaging (DTI) derived metrics, blood ammonia and inflammatory cytokines (interleukin-6 [IL6], tumor necrosis factor alpha [TNF-α]). In addition, the accuracy of MR-based investigations for diagnosis of MHE in comparison to neuropsychological tests was analysed. Thirty-four (50.7%) children with CLD had MHE on neuropsychological tests. MHE patients had higher BA (30.5 [6-74] vs. 14 [6-66]μmol/L; p=0.02), IL-6 (8.3 [4.7-28.7] vs. 7.6 [4.7-20.7]pg/ml; p=0.4) and TNF-α (17.8 [7.8-65.5] vs. 12.8 [7.5-35]pg/ml; p=0.06) than No-MHE. 1 HMRS showed higher glutamine (2.6 [2.1-3.3] vs. 2.4 [2.0-3.1]; p=0.02), and lower choline (0.20 [0.14-0.25] vs. 0.22 [0.17-0.28]; p=0.1) and myo-inositol (0.25 [0.14-0.41] vs. 0.29 [0.21-0.66]; p=0.2) in MHE patients than those without MHE. Mean diffusivity (MD) on DTI was significantly higher in 6/11 brain areas in patients with MHE vs. no MHE. Brain glutamine had a significant positive correlation with blood ammonia, IL-6, TNF-α and MD of various brain regions. Neuropsychological tests showed a negative correlation with blood ammonia, IL6, TNF-α, glutamine and MD. Frontal white matter MD had a sensitivity and specificity of 73.5% and 100% for diagnosing MHE. In children with CLD, 50% have MHE. There is a significant positive correlation between markers of hyperammonemia, inflammation and brain edema and these correlate negatively with neuropsychological tests. MD on DTI is a reliable tool for diagnosing MHE. Fifty percent of children with chronic liver disease

A new infectious encephalopathy syndrome, clinically mild encephalopathy associated with excitotoxicity (MEEX).

Science.gov (United States)

Hirai, Nozomi; Yoshimaru, Daisuke; Moriyama, Yoko; Yasukawa, Kumi; Takanashi, Jun-Ichi

2017-09-15

Acute infectious encephalopathy is often observed in children in East Asia including Japan. More than 40% of the patients remain unclassified into specific syndromes. To investigate the underlying pathomechanisms in those with unclassified encephalopathy, we evaluated brain metabolism by MR spectroscopy. Among seven patients with acute encephalopathy admitted to our hospital from June 2016 to May 2017, three were classified into acute encephalopathy with biphasic seizures and late reduced diffusion (AESD). The other four showed consciousness disturbance lasting more than three days with no parenchymal lesion visible on MRI, which led to a diagnosis of unclassified encephalopathy. MR spectroscopy in these four patients, however, revealed an increase of glutamine with a normal N-acetyl aspartate level on days 5 to 8, which had normalized by follow-up studies on days 11 to 16. The four patients clinically recovered completely. Among 27 patients with encephalopathy, including the present seven patients, admitted to our hospital from January 2015 to March 2017, seven (26%) were classified into this type, which we propose is a new encephalopathy syndrome, clinically mild encephalopathy associated with excitotoxicity (MEEX). MEEX is the second most common subtype, following AESD (30%). This study suggests that excitotoxicity may be a common underlying pathomechanism of acute infectious encephalopathy, and prompt astrocytic neuroprotection from excitotoxicity may prevent progression of MEEX into AESD. Copyright © 2017 Elsevier B.V. All rights reserved.

Bilirubin encephalopathy

Science.gov (United States)

Bilirubin encephalopathy is a rare neurological condition that occurs in some newborns with severe jaundice . ... Bilirubin encephalopathy (BE) is caused by very high levels of bilirubin. Bilirubin is a yellow pigment that is created ...

Successful Reversal of Chronic Incapacitating Post-TIPS Encephalopathy by Balloon Occlusion of the Stent

Directory of Open Access Journals (Sweden)

Daphna Fenyves

1994-01-01

Full Text Available Transjugular intrahepatic portosystemic shunt (TIPS placement is a new technique allowing decompression of the portal system without the need for abdominal surgery or general anesthetic. This promising procedure appears safe, and is being evaluated in the context of life threatening uncontrollable variceal hemorrhage as well as ascites refractory to medical treatment. Following TIPS, portal flow diversion is associated with hepatic encephalopathy in up to 25% of patients. This is most often mild and treatable but may become uncontrollable, incapacitating and even life threatening in up to 3 to 5% of cases. The authors present two patients in whom such life threatening encephalopathy and stupor was reversed by transjugular balloon occlusion of the TIPS.

CT findings in ischaemic hepatic failure due to intra-arterial embolisation: A case report

International Nuclear Information System (INIS)

Catalano, O.

1997-01-01

Liver infarction is relatively uncommon. It may be secondary to several conditions such as sepsis, shock, sickle-cell anaemia, eclampsia, vasculitis, metastatic disease, bacterial endocarditis, rheumatic heart disease, trauma, portal venous occlusion or compression, oral contraception, anaesthesia, hepatic artery thrombosis, therapeutical or inadvertent hepatic artery ligation, intra-arterial chemotherapy or embolisation. A case of hepatic infraction, unusual for iatrogenic pathogenesis, submassive extension with acute hepatic failure, and CT findings of an internally branching pattern due to intravascular gas was observed. (orig./AJ)

Disrupted thalamic resting-state functional connectivity in patients with minimal hepatic encephalopathy

International Nuclear Information System (INIS)

Qi, Rongfeng; Zhang, Long Jiang; Zhong, Jianhui; Zhang, Zhiqiang; Ni, Ling; Zheng, Gang; Lu, Guang Ming

2013-01-01

Background and purpose: Little is known about the role of thalamus in the pathophysiology of minimal hepatic encephalopathy (MHE). The purpose of this study was to investigate whether the thalamic functional connectivity was disrupted in cirrhotic patients with MHE by using resting-state functional magnetic resonance imaging (rs-fMRI). Materials and Methods: Twenty seven MHE patients and twenty seven age- and gender- matched healthy controls participated in the rs-fMRI scans. The functional connectivity of 11 thalamic nuclei were characterized by using a standard seed-based whole-brain correlation method and compared between MHE patients and healthy controls. Pearson correlation analysis was performed between the thalamic functional connectivity and venous blood ammonia levels/neuropsychological tests scores of patients. Results: The ventral anterior nucleus (VAN) and the ventral posterior medial nucleus (VPMN) in each side of thalamus showed abnormal functional connectivities in MHE. Compared with healthy controls, MHE patients demonstrated significant decreased functional connectivity between the right/left VAN and the bilateral putamen/pallidum, inferior frontal gyri, insula, supplementary motor area, right middle frontal gyrus, medial frontal gyrus. In addition, MHE patients showed significantly decreased functional connectivity with the right/left VPMN in the bilateral middle temporal gyri (MTG), temporal lobe, and right superior temporal gyrus. The venous blood ammonia levels of MHE patients negatively correlated with the functional connectivity between the VAN and the insula. Number connecting test scores showed negative correlation with the functional connectivity between the VAN and the insula, and between the VPMN and the MTG. Conclusion: MHE patients had disrupted thalamic functional connectivity, which mainly located in the bilateral ventral anterior nuclei and ventral posterior medial nuclei. The decreased connectivity between thalamus and many

Disrupted thalamic resting-state functional connectivity in patients with minimal hepatic encephalopathy

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Qi, Rongfeng [Department of Medical Imaging, Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing 210002 (China); Zhang, Long Jiang, E-mail: kevinzhanglongjiang@yahoo.com.cn [Department of Medical Imaging, Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing 210002 (China); Zhong, Jianhui [Department of Biomedical Engineering, Zhejiang University, Hangzhou, Zhejiang 310027 (China); Zhang, Zhiqiang; Ni, Ling; Zheng, Gang [Department of Medical Imaging, Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing 210002 (China); Lu, Guang Ming, E-mail: cjr.luguangming@vip.163.com [Department of Medical Imaging, Jinling Hospital, Clinical School of Medical College, Nanjing University, Nanjing 210002 (China)

2013-05-15

Background and purpose: Little is known about the role of thalamus in the pathophysiology of minimal hepatic encephalopathy (MHE). The purpose of this study was to investigate whether the thalamic functional connectivity was disrupted in cirrhotic patients with MHE by using resting-state functional magnetic resonance imaging (rs-fMRI). Materials and Methods: Twenty seven MHE patients and twenty seven age- and gender- matched healthy controls participated in the rs-fMRI scans. The functional connectivity of 11 thalamic nuclei were characterized by using a standard seed-based whole-brain correlation method and compared between MHE patients and healthy controls. Pearson correlation analysis was performed between the thalamic functional connectivity and venous blood ammonia levels/neuropsychological tests scores of patients. Results: The ventral anterior nucleus (VAN) and the ventral posterior medial nucleus (VPMN) in each side of thalamus showed abnormal functional connectivities in MHE. Compared with healthy controls, MHE patients demonstrated significant decreased functional connectivity between the right/left VAN and the bilateral putamen/pallidum, inferior frontal gyri, insula, supplementary motor area, right middle frontal gyrus, medial frontal gyrus. In addition, MHE patients showed significantly decreased functional connectivity with the right/left VPMN in the bilateral middle temporal gyri (MTG), temporal lobe, and right superior temporal gyrus. The venous blood ammonia levels of MHE patients negatively correlated with the functional connectivity between the VAN and the insula. Number connecting test scores showed negative correlation with the functional connectivity between the VAN and the insula, and between the VPMN and the MTG. Conclusion: MHE patients had disrupted thalamic functional connectivity, which mainly located in the bilateral ventral anterior nuclei and ventral posterior medial nuclei. The decreased connectivity between thalamus and many

Hepatic Lipodystrophy in Galloway Calves.

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Wieland, M; Mann, S; Hafner-Marx, A; Ignatius, A; Metzner, M

2017-05-01

Hepatic lipodystrophy in Galloway calves is a fatal liver disease affecting a small proportion of the Galloway breed described in different parts of Europe and North America during the past decades. The clinical findings include a diversity of neurological signs. Clinical pathology findings frequently indicate hepatobiliary disease. Postmortem examination reveals an enlarged, pale yellow, and firm liver. Histologic lesions include hepatic fibrosis, hepatic lipidosis, and bile duct hyperplasia. To date, the etiopathogenesis remains obscure. Infectious causes, intoxications, and a hereditary origin have been considered. We describe hepatic lipodystrophy in Galloway calves from an extensively farmed cow-calf operation in southern Germany. Main clinical findings in 6 calves were consistent with hepatic encephalopathy. Clinical pathology findings in 5 of 6 tested animals revealed increased concentration of total bilirubin (maximum value [MV], 54 μmol/l; reference range [RR], 250 U/g Hb). Postmortem examination in 6 calves revealed a firm, diffusely enlarged yellow liver with a finely nodular surface. Histologic lesions included hepatic fibrosis, hepatic lipidosis, and bile duct hyperplasia. Our findings add to the existing data on hepatic lipodystrophy in the Galloway breed and outline a protocol to aid in the diagnosis of this disorder.

Clinical manifestations and treatment response of steroid in pediatric Hashimoto encephalopathy.

Science.gov (United States)

Yu, Hee Joon; Lee, Jeehun; Seo, Dae Won; Lee, Munhyang

2014-07-01

Hashimoto encephalopathy is a steroid-responsive encephalopathy associated with elevated titers of antithyroid antibodies. Clinical symptoms are characterized by behavioral and cognitive changes, speech disturbance, seizures, myoclonus, psychosis, hallucination, involuntary movements, cerebellar signs, and coma. The standard treatment is the use of corticosteroids along with the treatment of any concurrent dysthyroidism. Other options are immunoglobulins and plasmapheresis. We described symptoms and outcomes on 3 teenage girls with Hashimoto encephalopathy. Presenting symptoms were seizure or altered mental status. One patient took levothyroxine due to hypothyroidism before presentation of Hashimoto encephalopathy. After confirmation of elevated antithyroid antibodies, all patients were treated with steroids. One patient needed plasmapheresis because of the lack of response to steroids and immunoglobulins. Hashimoto encephalopathy should be considered in any patient presenting with acute or subacute unexplained encephalopathy and seizures. Even though the use of steroids is the first line of treatment, plasmapheresis can rescue steroid-resistant patients. © The Author(s) 2013.

Hyperammonemia and systemic inflammatory response syndrome predicts presence of hepatic encephalopathy in dogs with congenital portosystemic shunts.

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Mickey S Tivers

Full Text Available Hepatic encephalopathy (HE is an important cause of morbidity and mortality in patients with liver disease. The pathogenesis of he is incompletely understood although ammonia and inflammatory cytokines have been implicated as key mediators. To facilitate further mechanistic understanding of the pathogenesis of HE, a large number of animal models have been developed which often involve the surgical creation of an anastomosis between the hepatic portal vein and the caudal vena cava. One of the most common congenital abnormalities in dogs is a congenital portosystemic shunt (cpss, which closely mimics these surgical experimental models of HE. Dogs with a cPSS often have clinical signs which mimic clinical signs observed in humans with HE. Our hypothesis is that the pathogenesis of HE in dogs with a cPSS is similar to humans with HE. The aim of the study was to measure a range of clinical, haematological and biochemical parameters, which have been linked to the development of HE in humans, in dogs with a cPSS and a known HE grade. One hundred and twenty dogs with a cPSS were included in the study and multiple regression analysis of clinical, haematological and biochemical variables revealed that plasma ammonia concentrations and systemic inflammatory response syndrome scores predicted the presence of HE. Our findings further support the notion that the pathogenesis of canine and human HE share many similarities and indicate that dogs with cPSS may be an informative spontaneous model of human HE. Further investigations on dogs with cPSS may allow studies on HE to be undertaken without creating surgical models of HE thereby allowing the number of large animals used in animal experimentation to be reduced.

Transjugular intrahepatic porto-systemic stent-shunt for therapy of bleeding esophageal varices due to extramedullary hematopoiesis in primary myelofibrosis: a case report.

Science.gov (United States)

Phillip, Veit; Berger, Hermann; Straub, Melanie; Saugel, Bernd; Treiber, Matthias; Einwächter, Henrik; Schmid, Roland M; Huber, Wolfgang

2012-01-01

Primary myelofibrosis belongs to the group of myeloproliferative syndromes. Extramedullary hematopoiesis in the liver can lead to portal hypertension. We report a case of a patient with life-threatening, endoscopically not treatable bleeding from esophageal varices due to extramedullary hematopoiesis of the liver that was successfully treated with placement of a transjugular intrahepatic porto-systemic stent-shunt (TIPS). Therapy of variceal bleeding by TIPS insertion was successful. During a 29-month follow-up, no hepatic failure, hepatic encephalopathy, or further variceal bleeding episode occurred. TIPS placement is a well-established procedure for the treatment of complications due to portal hypertension mainly due to liver cirrhosis. This report illustrates that TIPS placement can also be a promising treatment option in patients with primary myelofibrosis and portal hypertension due to extramedullary hematopoiesis. Copyright © 2012 S. Karger AG, Basel.

Connectivity of default-mode network is associated with cerebral edema in hepatic encephalopathy.

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Wei-Che Lin

Full Text Available Cerebral edema, a well-known feature of acute liver disease, can occur in cirrhotic patients regardless of hepatic encephalopathy (HE and adversely affect prognosis. This study characterized and correlated functional HE abnormalities in the brain to cerebral edema using resting-state functional magnetic resonance imaging (rs-fMRI and diffusion tensor imaging (DTI. Forty-one cirrhotic patients (16 without HE, 14 minimal HE, 11 overt HE and 32 healthy controls were assessed. The HE grade in cirrhotic patients was evaluated by the West Haven criteria and neuro-psychological examinations. Functional connectivity correlation coefficient (fc-CC of the default mode network (DMN was determined by rs-fMRI, while the corresponding mean diffusivity (MD was obtained from DTI. Correlations among inter-cortical fc-CC, DTI indices, Cognitive Ability Screening Instrument scores, and laboratory tests were also analyzed. Results showed that gradual reductions of HE-related consciousness levels, from "without HE" or "minimal HE" to "overt HE", correlated with decreased anterior-posterior fc-CC in DMN [F(4.415, p = 0.000]. The MD values from regions with anterior-posterior fc-CC differences in DMN revealed significant differences between the overt HE group and other groups. Increased MD in this network was inversely associated with decreased fc-CC in DMN and linearly correlated with poor cognitive performance. In conclusion, cerebral edema can be linked to altered cerebral temporal architecture that modifies both within- and between-network connectivity in HE. Reduced fc-CC in DMN is associated with behavior and consciousness deterioration. Through appropriate targets, rs-fMRI technology may provide relevant supplemental information for monitoring HE and serve as a new biomarker for clinical diagnosis.

Two-dimensional MR spectroscopy of minimal hepatic encephalopathy and neuropsychological correlates in vivo.

Science.gov (United States)

Singhal, Aparna; Nagarajan, Rajakumar; Hinkin, Charles H; Kumar, Rajesh; Sayre, James; Elderkin-Thompson, Virginia; Huda, Amir; Gupta, Rakesh K; Han, Steven-Huy; Thomas, M Albert

2010-07-01

To evaluate regional cerebral metabolic and structural changes in patients with minimal hepatic encephalopathy (MHE) using two-dimensional (2D) MR spectroscopy (MRS) and T( (1) )-weighted MRI, to correlate the observed MR changes with neuropsychological (NP) test scores, and to compare the diagnostic accuracy of MRI, 2D MRS, and NP tests in discriminating between patients and healthy subjects. Thirty-three MHE patients and 30 healthy controls were investigated. The 2D localized correlated spectroscopy (L-COSY) was performed in the frontal and occipital brain on a 1.5 Tesla (T) MR scanner. The NP test battery included 15 tests, grouped into 6 cognitive domains. Globus pallidus signal intensities were calculated from T(1)-weighted images. The 2D MRS showed significant differences in ratios of the following metabolite(s) peaks with respect to creatine (Cr): decreased myo-inositol (mI), choline (Ch), mICh, and increased (glutamate plus glutamine) (Glx) in patients compared with healthy subjects in both occipital and frontal lobes. Frontal lobe taurine also showed a decline in patients. The NP test results revealed declines in cognitive speed, motor function, executive function, and global cognitive status. Significant correlations were found between the altered metabolites and NP tests. Alteration in the mICh/Cr ratio was noted as a powerful discriminant between healthy subjects and the patients. The study demonstrates that relative metabolite levels determined by 2D MRS, in particular mICh/Cr, provide the best diagnostic prediction for MHE. The results suggest that depletions of myo-inositol, choline and taurine with respect to creatine correlate with measures of neuropsychological impairment. (c) 2010 Wiley-Liss, Inc.

USEFULNESS OF A NEW PROGNOSTIC INDEX FOR ALCOHOLIC HEPATITIS

Directory of Open Access Journals (Sweden)

Jazon Romilson de Souza ALMEIDA

2015-03-01

Full Text Available Background Alcoholic liver disease is a major cause of end-stage liver disease worldwide and severe forms of alcoholic hepatitis are associated with a high short-term mortality. Objectives To analyze the importance of age-bilirubin-INR-creatinine (ABIC score as an index of mortality and predictor for complications in patients with alcoholic hepatitis. To evaluate its correlation with those complications, with risk of death, as well as the scores model for end stage liver disease (MELD and Maddrey’s discriminat function. Methods A total of 46 medical records of patients who had been hospitalized with alcoholic hepatitis were assessed retrospectively with lab tests on admission and after seven days. Score calculations were carried out and analyzed as well. Results The scores showed positive reciprocal correlation and were associated with both hepatic encephalopathy and ascites. ABIC index, which was classified as high risk, presented as a risk factor for these complications and for death. In univariate logistic regression analysis of mortality, the ABIC index at hospital admission odds ratio was 19.27, whereas after 7 days, it was 41.29. The average survival of patients with ABIC of low and intermediate risk was 61.1 days, and for those with high risk, 26.2 days. Conclusions ABIC index is a predictor factor for complications such as ascites and hepatic encephalopathy, as well as for risk of death. Thus, it is a useful tool for clinical practice.

Treatment of hepatic encephalopathy by retrograde transcaval coil embolization of an ileal vein-to-right gonadal vein portosystemic shunt

International Nuclear Information System (INIS)

Nishie, Akihiro; Yoshimitsu, Kengo; Honda, Hiroshi; Kaneko, Kuniyuki; Kuroiwa, Toshiro; Fukuya, Tatsuro; Irie, Hiroyuki; Ninomiya, Toshiharu; Yoshimitsu, Takahiro; Hirakata, Hideki; Okuda, Seiya; Masuda, Kouji

1997-01-01

A 43-year-old non-cirrhotic woman suffered from encephalopathy caused by an extrahepatic portosystemic shunt between the ileal vein and inferior vena cava via the right gonadal vein. Percutaneous transcatheter embolization with stainless steel coils was performed by the retrograde systemic venous approach. Encephalopathy improved dramatically

MRI of neonatal encephalopathy

International Nuclear Information System (INIS)

Khong, P.L.; Lam, B.C.C.; Tung, H.K.S.; Wong, V.; Chan, F.L.; Ooi, G.C.

2003-01-01

We present the magnetic resonance imaging (MRI) findings in neonatal encephalopathy, including hypoxic-ischaemic encephalopathy, perinatal/neonatal stroke, metabolic encephalopathy from inborn errors of metabolism, congenital central nervous system infections and birth trauma. The applications of advanced MRI techniques, such as diffusion-weighted imaging and magnetic resonance spectroscopy are emphasized

MRI findings of Wernicke encephalopathy revisited due to hunger strike

Energy Technology Data Exchange (ETDEWEB)

Unlu, Ercument [Department of Radiology, Trakya University School of Medicine, Mimar Sinan m, Muammer Aksoy c, Yorulmaz apt, No 50, D-1 22030 Edirne (Turkey)]. E-mail: drercument@yahoo.com; Cakir, Bilge [Department of Radiology, Trakya University School of Medicine, Mimar Sinan m, Muammer Aksoy c, Yorulmaz apt, No 50, D-1 22030 Edirne (Turkey); Asil, Talip [Department of Neurology, Trakya University School of Medicine, Edirne (Turkey)

2006-01-15

Background and Purpose: The purpose of this study was to determine the characteristic magnetic resonance imaging (MRI) findings among a group of patients who presented with Wernicke encephalopathy (WE) due to the neurological complications of a long-term hunger strike (HS). Methods: MRI studies also including the fluid-attenuated inversion recovery (FLAIR) sequence and diffusion-weighted imaging (DWI) of six male patients with WE aged from 25 to 38 years (mean age 31 years) were evaluated. Results: In all subjects, T2-weighted sequences, FLAIR and DWI revealed a signal hyperintensity within the posteromedial thalami and surrounding the third ventricle. In particular, on coronal images, the hyperintense areas around the third ventricle showed a suggestive 'double wing' configuration. We observed an increased signal on proton-density and T2-weighted images in the mamillary bodies of three patients. Four patients demonstrated additional hyperintensities within the periaqueductal region and/or the tectal plate. At least one lesion area in five of six patients demonstrated contrast enhancement. Conclusion: The consistent imaging findings of our study suggest that MRI is a reliable means of diagnosing WE. Acute WE is sometimes underdiagnosed, yet early diagnosis and treatment of WE is crucial in order to avoid persistent brain damage. MRI, including postcontrast T1-weighted imaging, DWI beneath standardized T2-weighted imaging, and FLAIR sequences may prove to be a valuable adjunct to clinical diagnosis and to provide additional information in acute and/or subacute WE.

