A.M. Migliavacca Center for Liver Disease, 1st Division of Gastroenterology, Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Università degli Studi di Milano, Milan. firstname.lastname@example.org.
Background and Aims. Hepatitis C virus (HCV) infection is associated with insulin resistance (IR) occurrence, a condition known to influence liver fibrosis progression and response to pegylated interferon (PegIFN)/ribavirin (Rbv) therapy. We aimed to assess whether a sustained virological response (SVR) following antiviral therapy prevents development of IR in the long term. Methods. The MIST study cohort, who received Peg-IFN alfa2a or alfa2b/Rbv, underwent homeostasis model assessment (HOMA) at baseline and 24 months after treatment completion. All patients (n=431) had a liver biopsy scored for grading, staging (Ishak) and steatosis. Results. At baseline, IR (HOMA>2) was detected in 48 (12%) patients, and was associated with body weight (p=0.03), HCV load <0.6 × 10(6) IU/l (p=0.006), Fibrosis staging ≥ 4 (p=0.01), and moderate-severe steatosis (p=0.03). IR did not influence the rates of ETR (75% vs 69%, p=0.4), SVR (63% vs 60%, p=0.8) or relapse (19% vs 24%, p=0.5). Post treatment, IR developed in 49 of 384 (14%) non diabetic patients. While mean baseline and post treatment HOMA values were similar in SVR patients (1.11 ± 0.8 vs 1.18 ± 1.1, p=0.25), treatment failure patients showed a significant increase in mean HOMA at the follow-up visits (1.20 ± 0.85 to 1.49 ± 1.3, p=0.007), with an increased rate of de-novo IR in non-SVR compared to SVR patients (17% vs 7%, p=0.007). By logistic regression analysis, treatment failure (OR 2.81; 95% CI, 1.39-5.67; p=0.004) and 10% BMI increase (OR 6.42; 95% CI, 1.69-24.3; p=0.006) were significantly associated with the development of de-novo IR. Conclusions. In non diabetic patients with chronic hepatitis C, the achievement of an SVR to Peg IFN and Rbv prevents development of de-novo IR.