Predictive factors for success and failure of pegylated interferon/ribavirin therapy in chronic hepatitis C patients

The aim of this study was to determine the clinical, biological, virological and histological predictive factors for success and failure of pegylated interferon/Ribavirin therapy among Egyptian patients infected by hepatitis C virus [HCV]. This retrospective study included 100 patients with HCV infection who underwent clinical, biochemical and virological assessments before treatment and at 12, 24 and 48 weeks from the start of treatment. The selected patients were divided equally into two groups according to the seroconversion state after receiving a course of pegylated interferon and ribavirin. Group I: 50 patients with CHC who show seroconversion after 12, 24 and 48 weeks of treatment. Group II: 50 patients with CHC who did not show good virological response after 12 and 24 weeks of treatment and they further divided into two groups: Group II A: 25 patients who stop treatment at 12 weeks due to absence of virological response [S 2 log decline in HCV RNA by Quantitative PCR] and Group II B: 25 patients who siop treatment at 24 weeks due to presence of detected HCV RNA by Qualitative PCR. At the end of this study we found that the best positive predictor factors that associated with good virological response before treatment are male sex, younger patients, low BMI, low APP, low viremia and low grade of activity and fibrosis in liver biopsy. The positive predictive factors that associated with good virological response after 12 weeks of treatment are low liver enzymes low viremia and early virological response

Association between liver fibrosis and glucose intolerance in HCV-infected patients by measuring insulin sensitivity and B-cell function

HCV mainly affects the liver, but also several tissues outside the liver have been reported to be involved, resulting in a wide spectrum of extrahepatic manifestations. Several clinical studies have suggested a possible link between chronic hepatitis caused by hepatitis C [HCV] and the development of diabetes mellitus. We investigated the association between liver fibrosis and glucose intolerance in HCV-infected patients by measuring insulin sensitivity and beta-cell function. Untreated 38 chronic HCV-infected nondiabetic patients were recruited into this study [anti-HCV+]. Eighteen patients with chronic hepatitis other than HCV infection served as the control group [anti-HCV-]. We evaluated insulin sensitivity and beta-cell function of all patients in a fasting state [homeostasis model assessment of insulin resistance [HOMA-R] and homeostasis model assessment of beta-cell function [HOMA-beta]] and after an oral load of 75g glucose [whole -body insulin sensitivity index [WBISI] and delta-insulin/ delta-glucose 30]. For all included patients; histopathological changes in liver biopsies were evaluated. Severe fibrosis was a main factor associated with insulin resistance. There were significant differences in both HOMA-R [P< 0.01] and WBISI [P<0.05] between patients with mild fibrosis [N=17] and those with severe fibrosis [N=21]. Although HOMA-beta was increased significantly in the subjects with severe fibrosis compared with those with mild fibrosis [P<0.05], delta-insulin/ delta-glucose 30 showed no significant difference in stage of liver fibrosis. Last results suggest an uncertain association between liver fibrosis and beta cell function. Our findings suggest that the development of liver fibrosis is associated with insulin resistance in HCV-infected patients