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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients with multiple hepatotropic viral infections (B and C, or B, C and D), the reciprocal influence of each virus remains controversial. The aims of this study were twofold: first, to determine the impact of multiple infection on the replication status of B, C and D viruses and on histological features; and second, to compare patients with multiple infection to patients infected only with the hepatitis C virus (HCV). We retrospectively included 50 patients with multiple infection and 50 control HCV patients, who were matched on independent factors associated with fibrosis, such as age, gender, alcohol consumption and duration of infection. The replication status of hepatitis B virus (HBV), HCV and hepatitis D virus (HDV), and histological lesions, were determined. In patients with multiple infection, HCV RNA was present less frequently (44% vs 98%, P < 0.001) and the prevalence of cirrhosis was higher (35% vs 8%, P < 0.001). Among patients with triple infection (n = 16), HBV replication was observed in 25%, HCV RNA was detectable in only two (P < 0.0001) and HCV viremia was significantly lower than in the matched HCV patients (0 vs 54.7, P < 0.0001). Among patients with dual infection (n = 34), HCV RNA was present less frequently in those with serological markers of active HBV infection than in those without (30% vs 79%, P = 0.01). Hence, multiple infection is associated with a decrease of HCV replication. Cirrhosis seems to be more frequently observed in patients with multiple infection. In patients with triple infection, serum HCV RNA and markers of HBV replication were absent in 80%, suggesting that HDV acts as a dominant virus. In patients with dual infection, HBV and HCV exert an alternative, dominant replication.
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PMID:Replication status and histological features of patients with triple (B, C, D) and dual (B, C) hepatic infections. 1071 38

The treatment of chronic hepatitis C is aimed at eliminating viral replication in order to prevent further evolution towards cirrhosis and hepatocellular carcinoma. Virological parameters include hepatitis C virus (HCV) genotype, qualitative viraemia, quantitative viral load and the characteristics of HCV quasi-species heterogeneity. These parameters can be used to predict and monitor the response to therapy, in order to help clinicians to tailor treatment of chronic hepatitis C and to better understand the molecular mechanisms underlying HCV resistance to antiviral drugs. Current knowledge on these various issues is reviewed in the present article.
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PMID:Molecular tools for the treatment of hepatitis C. 1072 55

Hepatitis C virus (HCV) reinfection after liver transplantation is almost constant, assessed by the persistence of HCV RNA in 90% of cases. Acute hepatitis appeared in 75% of patients at a median of 4 months' post-transplantation. The 5-year actuarial rate of acute and chronic hepatitis on the graft is 75% and 60%, respectively. The rate of HCV cirrhosis on the graft is variable from 8 to 25% at 5 years. After transplantation, HCV viraemia is dramatically increased and correlates with the occurrence of acute hepatitis on the graft. Intrahepatic levels of HCV are high at the time of acute hepatitis, and decrease with constitution of chronic graft hepatitis lesions, implying an immunological response to the viral infection. A relationship between genotype 1b and the prevalence of HCV hepatitis on the graft has been suggested in European but not American series. The influence of the age of the recipient, quasispecies, viral compartmentalization, immunosuppressive treatment, and of HLA matching is being evaluated. The 5-year patient survival is around 65-80%. However, the occurrence of cirrhosis with a risk of graft failure may decrease the 10 and 15-year patient survival. Attempts to give prophylactic post-transplant antiviral treatment are under evaluation. Antiviral treatment of post-transplant graft lesions with combination therapy interferon-ribavirin gave promising results but indications and duration of treatment should be evaluated. In conclusion, HCV reinfection is frequent, but medium-term survival is good. However, the long-term graft and patient survival remains unknown, and efficient prevention and treatment of HCV graft is mandatory.
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PMID:Recurrent hepatitis C after liver transplantation: clinical and therapeutical issues. 1076 38

