Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immune complexes (IC) were investigated in sera from 208 individuals with various clinical types of viral hepatitis diagnosed by clinical and laboratory criteria, including liver biopsy. Immune complexes were assessed by platelet aggregation (PI A) and by radioimmunoassay (RIA). The data were related to autoimmune phenomena (especially rheumatoid factors) and to the role that the IgM class of hepatitis B (HB) antibody might have in IC formation. Although the highest frequency of P1 A was in the few sera from patients with cirrhosis or hepatoma, the next highest was in sera from acute hepatitis patients (71%), and the lowest in sera from chronic active (57%) and chronic persistent (46%) hepatitis patients. A proportional number of patients with IC's were positive for hepatitis B surface antigen (HBs). A parallel prevalence was noted between P1 A and autoantibodies, with anti-Ig's being found more frequently in sera from acute hepatitis and chronic active hepatitis patients. The relationship between RIA results for complexes and RIA results for anti-IgG was inverse, as though anti-IgG interfered with IC reactivity by RIA. Anti-IgM pre-incubated with sera increased the amount of P1 A in sera from patients with acute hepatitis as well as in those from patients with chronic persistent hepatitis, suggesting a more frequent IgM involvement in IC's in these diseases than in chronic active hepatitis. Whereas liver cell damage in acute and active hepatitis may reflect elevated autoantibodies, the IgM class of HBs antibody may be involved in acute as well as chronic persistent hepatitis.
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PMID:Autoimmune implications of immune complexes in clinical variants of hepatitis B. 49 83

Sera from patients with chronic liver disease were tested for antibody against hepatitis B surface antigen by radioimmunoassay. The antibody was found in 25% of patients with alcoholic cirrhosis and in 52% when alcoholic cirrhosis was associated with portal hypertension, these results being significantly higher than in a matched control population. Other forms of chronic liver disease did not differ from the control population. Hepatitis B virus infection might be a factor in determining which alcoholic patients go on to develop chronic liver disease and cirrhosis.
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PMID:Hepatitis Bs antibody in alcoholic cirrhosis. 51 37

Thirty-five male patients with decompensated hepatosplenic schistosomiasis were longitudinally studied and divided into 3 Groups; with hepatitis B surface antigen (HBsAg) or antibody (anti-HBs) and a control group negative to both. Patients with HBsAg were persistently carrying the antigen as estimated by radioimmunoassay (RIA) for up to 3 years and when compared with the other 2 groups, they had significantly higher serum glutamic transaminases, their liver biopsy showed more destructive liver cell lesions in the form of chronic active hepatitis or liver cirrhosis, they were refractory to diuretic treatment and had higher mortality rate (64% in 3 years compared to 22% and 33% in the other 2 groups). The majority of patients with dual infection are at greater risk in spreading hepatitis B as they proved to carry the 'e' antigen.
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PMID:Chronic hepatitis B antigenaemia in patients with hepatosplenic schistosomiasis. 52 49

Families of 11 patients with hepatitis B surface antigen (HBsAg)-positive cirrhosis were studied to evaluate the immunologic correlates and extent of intrafamilial HBsAg clustering. Of 76 family contacts, 12 were identified to be asymptomatic carriers of HBsAg and two were diagnosed to have HSsAg-positive cirrhosis. The over-all HBsAg prevalence for the 76 contacts was 18% and that for all 87 members studied 29.0%. Serologic evidence of hepatitis B virus (HBV) infection (either HBsAg, anti-HBs, or both) was detected in 59% of all family members. HBsAg was more prevalent in males (47%) compared with females (16%), and anti-HBs was more prevalent in females (42%) compared with males (18%). Evidence of an immunologic response in clinically unaffected HBsAg-negative family contacts consisted of elevated serum IgG levels (mean 1660 mg/100 ml) and increased prevalence of anti-smooth muscle and antimitochondrial antibodies (16% and 6%, respectively). The prevalence of one or more autoantibodies in all HBsAg-negative family contacts was 20%, and it was higher in females (25%) than in males (13%). The present study demonstrates that HBsAg clustering occurs in families of patients with cirrhosis in the Jerusalem area and indicates that HBsAg-negative family contacts may have increased B-cell activity.
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PMID:Familial clustering and immune response in family contacts of patients with HBsAg-positive liver cirrhosis. 67 91

In order to assess the frequency of significant liver disease in hepatitis B surface antigen carriers with normal liver tests, 54 such individuals were identified and prospectively followed for 4 to 48 months with monthly liver tests. Upon testing, 4 were found to carry e antigen and 14 carried e antibody (anti-e). During follow-up, only 4 patients, none of whom were e antigen-positive, developed persisting abnormalities in liver tests. Of the 23 patients who underwent percutaneous liver biopsies, normal histologies were found in 2, nonspecific changes (ground glass hepatocytes, focal necrosis, fatty changes, etc.) in 18, and chronic persistent hepatitis (with or without other nonspecific changes) in 3. Chronic active hepatitis and/or cirrhosis, lesions which may carry more serious prognostic implications, were not seen in any biopsies. Two of the 4 e antigen-positive patients consented to biopsy, both of whom had chronic persistent hepatitis. All 6 patients with anti-e who underwent biopsy had ground glass hepatocytes, which were found in only about 50% of the remaining patients. It is concluded that hepatitis B surface antigen carriers should be followed with serial liver tests, and those whom tests remain normal should not be considered for liver biopsy.
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PMID:Hepatitis B surface antigen carriers--to biopsy or not to biopsy. 70 Mar 27

