Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatitis E previously known as enterically transmitted non-A, non-B hepatitis, is a self limiting infectious viral disease of developing countries. Various issues regarding the pathogenesis of liver injury and its natural history remain unanswered after two decades of its discovery. A small proportion of patients develop fulminant hepatic failure. Mortality is very high if it is associated with pregnancy, especially during third trimester. After establishment of hepatitis A virus as a cause of decompensation of chronic liver disease, now there are reports that hepatitis E viruses also does the same. Acute hepatitis E in these patients has a protracted course with high morbidity and mortality. Many patients develop hepatorenal syndrome, hepatic encephalopathy and even liver failure after co-infection with hepatitis E virus. Now time has come to institute hepatitis E virus superinfection as one of the cause of acute on chronic liver failure. Hepatitis E is a problem of developing countries and Nepal is in the endemic zone. Sudden decompensation in chronic liver disease patient, who were otherwise stable and under regular follow up, should be carefully dealt with. Patient statistics at our unit shows that 7 cases of chronic liver diseases with superinfection with hepatitis E virus were dealt from April 2004 to August 2005. Two patients (29%) died and 5 recovered. In patients with recovery, there was deterioration of Child-Pugh grading and the duration of hospital stay was longer. Thus, hepatitis E in diagnosed chronic liver disease case should be taken apprehensively. Similarly patients of chronic liver disease traveling to endemic zone should take precaution. If vaccine against hepatitis E virus is developed, chronic liver disease patient would be the eligible candidate for vaccination beside pregnant ladies.
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PMID:Hepatitis E virus infection in chronic liver disease causes rapid decompensation. 1716 Jan

We evaluated the expression of human glucocorticoid receptor beta (hGRbeta) in patients with severe autoimmune hepatitis (AIH). The subjects were 27 patients with AIH, including 6 with severe type (prothrombin time [PT] < 40%) and 21 with non-severe type (PT>40%). Total RNA extracted from peripheral blood mononuclear cells (PBMCs) was reversed using reverse transcriptase. The resultant complementary DNA was amplified by reverse transcription polymerase chain reaction (RT-PCR) using specific primers for hGR alpha and beta. The six patients with severe AIH were female; three presented fulminant hepatic failure with hepatic encephalopathy. In all patients with AIH, hGR a was detected. The incidence of hGR beta expression in patients with non-severe type was 42.9% (9/21) ; it was 100% (6/6) in those with severe type. The positive ratio was significantly higher in severe-type patients. These results suggest that hGR beta expression in PBMCs is a novel predictor of AIH severity.
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PMID:Expression of human glucocorticoid receptor beta of peripheral blood mononuclear cells in patients with severe autoimmune hepatitis. 1742 57

Four hundred and twenty-three patients with chronic diffuse hepatic diseases (hepatitis and viral hepatic cirrhosis) underwent complex clinico-instrumental examination; the control group consisted of 30 healthy individuals. Hepatic encephalopathy syndrome was a much more frequent finding in patients with hepatic cirrhosis. Association of chronic viral hepatic lesion with alcohol abuse increased the frequency of latent central nervous system lesions.
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PMID:[Early symptoms of hepatic encephalopathy in patients with chronic diffuse hepatic diseases]. 1792 93

3 patients with liver failure developed hepatic encephalopathy. 2 patients, men aged 60 and 72 years, had chronic liver disease and presented with episodes of confusion. They recovered after being treated with lactulose. The third patient, a 37-year-old woman, became comatose shortly after the onset of acute liver failure due to acute autoimmune hepatitis. She died before a suitable donor liver became available. Hepatic encephalopathy is a syndrome of potential reversible neurological symptoms. Especially in the early stages of the condition, hepatic encephalopathy can be difficult to diagnose. Patients may present with mild cognitive impairment or episodes characterized by neurological symptoms. Hepatic encephalopathy is a clinical diagnosis. The pathophysiologic mechanism is only partly understood but toxicity of ammonia on the central nervous system seems to be of major importance. Raised ammonia concentrations or EEG findings consistent with metabolic encephalopathy may support but are not essential to the diagnosis. Episodes of hepatic encephalopathy are often elicited by an underlying disease such as infection or gastro-intestinal bleeding. It is important to recognize hepatic encephalopathy in its early stages because adequate treatment of the condition and any underlying disease reduces morbidity and mortality.
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PMID:[Confusion and abnormal liver enzyme levels: problems with diagnosing hepatic encephalopathy]. 1836 Nov 99

Acute hepatitis and hepatic encephalopathy are rare manifestations of dengue haemorrhagic fever (DHF). We report 4 children aged 8 months to 3 y who presented with severe hepatic dysfunction. Three male infants had in addition hepatic encephalopathy and 2 of them succumbed to their disease suggesting that hepatitis with encephalopathy has a very high mortality.
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PMID:Dengue and liver disease. 1860 99

Chronic liver disease results from a variety of causes such as hepatitis virus infections, autoimmune processes and alcohol consumption. Its complications include fat deposition, hemodynamic changes and fibrosis. Clinically there may be progression to portal-hypertension and porto-systemic encephalopathy. Pioneering research from the laboratory of Kunos at NIH has stressed the importance of endocannabinoids (ECs) as mediators of some of the pathological processes in chronic liver disease. The present review summarizes the literature on the association between ECs and liver disease, as well as the therapeutic potential of ECs and exogenous cannabinoids in liver disease with emphasis on hepatic encephalopathy.
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PMID:Endocannabinoids in liver disease and hepatic encephalopathy. 1878 86

