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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 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

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

The prevalence of hepatitis B surface antigen (HBsAg) was studied in 103 cases of hepatosplenic schistosomiasis (HSS), 134 control cases with a variety of illnesses including hepatointestinal schistosomiasis, and 600 blood donors, in an area endemic for both schisfosomiasis and viral hepatitis. The patients with HSS proved to be persistent carriers for HBsAg in a significantly higher proportion than the other two groups of cases. The HSS cases who were carriers of HBsAg had more clinical signs of chronic liver disease and strikingly more chronic inflammation of the portal spaces on liver biopsy. It is suggested that abnormal immunological responses in patients with HSS makes them more susceptible to become carriers of HBsAg and that the addition of this injurious factor makes their basic disease worse, and may be responsible for the development of cirrhosis in some cases.
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PMID:Hepatitis B surface antigen carrier state in hepatosplenic schistosomiasis. 95 51

To document the sequelae of acute hepatitis among recipients of commercial and volunteer blood and to assess factors influencing the development of chronic hepatitis (CH), 47 patients with post-transfusion hepatitis were followed prospectively from the time they received their transfusions. Twenty-nine had prolongation of at least 2-fold serum glutamic pyruvic transaminase (T) elevations for more than 20 weeks, and were classified as CH. When the patients with CH were compared to those with only acute hepatitis (abnormal T for less that 20 weeks), no difference was found with respect to age, sex, number of units transfused, incubation period, presence or absence of symptoms, occurrence of jaundice, maximum T, receipt or development of hepatitis B surface antigen or antibody, underlying illness, or area of the hospital where the patient was treated. Liver biopsies in 15 of the 29 revealed chronic-active hepatitis in 9, chronic persistent hepatitis in 2, unresolved hepatitis in 4. Five of the 9 patients with chronic active hepatitis were without symptoms. None of these died or have developed cirrhosis. Because chronic liver disease frequently developed after acute post-transfusion hepatitis among multiply transfused hepatitis B surface antigen negative blood recipients, close follow-up, including liver biopsy, is warranted in such patients with prolonged transaminase elevations.
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PMID:Post-transfusion chronic liver disease. 96 71

Sera were tested for autoantibodies in 98 patients with cryptogenic cirrhosis in Uganda and results correlated with serological tests for hepatitis B surface antigen (HBs Ag) and antibody to HBs Ag (HBs Ab). Smooth muscle antibodies (SMA) were detected in 23 (24%) of the patients but there was no difference in the incidence of SMA between HBs Ag-positive and negative cases. Antinuclear antibodies (ANA) were detected in five cases; mitochondrial, gastric and thyroid antibodies were not found in any patient. Unlike other geographical locations autoimmune mechanisms appear to play little part in the progression of chronic liver disease in Uganda Africans. Hepatitis B surface antigen was present in 36 (37%) and HBs Ab in 47 (48%) of the patients. Although evidence for past exposure to hepatitis B virus (as shown by detection of HBs Ab) was present in at least 30 out of the 62 HBs Ag-negative cases, there was no greater incidence of autoantibodies in HBs Ag-negative patients with or without HBs Ab. Persistent infection with hepatitis B virus and continuing liver damage may be an important factor but these results do not favor a role for the virus in causing chronic liver disease by triggering off an autoimmune reaction.
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PMID:Autoimmune factors in African cirrhosis. Correlation with hepatitis B surface antigen and antibody. 108 41


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