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)

The presence of hepatitis B surface (HBsAg) and core (HBcAg) antigens was investigated by immunofluorescence in specimens of liver tissue obtained at necrospy in 107 patients with primary hepatic carcinoma. HBsAg was detected in the cytoplasm of liver cells in 16 cases, and in eight of them the antigen was also found in malignant cells. HBcAg, which was present in the nuclei of liver cells in eight cases, was detected in the nuclei of tumour cells in six of these and also in two other cases showing HBsAg, but not HBcAg, in the nonneoplastic tissue. Although most of the primary hepatic carcinomas studied were associated with cirrhotic changes in the non-neoplastic tissue, HBsAg and HBcAg were also detected in the absence of underlying cirrhosis. Hepatitis B virus markers were demonstrated in non-neoplastic tissue, mainly in patients with a well-differentiated carcinoma, and only in these cases were they found also in the neoplastic tissue. These results show that hepatitis B virus antigens, including HBcAg, can be detected in the neoplastic cells of well-differentiated carcinoma of the liver. Although these cells could have been infected after the malignant transformation, a direct oncogenic role of the virus cannot be excluded.
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PMID:Hepatitis B virus antigens in primary hepatic carcinoma: immunofluorescent techniques on fixed liver tissue. 21 38

Among 7763 autopsies performed in Greater Copenhagen in 1973, there were 309 cases of cirrhosis of the liver and 52 cases of primary carcinoma of the liver (PCL). Of the latter, 45 were hepatocellular carcinoma (HCC), 4 combined HCC and cholangiocarcinoma (CCC) and 3 CCC. HCC was found in 7.8 per cent of the cirrhotic livers and was in 57.1 per cent accompagnied by cirrhosis. The criteria of WHO, Peters (modified) and Anthony were used for classification. The degree of differentiation of the tumours was estimated using the criteria of WHO and Edmondson. The apparently small number of CCC may be due to the fact that this tumour is often overdiagnosed at the expense of HCC. The incidence of combined tumours is probably higher than generally assumed. The reticulin stain was found very valuable in HCC, both for descriptive and diagnostic purposes. In contrast to the situation in sub-Saharan Africa where hepatitis B virus is incriminated as the most important etiologic factor of HCC, it was found in the present study that alcoholism was a very essential cause of cirrhosis and thereby of HCC.
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PMID:Primary carcinoma of the liver. A histological study of 52 cases from Denmark. 22 41

Liver cell dysplasia was noted on histological examination of nontumorous liver from 24 of 50 (48%) black southern African males with hepatocellular carcinoma (HCC). Macronodular cirrhosis was present in 40 (80%). There was no statistically significant difference between the frequency of dysplasia in 50% of 40 cirrhotic and 40% of 10 noncirrhotic livers, or in 52.6% of 38 hepatitis B antigen (HBAg) positive and 33.3% of 12 HBAg negative HCC patients. HBAg positivity was present in 80% of 40 cirrhotic and in 60% of 10 noncirrhotic HCC patients. This lack of significant correlation between liver cell dysplasia, and both cirrhosis and HBAg positivity in HCC patients in contrast to findings in Uganda and the United States, suggests a different pathogenetic mechanism for dysplasia in southern Africa. Liver cell dysplasia in man appears to be analogous to preneoplastic experimentally-induced hyperplastic foci or areas.
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PMID:Liver cell dysplasia: association with hepatocellular carcinoma, cirrhosis and hepatitis B antigen carrier status. 22 74

Until now, the hepatitis B virus has been thought to play a minor role in the aetiology of chronic liver disease in Australia. This is a report of 21 patients with cirrhosis and/or primary hepatocellular carcinoma with hepatitis B antigenaemia. Primary hepatocellular carcinoma occurred in six patients, five of whom had underlying cirrhosis. The disease occurred mainly in non-Australian born males, and was not often associated with a previous history of hepatitis. The death of 16 patients within 12 months of presentation is in contrast to previous concepts of the benign nature of hepatitis B associated cirrhosis.
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PMID:Emerging patterns of hepatitis B chronic liver disease in Australia. 22 47

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

Ninety-five patients with Hemophilia A, B and von Willebrand's disease followed over a three year period were evaluated for liver disease. Half of the patients were treated episodically and half received additional prophylactic treatment. Fifty-five per cent have significant transaminitis (elevated SGOT-SGPT), 42 per cent have biochemical evidence of chronic active liver disease and two per cent have subacute and active cirrhosis. There is an annual attack rate of Hepatitis B disease of 3.5 per cent and Hepatitis B antibody titres are present in 84 per cent. This asymptomatic liver disease requires close monitoring for clinical significance.
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PMID:Liver dysfunction in patients with hemophilia A, B, and von Willebrand's disease. 30 96

A Farr technique has been used to assay antibodies to double-stranded DNA in the serum of patients with acute and chronic liver disease and carriers of HBsAg from the United Kingdom and Iraq. These antibodies were found in all groups from both countries. The highest levels were found in chronic active hepatitis and cirrhosis. In the Iraqi patients there was a strongly positive correlation between DNA-binding antibody levels and the presence of hepatitis B markers but not with disease activity. In the patients from the United Kingdom there was little correlation with disease activity and none with autoantibodies. Ninety-five per cent of asymptomatic carriers of HBsAG had elevated DNA-binding antibodies. It is suggested that hepatitis B-specific DNA might be one trigger to DNA antibody formation, though in liver disease a variety of factors are clearly operative.
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PMID:DNA-binding antibodies and hepatitis B markers in acute and chronic liver disease. 30 8

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


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