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)

Three hundred and eighty-five patients mostly with chronic liver diseases and 729 apparently healthy adults were studied for hepatitis B surface antigen (HBsAg) with reversed passive hemagglutination and antibody (anti-HBs) with passive hemagglutination. In healthy adults around 15% was HBsAg positive and in 45% was anti-HBs positive, estimating hepatitis B virus (HBV) infection in nearly two thirds of the population. The infection already occurred before adulthood. The prevalences of HBsAg were invariably over 80% in chronic hepatitis, cirrhosis and hepatocellular carcinoma (hepatoma) indicating an intimate relationship to HBV. On the contrary, the positive rates of anti-HBs in these diseases were far lower than those in healthy people and patients with other diseases, this is similar to the situation in chronic HBsAg carriers. The prevalence of HBsAg in hepatoma patients was unusually high, being 82.7% in contrast to 11.9% in patients with other malignancies. Not only hepatoma patients with cirrhosis but also those without cirrhosis were found to have high prevalence of HBsAg. The fact indicates an even more intimate relationship between hepatoma and HBV.
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PMID:Hepatitis B virus infection and chronic liver disease in Taiwan. 21 87

Family member of 13 patients with hepatitis B surface antigen (HBsAg) positive primary hepatocellular carcinoma (PHC) were tested for the presence of hepatitis B virus-associated antigens and antibodies. Of the 122 members examined, circulating HGsAg was detected in 47 (39%), antibody to HBsAg (anti-HBs) was found in 37 (30%), and antibody to hepatitis B core antigen (anti-HBc) alone was present in 13 (11%). The relatives with the highest frequency of HBsAg positivity were the offspring of the propositus, followed by the nieces and nephews and the grandchildren. Anti-HBs and anti-HBc were detected most often in the spouses and non-blood relatives. Evidence for past and present hepatitis B virus (HBV) infection was more frequently found in the Asian family members when compared to the non-Asians. The e antigen (HBeAg) was present in 38% of the HBsAg positive individuals, including four with PHC; antibody to HBcAg (anti-HBe) was rarely detected. These results indicate that clustering of HBV infection was commonly present in family members of patients with PHC. The HBsAg positive individuals may be major contributors to the endemic pool of the virus, and may themselves be potential cases of chronic active type B hepatitis, cirrhosis, and PHC.
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PMID:Evidence for clustering of hepatitis B virus infection in families of patients with primary hepatocellular carcinoma. 22 43

Most series in Africa show a high percentage of hepatitis B surface antigen in hepatocellular carcinoma. Two groups of cases were investigated in this study. The one was derived from the autopsy material at Baragwanath hospital from subjects who had lived in Soweto, a large Black urban town. The second group consisted of male Black mineworkers generally originating from rural areas. A combination of the aldehydefuchsin stain and immunoperoxidase technique was used. The two groups showed totally different results. The Baragwanath series consisted of 24 hepatocellular carcinomas of which only 4 (17%) were HBsAg positive. Of the 24 cases, 14 had cirrhosis of which 9 were macronodular and 5 micronodular. Ten of these cases showed heavy iron overload. The series of male Black mineworkers comprised 22 cases of which 16 (72%) were HBsAg positive. Twelve of the 22 cases showed a macronodular cirrhosis and there were no micronodular cirrhoses. Only one case showed severe iron overload. These findings delineate two different populations of hepatocellular carcinoma in Southern Africa.
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PMID:Hepatitis B surface antigen and hepatocellular carcinoma in Southern Africa. 23 51

Liver specimens of 31 autopsied cases of liver cirrhosis who had had detectable levels of antibody to hepatitis B core antigen (anti-HBc) inthe serum were stained for hepatitis B core antigen (HBcAg) and hepatitis B surface antigen (HBSAg) by the direct immunofluorescence method. Their premortem serum samples were tested for HBSAg, antibody to HBSAg (anti-HBS) and anti-HBC. Persistent hepatitis B virus (HBV) infection as judged by circulating and/or liver HB antigens was identified in 18 patients, and all of them revealed a high titer of anti-HBC ranging from 2(11) to 2(16) by the immune adherence hemagglutination method. In contrast, anti-HBC titer of the remaining 13 patients without detectable HB antigens was less than 2(9), and the geometric mean titer of anti-HBC of the patients with persistent HBV infection was significantly higher than that of the patients without (13.9+/-1.55 versus 7.23+/-1.30; t test, P less than 0.001). A combination of circulating anti-HBS and hepatic HB antigens was found in one patient, whose serum revealed an anti-HBC titer of 2(12). On the basis of these results, a high titer of anti-HBC in the serum (immune adherence hemagglutination titer of 2(11) or more) seems to be a reliable indicator of persistent HBV infection in the liver.
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PMID:Correlation between titer of antibody to hepatitis B core antigen and presence of viral antigens in the liver. 33 Mar 6

Rapid progression of acute type B hepatitis to chronic active liver disease and cirrhosis in a young male with hypogammaglobulinemia is described. Absent circulating IgA, significantly low IgG, and normal IgM levels were detected during the acute phase of illness. Enumeration of peripheral lymphocytes revealed a decreased number of T cells and normal numbers of B cells. In vitro pokeweed stimulation of Ig synthesis correlated with the in vivo circulating levels of the three immunoglobulins. Cell-mediated immune responses were normal except for lymphocyte stimulation to hepatitis B surface antigen. It was concluded that the defective synthesis of IgG and IgA antibodies to hepatitis B surface antigen contributed to the accelerated progression to chronic active type B hepatitis in this person.
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PMID:Rapid progression of chronic active type B hepatitis in a patient with hypogammaglobulinemia. 33 24

