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)

A decade ago an antigen was identified by immunodiffusion and subsequently proved to be closely associated with hepatitis B virus. Further studies showed that hepatitis B virus circulates as a large particle containing a protein coat and a DNA core, and that excess coat particles are produced and circulate freely. Immunization with surface protein produced protective antibodies, and this led to the development of a prototype vaccine. Patients with hepatitis may develop a variety of extrahepatic manifestations, including polyarteritis, vasculitis, and glomerulonephritis. These associated symptoms may be due to immune complexes consisting of hepatitis B surface antigen and its antibody. The role of cellular immunity in hepatitis B is unknown. The relation between type B virus and the liver is both destructive (leading to severe acute hepatic disease and eventually to cirrhosis) and symbiotic (existing among carriers who have neither liver disease nor symptoms). If the factors that cause these divergent courses were delineated and understood, the results may lead to the prevention and cure of hepatitis B and its sequelae.
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PMID:The liver and the antigens of hepatitis B. 78 84

Among 134 patients with chronic active liver disease, selected by identical clinical, biochemical and morphologic criteria, assigned to standard treatment programs and followed at regular intervals, 21 of 105 failed treatment with standard regimens containing steroids. Treatment failure was more common in patients whose serum contained hepatitis B surface antigen, those with more severe liver disease as judged by liver function tests (prothrombin time) and hepatic morphology (subacute hepatitis or cirrhosis). Early diagnosis of treatment failure, based on changes in liver function tests rather than on clinical features of deterioration, coupled with the immediate administration of higher doses of prednisone with or without higher doses of azathioprine, resulted in disappearance of clinical and biochemical features of disease activity in the majority of patients. These results were greatly superior to those earlier reported by us from patients chosen by identical criteria but treated by conventional measures. However, when endogenous encephalopathy developed the outlook was grave, regardless of previous or subsequent therapy. We recommend that patients at risk for failing conventional treatment be identified early, followed carefully with serial liver function tests, and be treated promptly with higher doses of medication when deterioration occurs.
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PMID:Failure of customary treatment in chronic active liver disease: causes and management. 79 99

With an immunofluorescence technique using rabbit hepatocytes isolated by a non-enzymatic method an autoantibody directed against liver-cell-membrance was identified. Sera from 361 patients with various liver diseases and 274 patients with primary non-hepatic diseases-many associated with non-organ-specific auto-antibodies-were examined. The antibody (LMA) was found in 27 out of 72 patients with hepatitis-B-surgace antigen (HBsAg)-negative chronic active hepatitis and in 17 out of 28 patients with HBsAg-negative non-alcoholic cirrhosis. Only two patients had LMA and HBsAg, and both had chronic active hepatitis. One patient with extrhepatic disease was found to have LMA, and this patient had biochemical evidence of liver disease. Hence there is a close correlation between the presence of LMA and HBsAg-negative chronic inflammatory liver diseases and its detection may help in diagnosis.
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PMID:Liver-cell-membrane autoantibody specific for inflammatory liver diseases. 83 76

The cause of hyperamylasemia associated with chronic liver disease is unclear. In an attempt to identify the tissue of origin of hyperamylasemia in 3 patients with chornic active hepatitis their serum was isoelectrically focused. The isoamylase patterns obtained were compared to those of pancreatic and salivary amylase. The apparent salivary gland origin of the excessive blood amylase in the patients studied was substantiated by radiological demonstration of parotid sialoectasia in one patient and histological evidence of sialoadenitis in another. Further evidence was the coincident isoelectric points of the predominant isoamylase in the sera of the liver disease patients and of patients with parotid inflammatory disease. Hyperamylasemia associated with chronic liver disease may be of salivary gland origin and as such forms part of the spectrum of extrahepatic manifestations of chronic active hepatitis.
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PMID:A cause of hyperamylasemia associated with chronic liver disease. 83 1

Hepatic injury during long term dantrolene sodium therapy occurred in 19 of 1044 patients (1.8%) monitored for at least 60 days. Six had icteric hepatitis (0.6%) and 3 died (0.3%). After the marketing of the drug, an additional 31 cases of dantrolene-associated liver disease were available for analysis. Of these 16 had icteric hepatitis with a favorable outcome, whereas 11 died. The injury was mainly hepatocellular with a pattern of acute or subacute hepatic disease or chronic active hepatitis. Analysis of total of 50 cases showed a 28% case fatality rate. All the fatalities occurred in patients above 30 years of age and after at least 2 months of therapy, with 57% cases exposed for at least 6 months. Eleven of the 14 fatalities occurred in females (P is less than 0.05). No cases of hepatic disease occurred in patients exposed for less than 1 month or under the age of 10. The majority of adverse reactions (71%) occurred between 1 and 6 months of therapy. Daily dosage of 300 mg or more is associated with higher incidenceof hepatotoxic reactions and with the majority (85%) of the fatalities. The idiosyncratic hepatic injury does not appear to involve hypersensitivity to the drug. A careful assessment of the benefit-risk ratio in the therapeutic use of dantrolene sodium is proposed.
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PMID:Dantrolene-associated hepatic injury. Incidence and character. 83 13

