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Serum HCV RNA (serum + hcv_rna)
Selected AbstractsEight-week regimen of antiviral combination therapy with peginterferon and ribavirin for patients with chronic hepatitis C with hepatitis C virus genotype 2 and a rapid virological responseLIVER INTERNATIONAL, Issue 1 2009Hidenori Toyoda Abstract Background: It remains unclear how we can shorten the treatment duration of antiviral combination therapy with peginterferon and ribavirin for patients with chronic hepatitis C virus (HCV) genotype 2 infection who achieved a rapid virological response (RVR). Aim: We compared the efficacy of antiviral combination therapy with peginterferon and ribavirin for 8 vs. 24 weeks for the treatment of patients with HCV genotype 2 infection and with RVR. Methods: Sixty-one patients were enrolled. Serum HCV RNA was not detected at 4 weeks after the start of treatment in 32 patients with an RVR. These 32 patients were randomly assigned to 8-week (n=15) or 24-week (n=17) treatment regimens. Patients in the 8-week group who relapsed underwent a 24-week retreatment. Results: No significant difference in patient characteristics was observed between the 8- and the 24-week treatment groups. A sustained virological response (SVR) was seen in five of 15 patients (33.3%) in the 8-week treatment group and 14 of 17 (82.4%) in the 24-week treatment group; the rate was significantly higher in the 24-week treatment group (P=0.0140). Nine of 10 relapsed patients in the 8-week treatment group underwent a 24-week retreatment, and seven achieved an SVR. Conclusion: An 8-week regimen of combination antiviral therapy with peginterferon and ribavirin yielded an increase in the relapse rate, indicating the limitation of a reduction of treatment below 12 weeks in patients with genotype 2, after RVR. [source] Cholestatic syndrome with bile duct damage and loss in renal transplant recipients with HCV infectionLIVER INTERNATIONAL, Issue 2 2001Johanna K. Delladetsima Abstract:Background/Aims: Bile duct cells are known to be susceptible to hepatitis B and C virus, while it has been recently suggested that hepatitis B virus (HBV) and hepatitis C virus (HCV) infection may have a direct role in the pathogenesis of vanishing bile duct syndrome (VBDS) after liver transplantation. We report the development of a cholestatic syndrome associated with bile duct damage and loss in four HCV-infected renal transplant recipients. Methods: All four patients were followed up biochemically, serologically and with consecutive liver biopsies. Serum HCV RNA was quantitatively assessed and genotyping was performed. Results: Three patients were anti-HCV negative and one was anti-HCV/HBsAg positive at the time of transplantation and received the combination of methylprednisolone, azathioprine and cyclosporine A. Two patients became anti-HCV positive 1 year and one patient 3 years post-transplantation. Elevation of the cholestatic enzymes appeared simultaneously with seroconversion, or 2,4 years later, and was related to lesions of the small-sized interlobular bile ducts. Early bile duct lesions were characterized by degenerative changes of the epithelium. Late and more severe bile duct damage was associated with bile duct loss. The progression of the cholestatic syndrome coincided with high HCV RNA serum levels, while HCV genotype was 1a and 1b. Two patients (one with HBV co-infection) developed progressive VBDS and died of liver failure 2 and 3 years after biochemical onset. One patient, despite developing VBDS within a 10-month period, showed marked improvement of liver function after cessation of immunosuppression because of graft loss. The fourth patient, who had mild biochemical and histological bile duct changes, almost normalized liver function tests after withdrawal of azathioprine. Conclusion:Á progressive cholestatic syndrome due to bile duct damage and loss may develop in renal transplant patients with HCV infection. The occurrence of the lesions after the appearance of anti-HCV antibodies and the high HCV RNA levels are indicative of viral involvement in the pathogenesis. Withdrawal of immunosuppressive therapy may have a beneficial effect on the outcome of the disease. [source] A randomized, prospective trial of ribavirin 400 mg/day versus 800 mg/day in combination with peginterferon alfa-2a in hepatitis C virus genotypes 2 and 3,,HEPATOLOGY, Issue 6 2008Peter Ferenci We compared the efficacy and tolerability of 24 weeks of treatment with ribavirin 800 mg/day (group A) or 400 mg/day (group B) plus peginterferon alfa-2a 180 ,g/week in treatment-naive patients infected with hepatitis C virus (HCV) genotype 2 or 3. A total of 97 of 141 patients randomized to group A (68.8%, 95% confidence interval [CI] 60.5%-76.3%) and 90 of 141 patients randomized to group B (63.8; 95% CI 55.3%-71.7%) achieved a sustained virological response, defined as undetectable serum HCV RNA at the end of untreated follow-up (week 48). Among patients infected with genotype 3, the rate of sustained virological response was 67.5% (95% CI 58.4%-75.6%) in group A and 63.9% (95% CI 54.7%-72.4%) in group B, and among patients infected with genotype 2, the rate of sustained virological response was 77.8% (95% CI 54.2%-93.6%) in group A and 55.6% (95% CI 38.4%-83.7%) in group B. Relapse rates in the 2 treatment groups were similar (17% in group A and 20% in group B). The incidence of adverse events, laboratory abnormalities, and dose reductions was similar in the 2 treatment groups. Conclusion: The results suggest that when administered for 24 weeks with peginterferon alfa-2a, ribavirin doses of 400 and 800 mg/day produce equivalent outcomes in patients infected with HCV genotype 3. (HEPATOLOGY 2008.) [source] Maternal-infant transmission of hepatitis C virus infectionHEPATOLOGY, Issue 5B 2002Eve A. Roberts 555 University Ave. Mother-to-infant transmission of hepatitis C virus (HCV) is comparatively uncommon. The prevalence of antibody to HCV (anti-HCV) in pregnant women is 0.1% to 2.4%, although in some endemic areas it is much higher. The proportion of women with anti-HCV who have active infection with viremia is 60% to 70%. Transmission of HCV occurs only when serum HCV RNA is detectable and may be related to higher levels (above 106 copies per mL). The rate of mother-to-infant transmission is 4% to 7% per pregnancy in women with HCV viremia. Co-infection with human immunodeficiency virus (HIV) increases the rate of transmission 4 to 5 fold. The actual time and mode of transmission are not known. Elective Cesarean section is not recommended for women with chronic HCV infection alone. The role of treatment to prevent transmission is limited by the fetal toxicity of currently available medications for hepatitis C. Breast feeding poses no important risk of HCV transmission if nipples are not traumatized and maternal hepatitis C is quiescent. Pregnant women at high risk for HCV infection should be screened for anti-HCV, and HCV RNA testing should be performed if anti-HCV is positive. Infants of women with hepatitis C should be tested for HCV RNA on two occasions, between the ages of 2 and 6 months and again at 18 to 24 months, along with serum anti-HCV. The natural history of mother-to-infant hepatitis C remains uncertain, especially the course in the first year of life when some infants appear to have spontaneous resolution. [source] Maternal-infant transmission of hepatitis C virus infectionHEPATOLOGY, Issue S1 2002Eve A. Roberts M.D., FRCPC Mother-to-infant transmission of hepatitis C virus (HCV) is comparatively uncommon. The prevalence of antibody to HCV (anti-HCV) in pregnant women is 0.1% to 2.4%, although in some endemic areas it is much higher. The proportion of women with anti-HCV who have active infection with viremia is 60% to 70%. Transmission of HCV occurs only when serum HCV RNA is detectable and may be related to higher levels (above 106 copies per mL). The rate of mother-to-infant transmission is 4% to 7% per pregnancy in women with HCV viremia. Co-infection with human immunodeficiency virus (HIV) increases the rate of transmission 4 to 5 fold. The actual time and mode of transmission are not known. Elective Cesarean section is not recommended for women with chronic HCV infection alone. The role of treatment to prevent transmission is limited by the fetal toxicity of currently available medications for hepatitis C. Breast feeding poses no important risk of HCV transmission if nipples are not traumatized and maternal hepatitis C is quiescent. Pregnant women at high risk for HCV infection should be screened for anti-HCV, and HCV RNA testing should be performed if anti-HCV is positive. Infants of women with hepatitis C should be tested for HCV RNA on two occasions, between the ages of 2 and 6 months and again at 18 to 24 months, along with serum anti-HCV. The natural history of mother-to-infant hepatitis C remains uncertain, especially the course in the first year of life when some infants appear to have spontaneous resolution. (HEPATOLOGY 2002;36:S106,S113). [source] Predicting the response to 48-week combination therapy with peginterferon ,-2b plus ribavirin