الفهرس 
Introduction
Chronic hepatitis COnly 14 pages are availabe for public view
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Abstract
Chronic hepatitis C virus (HCV) infection is associated with an increased risk for the development of type 2 diabetes. In the current study, we evaluated the impact of HCV to induce insulin resistance and its relation to fibrosis progression. METHODS: Between July 2003 and August 2004 Among 60 patients with different aetiologies of chronic liver diseases were collected. Routine lab., viral markers, PCR for HCV infected patients, serum leptin, HOMAIR, Cpeptide, rectal snip examination, liver biopsy and pelviabdominal ultrasound were done. RESULTS: Insulin resistance is already present in early stages of HCV infected cases compared with control group (F0=3.9(R+(B1.01 and (F1+F2)=4.9(R+(B1.3) and also in CHB ( 3.10(R+(B0.73) compared with control (1.92(R+(B0.74). There was correlation between insulin resistance and fibrosis in CHC with elevated and normal enzymes (p<0.001 and p=0.002), and also in NASH patients (p=0.012). There was strong relation between serum leptin in CHC with elevated and normal enzymes (15(R+(B3.41 and 14.98(R+(B2.26) and in NASH patients (18.60(R+(B1.74) compared with control (10.88(R+(B3.20). There was correlation between seum leptin and fibrosis in CHC with elevated and normal enzymes (p<0.001 and p=0.002), and not in NASH patients. CONCLUSION: Insulin resistance is present in early stages of chronic hepatitis C. Insulin resistance and serum leptin seems to be associated with fibrosis in non diabetic patients with chronic hepatitis C, while insulin resistance but not leptin seems to be associated with fibrosis progression in NASH. The present data support the hypothesis that insulin resistance may increase the rat of fibrosis progression in non diabetic patients with chronic hepatitis C.