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)

Our aim was to verify whether the presence of antibodies to HCV envelope protein might mark the occurrence of liver damage, as recently suggested in the literature. Sera from 104 patients (62 male, 42 female) were tested: 84 were positive and 20 were negative to a second generation enzyme immunoassay for anti-HCV antibodies; 51 patients had mild chronic liver disease (44 chronic hepatitis, seven steatosis), 43 had liver cirrhosis (superimposed by hepatocellular carcinoma in 18) and ten were asymptomatic anti-HCV positive subjects with normal liver function tests. Besides, all sera were tested by means of an enzyme immunoassay for the presence of serum antibodies to the synthetic peptide S24A (SIYPGHVSGH RMAWDMMMNW SPTA) derived from amino acids 307-330 of HCV polyprotein. Anti-S24A antibodies were detected in 40/84 sera positive and 1/20 negative at anti-HCV testing (Pearson chi 2 12.29; p = 0.005). Among anti-HCV positive sera, no significant difference existed in anti-S24A status with regard to clinical evidence of liver disease, ALT concentration or HCV RNA positivity. Thus, anti-S24A antibodies are detectable in approximately half of HCV-positive sera, but they do not seem to add significant clinical information to existing tests or to be useful as putative markers of viraemia.
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PMID:Anti-envelope antibodies in anti-hepatitis C virus (HCV) positive patients with and without liver disease. 753 99

The prevalence of HBV recurrence after liver transplantation is higher in patients with viral B cirrhosis than in patients with viral B-D cirrhosis or fulminant hepatitis B and is related to the presence of HBV replication prior to transplantation. Long-term passive anti-HBs immunoprophylaxis is the best current way for prevention of HBV reinfection and improved long-term survival. The rate of recurrence of HCV infection is high, reaching 85%, and the rate of HCV hepatitis in the graft is approximately 75%. In most cases, HCV hepatitis leads to chronic hepatitis. The severity of graft hepatitis is related to the level of viremia at the time of the hepatitis and to the genotype 1b. The methods of prevention of HCV infection after liver transplantation are yet to be found. The treatment of graft HCV infection with interferon should be well evaluated and given cautiously. Other antiviral treatments without an immunostimulating effect are needed. Finally, patients transplanted for hepatitis B without HBV replication, receiving posttransplant long-term anti-HBs immunoprophylaxis, and those transplanted for HCV cirrhosis have a 5-year survival similar to other groups of transplanted patients. Patients belonging to these groups can be considered as candidates for transplantation. Patients with active HBV replication should be included in specific trials for prevention of HBV reinfection.
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PMID:Liver transplantation for viral hepatitis: the experience of the hepatobiliary center at Hospital Paul Brousse. 754 34

We tested for infection with hepatitis C virus (HCV) in 58 patients affected by humoral immunodeficiencies: 43 common variable immunodeficiency (CVI), two hyper IgM syndrome (HIM), two IgG subclass deficiency, four ataxia-telangiectasia (AT), and seven X-linked agammaglobulinaemia (XLA). While the assessment of serum specific HCV antibodies in some of these patients was not informative because of the impairment in specific antibody production, the reverse transcriptase polymerase chain reaction (RT-PCR) assay used to detect serum HCV RNA was a useful method for diagnosing infection. We found that 38% of late onset hypogammaglobulinaemic patients (CVI, HIM or IgG subclass deficiency) had evidence of HCV infection. HCV infection was not detectable in patients with XLA or AT. The majority of our patients had persistent viraemia, and those who underwent liver biopsy showed histological findings of chronic hepatitis. Moreover, we could demonstrate in vitro that eight of 18 HCV-infected patients were actively producing anti-HCV antibodies, despite their impaired antibody production. The high rate of HCV infection in hypogammaglobulinaemic patients could be related to several nosocomial routes of transmission, including intravenous immune globulin administration. Despite the persistent viremia only two patients had cirrhosis and none had hepatocarcinoma.
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PMID:HCV infection in patients with primary defects of immunoglobulin production. 755 76