MRI findings of Wernicke encephalopathy revisited due to hunger strike

International Nuclear Information System (INIS)

Unlu, Ercument; Cakir, Bilge; Asil, Talip

2006-01-01

Background and Purpose: The purpose of this study was to determine the characteristic magnetic resonance imaging (MRI) findings among a group of patients who presented with Wernicke encephalopathy (WE) due to the neurological complications of a long-term hunger strike (HS). Methods: MRI studies also including the fluid-attenuated inversion recovery (FLAIR) sequence and diffusion-weighted imaging (DWI) of six male patients with WE aged from 25 to 38 years (mean age 31 years) were evaluated. Results: In all subjects, T2-weighted sequences, FLAIR and DWI revealed a signal hyperintensity within the posteromedial thalami and surrounding the third ventricle. In particular, on coronal images, the hyperintense areas around the third ventricle showed a suggestive 'double wing' configuration. We observed an increased signal on proton-density and T2-weighted images in the mamillary bodies of three patients. Four patients demonstrated additional hyperintensities within the periaqueductal region and/or the tectal plate. At least one lesion area in five of six patients demonstrated contrast enhancement. Conclusion: The consistent imaging findings of our study suggest that MRI is a reliable means of diagnosing WE. Acute WE is sometimes underdiagnosed, yet early diagnosis and treatment of WE is crucial in order to avoid persistent brain damage. MRI, including postcontrast T1-weighted imaging, DWI beneath standardized T2-weighted imaging, and FLAIR sequences may prove to be a valuable adjunct to clinical diagnosis and to provide additional information in acute and/or subacute WE

Treatment of Epileptic Encephalopathies.

Science.gov (United States)

Balestrini, Simona; Sisodiya, Sanjay M

2017-01-01

Epileptic encephalopathies represent the most severe epilepsies, with onset in infancy and childhood and seizures continuing in adulthood in most cases. New genetic causes are being identified at a rapid rate. Treatment is challenging and the overall outcome remains poor. Available targeted treatments, based on the precision medicine approach, are currently few. To provide an overview of the treatment of epileptic encephalopathies with known genetic determinants, including established treatment, anecdotal reports of specific treatment, and potential tailored precision medicine strategies. Genes known to be associated to epileptic encephalopathy were selected. Genes where the association was uncertain or with no reports of details on treatment, were not included. Although some of the genes included are associated with multiple epilepsy phenotypes or other organ involvement, we have mainly focused on the epileptic encephalopathies and their antiepileptic treatments. Most epileptic encephalopathies show genotypic and phenotypic heterogeneity. The treatment of seizures is difficult in most cases. The available evidence may provide some guidance for treatment: for example, ACTH seems to be effective in controlling infantile spams in a number of genetic epileptic encephalopathies. There are potentially effective tailored precision medicine strategies available for some of the encephalopathies, and therapies with currently unexplained effectiveness in others. Understanding the effect of the mutation is crucial for targeted treatment. There is a broad range of disease mechanisms underlying epileptic encephalopathies, and this makes the application of targeted treatments challenging. However, there is evidence that tailored treatment could significantly improve epilepsy treatment and prognosis. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.

Glucocorticoids are ineffective in alcoholic hepatitis

DEFF Research Database (Denmark)

Christensen, E; Gluud, C

1995-01-01

The aim of this study was to perform a meta-analysis of controlled clinical trials of glucocorticoid treatment in clinical alcoholic hepatitis, adjusting for prognostic variables and their possible interaction with therapy, because these trials have given appreciably different results. Weighted...... logistic regression analysis was applied using the summarised descriptive data (for example, % with encephalopathy, mean bilirubin value) of the treatment and control groups of 12 controlled trials that gave this information. Despite evidence of publication bias favouring glucocorticoid treatment, its...... overall effect on mortality was not statistically significant (p = 0.20)--the relative risk (steroid/control) was 0.78 (95% confidence intervals 0.51, 1.18). There was indication of interaction between glucocorticoid therapy and gender, but not encephalopathy. Thus, the effect of glucocorticoid treatment...

FELINE HEPATIC LIPIDOSIS

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C. Masotti

2016-11-01

Full Text Available Since the first description of feline hepatic lipidosis occurred in 1977, it becames the most diagnosed liver disease in cats. Several factors have been proposed as causes of disease, and obesity being a predisposing factor. The disease can be considered primary or idiopathic when its underlying cause is unknown, or secondary when there is another concomitant disease lipidosis. Cats with hepatic lipidosis have anorexia usually ranging from several days to weeks and weight loss, followed by jaundice and varying degrees of dehydration, diarrhea and vomiting episodes may occur. A worsening of the disease shows signs of hepatic encephalopathy, drooling and retroflexion of the neck. In clinical examination can be observed depression, lethargy and hepatomegaly. The definitive diagnosis of the disease can be performed by fine needle aspiration biopsy guided by ultrasound and cytology or biopsy. The treatment of hepatic lipidosis is based on stabilizing the patient by supplying water and electrolyte losses and provide adequate nutritional support. The diet is usually provided through feeding tubes for a period ranging from 4 to 6 weeks may occur depending on the patient's condition. The prognosis for cats with hepatic lipidosis is favored in cases of identification followed by intensive treatment of underlying causes and for patients receiving therapy necessary in cases of idiopathic hepatic lipidosis.

Navigation skill impairment: Another dimension of the driving difficulties in minimal hepatic encephalopathy.

Science.gov (United States)

Bajaj, Jasmohan S; Hafeezullah, Muhammad; Hoffmann, Raymond G; Varma, Rajiv R; Franco, Jose; Binion, David G; Hammeke, Thomas A; Saeian, Kia

2008-02-01

Patients with minimal hepatic encephalopathy (MHE) have attention, response inhibition, and working memory difficulties that are associated with driving impairment and high motor vehicle accident risk. Navigation is a complex system needed for safe driving that requires functioning working memory and other domains adversely affected by MHE. The aim of this study was to determine the effect of MHE on navigation skills and correlate them with psychometric impairment. Forty-nine nonalcoholic patients with cirrhosis (34 MHE+, 15 MHE-; divided on the basis of a battery of block design, digit symbol, and number connection test A) and 48 age/education-matched controls were included. All patients underwent the psychometric battery and inhibitory control test (ICT) (a test of response inhibition) and driving simulation. Driving simulation consisted of 4 parts: (1) training; (2) driving (outcome being accidents); (3) divided attention (outcome being missed tasks); and (4) navigation, driving along a marked path on a map in a "virtual city" (outcome being illegal turns). Illegal turns were significantly higher in MHE+ (median 1; P = 0.007) compared with MHE-/controls (median 0). Patients who were MHE+ missed more divided attention tasks compared with others (median MHE+ 1, MHE-/controls 0; P = 0.001). Similarly, accidents were higher in patients who were MHE+ (median 2.5; P = 0.004) compared with MHE- (median 1) or controls (median 2). Accidents and illegal turns were significantly correlated (P = 0.001, r = 0.51). ICT impairment was the test most correlated with illegal turns (r = 0.6) and accidents (r = 0.44), although impairment on the other tests were also correlated with illegal turns. Patients positive for MHE have impaired navigation skills on a driving simulator, which is correlated with impairment in response inhibition (ICT) and attention. This navigation difficulty may pose additional driving problems, compounding the pre-existing deleterious effect of attention

Acute hepatitis due to Epstein–Barr virus with cross-reacting antibodies to cytomegalovirus

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Asli Karadeniz

2018-01-01

Full Text Available Epstein–Barr virus (EBV is the cause of systemic infection known as infectious mononucleosis with classic presentation of fever, oropharyngitis and lymphadenitis. EBV rarely causes acute hepatitis. In this report, we present a 19-year-old patient presented with nausea, fatigue and jaundice. Her physical examination and laboratory tests revealed the diagnosis as acute hepatitis due to EBV with cross-reacting antibodies to cytomegalovirus.

A Rare Case of Reversible Encephalopathy Syndrome Accompanying Late Postpartum Eclampsia or Hypertensive Encephalopathy-A Clinical Dilemma

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Shakuntala PN

2012-04-01

Full Text Available Posterior Reversible Encephalopathy Syndrome (PRES refers to a clinic-radiologic diagnosis. Clinically it is characterized by non specific symptoms such as headache, confusion, visual disturbances and seizures. The radiological findings in PRES are thought to be due to vasogenic oedema, predominantly in the posterior cerebral hemispheres, and are reversible with appropriate management. We report a case of reversible encephalopathy diagnosed by MRI scan occurring in atypical areas like the caudate and lentiform nuclei of the brain following an uneventful lower segment caesarean section in a normotensive patient, who was successfully treated with antihypertensives, anticonvulsants and supportive treatment. The differential diagnosis of convulsions in the post-partum period is discussed.

Diverse Neurological Manifestations of Lead Encephalopathy ...

African Journals Online (AJOL)

Three patients with lead encephalopathy due to industrial poisoning are presented. They all showed a wide spectrum of neurological manifestations, which mimic other neurological presentations. It is emphasised that lead poisoning still occurs in industry, despite efforts at prevention. S. Afr. Med. J., 48, 1721 (1974) ...

Posterior reversible encephalopathy syndrome: Some novel ...

African Journals Online (AJOL)

Two cases occurred following cerebral anoxia due to accidental strangulation and near-drowning, respectively. The third patient, a child known to have E-β thalassaemia, presented with transient encephalopathy following blood transfusion but involving the anterior brain rather than the posterior part classically described in ...

Detecção de encefalopatia hepática mínima através de testes neuropsicológicos e neurofisiológicos e o papel da amônia no seu diagnóstico Minimal hepatic encephalopathy detection by neuropsychological and neurophysiological methods and the role of ammonia for its diagnosis

Directory of Open Access Journals (Sweden)

Maurício Augusto Bragagnolo Jr.

2009-03-01

Full Text Available CONTEXTO: A encefalopatia hepática mínima vem sendo sistematicamente investigada em pacientes com cirrose hepática. Entretanto, existem controvérsias quanto aos melhores métodos, bem como o papel da amônia para seu diagnóstico. OBJETIVO: Avaliar a frequência de encefalopatia hepática mínima diagnosticada através de testes neuropsicológicos e neurofisiológicos em cirróticos, bem como os possíveis fatores de risco para esta condição, incluindo o papel da concentração arterial de amônia em seu diagnóstico. MÉTODOS: Indivíduos com cirrose hepática foram avaliados através do teste de conexão numérica partes A e B (TCN-A e TCN-B e potencial evocado relacionado a eventos (P300. O diagnóstico de encefalopatia hepática mínima foi feito quando da presença de anormalidade no P300 e em, pelo menos, um dos testes neuropsicológicos. As concentrações arteriais de amônia, a escolaridade e a gravidade da cirrose hepática também foram avaliadas em todos. RESULTADOS: Foram avaliados 48 pacientes cirróticos, com média de idade 50 ± 8 anos, sendo 79% do sexo masculino. As principais causas foram a alcoólica e a viral. O P300 foi anormal em 75% dos casos e o TCN-A e TCN-B anormais em 58% e 65% dos casos, respectivamente. Os resultados do TCN-B foram influenciados pela escolaridade. A frequência de encefalopatia hepática mínima foi de 50%. A concentração arterial de amônia não foi significantemente maior em pacientes com diagnóstico de encefalopatia hepática mínima (195 ± 152 mmol/L versus 148 ± 146 mmol/L; P>0,05. Não houve diferença significante entre os grupos com e sem encefalopatia hepática mínima quanto às demais variáveis estudadas. CONCLUSÃO:A encefalopatia hepática mínima é condição frequente em pacientes com cirrose hepática. A concentração arterial de amônia não parece ter papel importante no seu diagnóstico.CONTEXT: Minimal hepatic encephalopathy has been systematically investigated in

Avaliação dos potenciais evocados relacionados a eventos (ERP-P300 em pacientes com cirrose hepática sem encefalopatia Evaluation of the event-related potential (ERP-P300 in patients with hepatic cirrhosis without encephalopathy

Directory of Open Access Journals (Sweden)

Vinicius Teodoro

2008-03-01

Full Text Available RACIONAL: Na cirrose hepática ocorrem alterações na estrutura do fígado, levando à perda das funções do órgão, com conseqüências neuropsiquiátricas, como disfunções cognitivas. Um dos meios mais efetivos para avaliar objetivamente as funções cognitivas é medir a atividade eletrofisiológica do sistema nervoso central através do potencial evocado relacionado a eventos (ERP-P300. OBJETIVO: Estudar a utilidade do potencial evocado relacionado a eventos (ERP, para avaliar distúrbios cognitivos em pacientes com cirrose hepática e como auxiliar no diagnóstico da encefalopatia hepática mínima. MÉTODO: Foram selecionados 50 pacientes, diagnosticados com cirrose hepática sem sinais clínicos de encefalopatia hepática e 35 voluntários saudáveis de idades e sexo semelhantes. Em todos os pacientes foram realizados exames clínico-neurológico e laboratoriais. Para identificação do prejuízo cognitivo foi utilizado o ERP-P300 e obtida a média da latência da onda P300. RESULTADOS: Houve diferença significativa entre as médias da latência do ERP-P300 do grupo cirrótico e controle. CONCLUSÃO: A realização do ERP-P300 é simples, depende de fatores controláveis de variação e tem fácil reprodutibilidade, podendo ser útil para o rastreio de distúrbios cognitivos em pacientes com cirrose e auxiliar no diagnóstico de encefalopatia hepática mínima.BACKGROUND: In hepatic cirrhosis structural liver alterations occur leading to the loss of the organ functions with neuro-psychiatric consequence, as cognitive dysfunctions. One of the most effective ways of objectively evaluating cognition is to measure electrophysiological activity in the central nervous system trough event-related potentials (ERP-P300. AIM: To assess the value of the event-related potential (ERP in order to determine cognitive disturbances in patients with liver cirrhosis and to assist in the diagnosis of minimal hepatic encephalopathy. METHODS: Fifty

The effect of plasma exchange on entecavir-treated chronic hepatitis B patients with hepatic de-compensation and acute-on-chronic liver failure.

Science.gov (United States)

Yue-Meng, Wan; Yang, Li-Hong; Yang, Jin-Hui; Xu, Ying; Yang, Jing; Song, Gui-Bo

2016-05-01

Various studies showed that entecavir (ETV) failed to improve the short-term survival in chronic hepatitis B (CHB) patients with severe acute exacerbation (SAE) and hepatic de-compensation or acute-on-chronic liver failure (ACLF). One study concluded that plasma exchange (PE) significantly decreased the short-term mortality of CHB patients with ACLF who were treated with lamivudine (LAM). Our study was designed to examine the effect of PE on CHB patients with ACLF who were treated with ETV. From August 2010 to January 2015, 38 (PE group) and 120 (control group) consecutive CHB-naïve patients with hepatic de-compensation and ACLF treated with PE plus ETV and ETV, respectively, were recruited. The primary endpoint was liver-related mortality at week 12. Biochemical and virological responses were also studied. At baseline, the PE group had higher serum alanine aminotransferase (ALT) levels and model for end-stage liver disease (MELD) scores, and had lower albumin levels than the control group. The cumulative survival rate at week 4 and week 12 in the PE group and control group were, respectively, 37 and 18 %, and 29 and 14 % (p  0.05). Univariate analysis showed that the control group had a higher liver-related mortality (p = 0.038) at week 12 than the PE group. Multivariate analysis showed that hepatic encephalopathy, ascites, PE treatment, and MELD scores were independent factors for liver-related mortality at week 12. PE significantly improved the short-term survival of CHB patients with hepatic de-compensation and ACLF who were treated with ETV. Hepatic encephalopathy, ascites, PE treatment, and MELD scores were independent factors for liver-related mortality at week 12.

Contribution of altered signal transduction associated to glutamate receptors in brain to the neurological alterations of hepatic encephalopathy

Institute of Scientific and Technical Information of China (English)

Vicente Felipo

2006-01-01

Patients with liver disease may present hepatic encephalopathy (HE), a complex neuropsychiatric syndrome covering a wide range of neurological alterations,including cognitive and motor disturbances. HE reduces the quality of life of the patients and is associated with poor prognosis. In the worse cases HE may lead to coma or death.The mechanisms leading to HE which are not well known are being studied using animal models. The neurological alterations in HE are a consequence of impaired cerebral function mainly due to alterations in neurotransmission. We review here some studies indicating that alterations in neurotransmission associated to different types of glutamate receptors are responsible for some of the cognitive and motor alterations present in HE.These studies show that the function of the signal transduction pathway glutamate-nitric oxide-cGMP associated to the NMDA type of glutamate receptors is impaired in brain in vivo in HE animal models as well as in brain of patients died of HE. Activation of NMDA receptors in brain activates this pathway and increases cGMP. In animal models of HE this increase in cGMP induced by activation of NMDA receptors is reduced,which is responsible for the impairment in learning ability in these animal models. Increasing cGMP by pharmacological means restores learning ability in rats with HE and may be a new therapeutic approach to improve cognitive function in patients with HE.However, it is necessary to previously assess the possible secondary effects.Patients with HE may present psychomotor slowing,hypokinesia and bradykinesia. Animal models of HE also show hypolocomotion. It has been shown in rats with HE that hypolocomotion is due to excessive activation of metabotropic glutamate receptors (mGluRs) in substantia nigra pars reticulata. Blocking mGluR1 in this brain area normalizes motor activity in the rats, suggesting that a similar treatment for patients with HE could be useful to treat psychomotor slowing and

Hyperintensity of basal ganglia on T1-weighted images in patients with liver cirrhosis. Correlation with hepatic encephalopathy and liver function

International Nuclear Information System (INIS)

Maeda, Hiroko; Kita, Keisuke; Mizobata, Toshiharu; Kimura, Masashi; Sonomura, Tetsuo; Kishi, Kazushi; Tanaka, Kayo; Sato, Morio; Yamada, Ryosaku

1995-01-01

Brain MR imaging was performed in 38 liver cirrhosis (LC) patients and 9 normal volunteers. On T 1 -weighted images, the signal intensity of globus pallidus (S1) and frontal white matter (S2) was measured and S1/S2 ratio was explored. We examined the relationship between S1/S2 ratio and liver function parameters. High signal intensity in bilateral globus pallidus was noted on T 1 W1 in 28 of 38 LC patients. The S1/S2 ratio of 1.186±0.097 in the 38 LC patients was significantly higher than 0.987±0.062 in the 9 normal volunteers (p 2 -weighted images showed no abnormal intensity. Compared with the LC patients with hepatic encephalopathy (HE) (n=7) and without HE (n=31), the former S1/S2 ratio (1.239±0.057) was significantly higher than the latter (1.174±0.097) (p 15 (r=0.501, p 1 -WI and the degree of liver dysfunction. (author)

Clostridium difficile colonization and infection in patients with hepatic cirrhosis.

Science.gov (United States)

Yan, Dong; Chen, Yunbo; Lv, Tao; Huang, Yandi; Yang, Jiezuan; Li, Yongtao; Huang, Jianrong; Li, Lanjuan

2017-10-01

The aim of this study was to investigate the toxigenic Clostridium difficile colonization (CDC, colonization with toxigenic C. difficile but without symptoms) and C. difficile infection (CDI, active C. difficile infection resulting in disease symptoms) in hepatic cirrhosis patients, identify the risk factors of CDC, and determine the correlation between CDC and CDI. The strains of toxigenic C. difficile were isolated from patients with hepatic cirrhosis within 48 h after admission, followed by multilocus sequence typing (MLST). Patients were divided into toxigenic CDC group and noncolonized (NC) group according to the colonization. Logistic regression analysis was performed to analyse the risk factors for the CDC. Besides, the CDI incidence was compared between the two groups. Colonization of toxigenic C. difficile was identified in 104 cases (19.8 %). Eighteen sequence types (STs) were identified, among which ST-3, ST-54, ST-35 and ST-37 were the predominant types. Child-Pugh class C(relative risk, RR, 3.025; 95 % CI: 1.410-6.488), decrease of prothrombin time activity (PTA) (RR 2.180; 95 % CI: 1.368-3.476), decrease of platelet (RR 2.746; 95 % CI: 0.931-8.103) and concurrent hepatic encephalopathy (RR 1.740; 95 % CI: 1.012-2.990) were identified as the risk factors for the hepatic cirrhosis patients with CDC. The CDI incidence in the CDC group was also significantly higher than that of the NC group (26.0 % vs 1.7 %, Pdifficile colonization. Child's class C, decrease of PTA and platelet, and concurrent hepatic encephalopathy were the risk factors for the hepatic cirrhosis patients with C. difficile colonization. Hepatic cirrhosis patients with C. difficile colonization were more susceptible to CDI.

Probiotic and lactulose: influence on gastrointestinal flora and pH value in minimal hepatic encephalopathy rats.

Science.gov (United States)

Jiang, Shu-Man; Jia, Lin; Zhang, Mei-Hua

2015-01-01

The present study was conducted to investigate the influence on gastrointestinal flora, counts of bifidobacteria and Enterobacterceae in colon and pH value of gastrointestinal after lactulose and probiotic treatment on rat experimental minimal hepatic encephalopathy (MHE) induced by thioactamide (TAA). MHE was induced by intraperitoneal injection of TAA. 48 male MHE models were then randomly divided into 4 groups: control group (n = 12); MHE group (n = 12) received tap water ad libitum only; lactulose group (n = 12) and probiotics group (n = 12) gavaged respectively with 8 ml/kg of lactulose and 1.5 g/kg of probiotic preparation Golden Bifid (highly concentrated combination probiotic) dissolved in 2 ml of normal saline, once a day for 8 days. The latency of Brainstem auditory evoked potentials (BAEP) I was used as objective index of MHE. Counts of gastrointestinal flora, counts of bifidobacteria and Enterobacterceae in colon and pH value of gastrointestinal were examined respectively. Compared to MHE group, counts of gastrointestinal flora has greatly decreased, ratio of bifidobacteria and Enterobacterceae has greatly increased, pH value of colon has greatly descended (P 0.05). Both lactulose and probiotics can effectively prevent bacteria translocation and overgrowth, intensify CR, improved value of B/E, and acidify intestinal, decreased pH value of colon. Probiotic compound Golden Bifid is as useful as lactulose for the prevention and treatment of MHE. Probiotic therapy may be a safe, natural, well-tolerated therapy appropriate for the long-term treatment of MHE.

Loss of brain function - liver disease

Science.gov (United States)

Hepatic coma; Encephalopathy - hepatic; Hepatic encephalopathy; Portasystemic encephalopathy ... 2017:417-421. Nevah MI, Fallon MB. Hepatic encephalopathy, hepatorenal ... of liver disease. In: Feldman M, Friedman LS, Brandt LJ, ...

Multiple hepatic abscesses due to Yersinia enterocolitica infection secondary to primary haemochromatosis

DEFF Research Database (Denmark)

Bergmann, T K; Vinding, K; Hey, H

2001-01-01

A case of hepatic abscesses due to Yersinia enterocolitica in an immunocompetent male is presented. Re-examination after 3 months showed that the patient had primary haemochromatosis. Treatment with repeated phlebotomies was instituted. Two years after the patient was first admitted to hospital. 17...... showed that prior to this case only 45 cases of hepatic abscess secondary to Yersinia enterocolitica have been registered. Of the 45 reported cases, 64% had underlying haemochromatosis and 29% had diabetes mellitus. The overall mortality was 31%. Mortality before 1987 was 60% (n = 20) and since 1987...

Altered cerebral blood flow and glucose metabolism in patients with liver disease and minimal encephalopathy

International Nuclear Information System (INIS)

Lockwood, A.H.; Yap, E.W.; Rhoades, H.M.; Wong, W.H.

1991-01-01

We measured CBF and the CMRglc in normal controls and in patients with severe liver disease and evidence for minimal hepatic encephalopathy using positron emission tomography. Regions were defined in frontal, temporal, parietal, and visual cortex; the thalamus; the caudate; the cerebellum; and the white matter along with a whole-slice value obtained at the level of the thalamus. There was no difference in whole-slice CBF and CMRglc values. Individual regional values were normalized to the whole-slice value and subjected to a two-way repeated measures analysis of variance. When normalized CBF and CMRglc values for regions were compared between groups, significant differences were demonstrated (F = 5.650, p = 0.00014 and F = 4.58, p = 0.0073, respectively). These pattern differences were due to higher CBF and CMRglc in the cerebellum, thalamus, and caudate in patients and lower values in the cortex. Standardized coefficients extracted from a discriminant function analysis permitted correct group assignment for 95.5% of the CBF studies and for 92.9% of the CMRglc studies. The similarity of the altered pattern of cerebral metabolism and flow in our patients to that seen in rats subjected to portacaval shunts or ammonia infusions suggests that this toxin may alter flow and metabolism and that this, in turn, causes the clinical expression of encephalopathy

Hyperintense basal ganglia lesions on T1-weighted MR images in asymptomatic patients with hepatic dysfunction

Energy Technology Data Exchange (ETDEWEB)

Saatci, I. [Dept. of Radiology, Hacettepe Univ. Hospital, Ankara (Turkey); Cila, A. [Dept. of Radiology, Hacettepe Univ. Hospital, Ankara (Turkey); Dincer, F.F. [Dept. of Radiology, Hacettepe Univ. Hospital, Ankara (Turkey)

1995-12-31

Cranial MRI findings in four patients who had hepatic dysfunction, including one with sole hepatic form of Wilson`s disease, were reported. The MR examinations revealed bilateral, symmetric hyperintensity in the globus pallidus, subthalamic nuclei and mesencephalon on T1-weighted images with no corresponding abnormality on T2-weighted sequences. The basal ganglia were normal on CT examinations in all patients. None of the patients had the clinical findings of hepatic encephalopathy. The MR findings in our patients did not correlate with the degree or duration of hepatic dysfunction. (orig.)

