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 specific and sensitive radioimmunoassay was used to measure the levels of antibody to a liver-specific membrane lipoprotein in patients with acute and chronic liver disease. Antibody was detected in 29 of 30 patients with chronic active hepatitis (all of 15 HBsAg-negative and 14 of 15 HBsAg-positive cases), and in 10 of 17 patients with chronic persistent hepatitis but at significantly lower titer. The titer of antibody to the lipoprotein showed a significant correlation with activity of disease as judged histologically and biochemically. Transiently elevated levels were found in 20 of 21 patients with acute viral hepatitis, but there was no correlation with the degree of liver damage. Antibody to liver-specific membrane protein may be part of the final common pathway of liver-cell damage in both HBsAg-positive and HBsAg-negative chronic activite hepatitis, whereas other immune mechanisms determine the liver-cell injury in acute viral hepatitis.
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PMID:Detection of antibodies directed against a liver-specific membrane lipoprotein in patients with acute and chronic active hepatitis. 66 44

The probable etiology and outcome of bridging hepatic necrosis found on a liver biopsy performed within three months of the onset of clinical illness was evaluated in 42 consecutive patients with this finding. Eighteen of the patients (43%) had a probable drug etiology for their hepatitis. Ten patients had HBSAG-positive acute hepatitis. Fourteen patients had neither drug-induced disease nor proven HBSAg-positive hepatitis. One patient from the drug-induced group died, but the other 17 had complete clinical recovery. Eight of ten in the hepatitis B antigen-postive group cleared their antigen and had complete clinical recovery. Chronic hepatitis developed in two who remained persistently HGSAg positive. Eight of the patients in the group with unknown etiology recovered, while six developed evidence of active chronic liver disease. This incidence of active chronic liver disease is significantly greater than that found in the drug-induced group (P less than 0.02). We conclude that drug-induced hepatitiis accounts for a significant proportion of patients of acute hepatitis who have bridging hepatic necrosis on liver biopsy. However, in these drug-induced cases the finding of bridging hepatic necrosis does not appear to be associated with an increased risk of development of active chronic liver disease.
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PMID:Bridging hepatic necrosis. Etiology and prognosis. 73 15

329 patients with acute ouvert viral hepatitis which occurred in the Hannover area 1975 were classified according to virological data. The proportions of type A and type non A - non B hepatitis were each approximately 20 percent of the total cases (n = 60). Viral hepatitis B was the most frequent type of viral hepatitis (n = 209). 174 individuals of the 329 hepatitis patients were reexamined serologically two years after the onset of the acute disease. 7 out of 105 patients with hepatitis B (6,7%) and 5 out of 40 patients with hepatitis non A - non B (12,5%) revealed a serological pattern compatible with chronic hepatitis. In contrast none of 29 patients with hepatitis A indicated chronic liver disease. The frequency of anti-HAV was also determined in 41 patients with HBsAg positive and HBsAg negative histologically proven chronic hepatitis or liver cirrhosis. All patients were under 35 years of age. An equal proportion of anti-HAV was found in both groups. These results suggest that hepatitis A practically never results in chronic hepatitis, while hepatitis non A - non B can run a chronic course with a frequency similar to that of hepatitis B.
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PMID:[Chronic hepatitis as sequela of acute viral hepatitis A and hepatitis non A - non B (author's transl)]. 74 46

The clinical course is reported in 17 patients in whom the histological picture of subacute hepatic necrosis ("bridging hepatitis") was found on needle liver biopsy or at autopsy. The patients' ages ranged from 10-71 years, 12 patients being less than 40 years old. Ten patients were males. Jaundice lasted 2-4 months in nine cases and over six months in two, one of the latter having developed cirrhosis. In five patients a relapse of jaundice occurred within three months. Hepatitis B antigen was found in one of 13 patients tested. Two patients died in fulminant hepatic failure, one developed cirrhosis. These three patients and an additional two received prednisone therapy. Twelve of the remaining patients were followed for periods of 8-81 months; an additional two patients' follow-up was incomplete. None developed clinical evidence of chronic liver disease, and laboratory data at the last examination were normal except for slight elevation of alkaline phosphatase in six cases. Repeat biopsies showed persistent hepatitis in one case, slight portal fibrosis in one, cirrhosis in one and at autopsy in a patient who died of unrelated causes two years after hepatitis no evidence of chronic liver disease was found. This relatively good outome of subacute hepatic necrosis is probably due to the young average age of the patients, and the low incidence of B hepatitis in this series.
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PMID:The clinical course of subacute hepatic necrosis. 74 11