Chronic hepatitis C is a major health issue, affecting up to 1.4% of the US population. A high proportion of hepatitis C virus (HCV) infections are chronic. Significant liver disease (chronic hepatitis that is moderate to severe, fibrosis, or cirrhosis) develops in up to 50% of patients chronically infected with HCV. Progression of the disease is unpredictable but is typically slow and evolves over decades. Viral genotype, level of viremia, severity of liver disease, and hepatic iron content influence the response of chronic hepatitis C to therapy. Standard therapy is with interferon alfa-2b (Intron A), 3 million U given subcutaneously three times a week for 6 months. Forty percent of patients have an initial response to interferon therapy, but only half (or fewer) of these patients maintain a long-term sustained response. New treatment strategies are currently being evaluated; however, none, as yet, has emerged as a significant improvement over standard interferon therapy.
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PMID:Hepatitis C. Recent advances in understanding and management. 760 49

Serum HCV-RNA levels were determined by newly developed branched DNA probe (bDNA) assay in 87 patients with hepatocellular carcinoma (HCC), compared with 73 patients with chronic hepatitis active and 30 patients with liver cirrhosis. Patients with decompensated liver cirrhosis (LC-d) had a significant lower viremia (mean 3.2Meg.eq./ml, bDNA positive rate; 40%) than chronic hepatitis active (18.0; 64%) and compensated LC (LC-c, 17.9; 80%) (p < 0.05). Those data indicates that HCV replication may decrease as progression of LC. In contrast, there was no difference between the levels of HCC with LC-c (8.2; 85%) and LC-d (6.1; 89%), and their positive rate of bDNA assay were significantly higher than LC-d without HCC (p < 0.01). Therefore, patients undergoing LC in whom serum HCV-RNA sustained high level may correspond to the high risk group of HCC. In HCC of heavy drinker, serum HCV-RNA levels (11.3; 91%) were significantly higher than the levels (4.6; 79%) of HCC without heavy drink (p < 0.05). The result indicates that heavy drink may induced an increase in HCV replication.
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PMID:[Study of hepatocellular carcinoma type C by quantitation of serum HCV-RNA using branched DNA probe assay]. 760 18

To compare the levels of hepatitis C virus (HCV) viraemia in carriers of the same genotype in various stages of chronic HCV infection, we quantified the amount of HCV RNA by competitive polymerase chain reaction and determined HCV genotype using type-specific primers. The study population included 255 patients with chronic HCV infection (asymptomatic 33, chronic hepatitis 141, liver cirrhosis 50, hepatocellular carcinoma 31). Of these 255, the prevalence of HCV RNA genotype II was 67.8%, genotype III, 17.3% and genotype IV, 14.9%; no genotype I was found. The level of HCV RNA (logarithmic transformed copy numbers per 50 microliters of serum) was significantly higher in subjects of genotype II than in those of genotypes III or IV (mean titre 5.8 +/- 1.0 vs. 5.1 +/- 1.2 and 4.8 +/- 1.1, P < 0.05, respectively). There was no significant difference in the level of HCV RNA between genotypes III and IV. Of 173 patients of genotype II, there were no significant differences between the level of HCV RNA and the stage of liver disease or in the level of HCV RNA by age. Of the 129 with genotype II with a history of blood transfusion, there was no significant difference between the level of HCV RNA of patients with and without a history of transfusion or between that of patients with a history of blood transfusion and the time elapsed since blood transfusion. The level of HCV viraemia depended on the genotype of HCV RNA and did not correlate to age or to the stage of liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship of genotype to level of hepatitis C viraemia determined by competitive polymerase chain reaction. 767 48

Hepatitis B virus (HBV) infection in children is worldwide in distribution, but the features of HBV-associated liver disease differ depending on the route of transmission and the time of acquisition of the infection. The degree of liver injury varies from a mild disease to the development of cirrhosis and hepatocellular carcinoma, and depends on the replicative status of the viral genome. It is believed that the immune function plays a key role in the severity of HBV disease, and the impact of HBV mutants needs to be assessed. The goals of antiviral therapy in children are therefore, the clearance of viremia and HBV sequences from infected tissues, together with an improvement in the liver disease. Administration of 10 MU/m2 b.s. 3 times weekly over 6 months resulted in a significantly higher clearance of viremia, with normalization of ALT values and greater improvement in liver histology in treated than in untreated patients. Long-term follow-up of these cases reveals the presence of the viral genome in serum and liver by PCR without clearance of HBsAg. Complete eradication of HBV might need more years of evolution as for adult patients. The combination of more than one antiviral agent, as well as the potentiation of the immune system, needs to be assessed to improve the actual response rate obtained with interferon-alpha.
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PMID:Chronic hepatitis B in children. Natural history and treatment. 768 64