Economic impact of the use of rifaximin 550 mg twice daily for the treatment of overt hepatic encephalopathy in Italy.

Science.gov (United States)

Roggeri, Daniela Paola; Roggeri, Alessandro

2017-01-01

Hepatic encephalopathy (HE) is associated with a reduced survival, an increased risk of hospitalization for recurrences, and a reduced health-related quality of life. The purpose of the present economic analysis was to evaluate the impact on the Italian National Health Service (INHS) expenditure of the treatment with rifaximin 550 mg twice daily (Tixteller ® /Tixtar ® ) for the reduction of the recurrences of overt HE, with respect to the current treatment approach. Costs associated with patients treated with rifaximin 550 mg twice daily were estimated considering the reduction in hospitalizations for HE recurrences revealed by registrative clinical trial (-50%) applied to the hospitalization rate (42.5%) emerging from an Italian observational real-world study; costs associated with patients not treated with rifaximin were estimated based on the hospitalization rate, resulting from the same Italian observational study. Sensitivity analyses considering possible different discount levels to INHS structures for rifaximin were performed. The INHS perspective for a period of 3 years was considered. The treatment with rifaximin 550 mg twice daily, although increasing drug costs, is associated with a reduction in hospitalizations for HE recurrences that leads to an overall reduction of total costs charged to INHS, which could be estimated, based on the forecasted uptake of the treatment, at about €130,000 in the first year, reaching ~€260,000 in the third year. Considering a possible discount for rifaximin 550 mg to INHS structure of 20%, the total saving at the third year accounts for ~€3,000,000. Moreover, a relevant reduction in the number of hospitalizations and bed days is associated with rifaximin treatment. The treatment with rifaximin 550 mg twice daily, even if associated with an increase in drug expenditure, results in a reduction in total health care costs charged to INHS due to a reduction in hospitalizations for HE recurrences.

Endozepine-4 levels are increased in hepatic coma.

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Malaguarnera, Giulia; Vacante, Marco; Drago, Filippo; Bertino, Gaetano; Motta, Massimo; Giordano, Maria; Malaguarnera, Michele

2015-08-14

To evaluate the serum levels of endozepine-4, their relation with ammonia serum levels, the grading of coma and the severity of cirrhosis, in patients with hepatic coma. In this study we included 20 subjects with Hepatic coma, 20 subjects with minimal hepatic encephalopathy (MHE) and 20 subjects control. All subjects underwent blood analysis, Child Pugh and Model for End - stage liver disease (MELD) assessment, endozepine-4 analysis. Subjects with hepatic coma showed significant difference in endozepine-4 (P blood ammonia concentration was noted to be raised in patients with hepatic coma, with the highest ammonia levels being found in those who were comatose. We also found a high correlation between endozepine-4 and ammonia (P < 0.001). In patients with grade IV hepatic coma, endozepine levels were significantly higher compared to other groups. This study suggests that an increased level of endozepine in subjects with higher levels of MELD was observed. In conclusion, data concerning involvement of the GABA-ergic system in HE coma could be explained by stage-specific alterations.

Subcortical arteriosclerotic encephalopathy (Binswanger disease)

International Nuclear Information System (INIS)

Settanni, F.; Dumont, P.; Casella, C.L.; Pascuzzi, L.; Cecilio, S.; Caldas, J.G.

1992-01-01

Four patients with variable clinical and tomographic features were diagnosed as having subcortical arteriosclerotic encephalopathy (Binswanger disease). This diagnosis was done based on the presence of subacute progression of focal cerebral deficits, presence of hypertension, systemic vascular disease and dementia. The pathogenesis of subcortical arteriosclerotic encephalopathy is unknown; possible mechanism include diffuse ischemia and fluid transudation with subsequent gliosis related to subacute hypertensive encephalopathy. (author)

Sarcopenia Is Risk Factor for Development of Hepatic Encephalopathy After Transjugular Intrahepatic Portosystemic Shunt Placement.

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Nardelli, Silvia; Lattanzi, Barbara; Torrisi, Sabrina; Greco, Francesca; Farcomeni, Alessio; Gioia, Stefania; Merli, Manuela; Riggio, Oliviero

2017-06-01

Hepatic encephalopathy (HE) is an important complication in patients with cirrhosis who received transjugular intrahepatic portosystemic shunts (TIPS). We investigated whether a decrease in muscle mass was associated independently with the occurrence of HE after TIPS. We performed a prospective study of 46 consecutive patients with cirrhosis (mean age, 58.6 ± 9.1 y; mean model for end-stage liver disease score, 11.3 ± 3.3; mean Child-Pugh score, 7.6 ± 1.5) who received TIPS from January 2013 through December 2014 at a tertiary center in Rome, Italy. All patients underwent computed tomography analysis at the level of the third lumbar vertebrae to determine the skeletal muscle index; sarcopenia was defined by sex-specific cut-off values. We estimated the incidence of the first episode of HE after TIPS, taking into account the competing risk nature of the data (death or liver transplantation). Twenty-six patients (57%) were found to have sarcopenia. Twenty-one patients (46%) developed overt HE in the 7 ± 9 months after TIPS placement; all of these patients were sarcopenic, according to the skeletal muscle index. Of the 25 patients without HE after TIPS, only 5 had sarcopenia. In multivariate analysis, model for end-stage liver disease score (subdistribution hazard ratio, 1.16; 95% confidence interval, 1.01-1.34; P = .043) and sarcopenia (subdistribution hazard ratio, 31.3; 95% confidence interval, 4.5-218.07; P Sarcopenia should be considered in selecting patients for TIPS therapy. Nutritional status should be evaluated in patients with sarcopenia before TIPS placement, which might reduce the incidence of HE. Copyright © 2017 AGA Institute. Published by Elsevier Inc. All rights reserved.

Reduced TH expression and α-synuclein accumulation contribute towards nigrostriatal dysfunction in experimental hepatic encephalopathy.

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Suárez, Isabel; Bodega, Guillermo; Rubio, Miguel; Fernández, Benjamín

2017-01-01

The present work examines α-synuclein expression in the nigrostriatal system of a rat chronic hepatic encephalopathy model induced by portacaval anastomosis (PCA). There is evidence that dopaminergic dysfunction in disease conditions is strongly associated with such expression. Possible relationships among dopaminergic neurons, astroglial cells and α-synuclein expression were sought. Brain tissue samples from rats at 1 and 6 months post-PCA, and controls, were analysed immunohistochemically using antibodies against tyrosine hydroxylase (TH), α-synuclein, glial fibrillary acidic protein (GFAP) and ubiquitin (Ub). In the control rats, TH immunoreactivity was detected in the neuronal cell bodies and processes in the substantia nigra pars compacta (SNc). A dense TH-positive network of neurons was also seen in the striatum. In the PCA-exposed rats, however, a reduction in TH-positive neurons was seen at both 1 and 6 months in the SNc, as well as a reduction in TH-positive fibres in the striatum. This was coincident with the appearance of α-synuclein-immunoreactive neurons in the SNc; some of the TH-positive neurons also showed α-synuclein immunoreactivity. In addition, α-synuclein accumulation was seen in the SNc and striatum at both 1 and 6 months post-PCA, whereas α-synuclein was only mildly expressed in the nigrostriatal pathway of the controls. Astrogliosis was also seen following PCA, as revealed by increased GFAP expression from 1 month to 6 months post-PCA in both the SN and striatum. The astroglial activation level in the SN paralleled the reduced neuronal expression of TH throughout PCA exposure. α-synuclein accumulation following PCA may induce dopaminergic dysfunction via the downregulation of TH, as well as astroglial activation.

Peripheral benzodiazepine receptors in the brain of cirrhosis patients with manifest hepatic encephalopathy

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Iversen, Peter; Bender, Dirk; Munk, Ole L.; Cumming, Paul [Aarhus University Hospital, PET Centre, Aarhus (Denmark); Aagaard Hansen, Dorthe; Keiding, Susanne [Aarhus University Hospital, PET Centre, Aarhus (Denmark); Aarhus University Hospital, Department of Medicine V (Hepatology), Aarhus (Denmark); Rodell, Anders [Aarhus University Hospital, Centre of Functionally Integrative Neuroscience (CFIN), Aarhus (Denmark)

2006-07-15

It has been suggested that ammonia-induced enhancement of peripheral benzodiazepine receptors (PBRs) in the brain is involved in the development of hepatic encephalopathy (HE). This hypothesis is based on animal experiments and studies of post-mortem human brains using radiolabelled PK11195, a specific ligand for PBR, but to our knowledge has not been tested in living patients. The aim of the present study was to test this hypothesis by measuring the number of cerebral PBRs in specific brain regions in cirrhotic patients with an acute episode of clinically manifest HE and healthy subjects using dynamic {sup 11}C-PK11195 brain PET. Eight cirrhotic patients with an acute episode of clinically manifest HE (mean arterial ammonia 81 {mu}mol/l) and five healthy subjects (22 {mu}mol/l) underwent dynamic {sup 11}C-PK11195 and {sup 15}O-H{sub 2}O PET, co-registered with MR images. Brain regions (putamen, cerebellum, cortex and thalamus) were delineated on co-registered {sup 15}O-H{sub 2} {sup 15}O and MR images and copied to the dynamic {sup 15}O-H{sub 2}O and {sup 11}C-PK11195 images. Regional cerebral blood flow (CBF) ({sup 15}O-H{sub 2}O scan) and the volume of distribution of PK11195 ({sup 11}C-PK11195 scan) were calculated by kinetic analysis. There were regional differences in the CBF, with lowest values in the cortex and highest values in the putamen in both groups of subjects (p<0.05), but no significant differences between the groups. There were no significant differences in the volume of distribution of PK11195 (V{sub d}) between regions or between the two groups of subjects. Mean values of V{sub d} ranged from 1.0 to 1.1 in both groups of subjects. The results do not confirm the hypothesis of an increased number of PBRs in patients with HE. (orig.)

Role of dopaminergic and serotonergic neurotransmitters in behavioral alterations observed in rodent model of hepatic encephalopathy.

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Dhanda, Saurabh; Sandhir, Rajat

2015-06-01

The present study was designed to evaluate the role of biogenic amines in behavioral alterations observed in rat model of hepatic encephalopathy (HE) following bile duct ligation (BDL). Male Wistar rats subjected to BDL developed biliary fibrosis after four weeks which was supported by altered liver function tests, increased ammonia levels and histological staining (Sirius red). Animals were assessed for their behavioral performance in terms of cognitive, anxiety and motor functions. The levels of dopamine (DA), serotonin (5-HT), epinephrine and norepinephrine (NE) were estimated in different regions of brain viz. cortex, hippocampus, striatum and cerebellum using HPLC along with activity of monoamine oxidase (MAO). Cognitive assessment of BDL rats revealed a progressive decline in learning, memory formation, retrieval, exploration of novel environment and spontaneous locomotor activity along with decrease in 5-HT and NE levels. This was accompanied by an increase in MAO activity. Motor functions of BDL rats were also altered which were evident from decrease in the time spent on the rotating rod and higher foot faults assessed using narrow beam walk task. A global decrease was observed in the DA content along with an increase in MAO activity. Histopathological studies using hematoxylin-eosin (H&E) and cresyl violet exhibited marked neuronal degeneration, wherein neurons appeared more pyknotic, condensed and damaged. The results reveal that dopaminergic and serotonergic pathways are disturbed in chronic liver failure post-BDL which may be responsible for behavioral impairments observed in HE. Copyright © 2015 Elsevier B.V. All rights reserved.

Two siblings with early infantile myoclonic encephalopathy due to mutation in the gene encoding mitochondrial glutamate/H+ symporter SLC25A22.

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Cohen, Rony; Basel-Vanagaite, Lina; Goldberg-Stern, Hadassah; Halevy, Ayelet; Shuper, Avinoam; Feingold-Zadok, Michal; Behar, Doron M; Straussberg, Rachel

2014-11-01

To characterize a new subset of early myoclonic encephalopathy usually associated with metabolic etiologies with a new genetic entity. We describe two siblings with early myoclonic encephalopathy born to consanguineous parents of Arab Muslim origin from Israel. We used homozygosity mapping and candidate gene sequencing to reveal the genetic basis of the myoclonic syndrome. We found a rare missense mutation in the gene encoding one of the two mitochondrial glutamate/H symporters, SLC25A22. The phenotype of early myoclonic encephalopathy was first linked to the same mutation in 2005 in patients of the same ethnicity as our family. Owing to the devastating nature of this encephalopathy, we focus attention on its clinical history, epileptic semiology, distinct electroencephalography features, and genetic basis. We provide the evidence that an integrated diagnostic strategy combining homozygosity mapping with candidate gene sequencing is efficient in consanguineous families with highly heterogeneous autosomal recessive diseases. Copyright © 2014 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights reserved.

Hepatic Myelopathy in a Patient with Decompensated Alcoholic Cirrhosis and Portal Colopathy

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Madhumita Premkumar

2012-01-01

Full Text Available Cirrhotic or hepatic myelopathy is a rare neurological complication of chronic liver disease usually seen in adults and presents as a progressive pure motor spastic paraparesis which is usually associated with overt liver failure and a surgical or spontaneous systemic portocaval shunt. We describe the development of progressive spastic paraparesis, in a patient with alcoholic cirrhosis with portal hypertension and portal colopathy who presented with the first episode of hepatic encephalopathy. The patient had not undergone any shunt procedure.

A Critical Case of Wernicke's Encephalopathy Induced by Hyperemesis Gravidarum

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Byung Ju Kang

2015-05-01

Full Text Available Wernicke’s encephalopathy is a reversible but potentially critical disease caused by thiamine deficiency. Most patients complain of symptoms such as ophthalmoplegia, ataxia and confusion. Heavy alcohol drinking is commonly associated with the disease, but other clinical conditions also can provoke it. In pregnant women, hyperemesis gravidarum can lead to the depletion of body thiamine due to poor oral intake and a high metabolic demand. We report a case of Wernicke’s encephalopathy following hyperemesis gravidarum in a 36-year-old female at 20 weeks of pregnancy, who visited our hospital because of shock with vaginal bleeding. This case suggests that although the initial presentation may include atypical symptoms (e.g., shock or bleeding, Wernicke’s encephalopathy should be considered, and thiamine replacement should be performed in pregnant women with neurologic symptoms and poor oral intake.

Disease: H01506 [KEGG MEDICUS

Lifescience Database Archive (English)

Full Text Available H01506 Hepatic encephalopathy; Hepatic coma Hepatic encephalopathy (HE) is a brain...of current therapies for hepatic encephalopathy in liver cirrhosis. ... JOURNAL ... World J Gastroenterol 21:118... ... Wakim-Fleming J ... TITLE ... Hepatic encephalopathy: suspect it early in patients with cirrhosis. ... JOURNAL ... Cleve Clin J Med 78:597-605 (2011) DOI:10.3949/ccjm.78a10117

Expression and role of neuroglobin in rats with sepsis-associated encephalopathy.

Science.gov (United States)

Zhang, Li-Na; Ai, Yu-Hang; Gong, Hua; Guo, Qu-Lian; Huang, Li; Liu, Zhi-Yong; Yao, Bo

2014-01-01

To determine the role of neuroglobin in the pathology of sepsis-associated encephalopathy and ascertain if neuroglobin has any protective effects against sepsis-associated encephalopathy. Randomized laboratory animal study. Research university animal laboratory. Two hundred and forty adult male Sprague-Dawley rats. Rats received cecal puncture and ligation (or sham) surgery to induce sepsis, then broken up into groups based on whether or not the rat developed sepsis-associated encephalopathy as determined by electroencephalograph and evoked potential recordings. The rats were then left untreated to examine the effect of sepsis-associated encephalopathy on neuroglobin, treated with a neuroglobin antisense nucleotide to block gene expression, or given hemin, a neuroglobin inducer. Following sepsis induction, diagnosis, and treatment, the brains were analyzed for both gross and ultrastructural morphology. Also, neuronal neuroglobin immunoreactivity and apoptosis (via terminal uridine nucleotide end-labeling) were examined. Blood serum levels were then analyzed for neuroglobin, superoxide dismutase, and malondialdehyde levels. We determined that sepsis-associated encephalopathy induces damage evident when examining both gross and ultrastructural morphology, as well as induces neuronal neuroglobin expression. Also, blockade of neuroglobin expression via antisense treatment will exacerbate these pathological effects, while increasing neuroglobin levels via hemin will ameliorate them. Blood analysis found that levels of superoxide dismutase and malondialdehyde mirrored the level of pathology found in the brain, while plasma neuroglobin levels reflected the amount of neuronal neuroglobin immunoreactivity. We conclude that neuroglobin is involved in the pathogenesis of sepsis-associated encephalopathy and has neuroprotective effects. We also determined that hemin has protective effects against sepsis-associated encephalopathy as well, most probably due to its effect on

Treating hepatic encephalopathy in cirrhotic patients admitted to ICU with sodium phenylbutyrate: a preliminary study.

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Weiss, Nicolas; Tripon, Simona; Lodey, Marion; Guiller, Elsa; Junot, Helga; Monneret, Denis; Mayaux, Julien; Brisson, Hélène; Mallet, Maxime; Rudler, Marika; Imbert-Bismut, Françoise; Thabut, Dominique

2018-04-01

Hepatic encephalopathy (HE) influences short-term and long-term prognoses. Recently, glycerol phenylbutyrate (PB), that lowers ammonia by providing an alternate pathway to urea for waste nitrogen excretion, has shown that it was effective in preventing the occurrence of HE in RCT. The aim was to assess the benefits of sodium PB in cirrhotic patients admitted to ICU for overt HE, in terms of ammonia levels decrease, neurological improvement, and survival. Cirrhotic patients who presented with overt HE, ammonia levels >100 μmol/L, and did not display any contra-indication were included. Sodium PB was administered at 200 mg/kg/day. Control group included historical controls treated by standard therapy, matched for age, sex, MELD score, and severity of HE. Eighteen patients were included and treated with sodium PB (age: 59 [45-68], male gender: 15 [83%], Child-Pugh B: 8 [44%], Child-Pugh C: 10 [56%], and MELD score: 16 [13-23]). Ammonia levels significantly decreased in the PB as compared to the control group from inclusion to 12 h and from inclusion to 48 h (P = 0.0201 and P = 0.0230, respectively). The proportion of patients displaying neurological improvement was only higher in the PB-treated group as compared to controls at ICU discharge (15 [83%] vs. 9 [50%], P = 0.0339). ICU discharge survival was significantly higher in patients treated with PB (17 [94%] vs. 9 [50%], P = 0.0017). In cirrhotic patients with overt HE, sodium PB could be effective in reducing ammonia levels and might be effective in improving neurological status and ICU discharge survival. More extensive data, especially a RCT, are mandatory. © 2017 Société Française de Pharmacologie et de Thérapeutique.

[Hashimoto's encephalopathy and autoantibodies].

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Yoneda, Makoto

2013-04-01

Encephalopathy occasionally occurs in association with thyroid disorders, but most of these are treatable. These encephalopathies include a neuropsychiatric disorder associated with hypothyroidism, called myxedema encephalopathy. Moreover, Hashimoto's encephalopathy (HE) has been recognized as a new clinical disease based on an autoimmune mechanism associated with Hashimoto's thyroiditis. Steroid treatment was successfully administered to these patients. Recently, we discovered that the serum autoantibodies against the NH2-terminal of α-enolase (NAE) are highly specific diagnostic biomarkers for HE. Further, we analyzed serum anti-NAE autoantibodies and the clinical features in many cases of HE from institutions throughout Japan and other countries. Approximately half of assessed HE patients carry anti-NAE antibodies. The age was widely distributed with 2 peaks (20-30 years and 50-70 years). Most HE patients were in euthyroid states, and all patients had anti-thyroid (TG) antibodies and anti-thyroid peroxidase (TPO) antibodies. Anti-TSH receptor (TSH-R) antibodies were observed in some cases. The common neuropsychiatry features are consciousness disturbance and psychosis, followed by cognitive dysfunction, involuntary movements, seizures, and ataxia. Abnormalities on electroencephalography (EEG) and decreased cerebral blood flow on brain SPECT were common findings, whereas abnormal findings on brain magnetic resonance imaging (MRI) were rare. HE patients have various clinical phenotypes such as the acute encephalopathy form, the chronic psychiatric form, and other particular clinical forms, including limbic encephalitis, progressive cerebellar ataxia, and Creutzfeldt-Jakob disease (CJD)-like form. The cerebellar ataxic form of HE clinically mimics spinocerebellar degeneration (SCD) and is characterized by the absence of nystagmus, absent or mild cerebellar atrophy, and lazy background activities on EEG. Taken together, these data suggest that the possibility of

Hypoxic-Ischemic Encephalopathy after Bee Sting and Treatment with Zolpidem: A Case Report

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Turgay Demir

2016-09-01

Full Text Available Hypoxic-ischemic encephalopathy (HIE, a metabolic encephalopathy, develops as a result of cessation or reduction of oxygen and blood flow to the brain. The clinical picture may vary in severity from minimal neurologic deficits to coma. In living patients, permanent neuropsychological sequelae can develop. Herein, we present a case of HIE that occured after anaphylactic reaction due to bee sting, which was treatedm with zolpidem.

Single photon emission computed tomography and statistical parametric mapping analysis in cirrhotic patients with and without minimal hepatic encephalopathy

International Nuclear Information System (INIS)

Nakagawa, Yuri; Matsumura, Kaname; Iwasa, Motoh; Kaito, Masahiko; Adachi, Yukihiko; Takeda, Kan

2004-01-01

The early diagnosis and treatment of cognitive impairment in cirrhotic patients is needed to improve the patients' daily living. In this study, alterations of regional cerebral blood flow (rCBF) were evaluated in cirrhotic patients using statistical parametric mapping (SPM). The relationships between rCBF and neuropsychological test, severity of disease and biochemical data were also assessed. 99m Tc-ethyl cysteinate dimer single photon emission computed tomography was performed in 20 patients with non-alcoholic liver cirrhosis without overt hepatic encephalopathy (HE) and in 20 age-matched healthy subjects. Neuropsychological tests were performed in 16 patients; of these 7 had minimal HE. Regional CBF images were also analyzed in these groups using SPM. On SPM analysis, cirrhotic patients showed regions of significant hypoperfusion in the superior and middle frontal gyri, and inferior parietal lobules compared with the control group. These areas included parts of the premotor and parietal associated areas of the cortex. Among the cirrhotic patients, those with minimal HE had regions of significant hypoperfusion in the cingulate gyri bilaterally as compared with those without minimal HE. Abnormal function in the above regions may account for the relatively selective neuropsychological deficits in the cognitive status of patients with cirrhosis. These findings may be important in the identification and management of cirrhotic patients with minimal HE. (author)

Differential impact of hyponatremia and hepatic encephalopathy on health-related quality of life and brain metabolite abnormalities in cirrhosis.

