Chronic hepatitis C virus infection without cirrhosis induces insulin resistance in patients with beta-thalassaemia major

Aim The aim of this study was to investigate the cause of increased inciden ce of impaired glucose tolerance and diabetes mellitus in patients with bet a -thalassaemia major and chronic hepatitis C virus (HCV) infection without cirrhosis of the liver. Patients and methods The study included 28 beta -thalassaemic multi-transfu sed patients (14 females and 14 males; age, 25.7 +/- 6.3 years) with normal fasting glucose levels. Sixteen were seropositive for HCV and they had bio psy proven chronic hepatitis C without cirrhosis. An oral glucose tolerance test (OGTT) was performed. Glucose, insulin and C-peptide levels were meas ured every 30 min for 2 h. Fasting insulin resistance index (FIRI) was calc ulated according to the formula: FIRI = (fasting glucose x fasting insulin) /25. Results All patients had a normal OGTT except for two HCV positive and two HCV negative patients who had impaired glucose tolerance. HCV positive pati ents had higher fasting insulin levels (P = 0.02), higher fasting insulin/f asting glucose ratio (P = 0.017) and higher FIRI (P = 0.016) than HCV negat ive patients. During the OGTT, peak insulin levels occurred at 30 min in HC V negative patients but at 60 min in HCV positive. HCV infected patients ha d higher mean value of insulin at 60 (P = 0.017), 90 (P = 0.04), and 120 mi n (P = 0.04), and higher mean increment above basal at 60 (P = 0.015), 90 ( P = 0.018) and 120 min (P = 0.05). The area under the curve (AUC) of insuli n was also greater in HCV positive patients as compared to HCV negative (P = 0.04), although the AUC of glucose and the glucose levels at all time poi nts of the OGTT were similar in both groups. Conclusions The findings of this study show that beta -thalassaemic patient s with HCV infection without liver cirrhosis are more insulin resistant and have delayed insulin secretion compared to HCV negative beta -thalassaemic patients. These changes in insulin action and secretion are evident before the development of impaired glucose tolerance and may explain the higher p revalence of diabetes mellitus in this group. Eur J Gastroenterol Hepatol 1 3:1195-1199 (C) 2001 Lippincott Williams & Wilkins.