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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have induced acute hepatitis in rats with the amino sugar Galactosamine by i.p. injection. The development of the disease was controlled by measurements of several metabolites and enzymes in serum, and light and electronic microscopy. Tyrosine transaminase was induced by i.p. injection of Cortisol, that increases ten times enzyme activity in liver parenchyma of normal rats. This inductive phenomenon cannot be observed in animals with galactosamine hepatitis. We discuss the probable mechanism and their relationship with some forms of viral hepatitis in human beings.
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PMID:Induction of tyrosine aminotransferase in galactosamine hepatitis. 4 46

A study of the distribution of subtypes ad and ay among sera from hepatitis B antigen-positive subjects in North West England and North Wales revealed a marked contrast between symptomless carriers among whom ad predominated and patients with acute hepatitis the majority of whom were ay. Those with hepatitis associated with drug addiction or other forms of "needle transmission" were almost all of subtype ay. On the other hand in cases of "sporadic" hepatitis without evidence of parenteral exposure subtypes ad and ay are about equally distributed. These findings are similar to those reported from other countries in Northern Europe and North America. Although geographical and social factors clearly affect the distribution of the two subtypes it is suggested that the virus of subtype ay may be more readily transmitted than subtype ad by parenteral routes involving small amounts of blood.
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PMID:Subtypes of hepatitis B antigen among patients and symptomless carriers. 4 35

In three patients with malignant disease HBsAg was detected in the serum at least 6 months before the development of acute hepatitis type B, which in each case followed a fulminant course to death. It is suggested that suppression of the normal immunological responses to hepatitis-B viral antigens by cytotoxic drug therapy permitted widespread infection of hepatocytes. Subsequently, upon withdrawal of these drugs, recovery of immunocompetence resulted in rapid destruction of all infected hepatocytes and massive liver damage. Screening for HBsAg before cytotoxic drug therapy, careful monitoring of liver function during its withdrawal, and prompt treatment with corticosteroids should abnormalities occur may prevent this unfortunate sequence of events.
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PMID:Fulminant hepatic failure in leukaemia and choriocarcinoma related to withdrawal of cytotoxic drug therapy. 5 45

Chronic liver disease developing after acute hepatitis type B is well documented, but is not thought to occur after acute hepatitis due to other viruses. However, follow-up of 29 patients in a haemodialysis unit who contracted HBsAg-negative acute hepatitis during 1968-70 revealed 8 cases with raised serum-aminotransferase levels dating from that time. Liver biopsy in 7 of these disclosed chronic aggressive hepatitis in 3, of whom 2 had already progressed to advanced cirrhosis. Chronic persistent hepatitis was present in 2 others, and the remaining 2 had non-specific hepatitis in association with massive iron overload. Immunological studies demonstrated a higher frequency of cellular immunity to HBsAg in those who had previously had acute hepatitis than in those who had not, although the prevalence of humoral antibody was similar in the two groups. One possible explanation for these findings is the presence of immunological cross-reaction at a cellular level between the hepatitis B virus and that responsible for the initial outbreak.
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PMID:Chronic liver disease developing after outbreak of HBsAG-negative hepatitis in haemodialysis unit. 5 71

A modified immunofluorescent technique was used for the detection of HBSAg in formalin-fixed liver tissue, thereby allowing retrospective examination of paraffin sections and avoiding the need to split the sample at the time of biopsy. Comparison with two other methods, involving either orcein staining or standard haematoxylin and eosin (H and E) preparation for ground glass hepatocytes, showed slightly fewer positive hepatocytes in individual biopsies with the latter stain, but the specificity of both methods was high. In a series of 146 seropositive and 74 seronegative patients with a variety of liver disorders, hepatocytes positive for HBSAg were found in only one of 55 patients with acute hepatitis type B, whereas large numbers of positive cells were seen in all 22 healthy carriers of the surface antigen. In the 69 patients with chronic persistent or chronic aggressive hepatitis, the frequency of positive biopsies was 86% and 85% respectively. The positive cells in these cases were, in comparison with healthy carriers of HBSAg, much fewer in number and were scattered in random fashion throughout the lobule rather than occurring in discrete clumps or sheets. This variation in the intrahepatic expression of HBSAg may reflect differences in the immune response to hepatitis B viral antigens.
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PMID:Detection of HBSAG in fixed liver tissue - use of a modified immunofluorescent technique and comparison with histochemical methods. 5 4