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Ahluwalia, Vishwadeep; Wade, James B; Thacker, Leroy; Kraft, Kenneth A; Sterling, Richard K; Stravitz, R Todd; Fuchs, Michael; Bouneva, Iliana; Puri, Puneet; Luketic, Velimir; Sanyal, Arun J; Gilles, Hochong; Heuman, Douglas M; Bajaj, Jasmohan S

2013-09-01

Hyponatremia (HN) and hepatic encephalopathy (HE) together can impair health-related quality of life (HRQOL) and cognition in cirrhosis. We aimed at studying the effect of hyponatremia on cognition, HRQOL, and brain MR spectroscopy (MRS) independent of HE. Four cirrhotic groups (no HE/HN, HE alone, HN alone (sodium <130 mEq/L), HE+HN) underwent cognitive testing, HRQOL using Sickness Impact Profile (SIP: higher score is worse; has psychosocial and physical sub-scores) and brain MRS (myoinositol (mI) and glutamate+glutamine (Glx)), which were compared across groups. A subset underwent HRQOL testing before/after diuretic withdrawal. 82 cirrhotics (30 no HE/HN, 25 HE, 17 HE+HN, and 10 HN, MELD 12, 63% hepatitis C) were included. Cirrhotics with HN alone and without HE/HN had better cognition compared to HE groups (median abnormal tests no-HE/HN: 3, HN: 3.5, HE: 6.5, HE+HN: 7, p=0.008). Despite better cognition, HN only patients had worse HRQOL in total and psychosocial SIP while both HN groups (with/without HE) had a significantly worse physical SIP (p<0.0001, all comparisons). Brain MRS showed the lowest Glx in HN and the highest in HE groups (p<0.02). mI levels were comparably decreased in the three affected (HE, HE+HN, and HN) groups compared to no HE/HN and were associated with poor HRQOL. Six HE+HN cirrhotics underwent diuretic withdrawal which improved serum sodium and total/psychosocial SIP scores. Hyponatremic cirrhotics without HE have poor HRQOL despite better cognition than those with concomitant HE. Glx levels were lowest in HN without HE but mI was similar across affected groups. HRQOL improved after diuretic withdrawal. Hyponatremia has a complex, non-linear relationship with brain Glx and mI, cognition and HRQOL. Copyright © 2013 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

Hyperammonemia: A Report of Maternal Biliary Cirrhosis and Neonatal Outcome

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Deana J. Hussamy

2013-01-01

Full Text Available Although uncommon during pregnancy, cirrhosis results in multiple medical complications impacting both mother and fetus. Previous reports suggest liver dysfunction in pregnancy causes accumulation of neurotoxins within the maternal compartment that increases neonatal morbidity through placental transfer. We present a case of a 36-year-old G2P1 female with history of biliary cirrhosis presenting at 32-weeks' gestation with hepatic congestion progressing to hepatic encephalopathy prompting delivery. Umbilical cord sampling and postnatal infant testing demonstrated elevated ammonia levels which resolved by 12 hours of life without intervention. At discharge, the infant did not demonstrate evidence of neurologic deficit. We conclude that acute maternal hepatic encephalopathy and hyperammonemia due to chronic liver disease do not portend adverse neonatal outcomes, notably encephalopathy.

Hyaluronic acid levels predict risk of hepatic encephalopathy and liver-related death in HIV/viral hepatitis coinfected patients

DEFF Research Database (Denmark)

Peters, Lars; Mocroft, Amanda; Soriano, Vincent

2013-01-01

Whereas it is well established that various soluble biomarkers can predict level of liver fibrosis, their ability to predict liver-related clinical outcomes is less clearly established, in particular among HIV/viral hepatitis co-infected persons. We investigated plasma hyaluronic acid's (HA......) ability to predict risk of liver-related events (LRE; hepatic coma or liver-related death) in the EuroSIDA study....

Clinical research on alterations of brain MRI and 1H-MRS in chronic hepatic disease

International Nuclear Information System (INIS)

Long Liling; Li Xiangrong; Hong Zhongkui

2006-01-01

Objective: To study the abnormal findings and metabolic alterations of the brain in chronic hepatic disease with MRI and 1 H magnetic resonance spectroscopy ( 1 H-MRS) for better understanding the clinical significance of pallidal hyperintensity and the role in the diagnosis and treatment of hepatic encephalopathy (HE). Methods: Brain MRI and 1 H-MRS examination were performed in 50 patients with chronic hepatic disease and 20 healthy volunteers. The pallidus index (PI) was calculated and the height of resonance peaks of Glx was measured. The correlation between PI and Child/Pugh classification, and the association between blood ammonia and the spectroscopic alterations were studied. Pre-and post-therapeutic comparative study was also conducted in 5 cases with chronic HE. Results: PI was gradually increased from healthy volunteers to patients with chronic hepatitis and liver cirrhosis (1.01± 0.04, 1.06±0.09, and 1.18±0.09), and the differences in PI value among them were significant (F=22.294, P 1 -weighted MRI disappeared and the abnormal metabolic alterations returned to normal range 5 to 6 months after successful liver transplantation. However, the normalization of 1 H-MRS alterations preceded the disappearance of pallidal hyperintensities. Conclusion: PI can be an index of reference for liver dysfunction. Glx is more sensitive than blood ammonia in detecting the brain dysfunction. MRI and 1 H-MRS are reliable techniques in the diagnosis and evaluation of therapy for hepatic encephalopathy. (authors)

Altered dynamic functional connectivity in the default mode network in patients with cirrhosis and minimal hepatic encephalopathy

International Nuclear Information System (INIS)

Chen, Hua-Jun; Lin, Hai-Long; Chen, Qiu-Feng; Liu, Peng-Fei

2017-01-01

Abnormal brain intrinsic functional connectivity (FC) has been documented in minimal hepatic encephalopathy (MHE) by static connectivity analysis. However, changes in dynamic FC (dFC) remain unknown. We aimed to identify altered dFC within the default mode network (DMN) associated with MHE. Resting-state functional MRI data were acquired from 20 cirrhotic patients with MHE and 24 healthy controls. DMN seed regions were defined using seed-based FC analysis (centered on the posterior cingulate cortex (PCC)). Dynamic FC architecture was calculated using a sliding time-window method. K-means clustering (number of clusters = 2-4) was applied to estimate FC states. When the number of clusters was 2, MHE patients presented weaker connectivity strengths compared with controls in states 1 and 2. In state 1, decreased FC strength was found between the PCC/precuneus (PCUN) and right medial temporal lobe (MTL)/bilateral lateral temporal cortex (LTC); left inferior parietal lobule (IPL) and right MTL/left LTC; right IPL and right MTL/bilateral LTC; right MTL and right LTC; and medial prefrontal cortex (MPFC) and right MTL/bilateral LTC. In state 2, reduced FC strength was observed between the PCC/PCUN and bilateral MTL/bilateral LTC; left IPL and left MTL/bilateral LTC/MPFC; and left LTC and right LTC. Altered connectivities from state 1 were correlated with patient cognitive performance. Similar findings were observed when the number of clusters was set to 3 or 4. Aberrant dynamic DMN connectivity is an additional characteristic of MHE. Dynamic connectivity analysis offers a novel paradigm for understanding MHE-related mechanisms. (orig.)

Altered dynamic functional connectivity in the default mode network in patients with cirrhosis and minimal hepatic encephalopathy

Energy Technology Data Exchange (ETDEWEB)

Chen, Hua-Jun; Lin, Hai-Long [Fujian Medical University Union Hospital, Department of Radiology, Fuzhou (China); Chen, Qiu-Feng; Liu, Peng-Fei [Central South University, School of Information Science and Engineering, Changsha (China)

2017-09-15

Abnormal brain intrinsic functional connectivity (FC) has been documented in minimal hepatic encephalopathy (MHE) by static connectivity analysis. However, changes in dynamic FC (dFC) remain unknown. We aimed to identify altered dFC within the default mode network (DMN) associated with MHE. Resting-state functional MRI data were acquired from 20 cirrhotic patients with MHE and 24 healthy controls. DMN seed regions were defined using seed-based FC analysis (centered on the posterior cingulate cortex (PCC)). Dynamic FC architecture was calculated using a sliding time-window method. K-means clustering (number of clusters = 2-4) was applied to estimate FC states. When the number of clusters was 2, MHE patients presented weaker connectivity strengths compared with controls in states 1 and 2. In state 1, decreased FC strength was found between the PCC/precuneus (PCUN) and right medial temporal lobe (MTL)/bilateral lateral temporal cortex (LTC); left inferior parietal lobule (IPL) and right MTL/left LTC; right IPL and right MTL/bilateral LTC; right MTL and right LTC; and medial prefrontal cortex (MPFC) and right MTL/bilateral LTC. In state 2, reduced FC strength was observed between the PCC/PCUN and bilateral MTL/bilateral LTC; left IPL and left MTL/bilateral LTC/MPFC; and left LTC and right LTC. Altered connectivities from state 1 were correlated with patient cognitive performance. Similar findings were observed when the number of clusters was set to 3 or 4. Aberrant dynamic DMN connectivity is an additional characteristic of MHE. Dynamic connectivity analysis offers a novel paradigm for understanding MHE-related mechanisms. (orig.)

Color vision abnormality as the sole manifestation of posterior reversible encephalopathy due to post-partum HELLP syndrome.

Science.gov (United States)

Takahashi, Hironori; Matsubara, Teppei; Makino, Shinji; Horie, Kenji; Matsubara, Shigeki

2017-03-01

Posterior reversible encephalopathy syndrome (PRES) is associated with several symptoms; of those, visual acuity loss, light oversensitivity (photophobia), and light flashes (photopsia) are known as PRES-related eye symptoms. We report a post-partum woman with PRES associated with hemolysis, elevated liver enzymes, and low platelets syndrome (HELLP), in whom color vision abnormality (achromatopsia) was the sole manifestation. Cesarean section was performed at 28 weeks due to headache, epigastralgia, and severe hypertension. HELLP became evident after delivery. On post-partum day 1, she complained of achromatopsia, stating: "all things look brownish-gray". Ophthalmologic examination was normal, but brain magnetic resonance imaging showed occipital lobe lesions, indicative of PRES, and, interestingly, also color vision center (area V4) lesions, suggesting that the achromatopsia had been caused by brain damage. It may be prudent to question HELLP patients concerning achromatopsia. © 2017 Japan Society of Obstetrics and Gynecology.

S-100b and neuron-specific enolase in patients with fulminant hepatic failure

DEFF Research Database (Denmark)

Strauss, Gitte Irene; Christiansen, Michael; Møller, Kirsten

2001-01-01

, the cerebral flux of S-100b and NSE was measured. We included 35 patients with FHF, 6 patients with acute on chronic liver disease (AOCLD), 13 patients with cirrhosis of the liver without hepatic encephalopathy, and 8 healthy subjects. Blood samples were obtained from catheters placed in the radial artery...

Scoring system in cirrhotics due to viral hepatitis

International Nuclear Information System (INIS)

Abbasi, A.; Bhutto, A.R.; Butt, N.; Lal, K.; Munir, S.M.

2012-01-01

Objective: To determine the association of serum cholesterol levels with Child-Pugh class in patients with decompensated chronic liver disease due to viral hepatitis. Methodology: Consecutive patients attending outpatient department or admitted in medical unit III were eligible if they had a diagnosis of cirrhosis secondary to viral hepatitis. Patients were excluded if alcoholic, diabetic, hypertensive, or with non-alcoholic fatty liver disease, autoimmune, metabolic, cardiovascular, cerebrovascular or kidney diseases and recent use of lipid-regulating drugs. Serum lipid profile was determined after an overnight fast of 12 hours. On the basis of serum total cholesterol, patients were divided into four groups; Group I with serum total cholesterol = 100 mg/dl, Group II with level of 101-150 mg/dl, Group III with level of 151-200 mg/dl and Group IV with serum total cholesterol level of > 200 mg/dl. Hepatic dysfunction was categorized according to Child-Pugh scoring system. Chi-square and Spearman's correlation testing with p < 0.05 was accepted as significant. Results: One hundred and fourteen patients met the inclusion criteria with a mean age of 40.32 +- 13.59 years. Among these 32 were females (28.1%) while 82 were males (71.9%). According to Child-Pugh class; 34 patients (29.8%) presented with Child-Pugh class A, 34 (29.8%) in class B and 46 (40.4%) were in class C. Serum cholesterol (total) and triglycerides had significant association with Child-Pugh class (p = 0.0001 and p = 0.004 respectively) suggesting that as severity of liver dysfunction increases; serum cholesterol and triglycerides levels decrease. Results also revealed that males were significantly more hypocholesterolemic than females (p = 0.006). Conclusion: Hypocholesterolemia is a common finding in decompensated chronic liver disease and has got significant association with Child-Pugh class. It may increase the reliability of Child-Pugh classification in assessment of severity and prognosis in

Heavy flow autochtonic case of hepatitis E in elderly men

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S. V. Baramzina

2016-01-01

Full Text Available The article presents an analysis of the first clinical cases of acute hepatitis E autochtonic on the territory of the Kirov region. HEV-infection was diagnosed in 76 year old male, not to travel outside the region and the country for a long time, eat a lot of fresh fruit. A feature of the disease in non-endemic region was: severe course of hepatitis E in the elderly, with the development of clinic of acute liver failure and encephalopathy, the presence of the expressed syndrome cytolysis, cholestasis, hepatic-cell failure.Timely treatment of a patient for medical care, the lack of severe somatic diseases, chronic liver disease and adequate pathogenetic therapy helped to keep the patient’s life. In deciphering undifferentiated acute hepatitis in the elderly should be included in the scheme of examination and determination HEV RNA, a/HEV IgM and G.

Dramatic effect of levetiracetam in early-onset epileptic encephalopathy due to STXBP1 mutation.

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Dilena, Robertino; Striano, Pasquale; Traverso, Monica; Viri, Maurizio; Cristofori, Gloria; Tadini, Laura; Barbieri, Sergio; Romeo, Antonino; Zara, Federico

2016-01-01

Syntaxin Binding Protein 1 (STXBP1) mutations determine a central neurotransmission dysfunction through impairment of the synaptic vesicle release, thus causing a spectrum of phenotypes varying from syndromic and non-syndromic epilepsy to intellectual disability of variable degree. Among the antiepileptic drugs, levetiracetam has a unique mechanism of action binding SV2A, a glycoprotein of the synaptic vesicle release machinery. We report a 1-month-old boy manifesting an epileptic encephalopathy with clonic seizures refractory to phenobarbital, pyridoxine and phenytoin that presented a dramatic response to levetiracetam with full epilepsy control and EEG normalization. Genetic analysis identified a novel de novo heterozygous mutation (c.[922A>T]p.[Lys308(∗)]) in the STXBP1 gene that severely affects the protein. The observation of a dramatic efficacy of levetiracetam in a case of STXBP1 epileptic encephalopathy refractory to other antiepileptic drugs and considerations regarding the specific mechanism of action of levetiracetam modulating the same system affected by STXBP1 mutations support the hypothesis that this drug may be able to reverse specifically the disease epileptogenic abnormalities. Further clinical observations and laboratory studies are needed to confirm this hypothesis and eventually lead to consider levetiracetam as the first choice treatment of patients with suspected or confirmed STXBP1-related epilepsies. Copyright © 2015 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.

RiMINI - the influence of rifaximin on minimal hepatic encephalopathy (MHE) and on the intestinal microbiome in patients with liver cirrhosis: study protocol for a randomized controlled trial.

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Schulz, Christian; Schütte, Kerstin; Kropf, Siegfried; Schmitt, Friedhelm C; Vasapolli, Riccardo; Kliegis, Leon M; Riegger, Antonia; Malfertheiner, Peter

2016-02-29

Hepatic encephalopathy (HE) is a clinically significant complication of liver cirrhosis impacting on the patients' quality of life. Minimal hepatic encephalopathy (MHE) is diagnosed by psychometric tests, found in up to 80 % of patients with liver cirrhosis and carries a high risk of progression to overt HE. Continuous therapy with rifaximin in combination with lactulose significantly reduces the risk of overt HE, recurrence of HE and HE-related hospitalizations in randomized, double-blind, placebo-controlled clinical trials. Rifaximin is approved for the therapy of overt HE in Germany. Treatment with lactulose has been shown to improve cognitive functions in patients with liver cirrhosis. Data from prospective clinical trials comparing the efficacy of rifaximin alone against a combination of rifaximin and lactulose in the treatment of MHE are scarce. Changes in the microbiome of the upper and lower gastrointestinal tract as a result of therapy with rifaximin have not yet been addressed in clinical studies. RiMINI is a monocentric exploratory pilot study on 60 patients with MHE as assessed by critical flicker frequency (CFF). Additionally, visual evoked potentials' (VEP) testing, electroencephalography (EEG) and psychometric testing (NCT-A) will be carried out. Patients will be randomized to treatment either with rifaximin alone (550 mg twice daily (bid) continuously for a period of 3 months) or with rifaximin (550 mg bid continuously) in combination with lactulose (30-60 ml daily) for 3 months. An esophagogastroduodenoscopy (EGD) will be performed at baseline, at the end of treatment and 6 and 12 weeks after the end of treatment to obtain gastric and duodenal biopsies and aspirates. The samples will be analyzed for their content of specific bacterial taxae by applying next generation sequencing (NGS) after rRNA isolation to identify the microbiome of the stomach and duodenum, and of the gut, in patients with liver cirrhosis and MHE before and after therapy

Hashimoto's encephalopathy : epidemiology, pathogenesis and management.

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Mocellin, Ramon; Walterfang, Mark; Velakoulis, Dennis

2007-01-01

Hashimoto's encephalopathy is a term used to describe an encephalopathy of presumed autoimmune origin characterised by high titres of antithyroid peroxidase antibodies. In a similar fashion to autoimmune thyroid disease, Hashimoto's encephalopathy is more common in women than in men. It has been reported in paediatric, adult and elderly populations throughout the world. The clinical presentation may involve a relapsing and remitting course and include seizures, stroke-like episodes, cognitive decline, neuropsychiatric symptoms and myoclonus. Thyroid function is usually clinically and biochemically normal.Hashimoto's encephalopathy appears to be a rare disorder, but, as it is responsive to treatment with corticosteroids, it must be considered in cases of 'investigation negative encephalopathies'. Diagnosis is made in the first instance by excluding other toxic, metabolic and infectious causes of encephalopathy with neuroimaging and CSF examination. Neuroimaging findings are often not helpful in clarifying the diagnosis. Common differential diagnoses when these conditions are excluded are Creutzfeldt-Jakob disease, rapidly progressive dementias, and paraneoplastic and nonparaneoplastic limbic encephalitis. In the context of the typical clinical picture, high titres of antithyroid antibodies, in particular antithyroid peroxidase antibodies, are diagnostic. These antibodies, however, can be detected in elevated titres in the healthy general population. Treatment with corticosteroids is almost always successful, although relapse may occur if this treatment is ceased abruptly. Other forms of immunomodulation, such as intravenous immune-globulin and plasma exchange, may also be effective. Despite the link to autoimmune thyroid disease, the aetiology of Hashimoto's encephalopathy is unknown. It is likely that antithyroid antibodies are not pathogenic, but titres can be a marker of treatment response. Pathological findings can suggest an inflammatory process, but features

Diagnostic and prognostic factors for acute encephalopathy.

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Motojima, Yukiko; Nagura, Michiaki; Asano, Yoshitaka; Arakawa, Hiroshi; Takada, Eiko; Sakurai, Yoshio; Moriwaki, Koichi; Tamura, Masanori

2016-11-01

Acute encephalopathy has the possibility of sequelae. While early treatment is required to prevent the development of sequelae, differential diagnosis is of the utmost priority. The aim of this study was therefore to identify parameters that can facilitate early diagnosis and prediction of outcome of acute encephalopathy. We reviewed the medical charts of inpatients from 2005 to 2011 and identified 33 patients with febrile status epilepticus. Subjects were classified into an acute encephalopathy group (n = 20) and a febrile convulsion group (n = 13), and the parameters serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), ammonia (NH 3 ), cerebrospinal fluid (CSF) tau protein, and CSF interleukin-6 compared between them. Furthermore, the relationship between each parameter and prognosis was investigated in the encephalopathy group. Significant differences in serum AST, ALT, and LDH were observed between the febrile convulsion and acute encephalopathy group. Moreover, a significant difference in serum LDH was noted between the patients with and without developmental regression at the time of hospital discharge in the encephalopathy group. In particular, CSF tau protein was found to be highly likely to indicate progress, with CSF tau protein >1000 pg/dL associated with poor prognosis leading to developmental regression. Serum AST, ALT and LDH may be related to early diagnosis and prognosis, and should be carefully investigated in patients with encephalopathy. CSF tau protein could also be used as an indicator of poor prognosis in acute encephalopathy. © 2016 Japan Pediatric Society.

Does aetiology of neonatal encephalopathy and hypoxic-ischaemic encephalopathy influence the outcome of treatment?

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Mcintyre, Sarah; Badawi, Nadia; Blair, Eve; Nelson, Karin B

2015-04-01

Neonatal encephalopathy, a clinical syndrome affecting term-born and late preterm newborn infants, increases the risk of perinatal death and long-term neurological morbidity, especially cerebral palsy. With the advent of therapeutic hypothermia, a treatment designed for hypoxic or ischaemic injury, associated mortality and morbidity rates have decreased. Unfortunately, only about one in eight neonates (95% confidence interval) who meet eligibility criteria for therapeutic cooling apparently benefit from the treatment. Studies of infants in representative populations indicate that neonatal encephalopathy is a potential result of a variety of antecedents and that asphyxial complications at birth account for only a small percentage of neonatal encephalopathy. In contrast, clinical case series suggest that a large proportion of neonatal encephalopathy is hypoxic or ischaemic, and trials of therapeutic hypothermia are specifically designed to include only infants exposed to hypoxia or ischaemia. This review addresses the differences, definitional and methodological, between infants studied and investigations undertaken, in population studies compared with cooling trials. It raises the question if there may be subgroups of infants with a clinical diagnosis of hypoxic-ischaemic encephalopathy (HIE) in whom the pathobiology of neonatal neurological depression is not fundamentally hypoxic or ischaemic and, therefore, for whom cooling may not be beneficial. In addition, it suggests approaches to future trials of cooling plus adjuvant therapy that may contribute to further improvement of care for these vulnerable neonates. © The Authors. Journal compilation © 2015 Mac Keith Press.

Intrahepatic portal-hepatic venous shunt diagnosed by ultrasonography and computed tomography

International Nuclear Information System (INIS)

Shinagawa, Takashi; Iino, Yasuo; Ukaji, Haruyasu; Ishizuka, Masaharu

1986-01-01

Two cases of intrahepatic portal-hepatic venous shunt found by ultrasonography and computed tomography are reported. The first case came to the hospital because of hematuria. A large shunt between the portal vein and the hepatic vein was demonstrated by ultrasonography done for screening, and confirmed by percutaneous transhepatic portography (PTP). The second case was admitted because of cholelithiasis. Computed tomography with contrast enhancement revealed a dilated portal vein in the upper portion of the right lobe. It was subsequently shown by PTP to be a portal-hepatic venous shunt. Portal vein pressure and histological finding of the liver were normal in both cases. The etiology of the shunt was thought to be congenital in these cases for lack of liver disease, portal hypertension and history of trauma. Both cases had no history of hepatic encephalopathy and did not show any symptom attributable to the shunt. (author)

Hashimoto's encephalopathy

DEFF Research Database (Denmark)

Montagna, Giacomo; Imperiali, Mauro; Agazzi, Pamela

2016-01-01

Hashimoto's encephalopathy (HE) is a rare not well understood, progressive and relapsing multiform disease, characterized by seizures, movement disorders, subacute cognitive dysfunction, psychiatric symptoms and responsiveness to steroid therapy. The disorder is generally associated with thyroid ...... diseases and the most common feature is the presence of anti-thyroperoxidase antibodies (TPOAb). Patients are usually euthyroid or mildly hypothyroid at presentation. All age groups can be affected. The pathophysiology is still unclear, especially the link between elevated serum TPOAb...... and the encephalopathy. Most reported cases occurred in women and girls. Unspecific symptoms, non-pathognomonic laboratory neurophysiology and neuroimaging features make its diagnosis a real challenge for clinicians.The case of a 16 year old boy, with a clinical picture of HE associated with hypothyroidism...

Shunt occlusion for portosystemic shunt syndrome related refractory hepatic encephalopathy-A single-center experience in 21 patients from Kerala.