In Japan, patients with hepatitis are diagnosed as having fulminant hepatitis and late-onset hepatic failure (LOHF) when grade II or more severe hepatic encephalopathy develops within 8 weeks and between 8 and 24 weeks, respectively, of the disease onset, with a prothrombin time of less than 40% of the standardized value. Fulminant hepatitis patients are classified into the acute and subacute types, in which the encephalopathy occurs within 10 days and later than 11 days, respectively. According to the nation-wide survey by the Intractable Liver Disease Study Group of Japan, liver transplantation was performed in 14% and 26% of the patients with the acute and subacute types, respectively, and in 19% with LOHF between 1998 and 2003. Survival rate of these patients was 77%, which was greater than those of the patients treated without liver transplantation; 54%, 24% and 12% in the acute and subacute types and LOHF, respectively. The indications for liver transplantation in fulminant hepatitis patients are currently determined according to the Guideline of the Acute Liver Failure Study Group of Japan in 1996, which is based on assessment of the prognosis of the patients at the onset of hepatic encephalopathy and reassessed 5 days later. Predictive accuracy of the Guideline, assessed in the patients between 1998 and 2003, were 68% and 78% among the cases with the acute and subacute types, respectively, of fulminant hepatitis. Liver transplantation was considered in most of LOHF patients at 8 or more days before encephalopathy development. Although liver transplantation improved the prognosis of patients with acute liver failure, the Guideline should be modified to improve the accuracy for fulminant hepatitis patients, and the new criteria should be made for LOHF patients.
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PMID:Indication criteria for liver transplantation for acute liver failure in Japan. 1912 53

A 5-year-old male, drowsy, jaundiced child presented with fulminant hepatitis and had HAV and HEV infection. He had hepatic encephalopathy grade 1, fever, pallor, hypotension, crepitations in his right lung base and hepatosplenomegaly with dyspnoea. He had highly raised liver enzymes and hypoalbuminemia (2.8 g/dl) but anemia (hemoglobin of 7.7 g/dl and 5.7 g/dl 2 days later), reticulocytopenia and severe thrombocytopenia (44 x 10(9)/l) were unexplained. Parvovirus B19-specific IgM antibodies and B19 DNA were found in the serum of the child. Chest X-ray showed pleural effusion and bronchopneumonia, while blood culture isolated coagulase-negative staphylococci (BACTEC 9120) and he had low oxygen saturation. Hence, he was treated with IV amoxicillin+ clavulinic acid and oxygen inhalation. He had seizures and cardiac arrest but was revived. On the third day his condition worsened and the child died despite intensive care. Hence it is concluded that his anemia and thrombocytopenia were B19 induced and this might have aggravated or caused fulminant hepatitis.
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PMID:Parvovirus B19-induced thrombocytopenia and anemia in a child with fatal fulminant hepatic failure coinfected with hepatitis A and E viruses. 1920 89

Chronic intake of large quantities of alcohol causes damage to many organs, the liver being the most often affected one. In advanced countries, mortality due to liver diseases is directly proportional to alcohol consumption. 30 g of pure alcohol per day is regarded as a "safe" dose. Alcoholic liver disease may take the form of chronic illness (steatosis, steato-hepatitis, fibrosis and cirrhosis) or acute involvement (alcoholic hepatitis). Whereas steatosis is a relatively benign illness, the presence of cirrhosis of the liver means major life expectancy shortening. The actual stage of cirrhosis depends on the presence of complications--portal hypertension with bleeding oesophageal varices, ascites or hepatic encephalopathy. The median survival time of patients with advanced cirrhosis is 1-2 years. Serious alcoholic hepatitis has a mortality record of up to 50%. Absolute abstinence is a sine qua non condition for any treatment of alcoholic liver disease, the other therapeutic procedure are of a supportive nature and questionable significance. Corticoids can be used in the management of serious alcoholic hepatitis. Treatment in the stage of liver cirrhosis is similar to that in cirrhosis of any other aetiology. Cirrhotic patients who demonstrably abstain can be considered for transplantation leading to a markedly prolonged life expectancy.
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PMID:Alcoholic liver disease. 1965 94

Imatinib mesylate is a drug that has been approved for treatment of chronic myeloid leukemia, Philadelphia-positive acute lymphoblastic leukemia, and advanced gastrointestinal stromal tumors. Several cases of hepatotoxicity, including fatal liver failure, have been reported with the long-term use of imatinib mesylate. Generally hepatotoxicity resolves after discontinuation of imatinib. Despite discontinuation of imatinib, hepatotoxicity can be progressive. Steroid may be useful in these patients and should be started early. We report a 53-year-old woman with advanced gastrointestinal stromal tumors who developed hepatotoxicity while receiving imatinib and subsequently acute liver failure. Ten weeks after commencing imatinib treatment, hepatotoxicity was determined. Imatinib was immediately ceased. Subsequently, a week later hepatic encephalopathy, jaundice, and coagulopathy occurred. Prednisolone was commenced. Liver biopsy was performed five weeks after the determining of hepatotoxicity. Biopsy showed sinusoidal congestion, necrosis of hepatocytes, inflammation, and hepatocyte drop out around the hepatic venule consistent with drug toxicity. Her liver function tests normalized with a nine-week prednisolone treatment. The patient was discharged. Her liver enzymes remained in normal range following visits. In cases of imatinib-induced acute hepatitis, the administration of prednisolone may be useful in the resolution of the acute episode and allow the reintroduction of a drug without risking recurrence of hepatitis.
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PMID:Imatinib mesylate-induced acute liver failure in a patient with gastrointestinal stromal tumors. 1966 40


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