Viral hepatitis has been known to occur among the Greenland population endemically as well as in smaller and larger epidemics. A large epidemic of acute hepatitis comprising around 9% of the entire population, viz. more than 4000 notified cases, swept through Greenland between October 1970 and December 1972. 996 verified cases were seen in the Godthaab district and subjected to more detailed studies. Most of the Godthaab cases were seen among children and adolescents, and no disease was observed in children less than one year of age. Out of 996 diagnosed cases 9 showed acute hepatic failure with coma. Two further cases of hepatic coma were referred for treatment from outside the district. Three of these 11 patients recovered spontaneously. Of the residual 8 cases 6 were treated with exchange transfusions and steroids. Four of these survived and recovered completely. No lasting sequelae had been registered in any of the surviving cases of the epidemic up to June 1975 (2 1/2 years after cessation of the epidemic). Prophylaxis with gamma-globulin was undertaken in a medium-sized settlement in which practically the entire population received gamma-globulin when the first case of hepatitis was diagnosed. In this settlement only 7 out of 297 inhabitants contracted hepatitis. By contrast, in a similar settlement where no gamma-globulin was given, more than 30% of the population developed icteric hepatitis. The clinical features and the prophylactic effect of gamma-globulin seem to indicate that the epidemic was caused by the hepatitis A virus. In accordance with this, transitory Australia-antigenaemia was demonstrated in the acute phase in only 2.6% of the cases, possibly inidicating a small admixture of acute hepatitis type B to the epidemic predominantly caused by hepatitis A virus.
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PMID:The 1971-72 epidemic of acute viral hepatitis in Godthaab, Greenland. 5 37

F-antigen is a liver-specific antigen detected with antibody, raised in allogeneic (CBA) mice, to BALB/c mouse liver extract. The authors have confirmed the hepatic specificity of this antigen by showing it to be absent in extracts of extrahepatic organs of mouse and human origin. It is present in liver extracts of guinea pigs, rats, and rabbits, as well as in liver extracts from mouse and human sources. The antigen was present in the circulation of rabbits with acute carbon tetrachloride-induced hepatocellular injury. It was also demonstrated in the sera of 3 of 8 patients with acute hepatitis B antigen-positive hepatitis and in 1 of 4 patients with chronic active hepatitis. It was absent from the sera of 121 other patients with a variety of hepatic and nonhepatic diseases, and from the sera of 20 healthy subjects. The antigen is immunologically distinct from hepatitis B antigen, from the liver-specific lipoprotein antigen LP-2 of Meyer zum Buschenfeld, and from each of 15 individual human serum proteins tested.
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PMID:F-antigen: nature, liver specificity, and release in experimental liver injury. 5 3