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Philips, Cyriac Abby; Kumar, Lijesh; Augustine, Philip

2017-09-01

Large spontaneous portosystemic shunts (SPSS) are seen in a subset of patients with liver disease and medically refractory recurrent/persistent hepatic encephalopathy (MRHE). Shunt occlusion has been shown to improve clinical outcomes. We retrospectively analyzed patient characteristics, SPSS attributes, procedural features, baseline clinical and investigational parameters, neurological outcomes, adverse effects (procedure and portal hypertension related), and risk factors predicting outcomes in liver disease patients undergoing shunt occlusion procedure for MRHE. Between October 2016 and July 2017, 21 patients (Child-Pugh score, CTP 6 to 13) with mean model of end-stage liver disease (MELD) and MELD-sodium scores 15.7 and 19.3 respectively with MRHE [3-cirrhotic Parkinsonism (CP)] were diagnosed to have single or multiple large SPSSs. A total of 29 shunts were occluded (1 surgical, 20 non-surgical). Recurrent and persistent HE and CP markedly improved in the short (n=20, 1 to 3 months), intermediate (n=12, 3 to 6 months), and long (n=7, 6 to 9 months) follow up. None had spontaneous or persistent HE at a median follow up 105 (30 to 329) days (p11 predicted mortality post shunt occlusion (p=0.04). Embolization of large SPSS in liver disease patients with MRHE and modestly preserved liver function is safe and efficacious and associated with improved quality of life and can function as a bridge to liver transplantation in accurately selected patients.

Validation of a Paper and Pencil Test Battery for the Diagnosis of Minimal Hepatic Encephalopathy in Korea.

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Jeong, Jae Yoon; Jun, Dae Won; Bai, Daiseg; Kim, Ji Yean; Sohn, Joo Hyun; Ahn, Sang Bong; Kim, Sang Gyune; Kim, Tae Yeob; Kim, Hyoung Su; Jeong, Soung Won; Cho, Yong Kyun; Song, Do Seon; Kim, Hee Yeon; Jung, Young Kul; Yoon, Eileen L

2017-09-01

The aim of this study was to validate a new paper and pencil test battery to diagnose minimal hepatic encephalopathy (MHE) in Korea. A new paper and pencil test battery was composed of number connection test-A (NCT-A), number connection test-B (NCT-B), digit span test (DST), and symbol digit modality test (SDMT). The norm of the new test was based on 315 healthy individuals between the ages of 20 and 70 years old. Another 63 healthy subjects (n = 31) and cirrhosis patients (n = 32) were included as a validation cohort. All participants completed the new paper and pencil test, a critical flicker frequency (CFF) test and computerized cognitive function test (visual continuous performance test [CPT]). The scores on the NCT-A and NCT-B increased but those of DST and SDMT decreased according to age. Twelve of the cirrhotic patients (37.5%) were diagnosed with MHE based on the new paper and pencil test battery. The total score of the paper and pencil test battery showed good positive correlation with the CFF (r = 0.551, P cognitive function test. Also, this score was lower in patients with MHE compared to those without MHE (P cognitive test decreased significantly in patients with MHE compared to those without MHE. Test-retest reliability was comparable. In conclusion, the new paper and pencil test battery including NCT-A, NCT-B, DST, and SDMT showed good correlation with neuropsychological tests. This new paper and pencil test battery could help to discriminate patients with impaired cognitive function in cirrhosis (registered at Clinical Research Information Service [CRIS], https://cris.nih.go.kr/cris, KCT0000955). © 2017 The Korean Academy of Medical Sciences.

Logistic regression analysis of prognostic factors in 106 acute-on-chronic liver failure patients with hepatic encephalopathy

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CUI Yanping

2014-10-01

Full Text Available ObjectiveTo analyze the prognostic factors in acute-on-chronic liver failure (ACLF patients with hepatic encephalopathy (HE and to explore the risk factors for prognosis. MethodsA retrospective analysis was performed on 106 ACLF patients with HE who were hospitalized in our hospital from January 2010 to July 2013. The patients were divided into improved group and deteriorated group. The univariate indicators including age, sex, laboratory indicators ［total bilirubin (TBil, albumin (Alb, alanine aminotransferase (ALT, aspartate amino-transferase (AST, and prothrombin time activity (PTA］, the stage of HE, complications ［persistent hyponatremia, digestive tract bleeding, hepatorenal syndrome (HRS, ascites, infection, and spontaneous bacterial peritonitis (SBP］, and plasma exchange were analyzed by chi-square test or t-test. Indicators with statistical significance were subsequently analyzed by binary logistic regression. ResultsUnivariate analysis showed that ALT (P=0.009, PTA (P=0.043, the stage of HE (P=0.000, and HRS (P=0.003 were significantly different between the two groups, whereas differences in age, sex, TBil, Alb, AST, persistent hyponatremia, digestive tract bleeding, ascites, infection, SBP, and plasma exchange were not statistically significant (P＞0.05. Binary logistic regression demonstrated that PTA (b=-0097, P=0.025, OR=0.908, HRS (b=2.279, P=0.007, OR=9.764, and the stage of HE (b=1873, P=0.000, OR=6.510 were prognostic factors in ACLF patients with HE. ConclusionThe stage of HE, HRS, and PTA are independent influential factors for the prognosis in ACLF patients with HE. Reduced PTA, advanced HE stage, and the presence of HRS indicate worse prognosis.

Extremely elevated alpha-fetoprotein due to acute exacerbation of chronic hepatitis B without malignancy: a case report.

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Yoon, Young-Min; Kang, Da-Yeong; Kim, Da-Young; Seo, Jun-Won; Lim, Hyun-Jong; Lee, Hee-Jeong; Park, Sang-Gon

2016-06-01

Alpha-fetoprotein is produced by a variety of tumors such as hepatocellular carcinoma, hepatoblastoma, and germ cell tumors of the ovary and testes. However, we present a case of significantly elevated serum alpha-fetoprotein without evidence of malignant disease in a patient who is a carrier of chronic hepatitis B. A 60-year-old Korean man presented with markedly increased alpha-fetoprotein (2350 ng/mL; normal 7 × 105 IU/mL). Our patient was diagnosed with acute exacerbation of chronic hepatitis B, and we presumed that this condition might be related to extremely elevated alpha-fetoprotein. When our patient was treated with entecavir, the serum alpha-fetoprotein level immediately decreased, in parallel with the hepatitis B virus deoxyribonucleic acid copy number. We report a rare case of extremely elevated alpha-fetoprotein due to acute exacerbation of chronic hepatitis B without any malignancy, and a decrease in this tumor marker simultaneous with a decrease in hepatitis B virus deoxyribonucleic acid copy number on entecavir treatment. This case report is important due to the rarity of the case; furthermore, it provides details of a diagnostic process for a variety of benign diseases and malignant tumors that should be considered in patients with elevated alpha-fetoprotein. Thus, we present a case report, along with a review, that will be helpful for diagnosis and treatment of patients with elevated alpha-fetoprotein.

Treatment of Decompensated Cirrhosis Secondary to Hepatitis C with Antiviral Therapy

International Nuclear Information System (INIS)

Khokhar, N.; Qureshi, M.O.; Niazi, T.K.

2013-01-01

Objective: To treat decompensated hepatitis C patient with interferon, ribavirin and amantidine to ascertain the sustained viral response. Study Design: Descriptive study. Place and Duration of Study: Shifa International Hospital, Islamabad, from January 2007 to January 2012. Methodology: HCV PCR patients with decompensated hepatitis C, who had developed a complication like ascites, encephalopathy or variceal bleeding were included in the study. Those with uncontrolled ascites or other complications were excluded. Treatment with standard interferon 3 miU subcutaneously three times a week along with ribavirin 800 mg to 1200 mg and amantidine 100 mg b.i.d. was administered for 12 months. Patients were followed every month with CBC and ALT and HCV PCR was performed after 3 months to document early viral response. They had HCV PCR at the end of the treatment to document end of treatment response. All were further followed for another 6 months at monthly intervals and HCV PCR was performed at the end of this period to document sustained viral response. Results: In all, 165 patients were treated. Treatment had to be discontinued in 42 (26%) patients. Out of these, 16 patients died. Thus, 123 completed treatment. Sustained viral response was documented in 58 out of the 123 (47%) patients. Hepatic encephalopathy, gastrointestinal bleeding, sepsis and development of ascites were the major complications during treatment. Conclusion: Forty seven percent of patients with decompensated hepatitis C cirrhosis were able to achieve sustained viral response after one year treatment with anti-viral therapy. However, complications developed during treatment and, therefore, frequent and close monitoring is necessary in these patients. (author)

An iron-deficient diet stimulates the onset of the hepatitis due to hepatic copper deposition in the Long-Evans Cinnamon (LEC) rat

Energy Technology Data Exchange (ETDEWEB)

Sugawara, Naoki; Sugawara, Chieko [Sapporo Medical Univ. (Japan). Dept. of Public Health

1999-09-01

To study effects of dietary Cu and Fe levels on the onset of hepatitis in Long-Evans Cinnamon (LEC) rats, female rats (40 days old) were fed a semipurified diet containing 0.1 or 10 mg Cu/kg and 1.5 or 150 mg Fe/kg in a 2 x 2 factorial arrangement for 35 days. At 75 days after birth, LEC rats (+Cu-Fe) fed a Cu-sufficient but Fe-deficient diet (Cu, 10 mg/kg; Fe, 1.5 mg/kg) showed jaundice, with lethargy, anorexia, and malaise. The biochemical variables relating to liver function were significantly increased compared to three other groups, a Cu- and Fe-deficient (-Cu-Fe) group, a Cu-deficient but Fe-sufficient (-Cu+Fe) group, and a Cu and Fe sufficient (+Cu+Fe) group. Furthermore, the +Cu-Fe rat liver showed massive necrosis with huge nuclei. The other three groups presented no biochemical and histological findings of hepatitis. Hepatic Cu and metallothionein concentrations were 289 {+-} 87 (mean {+-} SD) {mu}g/g liver and 8.7 {+-} 1.8 mg/g liver, respectively, in the +Cu-Fe rats. However, in the +Cu+Fe group the values were 196 {+-} 28 {mu}g Cu/g liver and 10.8 {+-} 1.0 mg/g liver. Hepatic Fe deposition was not influenced significantly by the dietary Cu level. The +Cu-Fe group with jaundice showed the highest free Cu concentration in the liver among the four groups, but the hepatic free Fe concentration was similar to those in the -Cu+Fe and +Cu+Fe groups. Our results indicate that an Fe-deficient diet enhances the deposition of hepatic Cu due to increased absorption of Cu from the gastrointestinal tract. This deposition stimulated the onset of hepatitis. (orig.)

Subarachnoid hemorrhage due to ruptured intracranial aneurysm following posterior reversible encephalopathy syndrome

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Takamasa Nanba

2016-01-01

Full Text Available Although posterior reversible encephalopathy syndrome (PRES is rarely associated with subarachnoid hemorrhage, to our knowledge, rupture of a concomitant cerebral aneurysm following PRES has not been reported. We describe a patient with atypical PRES involving the brainstem, thalamus, and periventricular white matter without cortical or subcortical edema of the parietooccipital lobe on magnetic resonance imaging, with rupture of a concomitant cerebral aneurysm. Preexisting extremely high blood pressure may trigger atypical PRES, and failure to lower blood pressure may lead to a concomitant aneurysm rupture. In the future treatment of hypertensive urgency with a recurrence of symptoms and mean arterial blood pressure >150 mmHg, it is advisable to immediately hospitalize the patient for aggressive blood pressure management, especially if PRES is suspected based on clinical and radiological features.

Autism spectrum disorder and epileptic encephalopathy: common causes, many questions.

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Srivastava, Siddharth; Sahin, Mustafa

2017-01-01

Epileptic encephalopathies represent a particularly severe form of epilepsy, associated with cognitive and behavioral deficits, including impaired social-communication and restricted, repetitive behaviors that are the hallmarks of autism spectrum disorder (ASD). With the advent of next-generation sequencing, the genetic landscape of epileptic encephalopathies is growing and demonstrates overlap with genes separately implicated in ASD. However, many questions remain about this connection, including whether epileptiform activity itself contributes to the development of ASD symptomatology. In this review, we compiled a database of genes associated with both epileptic encephalopathy and ASD, limiting our purview to Mendelian disorders not including inborn errors of metabolism, and we focused on the connection between ASD and epileptic encephalopathy rather than epilepsy broadly. Our review has four goals: to (1) discuss the overlapping presentations of ASD and monogenic epileptic encephalopathies; (2) examine the impact of the epilepsy itself on neurocognitive features, including ASD, in monogenic epileptic encephalopathies; (3) outline many of the genetic causes responsible for both ASD and epileptic encephalopathy; (4) provide an illustrative example of a final common pathway that may be implicated in both ASD and epileptic encephalopathy. We demonstrate that autistic features are a common association with monogenic epileptic encephalopathies. Certain epileptic encephalopathy syndromes, like infantile spasms, are especially linked to the development of ASD. The connection between seizures themselves and neurobehavioral deficits in these monogenic encephalopathies remains open to debate. Finally, advances in genetics have revealed many genes that overlap in ties to both ASD and epileptic encephalopathy and that play a role in diverse central nervous system processes. Increased attention to the autistic features of monogenic epileptic encephalopathies is warranted for

Acute hyperammonemic encephalopathy after fluoropyrimidine-based chemotherapy: A case series and review of the literature.

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Mitani, Seiichiro; Kadowaki, Shigenori; Komori, Azusa; Sugiyama, Keiji; Narita, Yukiya; Taniguchi, Hiroya; Ura, Takashi; Ando, Masashi; Sato, Yozo; Yamaura, Hidekazu; Inaba, Yoshitaka; Ishihara, Makoto; Tanaka, Tsutomu; Tajika, Masahiro; Muro, Kei

2017-06-01

Acute hyperammonemic encephalopathy induced by fluoropyrimidines (FPs) is a rare complication. Its pathophysiology remains unclear, especially given the currently used regimens, including intermediate-doses of 5-fluorouracil (5-FU) or oral FP agents. We aimed to characterize the clinical manifestations in cancer patients who developed hyperammonemic encephalopathy after receiving FP-based chemotherapy.We retrospectively reviewed 1786 patients with gastrointestinal or primary-unknown cancer who received FP-based regimens between 2007 and 2012. Eleven patients (0.6%) developed acute hyperammonemic encephalopathy. The incidence according to the administered anticancer drugs were as follows: 5-FU (8 of 1176, 0.7%), S-1 (1 of 679, 0.1%), capecitabine (2 of 225, 0.9%), and tegafur-uracil (UFT) (0 of 39, 0%). Ten patients (90.9%) had at least 1 aggravating factor, including infection, dehydration, constipation, renal dysfunction, and muscle loss. All the 10 patients met the definition of sarcopenia. Median time to the onset of hyperammonemic encephalopathy in the cycle was 3 days (range: 2-21). Three patients (27.3%) developed encephalopathy during the first cycle of the regimen and the remaining 8 patients during the second or more cycles. Seven patients (63.6%) had received at least 1 other FP-containing regimen before without episodes of encephalopathy.All patients recovered soon after immediate discontinuation of chemotherapy and supportive therapies, such as hydration, infusion of branched-chain amino acids, and oral lactulose intake, with a median time to recovery of 2 days (range: encephalopathy due to S-1 monotherapy, received modified FOLFOX-6 therapy without encephalopathy later.FP-associated acute hyperammonemic encephalopathy is extremely rare, but a possible event at any time and even during the administration of oral FP agents. Particular attention is warranted when giving FP-based therapy for patients with aggravating factors, such as sarcopenia. This

Infecções bacterianas pioram o prognóstico da hepatite alcoólica Alcoholic hepatitis: bad prognosis due to concomitant bacterial infections

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Edna Strauss

2004-06-01

, from a single center during a six-year period, 52 (7.5% cases of alcoholic hepatitis were well documented, 73.1% by liver biopsy with histopathological analysis and the others by well characterized clinical-biochemical data. Males were predominant (ratio 3.3:1.0, mean age of 40 years and mean alcohol intake of 193g/day. Major complications were: Hepatic encephalopathy (n=5, renal insufficiency (n=4 and digestive bleeding (n=3. Bacterial infections were found in 11 (21% patients, distributed into: pulmonary (n=5, spontaneous bacterial peritonitis (n=2, urinary (n=3 and dermatological (n=1. Early hospital death occurred in eight (15.4% patients and comparative analysis between these and those who survived showed that poor prognostic factors were: presence of hepatic encephalopathy (p=0.012, total bilirubin > 20mg% (p=0.012 and the presence of severe infections (pulmonary and spontaneous bacterial peritonitis with statistical significance (p=0.004. In conclusion we have demonstrated that severe bacterial infections are poor prognostic factors for alcoholic hepatitis. Our recommendation, based on prophylaxis with antibiotics during digestive bleeding in cirrhosis and in acute hepatic insufficiency, is to extend this prophylaxis to alcoholic hepatitis, in its severe form, in order to prevent bacterial infections and early death.

Fulminant hepatic failure in children: Etiology, histopathology and MDCT findings

International Nuclear Information System (INIS)

Cakir, Banu; Kirbas, Ismail; Demirhan, Beyhan; Tarhan, Nefise Cagla; Bozkurt, Alper; Ozcay, Figen; Coskun, Mehmet

2009-01-01

Introduction: The purpose of this study is to determine the etiologies, histopathology and MDCT findings of children with fulminant hepatic failure admitted to our institution. Materials and methods: Between June 2004 and November 2006, 15 children with fulminant hepatic failure who underwent MDCT were included retrospectively in this study. Twelve patients had liver biopsies. The patients were divided into three groups as hyperacute (Group I), acute (Group II) and subacute (Group III) depending on onset of hepatic encephalopathy. Results: Hepatitis A in 4 patients, non-A, non-E hepatitis in 4; mushroom poisoning in 3; fulminant Wilson's disease in 2; autoimmune hepatitis in 1; and both hepatitis B and toxic hepatitis (with leflunomide treatment) in 1 patient were detected. MDCT of all three groups revealed diffuse reduction in hepatic attenuation in 11 patients; ascites in 9; periportal edema in 6; edema of gallbladder wall in 6; splenomegaly in 6; heterogeneous hepatic parenchyma in 6; hepatomegaly in 3; irregular contours of liver in 2; multiple micronodules in 1 and necrotic areas and regeneration in liver parenchyma in 2 patients. Histopathologic evaluation of liver biopsies showed massive hepatic necrosis, inflammatory cell infiltration and ductular proliferation in 8 patients, periportal edema in 6, edema of gallbladder wall in 5, regenerating nodules and fibrous septa consistent with cirrhotic pattern in 2, and regenerating nodules and necrotic areas in 2 patients. Conclusion: The most common MDCT findings in fulminant hepatic failure were diffuse reduction in hepatic attenuation and ascites. Massive hepatic necrosis was the most common histopathologic finding.

Fulminant hepatic failure in children: Etiology, histopathology and MDCT findings

Energy Technology Data Exchange (ETDEWEB)

Cakir, Banu [Baskent University Faculty of Medicine Department of Radiology, Fevzi Cakmak Cd. 10, Sok. No: 45, Bahcelievler, Ankara 06490 (Turkey)], E-mail: banutopcu@yahoo.com; Kirbas, Ismail [Baskent University Faculty of Medicine Department of Radiology, Fevzi Cakmak Cd. 10, Sok. No: 45, Bahcelievler, Ankara 06490 (Turkey)], E-mail: drismailk@yahoo.com; Demirhan, Beyhan [Baskent University Faculty of Medicine Department of Pathology, Fevzi Cakmak Cd. 10, Sok. No: 45, Bahcelievler, Ankara 06490 (Turkey)], E-mail: beyhand@baskent-ank.edu.tr; Tarhan, Nefise Cagla [Baskent University Faculty of Medicine Department of Radiology, Fevzi Cakmak Cd. 10, Sok. No: 45, Bahcelievler, Ankara 06490 (Turkey)], E-mail: caglat@gmail.com; Bozkurt, Alper [Baskent University Faculty of Medicine Department of Radiology, Fevzi Cakmak Cd. 10, Sok. No: 45, Bahcelievler, Ankara 06490 (Turkey)], E-mail: abozkurt78@hotmail.com; Ozcay, Figen [Baskent University Faculty of Medicine Department of Pediatric Gastroenterology, Fevzi Cakmak Cd. 10, Sok. No: 45, Bahcelievler, Ankara 06490 (Turkey)], E-mail: fozcay@baskent.edu.tr; Coskun, Mehmet [Baskent University Faculty of Medicine Department of Radiology, Fevzi Cakmak Cd. 10, Sok. No: 45, Bahcelievler, Ankara 06490 (Turkey)], E-mail: mcoskun@baskent-ank.edu.tr

2009-11-15

Introduction: The purpose of this study is to determine the etiologies, histopathology and MDCT findings of children with fulminant hepatic failure admitted to our institution. Materials and methods: Between June 2004 and November 2006, 15 children with fulminant hepatic failure who underwent MDCT were included retrospectively in this study. Twelve patients had liver biopsies. The patients were divided into three groups as hyperacute (Group I), acute (Group II) and subacute (Group III) depending on onset of hepatic encephalopathy. Results: Hepatitis A in 4 patients, non-A, non-E hepatitis in 4; mushroom poisoning in 3; fulminant Wilson's disease in 2; autoimmune hepatitis in 1; and both hepatitis B and toxic hepatitis (with leflunomide treatment) in 1 patient were detected. MDCT of all three groups revealed diffuse reduction in hepatic attenuation in 11 patients; ascites in 9; periportal edema in 6; edema of gallbladder wall in 6; splenomegaly in 6; heterogeneous hepatic parenchyma in 6; hepatomegaly in 3; irregular contours of liver in 2; multiple micronodules in 1 and necrotic areas and regeneration in liver parenchyma in 2 patients. Histopathologic evaluation of liver biopsies showed massive hepatic necrosis, inflammatory cell infiltration and ductular proliferation in 8 patients, periportal edema in 6, edema of gallbladder wall in 5, regenerating nodules and fibrous septa consistent with cirrhotic pattern in 2, and regenerating nodules and necrotic areas in 2 patients. Conclusion: The most common MDCT findings in fulminant hepatic failure were diffuse reduction in hepatic attenuation and ascites. Massive hepatic necrosis was the most common histopathologic finding.

Hashimoto's encephalopathy: Report of three cases

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Jan-Shun Chang

2014-11-01

Full Text Available Both severe thyrotoxicosis and hypothyroidism may affect brain function and cause a change in consciousness, as seen with a thyroid storm or myxedema coma. However, encephalopathy may also develop in patients with autoimmune thyroid diseases independent of actual thyroid function level, and this is known as Hashimoto's encephalopathy. Although most patients are found to have Hashimoto's thyroiditis, less frequently they have Graves' disease. Clinical manifestations include epilepsy, disturbance of consciousness, cognitive impairment, memory loss, myoclonus, hallucinations, stroke-like episodes, tremor, involuntary movements, language impairment, and gait impairment. Hashimoto's encephalopathy is a relatively rare disease. As a good response can be obtained with corticosteroid therapy, early diagnosis and treatment is very beneficial for patients. Here we report three patients with Hashimoto's encephalopathy with typical manifestations of hallucinations that were associated with hypothyroidism, hyperthyroidism, and euthyroid status, respectively. They all showed a dramatic response to methylprednisolone pulse therapy.

Treatment of Hyponatremic Encephalopathy in the Critically Ill.

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Achinger, Steven G; Ayus, Juan Carlos

2017-10-01

Hyponatremic encephalopathy, symptomatic cerebral edema due to a low osmolar state, is a medical emergency and often encountered in the ICU setting. This article provides a critical appraisal and review of the literature on identification of high-risk patients and the treatment of this life-threatening disorder. Online search of the PubMed database and manual review of articles involving risk factors for hyponatremic encephalopathy and treatment of hyponatremic encephalopathy in critical illness. Hyponatremic encephalopathy is a frequently encountered problem in the ICU. Prompt recognition of hyponatremic encephalopathy and early treatment with hypertonic saline are critical for successful outcomes. Manifestations are varied, depending on the extent of CNS's adaptation to the hypoosmolar state. The absolute change in serum sodium alone is a poor predictor of clinical symptoms. However, certain patient specific risks factors are predictive of a poor outcome and are important to identify. Gender (premenopausal and postmenopausal females), age (prepubertal children), and the presence of hypoxia are the three main clinical risk factors and are more predictive of poor outcomes than the rate of development of hyponatremia or the absolute decrease in the serum sodium. In patients with hyponatremic encephalopathy exhibiting neurologic manifestations, a bolus of 100 mL of 3% saline, given over 10 minutes, should be promptly administered. The goal of this initial bolus is to quickly treat cerebral edema. If signs persist, the bolus should be repeated in order to achieve clinical remission. However, the total change in serum sodium should not exceed 5 mEq/L in the initial 1-2 hours and 15-20 mEq/L in the first 48 hours of treatment. It has recently been demonstrated in a prospective fashion that 500 mL of 3% saline at an infusion rate of 100 mL per hour can be given safely. It is critical to recognize the early signs of cerebral edema (nausea, vomiting, and headache

Computerized tomography in acute toxic encephalopathy

International Nuclear Information System (INIS)

Aoki, Nobuhiko; Kaneshi, Kunio; Mizuguchi, Masashi; Kurihara, Eiji.

