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 study was performed on a family of 7 followed up over a 4-year period in which an outbreak of B-antigen-positive hepatitis occurred. Of the 5 male members who acquired HBsAg, 1 became a chronic asymptomatic carrier and 4 had episodes of acute icteric hepatitis during a 15-month period with development of histologically documented chronic hepatitis with persistent HBs antigenaemia in all. Of the 2 female members, 1 had an attack of acute HBsAg-positive hepatitis but recovered normally and cleared HBsAg from her serum, while the other was found to have anti-HBs with no evidence of liver disease. Serological and immunological studies carried out in all members of this family suggested that a sex-linked defect of T cell function itself could explain the differing host immune response to HBV infection in genetically related subjects.
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PMID:Clustering of HBsAg in a family. 30 17

In patients who have impaired hepatic reserve, the Warren shunt has been proposed as an effective operation because it decompresses the esophageal varices without disturbing portal perfusion of the liver. However, early reports of high operative mortality and technical difficulties have impeded acceptance of the procedure. The operation was done in a series of 17 patients. All patients in whom elective variceal decompression with a patent splenic vein was required and without clinical ascites were candidates for this operation. Follow-up ranged from 2 to 48 months. Six patients had alcoholic cirrhosis, two had primary biliary cirrhosis and seven had postnecrotic cirrhosis; in two the cause of the liver disease was unknown. Five patients were categorized as Child's class A, nine as class B and three as class C. No intraoperative or early postoperative deaths owing to hemorrhage occurred. However, there was one death two weeks postoperatively from pulmonary sepsis and one death five weeks postoperatively due to antigen-positive hepatitis. Two patients died from hepatic failure six weeks and five months after operation, respectively; in the first of these, chronic active hepatitis was diagnosed at the time of operation. In one patient hemorrhage recurred and transfusion was required. Although ascites, which eventually resolved, developed in eight patients after operation, the results in 76 percent of patients have been good without new episodes of hemorrhage or encephalopathy. We conclude that the Warren shunt is a safe and effective elective operation for the treatment of patients in whom hemorrhage from esophageal varices has occurred.
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PMID:The Warren shunt in treating bleeding esophageal varices. 31 64

The characterisation of lymphocytes from liver biopsies indicates that 'activated' T lymphocytes are present in the liver in alcohol induced hepatitis, chronic active hepatitis (HBS+ve and -ve), and in primary biliary cirrhosis but not in inactive cirrhosis, chronic persistent hepatitis, extrahepatic and drug induced cholestasis. A greater percentage of lymphocytes bear Fc-receptors in chronic active hepatitis than in alcohol induced hepatitis or cholestatic liver disease. The concentration of 'activated' T cells in the peripheral blood in all groups studied was within the normal range, suggesting that the 'activated' T cells found in the liver were reacting to either native or foreign antigens within the liver. The data on Fc-receptor bearing cells are consistent with the involvement of antibody assisted K cell mediated cytotoxicity in chronic active hepatitis.
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PMID:Lymphocyte populations in liver biopsy specimens from patients with chronic liver disease. 32 39

Rapid progression of acute type B hepatitis to chronic active liver disease and cirrhosis in a young male with hypogammaglobulinemia is described. Absent circulating IgA, significantly low IgG, and normal IgM levels were detected during the acute phase of illness. Enumeration of peripheral lymphocytes revealed a decreased number of T cells and normal numbers of B cells. In vitro pokeweed stimulation of Ig synthesis correlated with the in vivo circulating levels of the three immunoglobulins. Cell-mediated immune responses were normal except for lymphocyte stimulation to hepatitis B surface antigen. It was concluded that the defective synthesis of IgG and IgA antibodies to hepatitis B surface antigen contributed to the accelerated progression to chronic active type B hepatitis in this person.
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PMID:Rapid progression of chronic active type B hepatitis in a patient with hypogammaglobulinemia. 33 24

Frozen, unfixed sections of human liver biopsies from patients with acute, subchronic, and chronic hepatitis or fibrotic liver disease were studied in indirect immunofluorescence with specific antisera to type I and type III procollagen. In early stages of both hepatitis and fibrotic liver disease, intralobular type III collagen synthesis is increased. Maximum values are reached years after the onset of disease. Intralobular procollagen I content is not increased in the acute stage, but rises only later. An increase of procollagen I seems to herald irreversible liver changes. This approach allows for exact localization and semiquantitative analysis of the synthesis of type I and type III collagen, and adds a new parameter to the diagnostic approaches in liver diseases.
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PMID:The diagnostic application of specific antiprocollagen sera. II. Analysis of liver biopsies. 34 27

