Chronic coinfection with the hepatitis B (HBV) and hepatitis delta (HDV) viruses is known to cause severe liver disease, but the importance of coinfection with hepatitis C virus (HCV) and HBV has not been well documented. In the present study, the clinical and pathological severity of liver disease among patients with hepatitis resulting from multiple viruses was examined and an open trial of the efficacy of interferon-alpha 2b (IFN-alpha) treatment was conducted. Nineteen patients with chronic HBV and HCV infection and 17 with HBV, HCV and HDV infection were studied; 12 in each group underwent liver biopsy. For each coinfected patient, two patients infected with HCV alone were selected as controls, and these were matched for age and risk factor and were estimated to have been infected for a similar duration. Coinfection with HBV and HCV or HBV, HCV and HDV was associated with more severe liver disease than HCV alone (P < 0.01); total Scheuer score, portal and lobular inflammation and fibrosis were all worse in coinfected subjects. Eight patients with chronic HBV and HCV were treated with recombinant IFN-alpha 2b [3 million units (MU), thrice weekly for 6 months]. Liver function tests normalized in two patients and one lost hepatitis B surface antigen (HBsAg). Seven patients with hepatitis B, C and delta coinfection were treated with the same regimen and only one normalized serum alanine aminotransferase (ALT) during (and after) treatment. It is concluded that coinfection with multiple hepatitis viruses is associated with histologically more severe liver disease than HCV alone.(ABSTRACT TRUNCATED AT 250 WORDS)
To identify variables that are independent predictors of adverse outcomes in chronic hepatitis C, we analyzed a cohort of 455 patients followed for a median of 4.7 years. Associations were sought between demographic and behavioral factors, hepatitis C virus (HCV) genotype, liver histology and liver tests at entry, and development of liver complications, hepatocellular carcinoma (HCC), hepatic transplantation and liver-related death. Independent predictors were identified by multivariate analysis. The following were associated with a significantly higher rate of liver complications: age; birth in Asia, Europe, Mediterranean region, or Egypt; transmission by blood transfusion or sporadic cases; HCV genotypes 1b and 4 (compared with 1/1a); fibrosis stage 3 or 4 (cirrhosis); serum albumin; bilirubin; prothrombin time; and ␣-fetoprotein. However, the only independent predictors of liver-related complications were sporadic transmission (P F .001), advanced fibrosis (P ؍ .004), and low albumin (P F .001). The corresponding independent risk factors for HCC were male gender (P ؍ .07), sporadic transmission (P F .001), and albumin (P F .001); bilirubin (P ؍ .02) was an additional predictor of transplantation or liver-related death. It is concluded that only patients with advanced hepatic fibrosis or cirrhosis, are at risk of developing hepatic complications of chronic hepatitis C during 5-year follow-up. Among such patients, abnormalities in serum albumin, bilirubin, or prothrombin time indicate a high probability of complications. The rate of fibrotic progression in chronic hepatitis C is highly variable, 1 and the natural history of the disease usually extends over several decades. In some patients, it may culminate in the life-threatening liver complications of portal hypertension, hepatocellular carcinoma (HCC), and liver failure requiring hepatic transplantation or leading to liverrelated death. Such complications are rarely noted in the absence of cirrhosis. The factors that influence the rate of fibrotic progression in hepatitis C virus (HCV) include age at the time of HCV infection and at initial evaluation, male sex, HCV genotype, and alcohol consumption. [1][2][3][4][5][6][7][8] It is less clear as to whether any of these factors influence the onset of liver-related complications other than by their effects on the rate of fibrotic progression.The proportion of all patients with hepatitis C who develop life-threatening complications is also unclear. Many studies are confined to either the first 20 years of HCV infection when complications appear to be unusual, [8][9][10][11][12][13][14][15] or to the late stage of the disease when cirrhosis is present. [13][14][15][16] Thus some cohort studies have found low mortality rates at 17 to 20 years, particularly among younger individuals and among those who have a risk factor other than blood transfusion. 8,9,11,12,17 Others have indicated that approximately 18% of patients develop liver-related complications or HCC or succumb to liver-related death within 18 year...
Response to antiviral therapy, and particularly SVR, appears to reduce liver complications in chronic hepatitis C. However, in the absence of an antiviral treatment response, a course of interferon does not reduce risks of liver cancer or liver failure.
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