from the estimated HCV RNA load index after negative serum change in genotype 1b hepatitis C patientsHEPATOLOGY RESEARCH, Issue 6 2009Keiji Tsuji Aim:, We estimated viral dynamics after serum hepatitis C virus (HCV) RNA became negative and assessed the relation between the estimated viral load at the end of treatment (EVE) index and the response to the combination therapy with peginterferon ,-2b plus ribavirin. Methods:, Patients with chronic HCV, genotype 1b, and a high viral load were treated with this combination therapy for 48 weeks, and serum HCV RNA was measured frequently during the treatment period. In the patients showing an end-of-treatment response (ETR), the viral load profile from the start of treatment until serum HCV RNA became negative was expressed by an approximate curve. Then the EVE index was calculated by using the expression obtained from the curve, and differences between the sustained virologic response (SVR) and relapse groups were investigated. Results: The SVR rate increased as the EVE index became lower, and the EVE index was significantly lower in the SVR group than in the relapse group. The SVR rate was higher for those in whom the EVE index was below the cut-off point. Conclusion:, Prediction of SVR and relapse from the EVE index is more useful than prediction from viral dynamics at the time when HCV RNA becomes negative or when HCV RNA shows a decrease of 2-log or more. [source] Efficacy of interferon-, treatment in Japanese children with chronic hepatitis CJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 4 2003EISUKE NAKASHIMA Abstract Background: We investigated the efficacy of natural interferon (IFN)-, treatment in 34 Japanese children with chronic hepatitis C. Methods: Thirty-four children completed 6 months of therapy with natural IFN-, and were followed for 12 months or longer. We examined the serum hepatitis C virus (HCV) RNA titer and liver histology before, during, and after IFN treatment. Results: At 6 months after the cessation of IFN-, treatment, 16 patients (47%) had normal serum alanine aminotransferase concentration and no detectable serum HCV RNA. There were no major side-effects, excluding some influenza-like symptoms during the IFN-, treatment. Most genotype 2a patients had a complete response (80%). Moreover, patients who had a low HCV RNA titer (<102 copies/mL) after 1 month of IFN-, treatment became complete responders at 6 months after the cessation of treatment. Histological improvement was observed in almost all patients after IFN-, treatment. Conclusion: Interferon-, treatment is safe and effective for children with chronic hepatitis C and has no serious side-effects. A HCV RNA concentration of <102 copies/mL after 1 month of IFN-, treatment and genotype 2a may be useful predictors of long-term IFN efficacy. © 2003 Blackwell Publishing Asia Pty Ltd [source] Correlation of clinical characteristics with detection of hepatitis B virus X gene in liver tissue in HBsAg-negative, and HCV-negative hepatocellular carcinoma patientsLIVER INTERNATIONAL, Issue 5 2002Yoichiro Higashi Abstract: Purpose: We studied the clinical features and the etiology of hepatitis B virus surface antigen (HBsAg)-negative and antibody to hepatitis C virus (anti-HCV) negative patients with hepatocellular carcinoma. Methods: A total of 550 patients, hospitalized with an initial diagnosis of HCC were retrospectively studied. Eighty-one of these patients were HBsAg-positive (HB group), 404 patients were anti-HCV positive (HC group). The other 65 patients were negative for both HBsAg and for anti-HCV (NBNC group). We purified HBV-X gene from HCC or non-tumorous liver tissue of 23 NBNC patients using PCR. Results: Clinical features of NBNC as compared with HB and HC patients were as follows, respectively: non-cirrhosis rate (%): 57,37,15 (P = 0.02 for HB, P < 0.00001 for HC), the proportion of patients with normal ALT concentrations (%): 59,28,10 (P = 0.0002 for HB, P < 0.00001 for HC). Forty of 59 NBNC patients (68%) had anti-HBs and/or anti-HBc (healthy controls: 29%, P < 0.00001) and two of 56 had serum HBV DNA. Twelve of 23 NBNC patients had HBV-X gene in HCC and/or non-cancerous liver tissues (52%). None of 52 had serum HCV RNA. Conclusions: The NBNC patients with HCC had a higher frequency of non-cirrhotic liver without liver injury. The presence of the HBV-X gene in HCC suggests a possible role of past HBV infection in the development of HCC. About half of NBNC HCC is associated with seronegativity for HBsAg and positivity for the HBV-X gene in liver tissue. [source] | ||||||||||