The serum immunoglobulin (Ig) G, A, and M levels were investigated with respect to their differential diagnostic significance, pathogenesis and estimation of prognosis of different forms of liver disease. The sera of 204 patients with acute hepatitis, fatty liver I and II, and cirrhosis, and of 110 healthy adutls were quantitatively determined for immunoglobulins. 1. IgG- and IgA-concentrations higher than 2000 mg% and 330 mg%, respectively, indicate chronic aggressive hepatitis or cirrhosis, and exclude all other groups. 2. A clear correlation between HBsAG (Australia Antigen) and immunoglobulin content could not be demonstrated in any group; 3. A significantly elevated level of IgA was observed in alcoholic cirrhosis when compared to non-alcoholic cirrhosis. No such differences were found inhe other groups. 4. Acute and chronic persistent hepatitis show a similar increase of immunoglobulins. Thus persistent high levels of Ig following acute hepatitis indicate the development into a chronic hepatitis. 5. A relative increase of IgA rather than IgG corresponds to the degree of inflammatory activity of a liver process.
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PMID:[Quantitative serum immunoglobulin determination: differential diagnostic significance for liver disease (author's transl)s]. 84 Jan 24

A survey of significant pathological abnormalities of liver in the first two decades of life is presented; this is based on biopsy and autopsy specimens received in the histopathology service in Nairobi over five years. It includes conditions which one might expect in a diagnostic service in any country, some of which are attributable to known local conditions, and others which show distinctive features in their occurrence of frequency. There is an unexpected number of cases of chronic aggressive hepatitis and cirrhosis and the latter is notable for its frequency in the first decade of life. Hepatocellular carcinoma also occurs rather commonly, although most often in the second decade and as a complication of cirrhosis. There is a marked male preponderance in chronic aggressive hepatitis, cirrhosis, hepatocellular carcinoma and schistosomiasis. It is unlikely that this is due to selection of cases and the series shows no indication of tribal influence. The possible role of infections and toxins, particularly in the genesis of chronic aggressive hepatitis and cirrhosis, is discussed. In the search for clues to pathogenesis, detailed systematic investigation of children with liver disease is advocated, paying particular attention to cultural background, and exposure to infections and toxic agents.
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PMID:Liver disease in early life in Kenya. 84 46

Fifty Kenyan patients with chronic liver disease or hepatocellular carcinoma were tested for hepatitis B surface antigenaemia by radioimmunoassay. The hepatitis B surface antigen was detected in 77% of the patients with chronic persistent or chronic aggressive hepatitis, or cirrhosis confirmed by liver biopsy, compared with 15% in a control group. All six patients with hepatocellular carcinoma had detectable hepatitis B surface antigen or antibody. 50% of the controls had hepatitis B surface antibody in their plasma detectable by haemagglutination. Auto-immune associated liver disease appeared infrequent. The possibility that the hepatitis B virus is an important cause of cirrhosis in Kenya is discussed.
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PMID:Hepatitis B surface antigenaemia in Kenyans with chronic liver disease. 84 49

Kayser-Fleischer rings are pigmented corneal rings at the limbus of the cornea in Descemet's membrane that have been deemed pathognomonic of Wilson's disease. However, we have observed four exceptions in patients with non-Wilsonian liver disease. Three patients had primary biliary cirrhosis and one patient had chronic aggressive hepatitis with cirrhosis. Pigmented corneal rings were seen only by slit-lamp examination. Hepatic, serum, and urinary copper and serum ceruloplasmin levels were significantly elevated in the patients with primary biliary cirrhosis. Radiocopper (64Cu or 67Cu) studies in patients with primary biliary cirrhosis showed plasma disappearance curves which allowed a clear distinction from Wilson's disease in that all three patients with primary biliary cirrhosis showed a secondary rise in radiocopper that presumably represented copper incorporation into ceruloplasmin. In one patient, in whom 64Cu in ceruloplasmin was studied specifically, incorporation was found to be normal.
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PMID:Pigmented corneal rings in non-Wilsonian liver disease. 84 86

Essential cryoglobulinaemia was detected in 44 out of 150 patients (29%) screened on the basis of histological confirmation of chronic inflammatory liver disease (chronic persistent or aggressive hepatitis, or cirrhosis). Cryoglobulinemia prevailed in the patients whose hepatic tissue showed more features of active inflammation; also, a female prevalence was observed. There were no correlations between cryoglobulinaemia and either HBsAg positivity or alcoholic liver disease. Mixed cryoglobulins made of heterogeneous immunoglobulins without monotypic components were mostly associated with established cirrhosis, whereas monotypic cryoglobulins were exclusively found in patients with either persistent or aggressive chronic hepatitis. Mixed cryoglobulins with a monotypic component were associated with all histological grades of liver damage. This study affords an objective evaluation of both the frequency and immunochemical features of cryoglobulins associated with chronic inflammatory liver disease.
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PMID:Incidence and immunochemical features of serum cryoglobulin in chronic liver disease. 85 82


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