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  • There is increased awareness of HBV reactivation


    There is increased awareness of HBV reactivation in chronic HCV/HBV co-infected patients treated with DAAs [1], [2]. The recent emergence of this adverse event of DAA therapy is due to the exclusion of HBV co-infected subjects from registration clinical trials evaluating the safety of these treatments. A likely explanation for this adverse event is that the clearance of HCV infection due to effective anti-HCV therapy may remove the suppression exerted by HCV over HBV replication [16], thus inducing HBV reactivation [17]. Spontaneous fluctuations of HBV replication or of the immunological changes after HCV clearance have also been suggested rather than a direct HBV/HCV interference [18]. The severity of hepatic damage may range from HBV reactivation without hepatitis to fulminant hepatic failure requiring 81 5 sale liver transplantation [1]. The risk of HBV reactivation differs according to the HBV infection status: high in subjects with an overt infection, but low in those with an occult infection [1], [2]. The European Association for the Study of the Liver (EASL) guidelines focus on the management of subjects with HBV/HCV coinfection [18]. The EASL guidelines recommend testing for HBV markers before starting DAAs for HCV. HBsAg positive patients should be considered for concomitant NA prophylaxis, while the HBsAg-negative/anti-HBc-positive should be monitored and tested for HBV reactivation in the case of ALT elevation [18]. HBsAg positivity is found in nearly 3% of HCV-RNA-positive subjects, a rate more than three-fold higher than that observed in the general 81 5 sale [19]. This figure is not surprising because HBV and HCV share several modes of transmission. This proportion means that among the estimated one million HCV-RNA-positive subjects living in Italy, nearly 30,000 could be HBsAg-positive subjects at risk of DAA-induced HBV reactivation. Careful monitoring should also be addressed to the nearly 80,000 subjects with isolated anti-HBc also at risk of reactivation, albeit to a lesser extent. However, it should be considered that the real population target eligible for antiviral treatment is less as only part of these individuals will be identified and will have access to HCV therapy. Among the HCV-RNA-positive subjects investigated, the prevalence of liver cirrhosis resulted significantly higher than that of chronic hepatitis in HBsAg-positive subjects, but not in those positive for other HBV markers, confirming that overt HBV infection speeds up HCV chronic hepatitis to a more severe outcome [7], [8], [9], [16], [20].
    Conflict of interest
    Background and objectives An estimated 240 million people are chronically infected with hepatitis B virus (HBV) worldwide [1], [2], [3], and are at increased risk of developing cirrhosis, hepatic decompensation, and hepatocellular carcinoma (HCC) [1], [2], [3], [4], [5], [6]. Long-term elevations in HBV DNA viral levels >2000IU/mL, in addition to other factors including elevated alanine aminotransferase (ALT) and HBeAg status, have been shown to be associated with both risk of progression to cirrhosis and risk of HCC [7], [8], [9], [10]. An estimated 700,000 deaths every year are due to HBV related end stage liver disease or HCC [3]. Measurement of HBV viral loads (VL), in conjunction with other serological and biochemical markers, is an essential part of the decision to start treatment, for on-treatment monitoring and to determine treatment stopping points or treatment failure. Treatment goals are a sustained suppression of VL (virologic response (VR)), preferably below assay limit of detection (LOD). On treatment increases in VL of >1 log10 compared to nadir or values ≥100IU/mL in patients previously not detected (ND) on treatment may indicate virologic breakthrough (VB) and require a change in therapy. Use of real-time PCR quantification is recommended based on the sensitivity, specificity, accuracy and broad dynamic range of these assays [1], [2], [11].