1983-01-01

We experienced three cases of acute toxic encephalopathy, including a case of probable Reye syndrome, which had similar and unique CT findings in their acute stage; symmetrical low density area in the thalamus and the dentate nucleus, followed by changes in cerebellar hemispheres and around lateral ventricles. The CT findings, common to probable Reye syndrome and other acute toxic encephalopathy, may suggest the possibility of similar pathogenesis of brain damage in both disorders. The authors propose that present cases are a new subgroup in acute toxic encephalopathy, because of their similar and unique CT features. (author)

Persistent neurological deficit from iodinated contrast encephalopathy following intracranial aneurysm coiling. A case report and review of the literature.

LENUS (Irish Health Repository)

Leong, S

2012-03-01

Neurotoxicity from iodinated contrast agents is a known but rare complication of angiography and neurovascular intervention. Neurotoxicity results from contrast penetrating the blood-brain barrier with resultant cerebral oedema and altered neuronal excitability. Clinical effects include encephalopathy, seizures, cortical blindness and focal neurological deficits. Contrast induced encephalopathy is extensively reported as a transient and reversible phenomenon. We describe a patient with a persistent motor deficit due to an encephalopathy from iodinated contrast media administered during cerebral aneurysm coiling. This observation and a review of the literature highlights that contrast-induced encephalopathy may not always have a benign outcome and can cause permanent deficits. This potential harmful effect should be recognised by the angiographer and the interventionalist.

Chronic traumatic encephalopathy: The unknown disease.

Science.gov (United States)

Martínez-Pérez, R; Paredes, I; Munarriz, P M; Paredes, B; Alén, J F

2017-04-01

Chronic traumatic encephalopathy is a neurodegenerative disease produced by accumulated minor traumatic brain injuries; no definitive premortem diagnosis and no treatments are available for chronic traumatic encephalopathy. Risk factors associated with chronic traumatic encephalopathy include playing contact sports, presence of the apolipoprotein E4, and old age. Although it shares certain histopathological findings with Alzheimer disease, chronic traumatic encephalopathy has a more specific presentation (hyperphosphorylated tau protein deposited as neurofibrillary tangles, associated with neuropil threads and sometimes with beta-amyloid plaques). Its clinical presentation is insidious; patients show mild cognitive and emotional symptoms before progressing to parkinsonian motor signs and finally dementia. Results from new experimental diagnostic tools are promising, but these tools are not yet available. The mainstay of managing this disease is prevention and early detection of its first symptoms. Copyright © 2014 Sociedad Española de Neurología. Publicado por Elsevier España, S.L.U. All rights reserved.

MRI finding of ethylmalonic encephalopathy: case report

International Nuclear Information System (INIS)

Kim, Jin Yong; Lee, Shi Kyung; Han, Chun Hwan; Rho, Eun Jin

2002-01-01

Ethylmalonic encephalopathy is a rare syndrom characterized by developmental delay, acrocyanosis, petechiae, chronic diarrhea, and ethylmalonic, lactic, and methylsuccinic aciduria. We report the MRI finding of ethylmalonic encephalopathy including previously unreported intracranial hematoma

Myoclonic encephalopathy after exposure to trichloroethylene.

Science.gov (United States)

Sanz, Pere; Nogué, Santiago; Vilchez, Daniel; Salvadó, Elisa; Casal, Amparo; Logroscino, Giancarlo

2008-12-01

Trichloroethylene is a widely-used industrial solvent that is absorbed through the digestive or respiratory tracts or cutaneously. It has a selective tropism for the cardiovascular and central nervous systems and may cause death due to cardiac arrest or neurological sequelae. We present the case of a 25-yr-old women who was exposed to trichloroethylene in the workplace for 18 months and who developed a disabling myoclonic encephalopathy. Non-toxicological causes were excluded. Although the exposure ceased, the disease progressed with thalamic and cerebellar involvement. The patient, who had only a partial response to symptomatic treatment, suffered severe limitations in the activities of daily living and was registered as permanently disabled due to a work-related disability.

Hypercalcemia due to Primary Hepatic Lymphoma

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Andrew Hsu

2016-01-01

Full Text Available A 65-year-old female with a history of mixed connective tissue disease and pulmonary fibrosis on azathioprine, hydroxychloroquine, and prednisone (osteoporosis on teriparatide presented with a 1-month history of hypercalcemia. After discontinuation of teriparatide, the patient’s hypercalcemia persisted. Further evaluation revealed primary hepatic lymphoma as the source of her hypercalcemia.

Pure methotrexate encephalopathy presenting with seizures: CT and MRI features

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Loevblad, K.O.; Kelkar, P.; Ozdoba, C.; Remonda, L.; Schroth, G. [Department of Neuroradiology, Institute of Diagnostic Radiology, Inselspital, University of Bern, CH-3010 Bern (Switzerland); Ramelli, G. [Department of Pediatrics, Inselspital, University of Bern, Bern (Switzerland)

1998-02-01

With the advent of chemotherapy, mortality rates in acute lymphoblastic leukaemia (ALL) have decreased, but complications in the central nervous system have appeared. These include direct involvement of the brain itself and the development of chemotherapy-related encephalopathy as a delayed reaction. In most reported cases, this encephalopathy is believed to be due to necrotising angiitis arising from the combination of chemotherapy with adjuvant radiotherapy. We report the cases of four children with ALL who had been treated with high-dose intravenous and intrathecal chemotherapy but no radiation therapy, and who were admitted to hospital because of seizures. CT of the brain revealed the presence of diffuse periventricular white matter hypodensities in all cases and subcortical hyperdense foci in three cases. MRI showed diffuse hyperintense white matter lesions on T2-weighted images in all four patients; hypointense changes were observed on susceptibility-sensitive FLASH sequences in the hyperdense foci seen on CT as well as changes that were hyperintense on T1-weighted images. It was, therefore, concluded that the lesions corresponded to a leukoencephalopathy with calcific deposits. These findings are of a pure form of methotrexate encephalopathy causing seizures. (orig.) With 2 figs., 17 refs.

Pure methotrexate encephalopathy presenting with seizures: CT and MRI features

International Nuclear Information System (INIS)

Loevblad, K.O.; Kelkar, P.; Ozdoba, C.; Remonda, L.; Schroth, G.; Ramelli, G.

1998-01-01

With the advent of chemotherapy, mortality rates in acute lymphoblastic leukaemia (ALL) have decreased, but complications in the central nervous system have appeared. These include direct involvement of the brain itself and the development of chemotherapy-related encephalopathy as a delayed reaction. In most reported cases, this encephalopathy is believed to be due to necrotising angiitis arising from the combination of chemotherapy with adjuvant radiotherapy. We report the cases of four children with ALL who had been treated with high-dose intravenous and intrathecal chemotherapy but no radiation therapy, and who were admitted to hospital because of seizures. CT of the brain revealed the presence of diffuse periventricular white matter hypodensities in all cases and subcortical hyperdense foci in three cases. MRI showed diffuse hyperintense white matter lesions on T2-weighted images in all four patients; hypointense changes were observed on susceptibility-sensitive FLASH sequences in the hyperdense foci seen on CT as well as changes that were hyperintense on T1-weighted images. It was, therefore, concluded that the lesions corresponded to a leukoencephalopathy with calcific deposits. These findings are of a pure form of methotrexate encephalopathy causing seizures. (orig.)

Portal hemodynamics in chronic portal-systemic encephalopathy

International Nuclear Information System (INIS)

Takashi, Motohide; Igarashi, Masahiko; Hino, Shinichi; Takayasu, Kenichi; Goto, Nobuaki; Musha, Hirotaka; Ohnishi, Kunihiko; Okuda, Kunio

1985-01-01

A portal hemodynamic study was made in 7 consecutive patients with chronic portal-systemic encephalopathy by percutaneous transhepatic catheterization of the portal vein and injecting contrast medium into the superior mesenteric vein or by superior mesenteric arterial portography in comparison with patients without encephalopathy studied by percutaneous catheterization of these veins. It is suggested that chronic portal-systemic encephalopathy is a result of a large collateral route shunting a large proportion of the superior mesenteric venous blood into systemic circulation, and that development of such collaterals precludes formation of large esophageal varices. (Auth.)

Diffusion MR findings in cyclosporin-A induced encephalopathy

International Nuclear Information System (INIS)

Aydin, Kubilay; Minareci, Ozenc; Donmez, Fuldem; Tuzun, Umit; Atamer, Tanju

2004-01-01

Cyclosporin encephalopathy is a well-known entity, which is clinically characterized by altered mental status, vision problems, focal neurological deficits and seizures. The exact pathophysiology of the cyclosporin encephalopathy has not yet been defined. We report the diffusion-weighted MR imaging and proton MR spectroscopy findings in a case of cyclosporin encephalopathy. The white-matter lesions with reversible restricted diffusion supported the hypothesis of reversible vasospasm induced by the cyclosporin. (orig.)

DA Negatively Regulates IGF-I Actions Implicated in Cognitive Function via Interaction of PSD95 and nNOS in Minimal Hepatic Encephalopathy.

Science.gov (United States)

Ding, Saidan; Zhuge, Weishan; Wang, Xuebao; Yang, Jianjing; Lin, Yuanshao; Wang, Chengde; Hu, Jiangnan; Zhuge, Qichuan

2017-01-01

Insulin-like growth factor I (IGF-I) has been positively correlated with cognitive ability. Cognitive decline in minimal hepatic encephalopathy (MHE) was shown to be induced by elevated intracranial dopamine (DA). The beneficial effect of IGF-I signaling in MHE remains unknown. In this study, we found that IGF-I content was reduced in MHE rats and that IGF-I administration mitigated cognitive decline of MHE rats. A protective effect of IGF-I on the DA-induced interaction between postsynaptic density protein 95 (PSD95) and neuronal nitric oxide synthase (nNOS) was found in neurons. Ribosomal S6 protein kinase (RSK) phosphorylated nNOS in response to IGF-I by recruiting extracellular signal-regulated kinase (ERK1/2). In turn, DA inactivated the ERK1/2/RSK pathway and stimulated the PSD95-nNOS interaction by downregulating IGF-I. Inhibition of the interaction between PSD95 and nNOS ameliorated DA-induced memory impairment. As DA induced deficits in the ERK1/2/RSK pathway and the interaction between PSD95 and nNOS in MHE brains, IGF-I administration exerted a protective effect via interruption of the interaction between PSD95 and nNOS. These results suggest that IGF-I antagonizes DA-induced cognitive loss by disrupting PSD95-nNOS interactions in MHE.

DA Negatively Regulates IGF-I Actions Implicated in Cognitive Function via Interaction of PSD95 and nNOS in Minimal Hepatic Encephalopathy

Directory of Open Access Journals (Sweden)

Saidan Ding

2017-09-01

Full Text Available Insulin-like growth factor I (IGF-I has been positively correlated with cognitive ability. Cognitive decline in minimal hepatic encephalopathy (MHE was shown to be induced by elevated intracranial dopamine (DA. The beneficial effect of IGF-I signaling in MHE remains unknown. In this study, we found that IGF-I content was reduced in MHE rats and that IGF-I administration mitigated cognitive decline of MHE rats. A protective effect of IGF-I on the DA-induced interaction between postsynaptic density protein 95 (PSD95 and neuronal nitric oxide synthase (nNOS was found in neurons. Ribosomal S6 protein kinase (RSK phosphorylated nNOS in response to IGF-I by recruiting extracellular signal-regulated kinase (ERK1/2. In turn, DA inactivated the ERK1/2/RSK pathway and stimulated the PSD95–nNOS interaction by downregulating IGF-I. Inhibition of the interaction between PSD95 and nNOS ameliorated DA-induced memory impairment. As DA induced deficits in the ERK1/2/RSK pathway and the interaction between PSD95 and nNOS in MHE brains, IGF-I administration exerted a protective effect via interruption of the interaction between PSD95 and nNOS. These results suggest that IGF-I antagonizes DA-induced cognitive loss by disrupting PSD95–nNOS interactions in MHE.

[Risk of acute hepatic insufficiency in children due to chronic accidental overdose of paracetamol (acetaminophen)

NARCIS (Netherlands)

Hameleers-Snijders, P.; Hogeveen, M.; Smeitink, J.A.M.; Kramers, C.; Draaisma, J.M.T.

2007-01-01

Two girls aged 4 and 3 years, respectively, experienced acute liver failure due to accidental ingestion of supratherapeutic doses of paracetamol (90 mg/kg/day or more). Recognition of chronic paracetamol intoxication as a cause of acute hepatic failure is often delayed. It is important to consider

Altered regional homogeneity in the development of minimal hepatic encephalopathy: a resting-state functional MRI study.

Directory of Open Access Journals (Sweden)

Ling Ni

Full Text Available BACKGROUND: Little is known about how spontaneous brain activity progresses from non-hepatic encephalopathy (non-HE to minimal HE (MHE. The purpose of this study was to evaluate the evolution pattern of spontaneous brain activities in cirrhotic patients using resting-state fMRI with a regional homogeneity (ReHo method. METHODOLOGY/PRINCIPAL FINDINGS: Resting-state fMRI data were acquired in 47 cirrhotic patients (minimal HE [MHE], n = 20, and non-HE, n = 27 and 25 age-and sex-matched healthy controls. The Kendall's coefficient of concordance (KCC was used to measure the regional homogeneity. The regional homogeneity maps were compared with ANOVA tests among MHE, non-HE, and healthy control groups and t-tests between each pair in a voxel-wise way. Correlation analyses were performed to explore the relationships between regional ReHo values and Child-Pugh scores, number connection test type A (NCT-A, digit symbol test (DST scores, venous blood ammonia levels. Compared with healthy controls, both MHE and non-HE patients showed decreased ReHo in the bilateral frontal, parietal and temporal lobes and increased ReHo in the bilateral caudate. Compared with the non-HE, MHE patients showed decreased ReHo in the bilateral precuneus, cuneus and supplementary motor area (SMA. The NCT-A of cirrhotic patients negatively correlated with ReHo values in the precuneus, cuneus and lingual gyrus. DST scores positively correlated with ReHo values in the cuneus, precuneus and lingual gyrus, and negatively correlated with ReHo values in the bilateral caudate (P<0.05, AlphaSim corrected. CONCLUSIONS/SIGNIFICANCE: Diffused abnormal homogeneity of baseline brain activity was nonspecific for MHE, and only the progressively decreased ReHo in the SMA and the cuneus, especially for the latter, might be associated with the development of MHE. The ReHo analysis may be potentially valuable for detecting the development from non-HE to MHE.

Massive hemobilia due to hepatic arteriobiliary fistula during endoscopic retrograde cholangiopancretography: An extremely rare guidewir-related complication

Energy Technology Data Exchange (ETDEWEB)

Nam, Jeong Gu; Seo, Young Woo; Hwang, Jae Cheol; Weon, Young Cheol; Kang, Byeong Seong; Bang, Sung Jo; Bang, Min Seo [Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan (Korea, Republic of)

2015-05-15

Although endoscopic retrograde cholangiopancreatography (ERCP) is an effective modality for diagnosis and treatment of biliary and pancreatic diseases, the risk for procedure-related complications is high. Hemorrhage is one of major complications of ERCP. Most ERCP-associated bleeding is primarily a complication related to sphincterotomy rather than diagnostic ERCP. We are reporting a case of massive hemobilia due to hepatic arteriobiliary fistula caused by guidewire-associated injury during ERCP, which was successfully treated with transarterial embolization of the hepatic artery.

Birth defects in children with newborn encephalopathy

NARCIS (Netherlands)

Felix, JF; Badawi, N; Kurinczuk, JJ; Bower, C; Keogh, JM; Pemberton, PJ

2000-01-01

This study was designed to investigate birth defects found in association with newborn encephalopathy. All possible birth defects were ascertained in a population-based study of 276 term infants with moderate or severe encephalopathy and 564 unmatched term control infants. A strong association

Two cases of esophageal cancer with portal hypertension: esophagectomy with venous shunt procedure.

Science.gov (United States)

Kato, T; Motohara, T; Kaneko, Y; Shikishima, H; Okushiba, S; Kondo, S; Kato, H

2001-01-01

We performed venous shunt procedure in the reconstruction of the esophagus after esophagectomy using the gastric tube in two cases of esophageal cancer with portal hypertension due to liver cirrhosis. In both cases, the short-term postoperative course was uneventful, without congestion in the gastric tube. In Case 1 where the short gastric vein had been used as the shunt vein, the long-term postoperative course was also uneventful, without hepatic encephalopathy or hemorrhage from deterioration of the varices of the gastric tube. However, in Case 2 where the left gastroepiploic vein had been used, hepatic encephalopathy developed due to excessive shunt flow. These results suggested that appropriate shunt flow could be expected by using short gastric vein.

Bacopa monnieri Extract (CDRI-08 Modulates the NMDA Receptor Subunits and nNOS-Apoptosis Axis in Cerebellum of Hepatic Encephalopathy Rats

Directory of Open Access Journals (Sweden)

Papia Mondal

2015-01-01

Full Text Available Hepatic encephalopathy (HE, characterized by impaired cerebellar functions during chronic liver failure (CLF, involves N-methyl-D-aspartate receptor (NMDAR overactivation in the brain cells. Bacopa monnieri (BM extract is a known neuroprotectant. The present paper evaluates whether BM extract is able to modulate the two NMDAR subunits (NR2A and NR2B and its downstream mediators in cerebellum of rats with chronic liver failure (CLF, induced by administration of 50 mg/kg bw thioacetamide (TAA i.p. for 14 days, and in the TAA group rats orally treated with 200 mg/kg bw BM extract from days 8 to 14. NR2A is known to impart neuroprotection and that of NR2B induces neuronal death during NMDAR activation. Neuronal nitric oxide synthase- (nNOS- apoptosis pathway is known to mediate NMDAR led excitotoxicity. The level of NR2A was found to be significantly reduced with a concomitant increase of NR2B in cerebellum of the CLF rats. This was consistent with significantly enhanced nNOS expression, nitric oxide level, and reduced Bcl2/Bax ratio. Moreover, treatment with BM extract reversed the NR2A/NR2B ratio and also normalized the levels of nNOS-apoptotic factors in cerebellum of those rats. The findings suggest modulation of NR2A and NR2B expression by BM extract to prevent neurochemical alterations associated with HE.

Hepatitis Vaccines

OpenAIRE

Ogholikhan, Sina; Schwarz, Kathleen B.

2016-01-01

Viral hepatitis is a serious health problem all over the world. However, the reduction of the morbidity and mortality due to vaccinations against hepatitis A and hepatitis B has been a major component in the overall reduction in vaccine preventable diseases. We will discuss the epidemiology, vaccine development, and post-vaccination effects of the hepatitis A and B virus. In addition, we discuss attempts to provide hepatitis D vaccine for the 350 million individuals infected with hepatitis B ...

Liver transplant in ethylmalonic encephalopathy: a new treatment for an otherwise fatal disease.

Science.gov (United States)

Dionisi-Vici, Carlo; Diodato, Daria; Torre, Giuliano; Picca, Stefano; Pariante, Rosanna; Giuseppe Picardo, Sergio; Di Meo, Ivano; Rizzo, Cristiano; Tiranti, Valeria; Zeviani, Massimo; De Ville De Goyet, Jean

2016-04-01

Ethylmalonic encephalopathy is a fatal, rapidly progressive mitochondrial disorder caused by ETHE1 mutations, whose peculiar clinical and biochemical features are due to the toxic accumulation of hydrogen sulphide and of its metabolites, including thiosulphate. In mice with ethylmalonic encephalopathy, liver-targeted adeno-associated virus-mediated ETHE1 gene transfer dramatically improved both clinical course and metabolic abnormalities. Reasoning that the same achievement could be accomplished by liver transplantation, we performed living donor-liver transplantation in an infant with ethylmalonic encephalopathy. Unlike the invariably progressive deterioration of the disease, 8 months after liver transplantation, we observed striking neurological improvement with remarkable achievements in psychomotor development, along with dramatic reversion of biochemical abnormalities. These results clearly indicate that liver transplantation is a viable therapeutic option for ETHE1 disease. © The Author (2016). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

Current Management of Alcoholic Hepatitis and Future Therapies

Institute of Scientific and Technical Information of China (English)

Behnam Saberi; Alia S.Dadabhai; Yoon-Young Jang; Ahmet Gurakar; Esteban Mezey

2016-01-01

Alcohol is one of the most common etiologies of liver disease,and alcoholic liver disease overall is the second most common indication for liver transplantation in the United States.It encompasses a spectrum of disease,including fatty liver disease,alcoholic hepatitis (AH),and alcoholic cirrhosis.AH can range from mild to severe disease,with severe disease being defined as:Discriminant Function (DF) ≥ 32,or Model for End-stage Liver Disease (MELD) ≥ 21,or presence of hepatic encephalopathy.Management of the mild disease consists mainly of abstinence and supportive care.Severe AH is associated with significant mortality.Currently,there is no ideal medical treatment for this condition.Besides alcohol cessation,corticosteroids have been used with conflicting results and are associated with an inherent risk of infection.Overall steroids have shown short term benefit when compared to placebo,but they have no obvious long term benefits.Pentoxifylline does not improve survival in patients with severe AH and is no longer recommended based on the results of the STOPAH (Steroid Or Pentoxifylline for Alcoholic Hepatitis) trial.Anti-tumor necrosis factor (TNF) agents are associated with increased risk of life threatening infections and death.Currently,early stage trials are underway,mainly targeting novel pathways based on disease pathogenesis,including modulation of innate immune system,inhibition of gut-liver axis and cell death pathways,and activation of transcription factor farnesyl X receptor (FXR).Future treatment may lie in human induced pluripotent stem cell (iPSC)technology,which is currently under investigation for the study of pathogenesis,drug discovery,and stem cell transplantation.Liver transplantation has been reported with good results in highly selected patients but is controversial due to limited organ Suppply.

Electroencephalography and Brain MRI Patterns in Encephalopathy.

Science.gov (United States)

Wabulya, Angela; Lesser, Ronald P; Llinas, Rafael; Kaplan, Peter W

2016-04-01

Using electroencephalography (EEG) and histology in patients with diffuse encephalopathy, Gloor et al reported that paroxysmal synchronous discharges (PSDs) on EEG required combined cortical gray (CG) and "subcortical" gray (SCG) matter pathology, while polymorphic delta activity (PDA) occurred in patients with white matter pathology. In patients with encephalopathy, we compared EEG findings and magnetic resonance imaging (MRI) to determine if MRI reflected similar pathological EEG correlations. Retrospective case control study of 52 cases with EEG evidence of encephalopathy and 50 controls without evidence of encephalopathy. Review of clinical, EEG and MRI data acquired within 4 days of each other. The most common EEG finding in encephalopathy was background slowing, in 96.1%. We found PSDs in 0% of cases with the combination of CG and SCG abnormalities. Although 13.5% (n=7) had PSDs on EEG; 3 of these had CG and 4 had SCG abnormalities. A total of 73.1% (38/52) had white matter abnormalities-of these 28.9% (11/38) had PDA. PSDs were found with either CG or "SCG" MRI abnormalities and did not require a combination of the two. In agreement with Gloor et al, PDA occurred with white matter MRI abnormalities in the absence of gray matter abnormalities. © EEG and Clinical Neuroscience Society (ECNS) 2015.