Circulating complete and defective hepatitis B virus forms, as represented by full, DNA polymerase-positive and empty, DNA polymerase-negative Dane particles, respectively, were investigated in sera from patients with chronic hepatitis B virus infection and related to the presence of e antigen and antibody and to the histological findings on liver biopsy. Complete hepatitis B virus particles were detected in the serum of all patients postive for e antigen, their percentage ranging from 15 to 61% of the total Dane particle population. Although most of these cases had chronic persistent or chronic active hepatitis, complete viral particles were also found in serum of 3 healthy carriers of hepatitis B surface antigen who had e antigen. These results indicate that e antigen is a marker of active virus replication and support its association with infectivity. It is also associated with liver damage because production of complete virus is a feature of chronic hepatitis. In the presence of anti-e, detection of Dane particles in serum appeared to be related to the histological findings. Most of the healthy carriers had no Dane particles in serum, whereas 80% of the cases with chronic liver disease had circulating Dane particles. However, in contrast to the cases with e antigen, 98 to 100% of Dane particles in these cases appeared to be defective in nucleic acid material on electron microscopy after positive staining. All of the patients with chronic active hepatitis in this group had progressed to cirrhosis and it is possible that production of complete virus particles is reduced in the later stages of the illness.
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PMID:Full and empty Dane particles in chronic hepatitis B virus infection: relation to hepatitis B e antigen and presence of liver damage. 70 Mar 29

Hepatitis type B is hyperendemic in Greenland with serologic evidence of infection in 54% of adults and a hepatitis B surface antigen (HBsAg) carrier rate of 7--25%. The impact of this infection rate on the occurrence of cirrhosis and primary liver cancer (PLC) was studied. Mortality rates for cirrhosis were obtained from official mortality statistics, 1951--1975. PLC was identified by a study of all biopsy and necropsy material taken in the study area during the same period. Neither cirrhosis nor PLC was found to be a more prevalent cause of death in this population than in Northern Europe where hepatitis B is at least 10-fold less prevalent. It is concluded that hepatitis B infection per se does not contribute significantly to the development of cirrhosis or to PLC, at least in the Eskimo population of Greenland.
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PMID:Occurrence of cirrhosis and primary liver cancer in an Eskimo population hyperendemically infected with hepatitis B virus. 70 73

Immunosuppressive treatment with prednisolone and/or azathioprine has been assessed in three chronic liver diseases with immunological features, namely chronic active hepatitis, cryptogenic cirrhosis and primary biliary cirrhosis. In chronic active hepatitis, controlled prospective clinical trials have shown clinical, biochemical and hepatic histological improvement when prednisolone with or without azathioprine is employed. Azathioprine alone has no advantage over placebo tablets. Cirrhosis is probably not prevented. Selection of patients for treatment, the response and therapeutic regimes are discussed. Patients with hepatitis B surface antigen positive chronic active hepatitis have a worse therapeutic response than those patients with chronic active hepatitis who are HBsAg negative. In primary biliary cirrhosis, corticosteroid treatment is contra-indicated on account of bone thinning. Azathioprine has been used in controlled clinical trials and is of only marginal benefit.
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PMID:Immunosuppressive therapy in chronic liver disease. 71 60

Sera of 184 patients were examined to determine the incidence of hepatitis B surface antigen (HBsAg). Ninety-two patients had primary liver cancer (PLC) and there were 92 matched controls. Thirty-one of the 92 patients with PLC and 8 of the 92 patients with no clinical evidence of liver disease had radio-immunoassay-positive tests for HBsAg. The difference was significant (P less than 0,01). In 56 of the patients with PLC it was possible to assess the nature of associated liver disease histologically. HBsAg was found in the sera of 66,6% of patients with postcollapse cirrhosis and in 22,2% of patients with chronic Budd-Chiari syndrome. It is likely that the role played by hepatitis B infection in the pathogenesis of PLC varies according to local circumstances in different geographical areas.
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PMID:Hepatitis B surface antigen and primary liver cancer. 71 32

Evidence of chronic hepatitis was found on histological examination in nine out of 15 patients positive for hepatitis-B surface antigen (HBsAg) who had either chronic renal failure or a functioning renal transplant. Cirrhosis had already developed in three of the patients, who deteriorated rapidly and died. Liver biopsies from the remaining 12 patients showed the features of chronic aggressive hepatitis in two, chronic persistent hepatitis in four, and minor histological lesions in six. The persistence of HBsAg in patients with renal failure or in those receiving immunosuppressive drugs after a transplant must indicate some impairment of the normal immune response to hepatitis-B viral antigens. Nevertheless, cellular or humoral immunity to HBsAg was detected in all eight patients with chronic hepatitis tested compared with only one out of five with minimal liver lesions, which suggests that the severity of the liver damage may be directly related to the degree of immunocompetence.
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PMID:Immune response to HBsAg and the spectrum of liver lesions in HBsAg-positive patients with chronic renal disease. 77 35


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