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)

Forty patients with chronic liver disease and HCC were analyzed for infection with hepatitis C (HCV) and hepatitis B (HBV) viruses. All patients were negative for HBsAg, 16 were alcoholics, 6 had previous blood transfusions and 18 had sporadic chronic hepatitis. Antibodies to HCV were determined by EIA 2nd generation. HBV-DNA was detected by PCR using primers of the precore region. Analysis of HCV-RNA was done with nested PCR amplifying the 5' non-coding region of the HCV genome, using primers complementary to nucleotides 1-20 and 305-320 and nested primers complementary to nucleotides 21-31 and 271-286 of the HCV-J1. Anti-HCV were positive in 35/40 patients (87.5%). HCV-RNA was detected by PCR in 34 patients (85%) all of them positive for the anti-HCV. HCV-RNA was detected in 70.5% of the alcohol abusers, in 100% of patients with history of transfusion(s) and 94.1% of patients with cryptogenic chronic liver disease. HBV-DNA was detected in only 2 patients. In conclusion, there is a high rate of HCV and a low rate of HBV viremia detected by PCR in Spanish patients with HCC HBsAg negative. No patient without anti-HCV presents HCV-RNA. Our results suggest that persistent HCV replication may play a role in hepatic carcinogenesis, as HBV-DNA could be found in only 5% of our HCC patients.
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PMID:Demonstration of HCV-RNA and HBV-DNA in the serum of HBsAg negative patients with hepatocellular carcinoma. 781 97

Potential risk factors for the development of primary hepatocellular carcinoma and the prevalence and role of infection with viral hepatitis B and hepatitis C were investigated in 54 adult patients of Bangladeshi origin (45 male, age range 20-75 years), comprising 46 patients resident in Bangladesh (Group 1) and 8 patients who had emigrated to the UK 10-20 years previously (Group 2). Of the 46 patients in Group 1 (37 male), 16 had hepatocellular carcinoma, 10 had uncomplicated cirrhosis, and 20 had a clinical history of chronic viral hepatitis of more than 6 months' duration. Total hepatitis B virus marker positivity was 82.6%, significantly higher than in Group 2 patients (P < 0.001). Thirty-six per cent were hepatitis B surface antigen positive, 66% were hepatitis Be antigen positive and 45.3% were positive for hepatitis C virus antibody. Taking only the 16 patients with hepatocellular carcinoma, hepatitis B surface antigen positivity was 38%, hepatitis Be antigen 66% and positivity to hepatitis C virus antibody was 56%. The 8 patients with hepatocellular carcinoma in Group 2 were all male and aged between 45 and 56 years. Of these, 3 (38%) cases were positive for hepatitis B surface antibody and none was positive for hepatitis B surface antigen or antibody to hepatitis C virus (3 cases tested). Presenting features of HCC in the two groups differed with a short clinical history of tender abdominal mass in Group 1 and a gradual onset of jaundice in Group 2 UK-resident Bangladeshi subjects.
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PMID:Primary hepatocellular carcinoma and viral hepatitis B and C infection in Bangladeshi subjects. 786 82

Viral causes of acute or chronic hepatitis are the hepatitis A virus [HAV], the hepatitis B virus [HBV], the hepatitis C virus [HCV], the hepatitis delta virus [HDV], and the hepatitis E virus [HEV]. These viruses haven been characterized in great detail and can be detected by specific and sensitive serological or molecular assays. While HAV and HEV cause only acute hepatitis, infection with HBV, HCV or HDV frequently takes a chronic course. With time chronic viral hepatitis can progress to liver cirrhosis and its clinical sequelae as well as to hepatocellular carcinoma [HCC]. Apart from prophylactic measures aimed at the prevention of these viral infections, for those chronically infected natural or recombinant alpha-interferon may be a therapeutic option with the potential to prevent the development of liver cirrhosis and HCC.
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PMID:[Viral hepatitis A to E--diagnosis, clinical aspects and therapy]. 794 Apr 9

