Introduction During the past years, studies have provided evidence that hepatitis C virus (HCV) can independently contribute to insulin resistance (IR) and may interfere with insulin signalling pathway using genotype-specific mechanisms. HCV-associated insulin resistance may cause accelerated fibrogenesis, reduced response to IFN-based therapy and hepatocellutar carcinoma. Our aim was to evaluate the prevalence of insulin resistance in Egyptian patients infected with chronic hepatitis C virus genotype 4; being the most prevalent genotype, to assess factors associated with insulin resistance in those patients and to test the impact of insulin resistance on treatment outcome.
Method One hundred non diabetic adult patients with histologically proven chronic hepatitis C (CHC), genotype4 were randomly enrolled to test the prevalence of insulin resistanceusing the homeostasis model assessment-IR (HOMA-IR). Based on the results of the prevalence study, 71 consecutive treatment-naïve patients were chosen for testing treatment outcomes associated with various degrees of insulin resistance. All patients were given a combination of pegylated interferon and ribavirin for an intended duration of 48 weeks. Quantitative HCV RNA estimation and HOMA-IR testing were done at baseline, during therapy and at the end of treatment.
Results Insulin resistance (HOMA-IR >3) was detected in 31 patients (31%). HOMA-IR was positively correlated with age, basal viral load, BMI, triglycerides, fibrosis and steatosis with results regarding basal viral load and incidence of fibrosis mounting to a statistical significance (p = 0.029 and p = 0.026 respectively). When data were analysed by multivariate linear regression, viral load remained the only independent factor associated with elevated HOMA-IR levels (p = 0.001). Overall, 59 patients of those followed for assessing treatment outcomes achieved an end of treatment response (ETR) (59/71,83%). A univariate analysis showed that those were significantly younger, had lower HOMA-IR scores, less viral load and less steatosis compared with non-responders. However, after logistic regression, baseline viral load remained the only independent factor associated with ETR (odds ratio = 0.098, p = 0.006). A progressive significant decline in HOMA-IR scores was noted in this group of patients when comparing values before commencement of therapy, during therapy and at end of follow-up period.
Conclusion Insulin resistance is frequently encountered in genotype 4 CHC patients and is independently correlated with HCV viral load. Low baseline HOMA-IR is associated with favourable response to interferon-based therapy and may be a useful predictor for treatment responsiveness. Viral eradication leads to improvement in insulin sensitivity.
Disclosure of interest None Declared.