The records of 192 cadaver renal allotransplants were reviewed in order to evaluate the role of the hepatitis B antigen (HBsAg) carrier state on graft function, patient survival, and the incidence of severe hepatic dysfunction. Twenty-one allografts were placed into patients with hepatitis B antigenemia. After follow-up ranging from 1.5 to 8 years (mean 4.7), graft and patient survivals were not statistically different from antigen-negative patients. In addition, the acquisition of HBsAg after grafting did not seem to affect the rate of graft failuue or death. Neither cirrhosis not fatal hepatic failure developed in the HBsAg carrier group, whereas five HBsAg-negative recipients died of hepatic disease. Among HBsAg-positive recipients, nine with functioning renal allografts and five with graft failures, there was a low incidence of e antigen, suggesting low infectivity. This may explain the lack of correlation of the surface antigen with serious liver disease. Severe hepatic disease developing in renal graft recipients is most likely attributable to causes other than hepatitis B infection. The presence of hepatitis B antigenemia alone should not be a deterrent to renal transplantation.
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PMID:The effect of hepatitis B antigenemia on long-term success and hepatic disease in renal transplant recipients. 33 36

Kidney tissue from 99 unselected necropsy cases of various forms of hepatitis and liver cirrhosis was examined by histology and direct immunofluorescence. Glomerular deposits of hepatitis B surface antigen (HBsAg), IgG, IgM, and complement were found in nine of 59 cases (15%) of acute and subacute hepatitis and in seven of 40 cases (17%) of chronic aggressive hepatitis and liver cirrhosis. Different amounts of granular hepatitis B surface antigen immune deposits were distributed along glomerular capillary walls and/or in mesangial areas. Glomerular lesions found in these cases consisted of thickening of glomerular capillary walls, a slight increase in glomerular cellularity, and an increase of mesangial matrix. These glomerular lesions are considered to result from the humoral immune elimination of circulating viral surface antigen immune complexes.
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PMID:Kidney glomerular pathology in various forms of acute and chronic hepatitis. 36 29

A patient suffering from chronic active hepatitis with macronodular cirrhosis, positive for hepatitis B surface antigen (HBsAg), was treated with an orthotopic liver allograft. The HBs antigenemia, as measured with several precipitation tests and by complement fixation, became negative after transplantation and remained so for about 2 1/2 months. During the interval, very low titers of the antigen were detectable by radioimmunoassay. At about three months after transplantation, she had an attack of acute hepatitis, at which time HBsAg became detectable by all tests. She recovered, but progressive liver disease developed during the remaining 1 1/2 years of her life. She died of disseminated nocardiosis and candidiasis with deteriorating hepatic function. The homograft at autopsy showed no evidence of rejection, but was the site of chronic active liver disease, although of a different pathologic pattern than that affecting her native liver. The differences in histology may reflect the influence of chronic immunosuppression on the features of chronic active hepatitis.
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PMID:Liver allograft. Its use in chronic active hepatitis with macronodular cirrhosis, hepatitis B surface antigen. 36 34

Single liver biopsies from 102 clinically diagnosed hepatitis patients were examined by immunofluorescence for the presence of hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg), complement and immunoglobulin deposition, and for their capacity to fix human complement in vitro. Of the sixty-five HBsAg positive livers, fifty-three were histologically diagnosed as chronic hepatitis, three as acute hepatitis, five as acute hepatitis with signs of transition to chronicity, and four as 'near normal liver'. In the group with chronic hepatitis, HGcAg was observed in thirty-nine livers, all of which also had HBsAg. Thirty-five of these thirty-nine cases also had the ability to fix complement in vitro in the hepatocyte nuclei and/or cytoplasm. Of these thirty-five cases, twenty-nine were positive for immunoglobulin deposition on the nuclei. All of these cases had antibody to HBcAg in the blood, but only five had anti-HBs. The frequency of in vitro complement fixation and immunoglobulin deposition was higher in active forms of the disease, such as chronic aggressive hepatitis and active cirrhosis, than in non-active disease such as chronic persistent hepatitis and mild cirrhosis. By the application of double fluorescent staining techniques, complement fixation was observed in some HBcAg-positive nuclei. In the 'near normal liver' cases there was no intrahepatic accumulation of HBcAg, and despite the presence of anti-HBc in the blood, in vitro complement fixation and immunoglobulin deposition were both absent. The group of three HBsAg ositive 'acute hepatitis with signs of transition to chronicity' cases behaved similarly to those with chronic aggressive hepatitis and had circulating anti-HBc, in vitro complement fixation and immunoglobulin deposition in the hepatocytes. None had circulating anti-HBs. In the group sith HBs-positive acute hepatitis, anti-HGc in the blood was the only other evidence of hepatitis B virus infection.
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PMID:Hepatitis B core antigen immune complexes in the liver of hepatitis B patients. 38 86

Two hundred four volunteer blood donors with hepatitis B surface antigen found in their blood were followed for 3 to 44 months. The annual clearance rate of this antigen was 1.7%. Liver enzyme levels (aminotransferase) were elevated in 45 (22.1%) on at least one occasion, in 26 (12.7%) for one month or more, and in 13 for more than six months. Liver biopsies were performed on 17 chronic carriers with normal enzymes and nonspecific histologic abnormalities were found in 14 and mild diffuse hepatitis in three. Seventeen carriers with abnormal enzymes were biopsied, and specimens revealed chronic active hepatitis (CAH) in seven, including two with bridging necrosis and three with cirrhosis. CAH was found in 7 of 26 (26.9%) carriers with abnormal liver enzymes persisting for at least one month and 4 of 13 (30.8%) with abnormal liver enzymes for more than six months.
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PMID:The liver histology and frequency of clearance of the hepatitis B surface antigen (HBsAg) in chronic carriers. 42 95


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