The natural history of chronic hepatitis B virus (HBV) infection is highly variable, ranging from a benign course to one of shortened life expectancy. Liver histology represents an accurate tool for assessing progressive liver disease, and has been used in five recent Phase III clinical trials of the oral nucleoside analogue, lamivudine, 100 mg/day, in patients with chronic hepatitis B. Significant improvements in the Knodell histological activity index (HAI) score were reported with lamivudine, with greater decreases noted after 2 years of therapy, consistent with continued alanine transaminase (ALT) normalisation. Histological data showed that lamivudine therapy can resolve or lessen the progression of fibrosis, and reduce the progression to cirrhosis in patients with chronic hepatitis B. These trials also showed that lamivudine provoked significant enhancement of hepatitis B e antigen (HBeAg) seroconversion compared with placebo, and had a profound effect on serum HBV DNA, resulting in rapid suppression of viraemia. The emergence of variants with a mutation in the YMDD (tyrosine-methionine-aspartate-as-partate) motif did not cause significant worsening of the Knodell HAI score. In conclusion, lamivudine is the first oral antiviral therapy for the treatment of chronic hepatitis B. It reduces significantly the severity of liver disease and reduces progression to cirrhosis. In addition, because lamivudine is well tolerated it represents a viable therapeutic option that may improve the prognosis of patients with chronic hepatitis B.
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PMID:Liver disease-significant improvement with lamivudine. 1086 50

In the management of hepatitis B new therapeutic options have been established in the last years. Patients with fulminant course are rarely observed and should be submitted in a hepatological center. In chronic hepatitis B today we see mainly HBeAg negative/anti-HBe positive patients with replication of HBV-mutants. The tendency is to treat these cases with lamivudine (LAM) for some years. This is also true for HBV-cirrhosis in stage Child A. The progressed cirrhosis (Child B/C) without option for liver transplantation is not an indication for nucleosidanaloga and a contraindication for interferon. However before liver transplantation the viraemia should be diminished lower than 5 pg/ml. That means the HBV-hybridization test should become negative, which can be achieved with LAM in most cases. During and after liver transplantation the HBV-infected patients receive passive immunoprophylaxis with anti-HBs-hyperimmunoglobulin. In the situation of reinfection and hepatitis, nucleosidanaloga are indicated, in the first line LAM. In the case of LAM-resistance, interferon alpha is a further option. Patients after renal transplantation and HBV-infection should also be treated with LAM. In these patients IFN should be avoided, because graft rejection can be induced. Combined infection with HBV plus HDV, HCV or HIV need an individual concept for treatment. Extrahepatic manifestations of HBV-infection with clinical relevance, e.g. panarteriitis or glomerulonephritis are indications for antiviral treatment. If treatment with glucocorticosteroids is necessary in these situations, the steroids should be given only in combination with LAM. In non-cirrhotic patients with normal aminotransferases but quantify-able viraemia the liver histology is helpful for the indication of treatment.
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PMID:[Therapy of problem cases in hepatitis B]. 1089 96

TT virus (TTV) is transfusion-transmissible but its involvement in post-transfusion hepatitis is uncertain. To investigate the potential association of TTV with liver diseases, the prevalence of TTV DNA was tested by semi-nested PCR in 113 carriers of hepatitis C virus (HCV), 10 patients with acute liver failure, 11 patients with cryptogenic cirrhosis and 200 control blood donors. Thirty-seven of these patients underwent liver transplantation and were tested pre- and post-transplantation. TTV DNA was semi-quantified in serial samples from seven patients with unexplained post-transplant hepatitis. TTV genotyping was performed on samples from 28 patients by sequence analysis. The prevalence of TTV DNA in blood donors was 1.5% and 17% in HCV infected haemophiliacs. In patients with acute or chronic liver disease or hepatitis, 6 to 27% prevalence was observed. After liver transplantation, the prevalence of TTV DNA increased from 16 to 46% (P < 0.01). In patients who developed unexplained hepatitis post-transplantation, TTV viraemia did not parallel ALT levels. TTV DNA either increased in titre or became detectable shortly after transplantation, suggesting that either TTV was transfusion-transmitted, or, more likely, that immunosuppression caused a recurrence of low level or undetectable TTV viraemia. TTV had considerable genomic diversity in the N22 region, corresponding to at least 4 genotypes. Genotype 2 was found in 14/28 patients.
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PMID:Detection of TT virus DNA in patients with liver disease and recipients of liver transplant. 1089 63

