Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of antibodies to hepatitis C virus (anti-HCV) was studied in North East England in blood donors, local multiply transfused patients, local high risk individuals, and chronic liver disease patients. Anti-HCV was detected by enzyme-linked immunosorbent assay (ELISA) in 2/1120 (0.18%) blood donors; 1/84 chronic renal failure patients on haemodialysis who had received 1,992 units of blood (seroconversion rate of 0.05% per unit transfused), 1/207 cardiac patients 6 months post cardiac surgery transfused with 1,403 units of blood (1 anti-HCV pre-operatively, seroconversion rate 0.07%), 40/50 haemophilia A patients treated with commercial factor VIII, and 38/100 intravenous drug users. In addition anti-HCV was detected by ELISA in 5/35 cryptogenic chronic liver disease patients, 5/5 confirmed by recombinant immunoblot assay (RIBA) (14%); 3/30 patients with autoimmune chronic active hepatitis, 2/3 by RIBA (7%); 2/50 primary biliary cirrhosis patients, 1/2 by RIBA (2%); 0/30 alcoholic cirrhosis patients; and 2/9 patients with hepatocellular carcinoma, 1/2 by RIBA (11%). HCV is uncommon in North East England; it may be implicated in the aetiology of a minority of cases of cryptogenic liver disease and less than 5% of autoimmune chronic active hepatitis and primary biliary cirrhosis.
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PMID:Low prevalence of antibody to hepatitis C virus in north east England. 196 76

The rate of HBeAg clearance and the outcome were analyzed in 46 patients with asymptomatic chronic hepatitis B virus (HBV) infection whose condition was followed for 1-4 yr (mean 2.4). Mean age was 32.5 yr (range 10-68), and 28 (61%) were males. All had chronic hepatitis, on biopsy, and were positive for HBcAg on hepatocytes. Alcoholics, homosexuals, drug abusers, immunocompromised patients, and those with advanced liver disease were excluded. During the follow-up, 25 patients (54%) cleared HBeAg and became seronegative for HBV-DNAp. The estimated annual rate of seroconversion was 26%. One patient cleared HBsAg. After seroconversion, 18 patients had no evidence of ongoing liver disease, proved by biopsy in eight and by clinical follow-up in 10 that refused biopsy. A second liver biopsy was available in 15 patients, and HBcAg was negative in all; histology was normal in eight, unchanged in one, and compatible with cirrhosis in six. All six had clinical and/or biochemical evidence of advanced liver disease. These were significantly older at the start of the study, and had chronic active hepatitis with bridging necrosis on initial biopsy. Early identification of patients with silent chronic HBV infection and high levels of viral replication for antiviral therapy could prevent transmission of the infection and stop progression to liver cirrhosis and hepatocellular carcinoma.
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PMID:Development of cirrhosis after chronic type B hepatitis: a clinicopathologic and follow-up study of 46 HBeAg-positive asymptomatic patients. 202 45

The sera from patients with various liver diseases were investigated for the antibody against calmodulin (CaM) extracted from bovine brain by the enzyme linked immunosorbent assay. The specificity and purity of CaM were confirmed by the Western blot technique using anti-CaM antibody (anti-CaM) positive sera. IgA class antibody was frequently detected in patients with hepatocellular carcinoma (HCC), autoimmune hepatitis (AIH) and chronic active hepatitis (CAH). On the other hand, IgG class antibody was very often present in patients liver cirrhosis, AIH and acute viral hepatitis (AVH). Sixty seven percent of patients with AVH in the acute phase were positive for IgM class anti-CaM and 33% of patients with AVH in the convalescent phase positive respectively. In AVH, the titer of anti-CaM reached its peak on 26.3 days after the onset. The titer of anti-CaM in fulminant hepatitis was higher than that in AVH. Seventy percent of type A hepatitis patients were positive for IgM class anti-CaM, 33% of type B and 33% of type non-A non-B. These results suggest that the frequency and titer of anti-CaM may depend upon the type of hepatitis and the degree of liver cell injury.
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PMID:[Clinical significance of antibodies against calmodulin in patients with various liver diseases]. 203 May 58

Cirrhosis is the usual end-result of chronic active autoimmune hepatitis. Different immunological abnormalities divide chronic active hepatitis into 3 subgroups: type I with anti-smooth muscle antibody; type II with anti-liver/kidney microsome antibody type 1 (anti-LKM1 antibody) and type III with an antibody directed against a soluble hepatic antigen. Three quarters of the patients are young women. The liver disease is often diagnosed at the stage of chronic active hepatitis, during evaluation of the subject's general condition or during investigations for an episode of jaundice; it is seldom diagnosed at the stage of constituted or decompensated cirrhosis. Fulminant forms are rare. Extrahepatic autoimmune manifestations are frequently encountered. Treatment relies on immunosuppressants, in practice corticosteroids. Corticosteroid therapy significantly prolongs the patient's life, but it does not prevent the passage to cirrhosis. In the long term these patients are exposed to all the complications of cirrhosis, notably the occurrence of hepatocellular carcinoma.
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PMID:[Cirrhosis secondary to chronic autoimmune hepatitis]. 206 15

The concept of auto-immune hepatitis as a disease entity evolved from the descriptions of 'chronic active hepatitis' (CAH) in the 1950s. Several types of CAH are distinguished by disease-specific features. The distinctive (but not exclusive) markers for auto-immune CAH include: a negative test for HBsAg; female; Northern European ethnic background; multisystem disease expression; histological CAH with large areas of periportal piecemeal necrosis and plasmacytosis; pronounced hypergammaglobulinaemia; serum auto-antibodies the HLA B8-DR3 phenotype; responsiveness to corticosteroid therapy; and rarity of supervening hepatocellular carcinoma. Much weight is attached to the serological marker auto-antibodies to nuclear or smooth muscle (actin) antigens (ANA, SMA). However, these auto-antibodies do not have an absolute association with auto-immune CAH: the serological reactions are not yet standardized; titres decrease with remission of disease; and other auto-antibodies mark variant forms of auto-immune hepatitis. A more confident acceptance of auto-immune hepatitis as an entity requires detection of a liver-specific antigen, a valid experimental disease model in animals, and a better understanding of immune-mediated damage to liver cells.
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PMID:Auto-immune (lupoid) hepatitis: an entity in the spectrum of chronic active liver disease. 210 17