This paper reviews hepatic toxicity during chemoprophylactic treatment with isoniazid alone, and during the treatment or retreatment of active pulmonary tuberculosis with regimens containing one or more of the drugs isoniazid, rifampicin and pyrazinamide. Chemoprophylaxis with isoniazid carries a risk of drug-induced hepatitis, and this risk needs to be weighed against the advantages of preventing tuberculosis morbidity. The risks of hepatitis during standard treatment based on isoniazid are very small, and most patients who develop hepatitis recover. Moreover, it is often doubtful whether hepatitis is in fact drug-induced, and a proportion of patients who develop it already have liver disease at the time treatment is started. The risks are acceptable in the treatment of bacteriologically active disease. There is no consistent evidence that giving rifampicin with isoniazid in the initial treatment of tuberculosis increases the risk of hepatitis; in particular, transient abnormalities in the results of tests of liver function during the early weeks of treatment do not imply serious toxicity; patients who are rapid acetylators of isoniazid are not, as has been suggested, exposed to any special risk, and patients with known liver disease can also be treated without undue risk. Retreatment regimens based on rifampicin plus ethambutol carry a low risk of hepatitis, even though patients who need retreating have often experience toxicity during their initial treatment. Frist-line or second-line regimens containing pyrazinamide in currently accepted dosages, given daily or intermittently, carry a low and acceptable risk of hepatic toxicity. Finally, current studies of daily and intermittent short-course regimens based on isoniazid, rifampicin and pyrazinamide will extend our knowledge of hepatic toxicity. Because such regimens involve small total quantitites of drugs given over short periods they are likely to give rise to less hepatic toxicity than regimens of standard duration.
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PMID:The hepatic toxicity of antituberculosis regimens containing isoniazid, rifampicin and pyrazinamide. 34 72

We considered for bone marrow transplantation a boy whose only histocompatible donor was positive for hepatitis B surface antigen (HBsAg). He was conditioned for transplantation with cyclophosphamide and total body irradiation. Hepatitis hyperimmune gamma globulin was administered following the bone marrow infusion. Fourteen months after transplantation, the recipient remains a chronic HBsAg carrier, but he has neither developed fulminant liver disease nor has there been any evidence of graft failure.
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PMID:Transplantation of hepatitis B surface antigen positive bone marrow. 34 45

Many reports have demonstrated an elevation of circulating carcinoembryonic antigen (CEA) in the majority of patients with alcoholic liver disease and, less frequently, in patients with nonalcoholic liver disease. Several explanations for this finding have been proposed, eg, increased production or release of CEA by the damaged liver, decreased hepatic metabolism, or diminished excretion of CEA of extrahepatic origin. In an attempt to clarify the mechanism of CEA elevation in liver disease, we have compared the CEA plasma level as measured by radioimmunoassay with CEA demonstrable in liver tissue by the indirect fluorescent antibody technique in 7 patients without significant changes in the liver biopsy specimen, 23 patients with alcoholic liver disease, and 16 patients with miscellaneous liver diseases such as acute or chronic nonalcoholic hepatitis or extrahepatic biliary obstruction. The mean CEA plasma level in patients with alcoholic liver disease was significantly higher than in patients with nonalcoholic liver disease (8.8 +/- 9.5 vs 2.7 +/- 2.5 ng/ml; P less than 0.02). In normal liver tissue, CEA was observed in the apical cytoplasm and along the luminal surface of bile duct epithelial cells, suggesting that under normal conditions CEA accumulates in and is excreted by bile ducts. In patients with alcoholic hepatitis and/or cirrhosis there was marked bile ductular proliferation and prominent cytoplasmic CEA-specific staining and both were associated with elevated CEA plasma levels in more than 80% of cases. In the group of miscellaneous liver diseases, bile ductule counts and CEA-specific staining did not correlate with CEA plasma levels. These observations suggest that proliferating bile ductules contribute to elevated plasma CEA in alcoholic patients.
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PMID:Carcinoembryonic antigen in normal and diseased liver tissue. 35 25

The 'e antigen' (eAg) is specifically associated with hepatitis B virus infections and appears to be a marker for the infectivity and a prognostic indicator of the chronicity of liver disease. Therefore we examined by immunodiffusion the presence of eAg in the seum of HBsAg-positive patients on maintenance dialysis. The dialysis patients had a significantly higher incidence of positive eAg compared with a group of unselected HBsAg-positive patients without renal failure. In most of the dialysis patients the microscopic findings in the liver revealed only 'minimal changes'. Three eAg-positive patients received a renal transplant. Afterwards they displayed an appreciably increased eAg-yield on immunodiffusion and histology revealed chronic persistent hepatitis. It is assumed therefore that the immunodeficiency of patients undergoing chronic haemodialysis is possibly a supporting factor in the synthesis of eAg, and will perhaps induce a more subscute and prolonged course of hepatitis. The synthesis of eAg after renal transplantation may be enhanced by the additional immunosuppressive therapy.
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PMID:E antigen in the serum of HBs antigen-positive patients on maintenance dialysis and after transplantation. 36 77

Serological markers for hepatitis virus B (HBV) infection and the occurrence of hepatopathies were analyzed in 152 patients during the hemodialysis period and on average 3.8 years after receiving a renal allotransplant. At the beginning of hemodialysis, 25% of the patients showed signs of an ongoing or past infection with HBV (10% hepatitis virus B surface-antigen [HBsAG] positive and 15% anti-HBsAG positive). At the time of transplantation, 20% of the patients were positive for HBsAG and 25% had detectable anti-HBs. At the end of the study, 31% of the patients were positive for HBsAG and 25% had detectable anti-HBs. In 21 patients (14%) inflammatory liver disorders were observed: transitory hepatitis (7 patients), chronic persistent hepatitis (7 patients), chronic aggressive hepatitis (3 patients) and active cirrhosis (2 patients). Two patients had died in liver coma. All 21 patients with inflammatory hepatopathy had detectable HBsAG at the time of diagnosis, and all patients with chronic inflammatory liver disease were HBs carriers. In most of these patients the carrier state had been present for more than 3 years before diagnosis.
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PMID:[Hepatitis virus B infection and hepatopathy after kidney transplantation]. 39 Jun 93


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