A mouse monoclonal antibody directed against the protein of hepatitis B virus X open reading frame was prepared. After radiolabeled with sodium 131I-iodine and administration, imaging was performed with gamma camera and radioactivity of the tumor, organs, and blood were counted in a mini-gamma counter at day 1, 3, 5, 7 in nude mice bearing HCC xenografts, and the biodistribution and T: NT ratio was calculated. Selective accumulation was observed in tumor sites on day 3 and a clear image of tumor was shown in gamma camera on day 7. The image of tumor in the irrelevant IgG group was not obtained at any time. The tumor:blood ratio was 0.48 and tumor:liver was 1.2 on day 1, then increased to 1.5 and 4.5 on day 7 in experimental group, respectively. Specific mAb uptake by tumor was significantly greater than nonspecific IgG(P < 0.05) on day 7. The results were encouraging. The finding of this study indicates the possibility of using 131I-anti-HBx mAb to target cytostatic drugs to HCC.
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PMID:[Radioimmunoimaging with monoclonal antibody to HBV X protein in nude mice bearing human hepatocellular carcinoma]. 803 39

To examine the significance of mutation of the p53 tumour suppressor gene in the development of human hepatocellular carcinoma in a high-prevalence area for hepatitis B viral infection but a low-exposure area for aflatoxin B1, the spectrum of p53 gene mutations was examined in 21 tumour samples from Hong Kong Chinese patients, all of whom were HBsAg positive. DNA sequencing covering exons 5 to 9 of the p53 gene and Hae III restriction enzyme digestion for preliminary assessment of mutation at codon 249 were performed. Immunohistochemical staining with anti-p53 monoclonal antibodies was done on both tumour and nontumour liver tissues. Six tumours (28.6%) showed a p53 mutation and all were point mutations. Of the six point mutations, two (9.5%) were at codon 249 and both were G to T transversions (AGG-->ATG and AGG-->AGT transversions). The remaining point mutations were transversions scattered at codon 172 (exon 5), 214 (exon 6), 273 (exon 8) and 330 (exon 9). Mutated p53 protein was detected in five of these six cases with demonstrable point mutations by DNA sequencing, in contrast to none detected in all of the 15 cases without demonstrable point mutations. The presence of p53 mutations, including those at codon 249, did not show a significant association with tumour size, sex, age, tumour invasiveness in terms of liver invasion, microsatellites and venous permeation, cirrhosis and encapsulation, but tumours with low cellular differentiation tended to have a higher incidence (71%) of point mutations than those with high cellular differentiation (8%). In conclusion, both the overall p53 mutation rate and that a codon 249 in HCC in Hong Kong Chinese are lower than those reported in tumours from China and sub-Saharan Africa. The low mutation rate at codon 249 is compatible with a low aflatoxin exposure. A special type of p53 mutation has not been found to be associated with hepatitis B viral infection. Mutations of p53 gene tends to occur in tumours with low cellular differentiation, suggesting a late occurrence in the event of tumour progression.
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PMID:p53 gene mutation spectrum in hepatocellular carcinomas in Hong Kong Chinese. 810 45

A comparative analysis of preC sequences of hepatitis B virus (HBV) in human hepatoma (hepatocellular carcinoma; HCC) tissues and non-tumoral liver samples from HCC patients was performed. Ten out of 17 HCC tissue samples exhibited an amino acid substitution at the level of the distal cysteine residue of the HBV preC region, while generation of a TAG translational stop codon was observed in 4 of these samples. Interestingly, substitution of the distal cysteine residue was not observed in non-tumoral liver (available from 8 of the 17 patients), thus suggesting either that a selection among different HBV variants occurs in HCC cells, or that modifications to the conformation and stability of the HBV capsid protein may play a role in the process of selection and escape of transformed liver cells.
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PMID:Hepatitis B virus preC mutants in human hepatocellular carcinoma tissues. 821 Jul 12

Hepatocellular carcinoma samples obtained from 59 patients at surgical resection were examined for mutations of the third base at codon 249 of the p53 gene, using the polymerase chain reaction and oligonucleotide hybridization techniques. This point mutation, which is frequently observed in HCC cases from Southern Africa and Quidong in China, was not recognized in either 60 hepatocellular carcinomas or 53 noncancerous liver tissue samples from Japan. Thirty-four of 45 patients (75.6%) were positive for the hepatitis C virus, which was a higher rate than that for hepatitis B virus infection (9 of 55; 16.4%). The exposure to aflatoxin B1 was not considered to be remarkable. These results suggest that the point mutation of the third base at codon 249 is not common in Japanese patients, and it is suggested that numerous other factors affect the mutation of the p53 gene and the development of hepatocellular carcinoma.
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PMID:The mutation of codon 249 in the p53 gene is not specific in Japanese hepatocellular carcinoma. 825 41

