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)

Toga virus-like particles (typically 60-70 nm: enveloped with small surface spikes) were detected in the native hepatectomy specimens in 7 of 18 patients grafted for acute liver failure attributed to sporadic non-A, non-B hepatitis and in 2 patients grafted for fulminant hepatitis attributed to anti-epileptic drug hepatotoxicity. These particles were not detected in the hepatectomies from 12 other patients grafted for other causes of acute liver failure, 12 for various chronic liver diseases, and 2 histologically normal livers. Acute hepatic failure, characterized histologically by severe haemorrhagic necrosis, developed 7 days after grafting in 5 patients, all in the non-A, non-B group with toga virus-like particles in native liver. Similar virus-like particles were detected in all grafts and were in greater abundance than in the native livers. The agent may be novel because pre- and post-grafting sera were negative for antibodies against representative panels of arboviruses and in first and second generation antibody tests for hepatitis C virus.
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PMID:Toga virus-like particles in acute liver failure attributed to sporadic non-A, non-B hepatitis and recurrence after liver transplantation. 132 13

The Acute Hepatic Failure Study Group (AHFSG) has conducted a double-blinded, randomized evaluation of hydrocortisone in patients with acute hepatic failure. From July 1975 through August 1978, a 38-month period, 18 medical centers in the United States and one in Canada participated in this trial. A total of 64 patients were accessed and found eligible to participate in the study; two of them were subsequently eliminated from our analysis. Eighteen patients received placebo; 23 received 400 mg hydrocortisone per day, and 21 patients were administered 800 mg hydrocortisone per day. We did not observe any therapeutic effect of hydrocortisone, and the survival rates for placebo versus 400 mg and versus 800 mg hydrocortisone per day were 22%, 9%, and 24%, respectively. Fulminant hepatitis associated with drug hepatotoxicity or non-A, non-B hepatitis seemed to have a worse prognosis than fulminant B, although these differences were not significant. Serum alpha-fetoprotein had a modest prognostic value of survival and seemed to be limited to fulminant B. The AHFSG recommends, therefore, that corticosteroid use in acute hepatic failure with hepatic encephalopathy be discontinued.
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PMID:A double-blinded, randomized trial of hydrocortisone in acute hepatic failure. The Acute Hepatic Failure Study Group. 171 46

A case of aplastic anemia associated with non-A, non-B hepatitis was initially successfully treated by bone marrow transplantation. The patient subsequently developed fulminant hepatic failure. Fulminant hepatic failure is rare in bone marrow transplantation and only occurs in association with aplastic anemia associated with viral hepatitis. This case helps to highlight the relationships between the immune system, hepatitis, and bone marrow failure.
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PMID:Fulminant hepatic failure following bone marrow transplantation for hepatitis-associated aplastic anemia. 210 42

Fulminant hepatic failure accompanied by encephalopathy is a rare complication of acute liver disease, especially infection due to hepatitis A virus. We describe a 24-year-old woman and a 27-year-old man who developed this complication. One case presented with loss of consciousness and ended fatally. In the other the presenting symptoms were mental confusion and transient asterixis. Although hepatitis due to virus A is usually mild and the course favorable, one should be aware of the possibility of severe encephalopathy as a complication.
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PMID:[Fulminant hepatic failure due to hepatitis A]. 270 77

Fulminant hepatic failure occurred in an 11 week old baby of a Caucasian mother who was hepatitis B surface antigen positive, B e antigen negative, and B e antibody positive. Infants of hepatitis B e antigen positive mothers receive immunoprophylaxis against hepatitis, unlike those born to mothers who are B e antibody positive.
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PMID:Fatal hepatitis B in infant born to a HBsAg carrier with HBeAb. 398 61

A total of 293 sporadic cases of acute viral hepatitis were identified in Kashmir, India, from April 1979 to December 1981; 44 (15%) were found serologically to be hepatitis A, 94 (32%) hepatitis B, and 155 (53%) non-A, non-B type. The non-A, non-B hepatitis observed was a disease of young adults (29.8 +/- 15 years) with slight male predominance (1.4:1). Six of the 155 non-A, non-B cases had history of prior parenteral exposure, while 51 (33%) had a recent contact with another case of jaundice, suggesting that this form of hepatitis was spread by person-to-person contact. Fulminant hepatic failure occurred in 19 cases, and six (31.5%) of the 19 cases occurred in pregnant women. None of 90 non-A, non-B cases followed up six months later had developed chronic hepatitis. The acute sporadic non-A, non-B hepatitis described in Kashmir resembles epidemic non-A, non-B hepatitis epidemiologically and seems to be distinct from the non-A, non-B hepatitis described in the West.
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PMID:Acute sporadic non-A, non-B hepatitis in India. 641 42