Management and investigation of neonatal encephalopathy: 2017 update

Science.gov (United States)

Martinello, Kathryn; Hart, Anthony R; Yap, Sufin; Mitra, Subhabrata

2017-01-01

This review discusses an approach to determining the cause of neonatal encephalopathy, as well as current evidence on resuscitation and subsequent management of hypoxic-ischaemic encephalopathy (HIE). Encephalopathy in neonates can be due to varied aetiologies in addition to hypoxic-ischaemia. A combination of careful history, examination and the judicious use of investigations can help determine the cause. Over the last 7 years, infants with moderate to severe HIE have benefited from the introduction of routine therapeutic hypothermia; the number needed to treat for an additional beneficial outcome is 7 (95% CI 5 to 10). More recent research has focused on optimal resuscitation practices for babies with cardiorespiratory depression, such as delayed cord clamping after establishment of ventilation and resuscitation in air. Around a quarter of infants with asystole at 10 min after birth who are subsequently cooled have normal outcomes, suggesting that individualised decision making on stopping resuscitation is needed, based on access to intensive treatment unit and early cooling. The full benefit of cooling appears to have been exploited in our current treatment protocols of 72 hours at 33.5°C; deeper and longer cooling showed adverse outcome. The challenge over the next 5–10 years will be to assess which adjunct therapies are safe and optimise hypothermic brain protection in phase I and phase II trials. Optimal care may require tailoring treatments according to gender, genetic risk, injury severity and inflammatory status. PMID:28389438

STXBP1 encephalopathy

DEFF Research Database (Denmark)

Stamberger, Hannah; Nikanorova, Marina; Willemsen, Marjolein H

2016-01-01

OBJECTIVE: To give a comprehensive overview of the phenotypic and genetic spectrum of STXBP1 encephalopathy (STXBP1-E) by systematically reviewing newly diagnosed and previously reported patients. METHODS: We recruited newly diagnosed patients with STXBP1 mutations through an international networ......, and the degree of ID. Accordingly, we hypothesize that seizure severity and ID present 2 independent dimensions of the STXBP1-E phenotype. STXBP1-E may be conceptualized as a complex neurodevelopmental disorder rather than a primary epileptic encephalopathy....

Human transmissible spongiform encephalopathies in eleven countries: Diagnostic pattern across time, 1993-2002

NARCIS (Netherlands)

J. de Pedro-Cuesta (Jesús); M. Glatzel (Markus); J. Almazán (Javier); K. Stoeck (Katharina); V. Mellina (Vittorio); M. Puopolo (Maria); M. Pocchiari (Maurizio); I. Zerr (Inga); H.A. Kretszchmar (Hans); J-P. Brandel (Jean-Philippe); N. Delasnerie-Laupretre (Nicole); A. Alperovitch (Annick); C.M. van Duijn (Cornelia); P. Sanchez-Juan (Pascual); S.J. Collins (Steven); V. Lewis (Victoria); G.H. Jansen (Gerard); M.B. Coulthart (Michael); E. Gelpi (Ellen); H. Budka (Herbert); E. Mitrová (Eva)

2006-01-01

textabstractBackground: The objective of this study was to describe the diagnostic panorama of human transmissible spongiform encephalopathies across 11 countries. Methods: From data collected for surveillance purposes, we describe annual proportions of deaths due to different human transmissible

Malnutrition-induced Wernicke's encephalopathy following a water-only fasting diet.

Science.gov (United States)

Hutcheon, Deborah A

2015-02-01

Wernicke's encephalopathy is a critical condition of neurological dysfunction resulting from a deficiency in thiamine. Chronic alcoholism is recognized as the most common cause of Wernicke's encephalopathy, but other causes, including fasting/starvation and malnutrition, have been documented within the scientific literature. These causes may not be readily recognized by healthcare professionals and may lead to Wernicke's encephalopathy being overlooked as a diagnosis when a nonalcoholic patient presents with classic signs and symptoms of the disorder. A narrative review of thiamine and its relationship to the development, diagnosis, and treatment of Wernicke's encephalopathy is presented based on a review of evidence-based guidelines and published research. To heighten awareness of the development of Wernicke's encephalopathy in fasted/starved and malnourished patients and to contribute to the scientific body of knowledge for the identification and management of Wernicke's encephalopathy in these patients, the clinical course and treatment of an adult woman who developed Wernicke's encephalopathy following a 40-day water-only fasting diet is outlined. Clinical suspicion was required to identify the patient's condition and initiate immediate intervention through parenteral thiamine administration. Oral thiamine supplementation of 100 to 800 mg per day for 6 months was required to aid recovery. The patient's clinical course and response to treatment illustrate the necessity for clinical awareness and suspicion of Wernicke's encephalopathy among healthcare professionals, timely and adequate parenteral thiamine administration, and oral thiamine supplementation at therapeutic doses to correct the nutrient deficiency, halt the progression of Wernicke's encephalopathy, and promote recovery. © 2014 American Society for Parenteral and Enteral Nutrition.

Transient widespread cortical and splenial lesions in acute encephalitis/encephalopathy associated with primary Epstein–Barr virus infection

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Shuo Zhang

2016-01-01

Full Text Available Infection with Epstein–Barr virus (EBV is very common and usually occurs in childhood or early adulthood. Encephalitis/encephalopathy is an uncommon but serious neurological complication of EBV. A case of EBV-associated encephalitis/encephalopathy with involvement of reversible widespread cortical and splenial lesions is presented herein. An 8-year-old Chinese girl who presented with fever and headache, followed by seizures and drowsiness, was admitted to the hospital. Magnetic resonance imaging revealed high signal intensities on diffusion-weighted imaging in widespread cortical and splenial lesions. The clinical and laboratory examination results together with the unusual radiology findings suggested acute encephalitis/encephalopathy due to primary EBV infection. After methylprednisolone pulse therapy together with ganciclovir, the patient made a full recovery without any brain lesions. The hallmark clinical–radiological features of this patient included severe encephalitis/encephalopathy at onset, the prompt and complete recovery, and rapidly reversible widespread involvement of the cortex and splenium. Patients with EBV encephalitis/encephalopathy who have multiple lesions, even with the widespread involvement of cortex and splenium of the corpus callosum, may have a favorable outcome with complete disappearance of all brain lesions.

Bovine Spongiform Encephalopathy (BSE), or Mad Cow Disease

Science.gov (United States)

... the CDC Bovine Spongiform Encephalopathy (BSE), or Mad Cow Disease Note: Javascript is disabled or is not ... spongiform encephalopathy) is a progressive neurological disorder of cattle that results from infection by an unusual transmissible ...

Intrahepatic portal-hepatic venous shunt diagnosed by ultrasonography and computed tomography. Report of two cases

Energy Technology Data Exchange (ETDEWEB)

Shinagawa, Takashi; Iino, Yasuo; Ukaji, Haruyasu; Ishizuka, Masaharu

1986-02-01

Two cases of intrahepatic portal-hepatic venous shunt found by ultrasonography and computed tomography are reported. The first case came to the hospital because of hematuria. A large shunt between the portal vein and the hepatic vein was demonstrated by ultrasonography done for screening, and confirmed by percutaneous transhepatic portography (PTP). The second case was admitted because of cholelithiasis. Computed tomography with contrast enhancement revealed a dilated portal vein in the upper portion of the right lobe. It was subsequently shown by PTP to be a portal-hepatic venous shunt. Portal vein pressure and histological finding of the liver were normal in both cases. The etiology of the shunt was thought to be congenital in these cases for lack of liver disease, portal hypertension and history of trauma. Both cases had no history of hepatic encephalopathy and did not show any symptom attributable to the shunt.

Cerebral CT appearances of toxic encephalopathy of tetramine

International Nuclear Information System (INIS)

Zheng Wenlong; Wu Aiqin; Xu Chongyong; Ying Binyu; Hong Ruizhen

2003-01-01

Objective: To investigate the cerebral CT appearances of toxic encephalopathy of tetramine and improve the recognition on this disease. Methods: Four cases of toxic encephalopathy of tetramine were collected and their cerebral CT appearances were retrospectively analyzed. Results: Cerebral CT appearances in acute phase (within 8 days): (1) cerebral edema in different degree. CT abnormalities consisted of cortical hypodensities and complete loss of gray-white matter differentiation. The CT value were in 11-13 HU, and to be watery density in serious case, (2) subarachnoid hemorrhage. It demonstrated the signs of poisoning hypoxic ischemic encephalopathy in chronic phase. Conclusion: The cerebral CT appearances of toxic encephalopathy of tetramine had some character in acute phase and it can predict the serious degree of intoxication, but there was no characteristic findings in chronic phase

Hypertensive encephalopathy in a patient with neonatal thyrotoxicosis

NARCIS (Netherlands)

Pijnenburg, MWH; Zweens, MJ; Bink, MTE; Odink, RJ

1999-01-01

Neonatal hyperthyroidism may give rise to serious cardiovascular complications. A girl with severe thyrotoxicosis in whom hypertensive encephalopathy developed is described. Conclusion Neonatal thyrotoxicosis can give rise to hypertension and may lead to hypertensive encephalopathy.

Molecular & Genetic Investigation of Tau in Chronic Traumatic Encephalopathy

Science.gov (United States)

2015-10-01

AWARD NUMBER: W81XWH-14-1-0399 TITLE: Molecular & Genetic Investigation of Tau in Chronic Traumatic Encephalopathy PRINCIPAL INVESTIGATOR: John F...Include area code) October 2015 Annual Report 30 Sep 2014 - 29 Sep 2015 Molecular & Genetic Investigation of Tau in Chronic Traumatic Encephalopathy John... encephalopathy (CTE), but the underlying molecular changes remain unclear. Here, biochemical and genetic studies that deepen our understanding of the

Vegetable versus animal protein diet in cirrhotic patients with chronic encephalopathy. A randomized cross-over comparison.

Science.gov (United States)

Bianchi, G P; Marchesini, G; Fabbri, A; Rondelli, A; Bugianesi, E; Zoli, M; Pisi, E

1993-05-01

In a randomized cross-over comparison, the effects of a mainly vegetable protein diet were compared with an animal protein diet in eight patients with cirrhosis and chronic permanent encephalopathy, under optimum lactulose therapy. After a run-in period, patients were fed two equi-caloric, equi-nitrogenous diets for 7 days (71 g total proteins), containing either 50 g protein of animal origin or 50 g vegetable proteins. In the last 3 days of each period, nitrogen balance was significantly better during the vegetable protein diet (+0.2 (SD 1.4) g vs. -1.7 (2.4); P vegetable proteins, whereas insulin, plasma amino acids and ammonia were lower. The clinical grading of encephalopathy improved slightly on vegetable proteins, and psychometric tests improved significantly, but remained grossly abnormal. Compliance to dietary manipulation was good. The data prove that a mainly vegetable protein diet is worthwhile in cirrhotic patients with chronic encephalopathy under optimum lactulose therapy. Improved nitrogen balance may be related to more effective nitrogen use for protein synthesis, probably due to blunted hormonal response, and largely outweighs the effects on encephalopathy.

Wernicke's encephalopathy as a complication of gastroparesis after ...

African Journals Online (AJOL)

Wernicke's encephalopathy is a common complication of malnutrition, alcohol abuse and gastric outlet obstruction. We describe a patient who developed Wernicke's encephalopathy secondary to gastroparesis, with no significant evidence of malnutrition, alcohol abuse, or gastric outlet obstruction.

Genetics Home Reference: STXBP1 encephalopathy with epilepsy

Science.gov (United States)

... Resources (8 links) Boston Children's Hospital: Epilepsy and Seizure Disorder in Children Centers for Disease Control and Prevention: ... stxbp1 encephalopathy with epilepsy Merck Manual Consumer Version: Seizure Disorders Orphanet: Early infantile epileptic encephalopathy Patient Support and ...

Reversible dementia with psychosis: Hashimoto's encephalopathy.

Science.gov (United States)

Mocellin, Ramon; Lubman, Dan I; Lloyd, John; Tomlinson, E Bruce; Velakoulis, Dennis

2006-12-01

A case of presumed Hashimoto's encephalopathy (HE) is presented. The presentation included memory loss, delusions, functional decline and culminated in a generalized seizure. Anti-thyroid antibodies were detected and symptoms resolved with prednisolone. Patients with HE may present with prominent neuropsychiatric symptoms, attract psychiatric diagnoses and present to psychiatric services. Primarily a diagnosis of exclusion, HE should be considered in cases of encephalopathy in which standard investigations are negative.

[Follow-up of newborns with hypoxic-ischaemic encephalopathy].

Science.gov (United States)

Martínez-Biarge, M; Blanco, D; García-Alix, A; Salas, S

2014-07-01

Hypothermia treatment for newborn infants with hypoxic-ischemic encephalopathy reduces the number of neonates who die or have permanent neurological deficits. Although this therapy is now standard of care, neonatal hypoxic-ischaemic encephalopathy still has a significant impact on the child's neurodevelopment and quality of life. Infants with hypoxic-ischaemic encephalopathy should be enrolled in multidisciplinary follow-up programs in order to detect impairments, to initiate early intervention, and to provide counselling and support for families. This article describes the main neurodevelopmental outcomes after term neonatal hypoxic-ischaemic encephalopathy. We offer recommendations for follow-up based on the infant's clinical condition and other prognostic indicators, mainly neonatal neuroimaging. Other aspects, such as palliative care and medico-legal issues, are also briefly discussed. Copyright © 2013 Asociación Española de Pediatría. Published by Elsevier Espana. All rights reserved.

Wernicke’s encephalopathy following hyperemesis gravidarum

Directory of Open Access Journals (Sweden)

Leila Pourali

2016-06-01

Full Text Available Background: ″Wernicke’s Korsakoff″ syndrome is the most important complication of severe thiamine deficiency. The term refers to two different syndromes, each representing a different stage of the disease. Wernicke’s encephalopathy (WE is an acute syndrome requiring emergent treatment to prevent death and neurologic morbidity. Korsakoff syndrome (KS refers to a chronic neurologic condition that usually occurs as a consequence of WE. It is a rare complication of hyperemesis gravidarum that confusion, ocular signs, and gait ataxia are the most prevalent symptoms, respectively. Typical brain lesions of wernicke’s encephalopathy (WE are observed at autopsy in 0.4 to 2.8 percent of the general population in the western world and the majority of affected patients are alcoholic. The prevalence of wernicke’s encephalopathy lesions seen on autopsy was 12.5% of alcohol abusers in one report. Among those who with alcohol-related death, it has been reported to be even higher, 29 to 59%. The aim of this study was to report a case of wernicke’s encephalopathy following hyperemesis gravidarum. Case Presentation: A 28-year-old-pregnant woman in 19th weeks of gestation referred to the hospital with hyperemesis, gait ataxia, and dysarthria before that she had hyperemesis gravidarum with weight loss and unresponsive to outpatient and inpatient medical therapy. MRI showed hyperdense lesion around thalamus which was characteristic of wernicke’s encephalopathy. Rapid improvement in patient’s condition occurred after high dose thiamine infusion. Conclusion: In hyperemesis gravidarum, presence of either symptoms of ocular or mental disorder or ataxia must be considered to rule out and appropriate treatment of Wernicke’s syndrome which can cause maternal and fetal death.

The Frequency and Severity of Magnetic Resonance Imaging Abnormalities in Infants with Mild Neonatal Encephalopathy.

Science.gov (United States)

Walsh, Brian H; Neil, Jeffrey; Morey, JoAnn; Yang, Edward; Silvera, Michelle V; Inder, Terrie E; Ortinau, Cynthia

2017-08-01

To assess and contrast the incidence and severity of abnormalities on cerebral magnetic resonance imaging (MRI) between infants with mild, moderate, and severe neonatal encephalopathy who received therapeutic hypothermia. This retrospective cohort studied infants with mild, moderate, and severe neonatal encephalopathy who received therapeutic hypothermia at a single tertiary neonatal intensive care unit between 2013 and 2015. Two neuroradiologists masked to the clinical condition evaluated brain MRIs for cerebral injury after therapeutic hypothermia using the Barkovich classification system. Additional abnormalities not included in this classification system were also noted. The rate, pattern, and severity of abnormalities/injury were compared across the grades of neonatal encephalopathy. Eighty-nine infants received therapeutic hypothermia and met study criteria, 48 with mild neonatal encephalopathy, 35 with moderate neonatal encephalopathy, and 6 with severe neonatal encephalopathy. Forty-eight infants (54%) had an abnormality on MRI. There was no difference in the rate of overall MRI abnormalities by grade of neonatal encephalopathy (mild neonatal encephalopathy 54%, moderate neonatal encephalopathy 54%, and severe neonatal encephalopathy 50%; P= .89). Basal ganglia/thalamic injury was more common in those with severe neonatal encephalopathy (mild neonatal encephalopathy 4%, moderate neonatal encephalopathy 9%, severe neonatal encephalopathy 34%; P = .03). In contrast, watershed injury did not differ between neonatal encephalopathy grades (mild neonatal encephalopathy 36%, moderate neonatal encephalopathy 32%, severe neonatal encephalopathy 50%; P = .3). Mild neonatal encephalopathy is commonly associated with MRI abnormalities after therapeutic hypothermia. The grade of neonatal encephalopathy during the first hours of life may not discriminate adequately between infants with and without cerebral injury noted on MRI after therapeutic hypothermia

Hemolytic Uremic Syndrome-associated Encephalopathy Successfully Treated with Corticosteroids.

Science.gov (United States)

Hosaka, Takashi; Nakamagoe, Kiyotaka; Tamaoka, Akira

2017-11-01

The encephalopathy that occurs in association with hemolytic uremic syndrome (HUS), which is caused by enterohemorrhagic Escherichia coli (E. coli), has a high mortality rate and patients sometimes present sequelae. We herein describe the case of a 20-year-old woman who developed encephalopathy during the convalescent stage of HUS caused by E.coli O26. Hyperintense lesions were detected in the pons, basal ganglia, and cortex on diffusion-weighted brain MRI. From the onset of HUS encephalopathy, we treated the patient with methylprednisolone (mPSL) pulse therapy alone. Her condition improved, and she did not present sequelae. Our study shows that corticosteroids appear to be effective for the treatment of some patients with HUS encephalopathy.

CT diagnosis of hypoxic ischemic encephalopathy

International Nuclear Information System (INIS)

Zhao Xiang; Ma Jiwei; Wu Lide

2004-01-01

Objective: To explore CT characteristics of hypoxic ischemic encephalopathy (HIE), and to improve the accuracy of CT diagnosis. Methods: 50 cases of neonatal asphyxia in perinatal period diagnosed as hypoxic ischemic encephalopathy by CT was analyzed. Results: The main manifestation of hypoxic ischemic encephalopathy is cerebral edema and intracranial hemorrhage. Focal or diffuse hypo-dense lesion and hyper-dense area in various location and morphology were seen on CT images. (1) Localized diffuse hypo-dense area in 1 or 2 cerebral lobe were found in 17 cases, and the lesions were localized in frontal lobe (n=6), in frontotemporal lobe (n=5), and in temporo-occipital lobe (n=6). (2) Hypo-density region involving more than three cerebral lobes were found in 18 cases, and abnormalities were found in frontotemporal and parietal lobe (n=8), accompanying with subarachnoid hemorrhage (n=2); in frontal, temporal and occipital lobe (n=6), in which cerebral hemorrhage was complicated (n=1); and in other cerebral lobe (n=4). (3) Diffuse low-density region in all cerebral lobe were found in 15 cases, in which subarachnoid hemorrhage was complicated in 4 cases, and ventricular hemorrhage was found in 2 case. Conclusion: CT imaging plays an important role in diagnosis of hypoxic ischemic encephalopathy and has shown its clinical value

Characteristics, risk factors, and mortality of cirrhotic patients hospitalized for hepatic encephalopathy with and without acute-on-chronic liver failure (ACLF).

Science.gov (United States)

Cordoba, Juan; Ventura-Cots, Meritxell; Simón-Talero, Macarena; Amorós, Àlex; Pavesi, Marco; Vilstrup, Hendrik; Angeli, Paolo; Domenicali, Marco; Ginés, Pere; Bernardi, Mauro; Arroyo, Vicente

2014-02-01

In spite of the high incidence of hepatic encephalopathy (HE) in cirrhosis, there are few observational studies. We performed an analysis to define the characteristics of HE and associated features using the database of the Canonic Study. Clinical, laboratory and survival data of 1348 consecutive cirrhotic patients admitted with an acute decompensation were compared according to the presence (n=406) or absence of HE and of acute-on-chronic liver failure (ACLF) (n=301). HE development was independently associated with previous HE episodes; survival probabilities worsen in relation to the presence and grade of HE. There were marked differences between HE associated (n=174) and not associated (n=286) to ACLF. HE not associated with ACLF occurred in older cirrhotics, inactive drinkers, without severe liver failure or systemic inflammatory reaction and in relation to diuretic use. In contrast, HE associated with ACLF occurred in younger cirrhotics, more frequently alcoholics, with severe liver failure and systemic inflammatory reaction, and in relation to bacterial infections, active alcoholism and/or dilutional hyponatremia. Prognosis was relatively preserved in the first and extremely poor in the second group. Independent risk factors of mortality in patients with HE were age, bilirubin, INR, creatinine, sodium, and HE grade. In cirrhosis, previous HE identifies a subgroup of patients that is especially vulnerable for developing new episodes of HE. The course of HE appears to be different according to the presence of ACLF. Copyright © 2013 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

Potentially modifiable factors contributing to sepsis-associated encephalopathy.

Science.gov (United States)

Sonneville, Romain; de Montmollin, Etienne; Poujade, Julien; Garrouste-Orgeas, Maïté; Souweine, Bertrand; Darmon, Michael; Mariotte, Eric; Argaud, Laurent; Barbier, François; Goldgran-Toledano, Dany; Marcotte, Guillaume; Dumenil, Anne-Sylvie; Jamali, Samir; Lacave, Guillaume; Ruckly, Stéphane; Mourvillier, Bruno; Timsit, Jean-François

2017-08-01

Identifying modifiable factors for sepsis-associated encephalopathy may help improve patient care and outcomes. We conducted a retrospective analysis of a prospective multicenter database. Sepsis-associated encephalopathy (SAE) was defined by a score on the Glasgow coma scale (GCS) sepsis at ICU admission, of whom 1341 (53%) had sepsis-associated encephalopathy. After adjusting for baseline characteristics, site of infection, and type of admission, the following factors remained independently associated with sepsis-associated encephalopathy: acute renal failure [adjusted odds ratio (aOR) = 1.41, 95% confidence interval (CI) 1.19-1.67], hypoglycemia 10 mmol/l (aOR = 1.37, 95% CI 1.09-1.72), hypercapnia >45 mmHg (aOR = 1.91, 95% CI 1.53-2.38), hypernatremia >145 mmol/l (aOR = 2.30, 95% CI 1.48-3.57), and S. aureus (aOR = 1.54, 95% CI 1.05-2.25). Sepsis-associated encephalopathy was associated with higher mortality, higher use of ICU resources, and longer hospital stay. After adjusting for age, comorbidities, year of admission, and non-neurological SOFA score, even mild alteration of mental status (i.e., a score on the GCS of 13-14) remained independently associated with mortality (adjusted hazard ratio = 1.38, 95% CI 1.09-1.76). Acute renal failure and common metabolic disturbances represent potentially modifiable factors contributing to sepsis-associated encephalopathy. However, a true causal relationship has yet to be demonstrated. Our study confirms the prognostic significance of mild alteration of mental status in patients with sepsis.

