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Occult hepatitis B infection in egyptian chronic hepatitis C patients: prevalence, impact on pegylated interferon/ribavirin therapy

DOI: 10.1186/1743-422x-7-324

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Abstract:

In this study, occult hepatitis B infection occurs in 3.9% of Egyptian chronic HCV patients; tends to affect younger age patients, associated with higher base line HCV viral load, less hepatic fibrosis than monoinfected patients. This occult hepatitis B infection is not a statistically significant cause of non-response to pegylated interferon/ribavirin therapy. Anti-HBs was not associated with any biochemical, histological or virological abnormalities in those patients, contrary to low response rate to therapy and higher HCV viral load that was observed with anti-HBc.Detection of HBV DNA in HBsAg negative chronic HCV patients plays a non significant role in non-response of Egyptian patients to pegylated interferon/ribavirin therapy.Chronic hepatitis C (HCV) affects more than 170 million people worldwide, causing cirrhosis and liver cancer [1]. In Egypt, high HCV rates were reported reaching up to 20% [2]. The currently recommended therapy for chronic HCV is the combination of pegylated interferon alpha and ribavirin (Peg-IFN/RBV) that proved to be superior to standard interferon alpha and ribavirin [3]. More than 50% of patients can achieve a sustained virological response (SVR) after 24-48 weeks of this combination therapy, making HCV a potentially curable disease [1]. For patients with HCV genotype 4 infections (the prevalent genotype in Egypt), combination treatment with pegylated interferon alpha and weight based ribavirin administered for 48 weeks seems to be an appropriate regimen [4]. Occult hepatitis B virus infection (OBI) is defined as the presence of HBV DNA, in serum and/or the liver tissue without detectable HBsAg with or without anti-HBc or anti-HBs outside the pre-seroconversion window period [5]. Both HBV and HCV share common routes of transmission and hence there is a consensus that patients with chronic HCV liver disease, are at high risk of OBI [6,7]. OBI may contribute to liver inflammation through episodes of increased viral replication, increas

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