Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

Acute viral B-hepatitis is the consequence of an effective specific immune response against the hepatitis B-virus with elimination of the virus. Corticosteroids decrease this immune reaction and thereby inhibit virus elimination. In principle, therefore, corticosteroid therapy promotes a transition to chronicity. This theoretical concept is documented practically by 8 patients treated with steroids in the early phase of acute viral hepatitis. Transition to some form of chronic liver disease is documented by serial liver biopsies in all 8 patients. The immunohistological findings showed the presence of HBsAg and HBcAg, as theoretically expected. These 8 selected cases, although uncontrolled, together with the theoretical concept of B-virus elimination, provide evidence against the use of corticosteroids in acute B-hepatitis.
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PMID:[Immunological aspects of acute viral hepatitis treated with corticosteroids]. 92 38

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

Of sixty patients with chronic liver disease, eight with cirrhosis or chronic hepatitis had very low serum CH50 but normal plasma CH50. The complement component profiles of these sera revealed markedly decreased C4 and C2 activities and normal C3T (C3-C9) activities. From these results, it is suggested that the early acting complement components had been non-specifically activated during blood coagulation in these patients. No difference between plasma and serum CH50 was found in patients with hepatitis B(s) antigen.
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PMID:Differences between plasma and serum complement in patients with chronic liver disease. 96 9

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

Among the several methods employed for the detection of hepatitis B antigen (HBAg) and hepatitis B antibody (HBAb), radioimmunoassay is considered to be the most sensitive and specific. This paper describes a radioimmunoprecipitation test (RIP) for HBAg and HBAb standardized in our laboratory; it consists of a double-antibody precipitation test in a micro-titer system employing 125I-labeled HBAg. The test is compared with double immunodiffusion (ID) and with counterimmunoelectrophoresis (CEP) in the detection of HBAg and HBAb in healthy persons and in patients with acute and chronic liver disease. RIP is 20,000 times more sensitive than ID and 2,500 times than CEP when HBAg is tested, and 40,000 times more sensitive than ID and 10,000 times than CEP for the antibody detection. Moreover the method is reproducible and specific for HBAg and HBAb. With this test the frequency of HBAg in healthy persons was 0% in subjects without any known contact with antigenic material, 0.80% in hospital personnel and 1.17% in high risk personnel (laboratory technicians, blood products workers, ecc.). In acute viral hepatitis the frequency of HBAg was 90% at the admittance to the hospital and 70% at the dimission, while CEP detected a frequency of 85% and 20% respectively. In chronic liver disease the frequency of HBAg with the RIP method was 83.3% in chronic persistent hepatitis, 42.8% in chronic aggressive hepatitis, 23% in cryptogenic cirrhosis and 16.6% in alcoholic cirrhosis. The frequency of HBAb detected with RIP was 4.50% in subjects without any known contact with antigenic material, 6.45% in hospital personnel, 0.41% in high risk personnel, 20% in acute viral hepatitis at the admittance to the hospital and 50% at the discharge, 25% in chronic persistent hepatitis, 14.2% in chronic aggressive hepatitis, 15.3% in cryptogenic cirrhosis and 50% in alcoholic cirrhosis. The high frequency of antibody in healthy persons with no history of hepatitis or parenteral exposure to blood transfusion suggests a widespread diffusion of hepatitis B infection and the possibility of a nonparenteral route transmission. The frequency of HBAg and HBAb in chronic liver disease as detected by a very sensitive method rises the question of a possible role of hepatitis B virus in the pathogenesis of the disease.
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PMID:[Frequency of antigen associated to hepatitis due to virus B (HBAg) and of antibody (HBAc) in healthy subjects and during of course of acute and chronic hepatitis. Radioimmunologic study]. 122 46

The extent of involvement of hepatitis C, as compared to hepatitis A and hepatitis B, virus infection in acute and chronic liver disease in the Asir Region, southwestern Saudi Arabia, was assessed in 898 patients hospitalized during the period from June 1990 to November 1991. Acute icteric hepatitis cases with severe onset were distinguished by their referral to the fever hospital while cases with milder onset and those with chronic hepatitis were followed at two general hospitals. Antibodies to the c-100-3 antigen of hepatitis C virus (anti HCV) were detected in a significant proportion of patients with chronic liver disease (chronic active hepatitis (65%), cirrhosis (44%)). Anti HCV was also detected in patients with acute hepatitis with milder onset at the general hospitals (10.9%) but proportionately much less in patients at the fever referral hospital (< 1%) where hepatitis A (52%) and, to a lesser extent hepatitis B (11%), were mostly diagnosed. These results indicate that HCV is a major identifiable infection in hospitalized patients with chronic liver disease in this region but that anti HCV antibodies (c-100-3) are not detected, at least at onset, in sporadic cases with acute manifestations. Testing for additional viral antigens or RNA and a longer follow-up period would be required before exclusion of a role for HCV in acute disease. Alternatively, other viral and non-viral agents may be sought in this illness.
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PMID:Serodiagnosis of hepatitis C in acute and chronic liver disease in southwestern Saudi Arabia. 128 Dec 39


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