Prediction of sustained virologic responses to combination therapy of pegylated interferon-alpha and ribavirin in patients with chronic hepatitis C infection

ABSTRACT

Hepatitis C virus [HCV] infection is a major health problem worldwide. Genotype-4 is the most common genotype in Saudi Arabia. The response to treatment with pegylated interferon-alpha combined with ribavirin in chronic HCV infection varies. This study aimed at investigating the pre- and on-treatment predictors of sustained virologic response [SVR] in patients with chronic hepatitis C [CHC] infection. Clinical data of 48 patients with CHC treated with standard HCV antiviral combination therapy, between January 2005 and December 2010, at a Saudi University hospital, were retrospectively reviewed for age, sex, body mass index, liver enzymes, HCV-RNA viral load, liver biopsy, and response to treatment. The primary end point was SVR defined as undetectable HCV-RNA by polymerase chain reaction [PCR] 24 weeks after the end of treatment. Univariable logistic regression was used to explore the association between the different variables and SVR. These independent predictors of SVR were then analyzed with multivariable logistic regression analysis. Of the 48 treated patients, 25 [52%] were females and 27 [56%] were Saudi. The mean age was 43 years [43 +/- 10 years]. Twenty-four [50%] had genotype-4, and 26 [54%] had liver biopsy. The overall SVR rate was 75% [36/48] and was 83.3% [20/24] among genotype-4 patients. Baseline factors associated with SVR identified by univariate logistic regression were genotype-4 and early viral response [EVR], defined as a drop of >/= 2 log in serum HCV viral load after 12 weeks of initiation of combination therapy [P = 0.001]. However, in stepwise regression analysis, the independent factor associated with the effect of antiviral therapy was genotype-4. When on-treatment variables were included, EVR [P = 0.003] and low baseline viral load [P = 0.048] were highly predictive of SVR. Of our HCV-treated patients, 75% had SVR. HCV genotype-4, EVR, and low baseline viral load were predictive of SVR