A larger follow-up of the cohort will definitely rule out or confirm if LS also predicts overall mortality. Other prognostic factors found in this study were hepatitis B coinfection, high HCV RNA viral load, Selleck Pexidartinib and CTP score. Also, MELD score predicted the development of liver events

but its independent predictive value could not be assessed as a statistical interaction with CTP stage was found. Interestingly, MELD score was associated with overall mortality but not with liver-related mortality after multivariate analyses in our study. In fact, the predictive value of MELD score in HIV/HCV-coinfected patients remains controversial, with previous studies reporting no independent association with survival6, 33 and others finding such an association.34, 35 In our opinion, the lack of an independent association of MELD with liver-related mortality in our cohort could reflect a weaker Selleck Fostamatinib predictive value in the long term, as is the case in this study, than in the short- and mid-term. Achievement of SVR after treatment of hepatitis C is associated with a reduction in liver-related mortality in HIV-negative36 and HIV-positive patients.37 The impact of anti-HCV therapy on the survival or the risk of decompensations

in HIV/HCV-coinfected patients with compensated cirrhosis has been only assessed in two previous cohort studies with apparent conflicting data.33, 38 In the present study, neither exposure to HCV therapy nor achieving SVR during follow-up were associated with a lower risk of developing decompensations. On the contrary, achieving

SVR during follow-up tended to be associated with an improved survival in univariate analyses and exposure to therapy during follow-up was associated with a lower risk of death of any cause. However, these associations did not reach statistical significance, probably due to lack of power and insufficient follow-up. Finally, previous exposure to HCV therapy before enrolment was associated with increased mortality. In our opinion, this association probably reflects a longer time of evolution and an advanced stage of liver disease ADAMTS5 in previous nonresponder patients rather than a worrisome effect of therapy. Additionally, we cannot definitely exclude that selection bias of patients who received prior HCV therapy may have affected our results. Our study may have some limitations. The follow-up period was somewhat short, and the number of some events, particularly liver-related deaths, was relatively low. This might have precluded identifying some potential predictors of mortality as the consecution of SVR. However, the follow-up was long enough to identify other stronger predictors of clinical outcomes such as CTP score or HBV coinfection.