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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper describes immunofluorescence studies on liver cell surface localization of hepatitis B surface antigen (HBsAg) and of IgG in acute and chronic hepatitis and in cirrhosis. In acute hepatitis B, HBsAg was found at the surface of hepatocytes in an early phase of the disease, but not during the recovery. This finding is consistent with the hypothesis that immune reactions to HBsAg may be responsible for the liver cell lysis. In HBsAg-positive chronic hepatitis and cirrhosis the antigen was found in the cytoplasm, but not on the surface of the hepatocytes, while in HBsAg-negative cases the antigen could not be detected in the liver cells. Both in HBsAg-positive and in HBsAg-negative chronic active hepatitis (CAH) and cryptogenic cirrhosis IgG bound to the membrane of the hepatocytes could be detected, suggesting a role of antibodies in the pathogenesis of the disease.
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PMID:Liver cell surface localization of hepatitis B antigen and of immunoglobulins in acute and chronic hepatitis and in liver cirrhosis. 78 18

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

The lymphocyte delayed hypersensitivity response to phytohaemagglutinin (PHA) and hepatitis B antigen (HBsAG) was evaluated by two in vitro tests-leucocyte migration inhibition and DNA synthesis. Patients convalescing from HBsAG-positive hepatits showed the presence of a state of cell-mediated immune responsiveness to the antigen. In Indian childhood cirrhosis, there was a failure of response to HBsAG and a slight but significant depression of reaction to PHA. It is suggested that the lack of immune reactivity to HBsAG, perhaps determined genetically, may be a significant factor in the evolution of cirrhosis in Indian children.
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PMID:Lymphocyte response to hepatitis B surface antigen. Findings in hepatitis and Indian childhood cirrhosis. 81 95

The sensitivities of three technqiues used to detect serum hepatitis B surface antigen (HBsAg) were compared in 411 patients with various types of chronic liver disease. Counterimmunoelectrophoresis proved an unreliable test. Two haemagglutination technqiues were slightly less sensitive than radioimmunoassay but were more rapidly performed. Less sensitive techniques were particularly unreliable in active liver disease where HBsAg titres were low. HBsAg was detected in patients with chronic persistent hepatitis, alcoholic liver disease, chronic active liver disease with or without cirrhosis, and primary liver cell carcinoma. Forty-six of the 68 (68%) HBsAg positive subjects were males coming from outside the United Kingdom. The HBsAg titres in 13 subjects with chronic persistent hepatitis were significantly higher (P less than 0-001) than those in 43 subjects with chronic active liver disease. Corticosteroid therapy did not alter the HBsAg titre significantly. None of the 28 HBsAg positive subjects studied serially for up to two years cleared HBsAg from the serum. Anti-HBs was examined by passive haemagglutination and found in 35 subjects, 26 of whom had no evidence of liver disease, 80% came from abroad. Anti-HBs was believed to be of epidemiological rather than of pathological importance.
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PMID:Detection, by three techniques, of hepatitis B surface antigen (HBsAg) and determination of HBsAg and anti-HBs titres in patients with chronic liver disease. 83 98

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

Thirty-five Black patients with cirrhosis of the liver were admitted to the professorial unit over a 1-year period and were included in a carefully planned prospective study. Men predominated over women in a ratio of 3:1. Alcohol consumption in the form of African beer was significantly higher in cirrhotic patients than in a control population. The clinical picture was neither predominantly that of alcoholic nor of cryptogenic cirrhosis. Hepatomegaly, porphyria cutanea tarda, ascites, splenomegaly and oesophageal varices were common. There was a complete absence of gynaecomastia, spider naevi and liver palms. Histologically, the majority of patients had macronodular cirrhosis, and only 1 patient had micronodular cirrhosis and minimal fatty change. Hepatitis B surface antigen (HbsAg) was not detected in any patient, despite a positive HbAg rate of 4% in Black African blood donors, determined by means of the same laboratory technique.
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PMID:Cirrhosis of the liver in Rhodesian Blacks. 88 20

Serial measurements of complement components were performed in fifty-nine patients with acute, uncomplicated hepatitis and twelve with alcoholic cirrhosis. Thirty-one of the former group had detectable hepatitis B antigen. Abnormal complement profiles were observed in nine patients with hepatitis B and seven with antigen-negative hepatitis. Low levels of C4, C3 and factor B were common in the subjects with cirrhosis and confined to those cases with severe reduction in serum albumin and/or prothrombin index. By contrast, the complement changes in the patients with hepatitis occurred without significant alteration in these parameters; certain subjects also had reduction in C1q and C5 and a significant number had C3d detectable in fresh plasma. The pattern of abnormality suggests predominant involvement of the classical pathway and it is concluded that this results, at least in part, from an immune process evident only in the early clinical phase of hepatitis. Such gross changes in complement are likely to reflect immune-complex activity and it is proposed that these complexes may be important in the clearance of virus material. The data supports a previous suggestion that recovery from acute hepatitis is primarily dependent on host immune competence rather than viral cytotoxicity or generation of immune complexes.
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PMID:Acute hepatitis: significance of changes in complement components. 89 Oct 25

A study of liver abnormalities in 36 patients with mixed cryoglobulinemia in the absence of underlying infectious, connective tissue, or lymphoproliferative disorders revealed clinical or biochemical evidence of liver dysfunction in 84%. Hepatomegaly was detected in 77%, splenomegaly in 54%, and abnormalities in bilirubin, alkaline phosphatase, or serum glutamic oxalacetic transaminase in 77%. Only four of the patients had overt liver disease. Of 15 biopsies from 12 patients, there was normal tissue structure in two, minimal nonspecific changes in one, portal fibrosis in three, chronic persistent hepatitis in one, chronic active hepatitis in two, chronic active hepatitis with cirrhosis in four, and postnecrotic cirrhosis in two. These findings, together with the previously reported high incidence of serologic evidence of hepatitis B virus (HBV) infection, support the view that the syndrome of purpura, arthritis, and nephritis is often a consequence of immune-complex vasculitis secondary to HBV infection.
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PMID:Liver involvement in the syndrome of mixed cryoglobulinemia. 90 Jun 72

This study was designed to compare the clinical and immunological characteristics of the hepatitis B surface antigen (HBsAg)-positive and HBsAg-negative (cryptogenic) forms of chronic active hepatitis. The data of 48 patients with chronic active hepatitis, 24 with persistent HBs antigenemia and 24 without HBsAg, were analysed. HBsAg was detected by counter-immunoelectrophoresis and radioimmunoassay. The clinical features, biochemical liver function tests, immunoglobulins, complement C3, antoantibodies, and cell-mediated immunoreactivity of the two forms of the disease were compared. Cirrhosis was found to occur more frequently at the time of diagnosis in the HBsAg-negative group, and the serum alkaline phosphatase level was raised significantly compared to the HBsAg-positive form. The elevation of the IgG level was greater in the cryptogenic form, but the difference was not statistically significant compared to the HBsAg-positive patients. There was a marked difference in the frequency of the mitochondrial antibodies, but not of the antinuclear factor and other autoantibody-like serum factors. Lymphoblastic transformation revealed a similar diminution in response to phytohaemagglutinin stimulation in both groups of patients compared to the normal controls. An increase of the 3H-thymidine incorporation was seen after stimulation with human liver mitochondrial antigen, and leukocyte migration inhibition could be observed with this antigen in both forms of chronic active hepatitis.
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PMID:Chronic active hepatitis in patients with and without hepatitis B surface antigenemia. 91 64


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