The aim of the study was to evaluate epidemiology and clinical course of HCV infection in children and adolescents with end-stage renal disease. The study involved 70 patients, aged 1-25 years, 31 M, 39 F: group of 40 dialysed (27 HD, 13 CAPD) and 30 patients suffering from different chronic renal disease as a control group. Anti-HCV antibodies were assayed by EIA 3rd gene (Abbott Diagnostic) and were sought by LIATEK HCV 3rd gene. HCv RNA was detected and measured by a standardised HCV RNA PCR assay (Amplicor Roche). HCV genotypes were identified by InnoLIPA (Innogenetics). HCV infection was diagnosed in 20 (50%) dialysed and in 3 (10%) non-dialysed patients. None of the HCV infected patients presented the clinical symptoms of hepatitis; the mild activity of ALT was observed in 8 cases only. HCV viremia was relatively low: 365 x 103 copies/mL in PD and 110,9 x 103 copies/mL in HD patients. 3 genotypes of HCV were identified: 1a, 1b and 4c/4d. In 3 cases liver biopsy was performed, no cirrhosis was diagnosed.
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PMID:[Epidemiology and clinical course of HCV infection in children and adolescents with chronic renal failure]. 1089 36

The majority of patients undergoing orthotopic liver transplantation (OLT) have end-stage liver disease secondary to hepatitis C virus (HCV) infection. Although OLT does not cure the disease and recurrent virus is present in all patients, relatively few patients with recurrent viremia develop clinical disease. When the disease recurs, however, the results can be devastating. Factors associated with increased risk for recurrent HCV disease remain controversial. We hypothesized that preservation injury may predispose to the severity of HCV disease after OLT. We reviewed our series of OLTs performed for HCV cirrhosis between January 1994 and December 1998 (n = 56; 62 transplants). Patients were grouped according to the severity of recurrent hepatitis C. Group 1 had no or mild HCV disease (n = 36), and group 2 had moderate to severe HCV disease (n = 20). The duration of ischemic rewarming during graft implantation was significantly associated with the severity of recurrent hepatitis C (P <.04). The estimated chances of severe disease within the first year post-OLT after 30, 60, or 90 minutes of ischemic rewarming time were 19%, 40%, and 65%, respectively. Cold ischemia time, transaminase levels, and prothrombin time did not correlate with the severity of hepatitis C. In conclusion, our data suggest that the duration of ischemic rewarming predisposes to severe recurrent hepatitis C. This finding warrants the investigation of the pathogenesis of recurrent HCV disease after ischemic injury. Reduction of rewarming time should be stressed in OLT, particularly in patients with HCV cirrhosis.
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PMID:Prolonged rewarming time during allograft implantation predisposes to recurrent hepatitis C infection after liver transplantation. 1091 61

(1) Hepatitis C can progress over decades, leading in some cases to cirrhosis or liver cancer. (2) The only treatment currently approved for preventing long-term complications of hepatitis C is interferon alfa (2a or 2b) at 3 MU 3 times a week for 12 months. It is recommended only for patients with chronic active hepatitis C. (3) The assessment of interferon alfa in clinical trials is based on surrogate end points (transaminase levels, histopathological changes, clearance of viraemia), and the results sometimes conflict. (4) There is no firm evidence that interferon alfa prevents cirrhosis. (5) Treatment with interferon alfa can be stopped after 3 months when patients fail to respond. (6) Thyroid disorders are the most important adverse effect of interferon alfa.
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PMID:Hepatitis C: limits and dose regimen of interferon alfa. 1091 23

Chronic hepatitis C (CHC) is a major health problem worldwide, with approximately 200 million affected individuals and a significant rate of progression to end-stage cirrhosis and hepatocellular carcinoma (HCC). If hepatitis C virus (HCV) infection is left untreated in the population, then the number of liver-related deaths will soon double and the need for liver transplantation may increase to five times that seen today. Available therapies for CHC are restricted to interferon alpha (IFN alpha) monotherapy and to the combination of IFN alpha and ribavirin. Despite their high cost and side effects, both of these therapies have proved to be cost effective, particularly combination therapy. IFN alpha monotherapy for one year can induce sustained response (SR) rates of approximately 10% in naive patients infected with HCV genotype 1, and above 50% in those infected with other genotypes. Combination therapy can double or even triple the rate of SR in genotype 1 infections and may further increase the SR rate in the other HCV genotypes. Combination therapy has also been proven to be effective in approximately 50% of relapsed responders to IFN alpha monotherapy. In clinical practice, the decision to treat should be individualized and tailored on the basis of several virus- and host-related factors, particularly the grade and stage of liver disease, HCV genotype and levels of viremia. Appropriate monitoring of therapy by careful clinical evaluation, liver biochemistry and serum HCV RNA testing is mandatory. IFN alpha therapy may also prove to be effective in reducing the rate of HCC development in CHC regardless of whether a virological response is achieved, but this remains to be established.
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PMID:Why and how to treat chronic hepatitis C. 1093 5


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