One hundred liver biopsies from 100 patients with clinical presumptive diagnosis of hepatitis were examined by immunofluorescence for the presence of hepatitis B surface antigen (HBSAg) and hepatitis B core antigen (HBcAg). Of the 60 HBsAg-positive livers, 51 were diagnosed as chronic hepatitis on histological grounds, 6 as acute hepatitis, and 3 as "near-normal liver." From the 60 tissue-positive cases, 3 subjects were HBsAg seronegative. HBcAg was detected in 44 livers, all of which also had HBcAg in the localized in the cytoplasm and the membranes of the hepatocytes, and HBcAg in the nuclei and in 4 cases also in the cytoplasm. Predominant HBsAg expression in the cytoplasm was observed in near-normal liver, chronic persistent hepatitis, and cirrhosis with little activity. This correlated with the amount of ground glass hepatocytes in the biopsies. HBcAg and membrane-localized HBsAg were minimal in those conditions. HBcAg was most prevalent in patients with chronic aggressive hepatitis and active cirrhosis treated with immunosuppressive drugs, whereas the amounts of HBsAg and HBcAg in nontreated patients of those two groups and in acute hepatitis with signs of transition to chronicity were almost equal. HBsAg expression in liver cell membranes was most prominent in active forms of chronic hepatitis (chronic aggressive hepatitis and in active cirrhosis) and in acute hepatitis with signs of transition to chronicity. This observation correlated in the presence of HBcAg in the biopsies of those patients. In acute hepatitis both HBsAg and HBcAg were detected rarely and no membrane expression of HBsAg was observed. The over-all results show a significant relationship between the different degrees of accumulation of HBsAg and HBcAg in the liver and the various histological types of hepatitis and further suggest an interplay of both hepatitis B virus and host immune response in the development and pathogenesis of hepatitis B.
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PMID:Differential distribution of hepatitis B surface antigen and hepatitis B core antigen in the liver of hepatitis B patients. 5 75

The effect on abnormal coagulation tests of infusions of fresh-frozen plasma (F.F.P), prothrombin complex concentrates, and a combination of these treatments was compared in 30 patients with chronic liver disease undergoing needle biopsy. A single dose of F.F.P. (12 ml/kg body-weight) was found to be the least effective therapeutic regimen. The concentrate containing factors II, IX, and X was also not adequate, but the additional administration of factor-VII concentrate corrected the prothrombin-time (P.T.) and "Normotest" (N.T.) in most patients. However, this regimen did not correct the prolonged kaolin activated partial thromboplastin-time (K.P.T.T.). The results of tests for exploring both the extrinsic (P.T. and N.T.) and intrinsic (K.P.T.T.) coagulation systems only became normal after the combined administration of a lower dose of F.F.P. (8 ml/kg body-weight) and of both concentrates (12 units/ml). There was no clinical or laboratory evidence of thrombotic complications. No patient developed acute hepatitis or hepatitis-B surface antigen in the twelve months after biopsy. These results indicate that prothrombin-complex concentrates in combination with F.F.P. may therefore be used to allow liver biopsy to be performed safely in patients presenting with severe coagulation defects.
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PMID:Correction of abnormal coagulation in chronic liver disease by combined use of fresh-frozen plasma and prothrombin complex concentrates. 6 Jun 23

Progression of acute type B hepatitis to chronic liver disease and cirrhosis is well recognized, whereas no progression of acute type A hepatitis has as yet been documented. The natural history of acute non-A, non-B hepatitis has not been previously characterized. Ten cases of chronic liver disease were identified in 44 cases of acute non-A, non-B post-transfusion hepatitis. Age, sex, severity of acute illness, and prevalence of preoperative antibodies to known hepatitis-producing agents did not differ between the group whose hepatitis progressed to chronicity and the group whose hepatitis resolved. Less progression of acute hepatitis to chronic liver disease was seen in those patients receiving immune serum globulin preoperatively than in those receiving an albumin placebo (P = 0.009). Only 3 patients had clinical symptoms of hepatitis at the time of liver biopsy, and elevations of liver enzymes and gamma-globulin were mild. However, liver biopsy specimens in 8 of 10 patients showed chronic active hepatitis and an additional biopsy specimen showed cirrhosis. Acute non-A, non-B post-transfusion hepatitis often progresses to chronic active hepatitis. Preoperative gamma-globulin prophylaxis significantly reduces this progression. Identification and characterization of this viral agent(s) will further aid in the prevention of this undesirable complication of blood transfusion.
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PMID:Development of chronic liver disease after acute non-A, non-B post-transfusion hepatitis. Role of gamma-globulin prophylaxis in its prevention. 6 67


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