Fulminant hepatic failure is a relatively rare disease. It develops in approximately 400 patients per year in the Federal Republic of Germany after viral hepatitis, toxic hepatitis or hypoxia of the liver. The mortality ranges between 80 - 90%. Therapy must start early. It consists mainly of intensive conservative care. Of the variety of invasive therapeutic measures only baboon liver perfusion and plasma exchange applied early in the disease seem to be of any benefit.
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PMID:[Acute liver failure--therapeutic aspects 1982]. 698 72

Fulminant hepatic failure (FHF) is characterized by massive necroinflammation of the liver tissue and is associated with high mortality. Serum concentrations of IL-1 beta, tumour necrosis factor-alpha (TNF-alpha), IL-6 and IL-1 receptor antagonist (IL-1Ra) were measured in 30 patients with FHF and in 23 patients with acute hepatitis (AH) before start of treatment and in 23 healthy controls. Levels of all four molecules were increased significantly in FHF compared with AH, in which values were higher than in the healthy controls. High serum levels of IL-1 beta and a significantly reduced ratio of IL-1Ra to IL-1 beta (IL-1Ra/IL-1 beta) were observed in FHF patients who subsequently died compared with subjects who survived. TNF-alpha and IL-6 concentrations were correlated with levels of human hepatocyte growth factor (hHGF), an index of hepatocyte regeneration. Although serum cytokine levels varied considerably between patients within each group studied, it is suggested that the striking elevation in proinflammatory cytokine levels in FHF may reflect both the insufficiency of hepatitis virus elimination and a failure to control a vicious cytokine cascade leading to overwhelming hepatocyte destruction rather than regeneration. The high cytokine levels observed in these patients and the significantly elevated IL-1Ra/IL-1 beta ratio in FHF patients who survived compared with those who did not suggest the possible therapeutic use of cytokine antagonists for the control of this life-threatening disease.
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PMID:Circulating proinflammatory cytokines (IL-1 beta, TNF-alpha, and IL-6) and IL-1 receptor antagonist (IL-1Ra) in fulminant hepatic failure and acute hepatitis. 792 88

Fulminant hepatic failure resulting from hepatitis E and coexistent Wilson's disease was diagnosed in a six year old girl six weeks after returning from a holiday in India. Wilson's disease was diagnosed on the basis of histological evidence of hepatocellular copper deposition, confirmed by biochemical estimation of liver copper concentration. Although severely damaged, the liver was non-cirrhotic. Hepatitis E virus (HEV) was diagnosed by nested polymerase chain reaction, the specificity of which was confirmed by direct sequencing of amplified DNA. Replication of HEV within the liver at the time of diagnosis was confirmed by selective amplification of the antigenomic strand of the virus obtained from total liver RNA. The patient had an orthotopic liver transplantation without recurrence of hepatitis and remains well at 19 months. Viral excretion, recorded by serial amplification of HEV RNA extracted from stool samples, persisted for 30 days after liver grafting. Severe vitiligo, present preoperatively, dramatically improved after liver grafting and institution of immunosuppressive treatment. This case suggests that viral infection may play a part in the acute decompensation seen in some cases of Wilson's disease.
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PMID:Fulminant hepatic failure resulting from coexistent Wilson's disease and hepatitis E. 802 Aug 19

Fulminant hepatic failure may develop as a complication of liver disease of various etiology. Infectious agents, drugs and liver toxins represent the major causes of fulminant hepatitis. The function of many organ systems may be impaired during acute hepatic failure because of the crucial role of the liver in intermediary metabolism. The mortality of 50% or more is mainly due to cerebral edema, bleeding from the gastrointestinal tract or disseminated infections. In this review the causes, complications and pathophysiology of fulminant hepatitis are discussed, with particular reference to the prevention of complications and to therapeutic strategies. Moreover, criteria for assessment of prognosis are discussed. A case report illustrates the complex clinical picture and frequently fatal outcome of the disease.
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PMID:[Fulminant hepatitis: pathogenesis, clinical aspects and management]. 814 Apr 5


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