Although blood banks in this country have been testing every unit of blood for hepatitis B surface antigen (HBSAg) by one of the highly sensitive "third generation" methods (radioimmunoassay or reversed passive hemagglutination) since September, 1975, post-transfusion hepatitis (PTH) still remains the major hazard to patients who require transfusion with blood and blood products. Since there may be an interval of many months between transfusion and onset of PTH and many cases are subclinical, the best data on the incidence of PTH have come from prospective studies with careful follow-up of transfused patients. Such studies first established the validity of HBSAg as a marker for the presence of hepatitis B virus (HBV), and they have shown a dramatic reduction in the incidence of post-transfusion type B hepatitis following the elemination of HBSAg positive blood from transfusion. Nevertheless, PTH cases not associated with HBV or HAV, which are termed non-A, non-B hepatitis, continue to occur commonly among transfused patients. Non-A, non-B hepatitis appears to be subclinical in many instances, but it can produce prolonged persistence of abnormal liver function tests, which may be associated with chronic liver disease. The outstanding risk factor responsible for the development of PTH has been shown to be blood from paid donors in every study which has evaluated this factor. HBSAg and anti-HBS prevalences were found to be much higher in paid donor groups than in voluntary donors. Accordingly, the Food and Drug Administration has proposed that all units of blood be labeled to indicate whether they were collected from voluntary or paid donors in order to inform consumers of the relative hepatitis risks of blood units from these different donor populations. In addition to HBSAg testing and reduced use of blood from paid donors, measures which may provide future reduction of the hepatitis hazard associated with blood transfusion include avoidance of unnecessary transfusions, identification of the agent(s) responsible for non-A non-B hepatitis and development of tests for these agents, idenfification and avoidance of blood from donors implicated in PTH cases, development of methods for immunizing transfused patients against the various agents responsible for PTH, and use of frozen-washed red blood cells for transfusion. Efforts to develop and/or evaluate these various approaches are currently being actively pursued in many laboratories.
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PMID:The clinical problem of hepatitis transmission;. 79 7

Screening for hepatitis B antigen (HB-sAg) in the serum of blood donors and exclusion of antigen-positive blood units have reduced the frequency of post-transfusion hepatitis but several cases of hepatitis B still occur in association with transfusions. One explanation for this is probably that HB-sAg is not an indicator of infectivity. Thus healthy carriers of the antigen seem to have low infectivity while carriers with chronic liver disease as well as donors incubating hepatitis B probably present a great risk.
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PMID:Hepatitis B antigen and prevention of post-transfusion hepatitis B. 80 65

Plasma amino acids were measured in 18 patients with hepatic encephalopathy on a protein-restricted diet of 20 g or less daily. Plasma aminograms tended to group into two distinct patterns depending on the etiology of the patients' hepatic pathology. Patients with chronic liver disease with superimposed acute insults, i.e., gastrointestinal bleeding, infection, alcoholic hepatitis, had elevated levels of the aromatic amino acids, phenylalanine, tyrosine, and tryptophan, as well as methionine, glutamate, and aspartate, whereas levels of the branched chain amino acids, valine, leucine, and isoleucine, were consistently depressed. Those patients with previously normal livers and acute hepatic necrosis, i.e., "fulminant hepatitis," had grossly elevated levels of all amino acids except the branched chain amino acids, which were normal. Elevations of amino acid levels in this patient group tended to correlate with extent of hepatic necrosis and hence had prognostic significance. Additionally, the different patterns seen in these two groups tend to suggest the indicated therapy as well as predict its efficacy.
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PMID:Plasma amino acid patterns in hepatic encephalopathy of differing etiology. 83 96

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

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

The different types of immune responses occurring during hepatitis B virus infection are reviewed. The responses specific for HBsAg (hepatitis B surface antigen) are important in the pathogenesis of chronic liver disease. The cell-mediated immunity specific for this antigen seems to be responsible for cytolysis occurring when the antigen is located within the hepatocyte (acute and persistent hepatitis). It is also responsible for the subsequent elimination of the virus. Immune complexes in antibody excess probably provoke the lesion of fulminant hepatitis. Complexes in the zone of antigen excess, which are responsible for the extrahepatic lesions of the prodromic phase, may perhaps also play a pathogenetic role in some forms of chronic active hepatitis.
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PMID:[Immune mechanisms in hepatitis B. New aspects and consequent practices]. 85 20


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