Minimal hepatic encephalopathy in children with liver cirrhosis: diffusion-weighted MR imaging and proton MR spectroscopy of the brain

Energy Technology Data Exchange (ETDEWEB)

Abdel Razek, Ahmed Abdel Khalek; Ezzat, Amany [Mansoura University Hospital, Department of Diagnostic Radiology, Mansoura Faculty of Medicine, Mansoura (Egypt); Abdalla, Ahmed; Megahed, Ahmed; Barakat, Tarek [Mansoura Children Hospital, Gastroenterology and Hepatology Unit, Mansoura Faculty of Medicine, Mansoura (Egypt)

2014-10-15

The aim of this work was to detect minimal hepatic encephalopathy (minHE) in children with diffusion-weighted MR imaging (DWI) and proton magnetic resonance spectroscopy ({sup 1}H-MRS) of the brain. Prospective study conducted upon 30 consecutive children (age range 6-16 years, 21 boys and 9 girls) with liver cirrhosis and 15 age- and sex-matched healthy control children. Patients with minHE (n = 17) and with no minHE (n = 13) groups and control group underwent DWI, {sup 1}H-MRS, and neuropsychological tests (NPTs). The glutamate or glutamine (Glx), myoinositol (mI), choline (Cho), and creatine (Cr) at the right ganglionic region were determined at {sup 1}H-MRS. The apparent diffusion coefficient (ADC) value and metabolic ratios of Glx/Cr, mI/Cr, and Cho/Cr were calculated. There was elevated ADC value and Glx/Cr and decreased mI/CI and Ch/Cr in patients with minHE compared to no minHE and control group. There was significant difference between minHE, no minHE, and control group in the ADC value (P = 0.001 for all groups), GLx/Cr (P = 0.001 for all groups), mI/Cr (P = 0.004, 0.001, and 0.001, respectively), Ch/Cr (P = 0.001 for all groups), and full-scale IQ of NPT (P = 0.001, 0.001, and 0.143, respectively). The NPT of minHE had negative correlation with ADC value (r = -0.872, P = 0.001) and GLx/Cr (r = -0.812, P = 0.001) and positive correlation with mI/Cr (r = 0.732, P = 0.001). DWI and {sup 1}H-MRS are imaging modalities that can detect minHE in children with liver cirrhosis and correlate well with parameters of NPT. (orig.)

Minimal hepatic encephalopathy in children with liver cirrhosis: diffusion-weighted MR imaging and proton MR spectroscopy of the brain

International Nuclear Information System (INIS)

Abdel Razek, Ahmed Abdel Khalek; Ezzat, Amany; Abdalla, Ahmed; Megahed, Ahmed; Barakat, Tarek

2014-01-01

The aim of this work was to detect minimal hepatic encephalopathy (minHE) in children with diffusion-weighted MR imaging (DWI) and proton magnetic resonance spectroscopy ( 1 H-MRS) of the brain. Prospective study conducted upon 30 consecutive children (age range 6-16 years, 21 boys and 9 girls) with liver cirrhosis and 15 age- and sex-matched healthy control children. Patients with minHE (n = 17) and with no minHE (n = 13) groups and control group underwent DWI, 1 H-MRS, and neuropsychological tests (NPTs). The glutamate or glutamine (Glx), myoinositol (mI), choline (Cho), and creatine (Cr) at the right ganglionic region were determined at 1 H-MRS. The apparent diffusion coefficient (ADC) value and metabolic ratios of Glx/Cr, mI/Cr, and Cho/Cr were calculated. There was elevated ADC value and Glx/Cr and decreased mI/CI and Ch/Cr in patients with minHE compared to no minHE and control group. There was significant difference between minHE, no minHE, and control group in the ADC value (P = 0.001 for all groups), GLx/Cr (P = 0.001 for all groups), mI/Cr (P = 0.004, 0.001, and 0.001, respectively), Ch/Cr (P = 0.001 for all groups), and full-scale IQ of NPT (P = 0.001, 0.001, and 0.143, respectively). The NPT of minHE had negative correlation with ADC value (r = -0.872, P = 0.001) and GLx/Cr (r = -0.812, P = 0.001) and positive correlation with mI/Cr (r = 0.732, P = 0.001). DWI and 1 H-MRS are imaging modalities that can detect minHE in children with liver cirrhosis and correlate well with parameters of NPT. (orig.)

The GABAA receptor complex in hepatic encephalopathy. Autoradiographic evidence for the presence of elevated levels of a benzodiazepine receptor ligand

Energy Technology Data Exchange (ETDEWEB)

Basile, A.S.; Ostrowski, N.L.; Gammal, S.H.; Jones, E.A.; Skolnick, P. (National Institutes of Health, Bethesda, MD (USA))

1990-02-01

Autoradiographic analysis was used to examine radioligand binding to benzodiazepine (BZ) and GABAA receptors in the brains of rabbits with hepatic encephalopathy (HE). Thin sections of whole brain from normal rabbits and rabbits with HE were mounted on slides and subdivided into two groups. One group was washed before incubation with radioligand, while the second group was not prewashed. (3H)Flunitrazepam binding to BZ receptors was decreased by 22% to 42% (p less than 0.05) in the cerebral cortex, superior and inferior colliculi, and cerebellum of unwashed sections from rabbits with HE compared to all other groups. The binding of (3H)Ro 15-1788 to unwashed sections from rabbits with HE was reduced by a similar degree (18% to 37%, p less than 0.05) in the cerebral cortex, hippocampus, superior colliculus, and cerebellar cortex. Incubation of sections with the GABA-mimetic muscimol and NaCl produced an additional decrease in (3H)flunitrazepam binding to the cortex and hippocampus (25% to 31%, p less than 0.05) in unwashed HE rabbit brain, but increased radioligand binding (27% to 71%, p less than 0.05) to several regions in control rabbits. No changes in radioligand binding to either GABAA or peripheral benzodiazepine receptors was observed between HE and control rabbit sections. These findings are consistent with previous electrophysiologic and neurochemical observations indicating no significant changes in either the function or density of GABAA or BZ receptors in this model of HE. Further, they indicate that a reversible BZ receptor ligand with agonist properties is present in the brain in HE. This substance may contribute to the enhancement of GABAergic tone observed in this syndrome.

Dengue viral infections as a cause of encephalopathy

Directory of Open Access Journals (Sweden)

Malavige G

2007-01-01

Full Text Available The aim of this study was to determine the clinical characteristics and poor prognostic factors associated with high mortality in dengue encephalopathy. Fifteen patients with confirmed dengue infections, who developed encephalopathy, were recruited from two tertiary care hospitals in Colombo, Sri Lanka. Among the factors that contributed to encephalopathy were: Acute liver failure (73%, electrolyte imbalances (80% and shock (40%. Five (33.3% patients developed seizures. Disseminated intravascular coagulation was seen in five (33.3%. Secondary bacterial infections were observed in 8 (53.3% of our patients. The overall mortality rate was 47%.

Arterial hypoxaemia in cirrhosis: fact or fiction?

DEFF Research Database (Denmark)

Møller, S; Hillingsø, J; Christensen, E

1998-01-01

characteristics. PATIENTS: One hundred and forty two patients with cirrhosis without significant hepatic encephalopathy (grades 0-I) (41 patients in Child class A, 57 in class B, and 44 in class C) and 21 patients with hepatic encephalopathy. RESULTS: Mean Po2 in kPa was 11.3 in Child class A, 10.8 in class B, 10...... resistance, and a low indocyanine green clearance (p hepatic dysfunction. Arterial hypoxaemia in patients with cirrhosis of differing.......6 in class C, and 10.6 in patients with encephalopathy (p C, and in patients with encephalopathy (p

Arterial hypoxaemia in cirrhosis

DEFF Research Database (Denmark)

Møller, S; Hillingsø, Jens; Christensen, E

1998-01-01

characteristics. PATIENTS: One hundred and forty two patients with cirrhosis without significant hepatic encephalopathy (grades 0-I) (41 patients in Child class A, 57 in class B, and 44 in class C) and 21 patients with hepatic encephalopathy. RESULTS: Mean Po2 in kPa was 11.3 in Child class A, 10.8 in class B, 10...... resistance, and a low indocyanine green clearance (p hepatic dysfunction. Arterial hypoxaemia in patients with cirrhosis of differing.......6 in class C, and 10.6 in patients with encephalopathy (p C, and in patients with encephalopathy (p

Topiramate increases the risk of valproic acid-induced encephalopathy.

Science.gov (United States)

Noh, Young; Kim, Dong Wook; Chu, Kon; Lee, Soon-Tae; Jung, Keun-Hwa; Moon, Hye-Jin; Lee, Sang Kun

2013-01-01

Metabolic encephalopathy is a rare but serious complication of valproic acid (VPA) therapy that usually presents with impaired consciousness or increased seizure frequency. Although it has been suggested that topiramate (TPM) increases the risk of VPA-induced encephalopathy, the additional risk in patients receiving TPM therapy has not been evaluated. We reviewed all adult patients who took VPA between January 2005 and February 2009 at the Seoul National University Hospital and identified patients with VPA-induced encephalopathy based on clinical and electroencephalography (EEG) data. Information on sex, age, serum ammonia level, serum VPA level, liver function test, and EEG was collected from patient registry and medical data. We enrolled 8,372 patients who received VPA therapy and 1,236 patients who received VPA/TPM combination therapy. We identified 11 patients with VPA-induced encephalopathy (0.13%), 7 of whom received a combination therapy of VPA and TPM. The odds ratio of VPA-induced encephalopathy with TPM over that without TPM was 10.16. There were no significant differences in sex distribution, number of antiepileptic agents, ammonia level, VPA serum level, underlying diseases, dosage of VPA, duration of VPA treatment, treatment of encephalopathy, and outcomes between the two groups. Our study showed that the prevalence of VPA-induced encephalopathy is approximately 0.1% among patients treated with VPA and that the risk of this condition, although still low, can increase by approximately 10 times in the presence of TPM therapy. Based on these results, we suggest that TPM should be carefully used in patients receiving VPA treatment. Wiley Periodicals, Inc. © 2012 International League Against Epilepsy.

Wernicke encephalopathy in children and adolescents.

Science.gov (United States)

Lallas, Matt; Desai, Jay

2014-11-01

Wernicke encephalopathy is caused by thiamine (vitamin B1) deficiency. It is generally considered to be a disease of adult alcoholics. However, it is known to occur in the pediatric population and in non-alcoholic conditions. We searched PubMed with the key words Wernicke, thiamine, pediatric, children and adolescents and selected publications that were deemed appropriate. The global prevalence rates of hunger, poverty and resultant nutrient deprivation have decreased in the 21st century. However, several scenarios which may predispose to Wernicke encephalopathy may be increasingly prevalent in children and adolescents such as malignancies, intensive care unit stays and surgical procedures for the treatment of obesity. Other predisposing conditions include magnesium deficiency and defects in the SLC19A3 gene causing thiamine transporter-2 deficiency. The classic triad consists of encephalopathy, oculomotor dysfunction and gait ataxia but is not seen in a majority of patients. Treatment should be instituted immediately when the diagnosis is suspected clinically without waiting for laboratory confirmation. Common magnetic resonance findings include symmetric T2 hyperintensities in dorsal medial thalamus, mammillary bodies, periaqueductal gray matter, and tectal plate. Wernicke encephalopathy is a medical emergency. Delay in its recognition and treatment may lead to significant morbidity, irreversible neurological damage or even death. This article aims to raise the awareness of this condition among pediatricians.

Genetics Home Reference: familial encephalopathy with neuroserpin inclusion bodies

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... Home Health Conditions FENIB Familial encephalopathy with neuroserpin inclusion bodies Printable PDF Open All Close All Enable ... expand/collapse boxes. Description Familial encephalopathy with neuroserpin inclusion bodies ( FENIB ) is a disorder that causes progressive ...

Effects of hepatic ischemia-reperfusion injury on the blood-brain barrier permeability to [14C] and [13C]sucrose.

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Miah, Mohammad K; Bickel, Ulrich; Mehvar, Reza

2017-12-01

Hepatic encephalopathy that is associated with severe liver failure may compromise the blood-brain barrier (BBB) integrity. However, the effects of less severe liver diseases, in the absence of overt encephalopathy, on the BBB are not well understood. The goal of the current study was to investigate the effects of hepatic ischemia-reperfusion (IR) injury on the BBB tight junction permeability to small, hydrophilic molecules using the widely used [ 14 C]sucrose and recently-proposed alternative [ 13 C]sucrose as markers. Rats were subjected to 20 min of hepatic ischemia or sham surgery, followed by 8 h of reperfusion before administration of a single bolus dose of [ 14 C] or [ 13 C]sucrose and collection of serial (0-30 min) blood and plasma and terminal brain samples. The concentrations of [ 14 C] and [ 13 C]sucrose in the samples were determined by measurement of total radioactivity (nonspecific) and LC-MS/MS (specific), respectively. IR injury significantly increased the blood, plasma, and brain concentrations of both [ 14 C] and [ 13 C]sucrose. However, when the brain concentrations were corrected for their respective area under the blood concentration-time curve, only [ 14 C]sucrose showed significantly higher (30%) BBB permeability values in the IR animals. Because [ 13 C]sucrose is a more specific BBB permeability marker, these data indicate that our animal model of hepatic IR injury does not affect the BBB tight junction permeability to small, hydrophilic molecules. Methodological differences among studies of the effects of liver diseases on the BBB permeability may confound the conclusions of such studies.

Reducing Peripheral Inflammation with Infliximab Reduces Neuroinflammation and Improves Cognition in Rats with Hepatic Encephalopathy

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Dadsetan, Sherry; Balzano, Tiziano; Forteza, Jerónimo; Cabrera-Pastor, Andrea; Taoro-Gonzalez, Lucas; Hernandez-Rabaza, Vicente; Gil-Perotín, Sara; Cubas-Núñez, Laura; García-Verdugo, José-Manuel; Agusti, Ana; Llansola, Marta; Felipo, Vicente

2016-01-01

Inflammation contributes to cognitive impairment in patients with hepatic encephalopathy (HE). However, the process by which peripheral inflammation results in cognitive impairment remains unclear. In animal models, neuroinflammation and altered neurotransmission mediate cognitive impairment. Taking into account these data, we hypothesized that in rats with HE: (1) peripheral inflammation is a main contributor to neuroinflammation; (2) neuroinflammation in hippocampus impairs spatial learning by altering AMPA and/or NMDA receptors membrane expression; (3) reducing peripheral inflammation with infliximab (anti-TNF-a) would improve spatial learning; (4) this would be associated with reduced neuroinflammation and normalization of the membrane expression of glutamate receptors. The aims of this work were to assess these hypotheses. We analyzed in rats with portacaval shunt (PCS) and control rats, treated or not with infliximab: (a) peripheral inflammation by measuring prostaglandin E2, IL10, IL-17, and IL-6; (b) neuroinflammation in hippocampus by analyzing microglial activation and the content of TNF-a and IL-1b; (c) AMPA and NMDA receptors membrane expression in hippocampus; and (d) spatial learning in the Radial and Morris water mazes. We assessed the effects of treatment with infliximab on peripheral inflammation, on neuroinflammation and AMPA and NMDA receptors membrane expression in hippocampus and on spatial learning and memory. PCS rats show increased serum prostaglandin E2, IL-17, and IL-6 and reduced IL-10 levels, indicating increased peripheral inflammation. PCS rats also show microglial activation and increased nuclear NF-kB and expression of TNF-a and IL-1b in hippocampus. This was associated with altered AMPA and NMDA receptors membrane expression in hippocampus and impaired spatial learning and memory in the radial and Morris water maze. Treatment with infliximab reduces peripheral inflammation in PCS rats, normalizing prostaglandin E2, IL-17, IL-6, and

Validation of EncephalApp, Smartphone-Based Stroop Test, for the Diagnosis of Covert Hepatic Encephalopathy.

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Bajaj, Jasmohan S; Heuman, Douglas M; Sterling, Richard K; Sanyal, Arun J; Siddiqui, Muhammad; Matherly, Scott; Luketic, Velimir; Stravitz, R Todd; Fuchs, Michael; Thacker, Leroy R; Gilles, HoChong; White, Melanie B; Unser, Ariel; Hovermale, James; Gavis, Edith; Noble, Nicole A; Wade, James B

2015-10-01

Detection of covert hepatic encephalopathy (CHE) is difficult, but point-of-care testing could increase rates of diagnosis. We aimed to validate the ability of the smartphone app EncephalApp, a streamlined version of Stroop App, to detect CHE. We evaluated face validity, test-retest reliability, and external validity. Patients with cirrhosis (n = 167; 38% with overt HE [OHE]; mean age, 55 years; mean Model for End-Stage Liver Disease score, 12) and controls (n = 114) were each given a paper and pencil cognitive battery (standard) along with EncephalApp. EncephalApp has Off and On states; results measured were OffTime, OnTime, OffTime+OnTime, and number of runs required to complete 5 off and on runs. Thirty-six patients with cirrhosis underwent driving simulation tests, and EncephalApp results were correlated with results. Test-retest reliability was analyzed in a subgroup of patients. The test was performed before and after transjugular intrahepatic portosystemic shunt placement, and before and after correction for hyponatremia, to determine external validity. All patients with cirrhosis performed worse on paper and pencil and EncephalApp tests than controls. Patients with cirrhosis and OHE performed worse than those without OHE. Age-dependent EncephalApp cutoffs (younger or older than 45 years) were set. An OffTime+OnTime value of >190 seconds identified all patients with CHE with an area under the receiver operator characteristic value of 0.91; the area under the receiver operator characteristic value was 0.88 for diagnosis of CHE in those without OHE. EncephalApp times correlated with crashes and illegal turns in driving simulation tests. Test-retest reliability was high (intraclass coefficient, 0.83) among 30 patients retested 1-3 months apart. OffTime+OnTime increased significantly (206 vs 255 seconds, P = .007) among 10 patients retested 33 ± 7 days after transjugular intrahepatic portosystemic shunt placement. OffTime+OnTime decreased significantly (242 vs

The Spectrum of Disease in Chronic Traumatic Encephalopathy

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McKee, Ann C.; Stein, Thor D.; Nowinski, Christopher J.; Stern, Robert A.; Daneshvar, Daniel H.; Alvarez, Victor E.; Lee, Hyo-Soon; Hall, Garth; Wojtowicz, Sydney M.; Baugh, Christine M.; Riley, David O.; Kubilus, Caroline A.; Cormier, Kerry A.; Jacobs, Matthew A.; Martin, Brett R.; Abraham, Carmela R.; Ikezu, Tsuneya; Reichard, Robert Ross; Wolozin, Benjamin L.; Budson, Andrew E.; Goldstein, Lee E.; Kowall, Neil W.; Cantu, Robert C.

2013-01-01

Chronic traumatic encephalopathy is a progressive tauopathy that occurs as a consequence of repetitive mild traumatic brain injury. We analysed post-mortem brains obtained from a cohort of 85 subjects with histories of repetitive mild traumatic brain injury and found evidence of chronic traumatic encephalopathy in 68 subjects: all males, ranging…

Need for early diagnosis of mental and mobility changes in Wernicke encephalopathy.

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Wijnia, Jan W; Oudman, Erik; Bresser, Esmay L; Gerridzen, Ineke J; van de Wiel, Albert; Beuman, Carla; Mulder, Cornelis L

2014-12-01

Korsakoff syndrome is a chronic form of amnesia resulting from thiamine deficiency. The syndrome can develop from unrecognized or undertreated Wernicke encephalopathy. The intra-individual course of Wernicke-Korsakoff syndrome has not been studied extensively, nor has the temporal progression of gait disturbances and other symptoms of Wernicke encephalopathy. Here we present the detailed history of a patient whose acute symptoms of Wernicke encephalopathy were far from stable. We follow his mobility changes and the shifts in his mental status from global confusion and impaired consciousness to more selective cognitive deficits. His Wernicke encephalopathy was missed and left untreated, being labeled as "probable" Korsakoff syndrome. Patients with a history of self-neglect and alcohol abuse, at risk of or suffering with Wernicke encephalopathy, should receive immediate and adequate vitamin replacement. Self-neglecting alcoholics who are bedridden may have severe illness and probably active Wernicke encephalopathy. In these patients, mobility changes, delirium, or impaired consciousness can be an expression of Wernicke encephalopathy, and should be treated to prevent further damage from the neurologic complications of thiamine deficiency.

Hyperintensity of basal ganglia on T{sub 1}-weighted images in patients with liver cirrhosis. Correlation with hepatic encephalopathy and liver function

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Maeda, Hiroko; Kita, Keisuke; Mizobata, Toshiharu; Kimura, Masashi; Sonomura, Tetsuo; Kishi, Kazushi; Tanaka, Kayo; Sato, Morio; Yamada, Ryosaku [Wakayama Medical Coll. (Japan)

1995-04-01

Brain MR imaging was performed in 38 liver cirrhosis (LC) patients and 9 normal volunteers. On T{sub 1}-weighted images, the signal intensity of globus pallidus (S1) and frontal white matter (S2) was measured and S1/S2 ratio was explored. We examined the relationship between S1/S2 ratio and liver function parameters. High signal intensity in bilateral globus pallidus was noted on T{sub 1} W1 in 28 of 38 LC patients. The S1/S2 ratio of 1.186{+-}0.097 in the 38 LC patients was significantly higher than 0.987{+-}0.062 in the 9 normal volunteers (p<0.001), while T{sub 2}-weighted images showed no abnormal intensity. Compared with the LC patients with hepatic encephalopathy (HE) (n=7) and without HE (n=31), the former S1/S2 ratio (1.239{+-}0.057) was significantly higher than the latter (1.174{+-}0.097) (p<0.05). There was a significant correlation between the value of the S1/S2 ratio and deterioration of ICG R{sub 15} (r=0.501, p<0.005), prolongation of prothrombine time (r=-0.392, p<0.05) and decrease of choline esterase (r=-0.336, p<0.05). There was, however, little correlation between the value of the S1/S2 ratio and ammonia and Fisher ratio. In conclusion, there is a significant relationship between high intensity of globus pallidus on T{sub 1}-WI and the degree of liver dysfunction. (author).

77 FR 29914 - Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products

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2012-05-21

... Spongiform Encephalopathy; Importation of Bovines and Bovine Products AGENCY: Animal and Plant Health... derived from bovines with regard to bovine spongiform encephalopathy. This action will allow interested... importation of live bovines and products derived from bovines with regard to bovine spongiform encephalopathy...

Hyperammonemia: What Urea-lly Need to Know: Case Report of Severe Noncirrhotic Hyperammonemic Encephalopathy and Review of the Literature

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Ruby Upadhyay

2016-01-01

Full Text Available Purpose. A 66-year-old man who presented with coma was found to have isolated severe hyperammonemia and diagnosed with a late-onset urea-cycle disorder. He was treated successfully and had full recovery. Methods. We report a novel case of noncirrhotic hyperammonemia and review the literature on this topic. Selected literature for review included English-language articles concerning hyperammonemia using the search terms “hyperammonemic encephalopathy”, “non-cirrhotic encephalopathy”, “hepatic encephalopathy”, “urea-cycle disorders”, “ornithine transcarbamylase (OTC deficiency”, and “fulminant hepatic failure”. Results. A unique case of isolated hyperammonemia diagnosed as late-onset OTC deficiency is presented. Existing evidence about hyperammonemia is organized to address pathophysiology, clinical presentation, diagnosis, and treatment. The case report is discussed in context of the reviewed literature. Conclusion. Late-onset OTC deficiency presenting with severe hyperammonemic encephalopathy and extensive imaging correlate can be fully reversible if recognized promptly and treated aggressively.

Evaluation of the zoonotic potential of transmissible mink encephalopathy

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Successful transmission of Transmissible Mink Encephalopathy (TME) to cattle supports the bovine hypothesis to the still controversial origin of TME outbreaks. Human and primate susceptibility to classical Bovine Spongiform Encephalopathy (c-BSE) and the transmissibility of L-type BSE to macaques as...

Maternal or neonatal infection: association with neonatal encephalopathy outcomes.

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Jenster, Meike; Bonifacio, Sonia L; Ruel, Theodore; Rogers, Elizabeth E; Tam, Emily W; Partridge, John Colin; Barkovich, Anthony James; Ferriero, Donna M; Glass, Hannah C

2014-07-01

Perinatal infection may potentiate brain injury among children born preterm. The objective of this study was to examine whether maternal and/or neonatal infection are associated with adverse outcomes among term neonates with encephalopathy. This study is a cohort study of 258 term newborns with encephalopathy whose clinical records were examined for signs of maternal infection (chorioamnionitis) and infant infection (sepsis). Multivariate regression was used to assess associations between infection, pattern, and severity of injury on neonatal magnetic resonance imaging, as well as neurodevelopment at 30 mo (neuromotor examination, or Bayley Scales of Infant Development, second edition mental development index encephalopathy, chorioamnionitis was associated with a lower risk of brain injury and adverse outcomes, whereas signs of neonatal sepsis carried an elevated risk. The etiology of encephalopathy and timing of infection and its associated inflammatory response may influence whether infection potentiates or mitigates injury in term newborns.