The prevalence of glucose intolerance has been studied by oral glucose tolerance test in 670 patients affected by chronic liver disease. The glycometabolic status was evaluated by criteria given by WHO in 1980. Sixty-nine subjects appeared to be affected by chronic persistent hepatitis and 140 by chronic active hepatitis. In these patients the prevalence of diabetic responses (DR) did not differ much from that of the general population in our geographic area. In contrast, a markedly higher frequency of DR appeared in a cirrhotic group of 401 patients compared to non-cirrhotic subjects. The cirrhotics, divided according to different disease stages, showed a higher DR frequency in decompensated patients than in well compensated patients, the prevalence reaching 63% in the former subgroup. The coincident presence of hepatocarcinoma - documented in 60 other cirrhotic patients - does not modify the prevalence of diabetes. Other risk factors for diabetes such as age, sex, and family history have been considered. Our results suggest that: (1) all these factors seem not to play a major role in the pathogenesis of alterations of glucose metabolism in patients suffering from chronic liver disease, and therefore (2) liver cirrhosis by itself might be a risk factor in the disturbance of glucose tolerance.
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PMID:Alterations of glucose metabolism in chronic liver disease. 215 13

The phenotypes of alpha-1-antitrypsin have been analyzed by isoelectric focusing on polyacrylamide gels in 232 healthy Japanese blood donors and in 240 Japanese patients with chronic liver diseases: 69 with chronic active hepatitis, 122 with liver cirrhosis, 41 with hepatocellular carcinoma and 8 with primary biliary cirrhosis. The liver cirrhosis patients had a gene frequency of 0.07 for P1*M3, which was significantly higher (P less than 0.01) than that (0.03) in blood donors. The gene frequency of P1*M3 was significantly increased in cryptogenic liver cirrhosis (P less than 0.05), and there was a tendency toward an increased frequency of P1*M3 in post-transfusion groups, and in primary biliary cirrhosis. There were also tendencies toward increased frequencies of P1*M3 in cryptogenic and post-transfusion groups of patients with chronic active hepatitis. The present study indicates that P1*M3 is a genetic or predisposing factor for chronic liver diseases, especially for cryptogenic and/or non A-non B viral chronic liver disease and also for primary biliary cirrhosis.
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PMID:An association between alpha 1-antitrypsin phenotype and chronic liver disease. 215 26

During the period 1986-1988, the expression of anti-HDV in different high-risk groups and its clinical impact on patients with HBV-related chronic liver disease and hepatocellular carcinoma was investigated in Iran. Using the ELISA technique, we observed a 2.5% anti-HDV positivity in asymptomatic chronic HBsAg carriers (3 of 120); in hemophiliacs, two of six HBsAg carriers were positive for anti-HDV and zero of 50 anti-HBs positives. Anti-HBs positive dialysis patients were positive for anti-HDV in 2.0% of the cases (1 of 50), whereas the rate of anti-HDV positivity was 44.5% in hemodialysis patients positive for HBsAg (16 of 36). The figures were comparable in HBsAg positive patients with chronic active hepatitis and cirrhosis (49.2%; 31 of 63). Moreover, anti-HDV was detected in five of eight patients with hepatocellular carcinoma. These data indicate the endemicity of delta infection in Iran. The increased incidence among hepatocellular carcinoma patients is an interesting finding to be further investigated with larger groups of patients in this region.
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PMID:A study on delta virus infection and its clinical impact in Iran. 215 76

A total 1400 hepatitis B surface antigen-positive Alaska natives, 824 men and 576 women of all ages, were followed up prospectively over a period of 7815 carrier years for the development of sequelae related to chronic hepatitis B virus infection. During the observation period, 20 cases of hepatocellular carcinoma, 14 cases of chronic active hepatitis, 8 cases of cirrhosis, and 1 case of glomerulonephritis developed in this cohort. The annual incidence of hepatocellular carcinoma was 387 per 100,000 for men and 63 per 100,000 for women. The incidence of chronic active hepatitis and cirrhosis was 193 and 107 per 100,000 in men and 158 and 95 per 100,000 in women, respectively. No cases of either essential mixed cryoglobulinemia or necrotizing vasculitis were seen. Sixty of the hepatitis B surface antigen-positive carriers died, with 13 (21.7%) of the deaths due to hepatocellular carcinoma. The leading cause of death in this group was malignant neoplasms compared with accidents in the general Alaska native population.
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PMID:Hepatitis B-related sequelae. Prospective study in 1400 hepatitis B surface antigen-positive Alaska native carriers. 215 73

Primary hepatocellular carcinoma, one of the most common malignancies in the world, develops in chronic liver diseases of different etiologies. Hepatitis B and non-A, non-B infections, alcoholic cirrhosis, hemochromatosis, contamination with aflatoxins, and oral contraceptives are just a few of the conditions that have been associated with this carcinoma. To our knowledge, few cases of autoimmune chronic active hepatitis and hepatocellular carcinoma have been reported in the literature. We describe a patient who developed hepatocellular carcinoma 21 years after the onset of the autoimmune hepatitis.
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PMID:Hepatocellular carcinoma associated with autoimmune chronic active hepatitis. 216 43


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