A review of the histopathology and demonstration of alpha-interferon with a monoclonal anti-alpha-interferon antibody reagent were carried out in 71 consecutive cases of acute and chronic hepatitis, and also in some cases of cirrhosis and HCC. The main cells expressing alpha-interferon were lymphocytes, plasma cells, fibroblasts and polymorphonuclears. There was no evidence for local alpha-interferon production near the site of virus replication in hepatitis B infection. Eleven cases of hepatitis were positive for alpha-interferon. The carrier state showed the highest positive rate in the different types of hepatitis. The positive rate in acute and chronic persistent hepatitis was lower than that in carrier state but higher than that in cirrhosis and HCC. The alpha-interferon positive cells were mainly located in the portal area and in the fibrotissue band around the necrotic and/or carcinomatous cells. These suggest that the function of the interferon system was related mainly to the pathological changes of liver tissue. Early use of interferon might be of therapeutic value to protect liver tissue from injury and to improve the interferon response of the host.
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PMID:[Detection of alpha-interferon positive cells in liver tissue from patients with hepatitis]. 839 41

Viral hepatitis has a high prevalence in East Asia and is an important problem. Identification of the individual hepatitis viruses. A-E, has enabled researches to investigate the epidemiology and pathogenesis of viral hepatitis and its sequelae, and possible means of prevention. Because of improvement in hygiene in East Asia in recent decades, hepatitis A virus infection has decreased markedly. However, this has resulted in the younger population being susceptible to hepatitis A. Fortunately, effective active immunization for hepatitis A has become available. Hepatitis B is still rampant, especially in the southern part of East Asia where chronic infection is common. Patients who are chronic hepatitis B virus carriers are reservoirs for the virus and have a much higher risk of chronic liver disease and hepatocellular carcinoma (HGC). Currently, hepatitis B infection is being brought under control in East Asia through mass immunization. Serologic and molecular epidemiologic studies have also revealed that Hepatitis C is prevalent in the region. Hepatitis C virus also contributes to the development of cirrhosis and HCC. No effect immunization is currently available, and hepatitis C can only be controlled by preventative measures. The epidemiology and pathogenesis of viral hepatitis is discussed in this review, including new viral hepatitis agents possibly responsible for non-A-E hepatitis.
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PMID:Viral hepatitis in East Asia. 864 98

Two hundred and twenty-eight patients who underwent orthotopic liver transplantation for hepatitis B-related cirrhosis in 11 European Liver Transplant Centers were collected. The male/female ratio was 184/44, with a median age of 41 years (13-66). In 55 patients (24%) hepatocellular carcinoma was associated with liver disease. All cases were stratified for pre-orthotopic liver transplantation viral characteristics: HBV-DNA neg/HBeAg neg: 106 patients (47%), HBV-DNA neg/Delta pos: 80 (35.5%), HBV-DNA pos/HBeAg pos: 28 (12.5%), other 14 (5%). In 49 patients (21.4%) post-orthotopic liver transplantation passive prophylaxis with anti-HBs immunoglobulins was not followed, while in 179 patients the anti-HBs serum titer was kept above 100-200 mU/ml. Overall 5-year actuarial survival of the series was 54%. One hundred and eighty-five patients were evaluable for HBsAg reappearance in the serum at various intervals after orthotopic liver transplantation. Overall 3-year HBV-free survival of these patients was 55%. There was a significant difference in 3-year HBV-free survival between HBV-DNA neg (52%), HBV-DNA pos (13%) and Delta pos (73%) patients (p: 0.03). Sixty-three percent of patients in the prophylaxis group were HBV-free, compared to only 25% of untreated patients (p < 0.001). Three-year HBV-free survival in patients with or without HCC was 44% and 59%, respectively. Cox-multivariate analysis revealed that only post-transplantation prophylaxis (p: 0.003) and pre-transplantation viral activity (p: 0.004) can be considered as independent factors affecting HBV recurrence. Candidates with hepatocellular carcinoma in HBV-cirrhosis should not be excluded from orthotopic liver transplantation, supporting the idea of a higher risk of post-transplantation viral reactivation.
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PMID:Risk of HBV reinfection after liver transplantation in HBsAg-positive cirrhosis. Primary hepatocellular carcinoma is not a predictor for HBV recurrence. The European Cooperative Study Group on Liver Cancer and Transplantation. 874 Aug 45


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