Author(s)

Inas Kostandi, Magy Bahgat, Naglaa Zayed, Laila Rashed

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Introduction: Insulin resistance (IR) is documented in patients with chronic hepatitis C(CHC), plays an important factor in disease progression and predicting poor response to treatment. In chronic liver disease, levels of insulin-like growth factor-1 (IGF-1) were correlated with IR. Aim: To evaluate IR and serum levels of IGF-1 in Egyptian patients with CHC after anti-viral therapy. Patients and Methods: Forty biopsy-proven, non-diabetic, CHC patients, who received combined IFN/ribavirin therapy, in addition to 10 healthy controls were studied. Serum levels of IGF-1, growth hormone (GH) were measured and HOMA-IR(homeostasis model assessment of IR), body mass index (BMI) were calculated. Baseline data, retrieved from patients’ files before initiation of therapy, together with response to antiviral therapy were analyzed with respect to the measured variables. Results: All patients possessed a significant higher HOMA-IR score (p = 0.02), GH levels (p < 0.001) and blood glucose levels (p < 0.001) than controls while significantly lower levels of IGF-1 were found in patients (p = 0.008)with no significant difference between responders and non-responders as regards the previously mentioned variables. HOMA-IR score was significantly correlated with GH levels, p = 0.003 and with IGF-1 levels in both responders and non responders. Low IGF-1 levels were associated with increase in fibrosis stages and were significantly correlated with insulin(r = –0.499, p = 0.001). Conclusion: CHC patients exhibit an increased HOMA-IR score reflecting the existence of IR irrespective of treatment response. Low IGF-1 levels were associated with advanced stages of fibrosis and thus could contribute to the progression of hepatic fibrosis in CHC.

Hepatitis C, Insulin Resistance, Interferon, Ribavirin, IGF-1

I. Kostandi, M. Bahgat, N. Zayed and L. Rashed, "Assessment of Insulin Resistance and Insulin Growth Factor-1 in Egyptian Patients with Chronic Hepatitis C," Open Journal of Endocrine and Metabolic Diseases, Vol. 1 No. 1, 2011, pp. 1-8. doi: 10.4236/ojemd.2011.11001.