We would like to congratulate the investigators and the editors for the article by Ioannou et al. recently published in HEPATOLOGY.1
Despite the valuable information added by the study, some issues caught our attention and, if clarified by the investigators, may greatly contribute to the knowledge on human immunodeficiency virus/hepatitis C virus (HIV/HCV) coinfection.
In Table 3, HCV antiviral treatment and sustained virological response (SVR) are additionally adjusted for HCV genotype. Because these data have a major influence in the study endpoints,2, 3 we agreed with this strategy, but we missed the information on the HCV genotype prevalence in the sample. Was HCV genotype prevalence different among patients who achieved the endpoints (i.e., cirrhosis or hepatocellular carcinoma)? If not, why was this additional adjustment performed?
Another issue that caused much surprise was why had only 18% of HIV/HCV-coinfected patients ever been treated for HCV? Did these patients have other comorbidities that prevented them from been treated? In this case, were these morbidities associated with the endpoints?
Finally, the very low SVR rate in treated patients (17%) was very disappointing and is lower than rates previously reported. In an extensive systematic review, Shire et al. found SVR rates with pegylated interferon (IFN) and ribavirin treatment between 27% and 44%.4
Because patients who received two or more doses of IFN were considered as having been treated, we believe that these may be responsible, at least in part, for the low SVR rates reported. The absence of efficacy data (on treatment SVR results in addition to the reported intention-to-treat data) prevented the readers from better understanding these results.