Background:  Insulin resistance diminishes the likelihood of achieving a sustained virological to hepatitis C virus (HCV) antiviral therapy in HCV⁺/HIV^­ patients, but there is no information about the association of insulin resistance with the efficacy of such treatment in HCV⁺/HIV⁺ patients. Our objectives was to evaluate the independent predictors of sustained virological response.

Methods:  In a cohort or 198 patients (113 HCV⁺/HIV⁺ and 85 HCV⁺/HIV^­), all were naïve for HCV antiviral therapy and received peg-interferon-alpha 2a (pegINF-a2a; 180 µg/week) + ribavirin (RBV; 800 to 1200 mg/day). Patients’ characteristics were were recorded:  baseline HCV and HIV RNA, CD4⁺ count, HCV genotype, and liver fibrosis stage. Homeostasis model assessment (HOMA)-insulin resistance and HOMA-β were calculated as:  insulin resistance = fasting insulin (mUI/l) × fasting glucose (mmol/)/22.5 and β-cell function (HOMA-β)=20×fasting insulin (mUI/l)/fasting glucose (mmol/l)- 3.5.

Results:  There were significant differences in sex, body mass index, liver fibrosis stage, HCV genotype distribution, and baseline HCV RNA between HCV⁺/HIV^­ and HCV⁺/HIV⁺. Moreover, co-infected patients showed higher baseline insulinemia, lower glycemia, and thus higher degree of insulin resistance (HOMA-insulin resistance) and β-cell function than HCV mono-infected patients. Sustained virological response rate was achieved in 57% of HCV⁺/HIV^­ and in 51% of HCV⁺/HIV⁺ patients (by on treatment analyses) (p = NS). Overall, the factors independently associated with the achievement of a sustained virological response were HIV (OR 0.45, 95%CI 0.21 to 0.58), age (OR 1.05, 95%CI 1.00 to 1.11), HCV genotype 2 and 3 (OR 5.90, 95%CI 2.62 to 13.29), fibrosis (OR 0.7, 95%CI 0.51 to 0.97), and HOMA-insulin resistance (OR 0.43, 95%CI 0.19 to 0.98). Among patients harboring genotype 1 and 4 (82 HCV⁺/HIV⁺, 63 HCV⁺/HIV^­), in multivariate analysis using Backward LR, HOMA-insulin resistance was the only independent variable associated with the chance of achieving a sustained virological response when all these patients were considered (OR 1.30, 95%CI 1.07 to 1.59) and also when the analysis was preformed only within the co-infected population (OR 1.49, 95%CI 1.08 to 2.07). Sustained response was achieved in 22.5% HCV genotype 1 and 4 patients showing HOMA-insulin resistance >4 and in 51% of patients with HOMA £4; p = 0.005.

Conclusions:  Insulin resistance is a independent factor associated with the possibility of achieving a sustained virological response in HIV⁺ patients co-infected by HCV genotype 1.