Eighty patients with chronic hepatitis C who completed a previously reported randomized controlled trial on the efficacy of interferon-alpha 2b were followed up for at least 36 mo after therapy discontinuation. Seventeen patients (21.2%) maintained normal ALT values throughout the follow-up; 63 (78.8%) either did not normalize the levels of ALT or relapsed during the follow-up. A significantly greater proportion of patients treated with 3 million units of interferon three times a week subcutaneously for 48 wk were long-term responders compared with patients treated for 24 wk. Sex, age, hepatitis C virus antibody status, source of infection and pretreatment levels of ALT were not predictive of long-term response. Cirrhosis was found to be an unfavorable predictive factor. After 3 yr of follow-up, clearance of viremia was observed in 58.9% of the 17 long-term responders but in none of the non-responders (p = 0.002). E2-NS1 antibody tested negative in 88.2% of long-term responders and in 14.3% of nonresponders (p = 0.001). Fifty-nine percent of long-term responders tested negative for C100-NS4 antibody compared with 14.3% of nonresponders (p = 0.031). No significant change was observed in other antibodies. Four long-term responders underwent liver biopsy 2 yr after discontinuation of therapy. All four patients had normal liver histology compared with baseline assessment of chronic active hepatitis in three and chronic persistent hepatitis in the other. Three of the four were negative for serum hepatitis C virus RNA.
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PMID:Long-term follow-up of patients with chronic hepatitis C treated with different doses of interferon-alpha 2b. 769 94

The authors compared the diagnostic performance of a second-generation recombinant immunoblot assay (RIBA) (RIBA HCV 2.0 SIA) and the recently introduced third-generation RIBA (RIBA HCV 3.0 SIA) with that of hepatitis C virus (HCV) RNA by the polymerase chain reaction (PCR) in 55 patients on chronic hemodialysis. Compared with HCV RNA by PCR, RIBA 3.0 increased the sensitivity of HCV detection to 72% as compared with 56% of RIBA 2.0. Both assays underestimated the prevalence of HCV infection as determined by PCR. However, RIBA HCV 3.0 outperformed RIBA HCV 2.0, detecting all of the RIBA 2.0-positive patients plus an additional eight (8 of 22 RIBA 2.0 negative; confidence interval [CI] = [17.2%, 59.3%]). Forty-three of 51 patients with positive RIBA 3.0 or positive HCV RNA by PCR underwent a liver biopsy. Thirty (70%) had chronic hepatitis (three with cirrhosis), 10 (23%) had nonspecific changes, and three (7%) had normal liver histology. Thirty of 37 patients (81%) with hepatitis C viremia and positive anti-HCV had chronic hepatitis, whereas none of the viremic patients with negative anti-HCV had chronic hepatitis. Among the reactive antigens on RIBA 3.0, c33c was found to be most predictive of chronic hepatitis (P = 0.0002). Detection of HCV RNA continues to be the method of choice in the early phase of HCV infection. In places where a validated HCV RNA assay is not available, RIBA HCV 3.0 (soon to be commercially available) is a better alternative. Early detection of HCV infection and the implementation of an isolation strategy might be important in preventing the spread of HCV infection among hemodialysis patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New insights into hepatitis C virus infection of hemodialysis patients: the implications. 770 52

This article covers several dilemmas posed by hepatitis C for the family physician. It is proposed that patients with known risk factors, such as injecting drug use or blood transfusion, be treated for an anti HCV. The problems of counselling the patient with an incidental positive anti HCV test are discussed; at present, the history of risk factors and liver test results are the most important aspects as there is no gold standard for hepatitis C diagnosis. Family and sexual transmission of HCV are rare; only mothers with extremely high levels of HCV viraemia are likely to transmit HCV to their offspring. Decisions about interferon treatment for hepatitis C require consideration of the natural history of this disease, the chances of a long-term response to treatment, and the adverse affects of interferon. Screening for hepatocellular carcinoma is proposed for patients who already have cirrhosis.
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PMID:Hepatitis C: a current perspective. 767 29


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