الفهرس 
Introduction and Aim of the WorkOnly 14 pages are availabe for public view
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Abstract
Several clinical studies have suggested a possible link between chronic hepatitis caused by hepatitis C virus (HCV) infection and the development of diabetes mellitus. The pathogenic mechanisms causing DM in patients with HCV infection are not well understood, although both insulin resistance and impaired insulin secretion have been considered to play an important role in the development of diabetes. This study included 42 chronic hepatitis C patients confirmed by PCR. According to the results of their OGTT, they were divided into 3 groups: group (A) included 28 patients with normal OGTT, group (B) included 8 patients with impaired OGTT and group (C) included 6 patients with DM (Table 6, Figure 3). In addition, 10 healthy subjects were selected as control group. The following investigations were done to the studied groups: - Serum glucose levels. - Liver function tests (AST, ALT, albumin, bilirubin and INR). - Serum creatinine - Serum cholesterol and triglycerids. - Serum iron and ferritin. - Serum insulin and C-peptide. The following indices were calculated for each subject: - HOMA-R. - HOMA-B. - Insulinogenic index. - ∆ C-peptide. - Hepatic insulin extraction. In the present study, age and BMI showed no significant change among various studied groups (Table 1, Figure 1). Both ALT and AST were elevated in the three studied groups (Table 2), when compared to the control group. Serum triglyceride levels (Table 3) were significantly higher in HCV patients with diabetes while serum cholesterol levels showed insignificant changes in the diseased groups in comparison to the control group. Serum iron (Table 4) showed significant increase in the diabetic group when compared to HCV group with impaired OGTT group. Serum ferritin levels showed a highly significant increase in its levels in all diseased groups when compared to control group (P<0.01). Also, there was a significant increase in serum ferritin levels in diabetic group when compared to HCV with normal OGTT and HCV with impaired OGTT. In this study,there was a significant positive correlation between the HCV viral load and HOMA-R (Table 15). The insulin resistance was measured by the homeostatic model assessment of insulin resistance (HOMA-R) (Table 9). HOMA-R in CHC patients with diabetes was significantly higher than those with both normal and impaired glucose tolerance. Insulin resistance increased with the development of glucose intolerance. The β-cell function was assessed by the homeostatic model for assessment of β-cell function (HOMA-B) (Table 10). HOMA-B was significantly lower in diabetic group when compared to other diseased groups. Also, there was a significant decrease in HOMA-B in impaired and normal OGTT groups when compared to the control group. HOMA-B decreased in CHC patients with glucose intolerance. The insulinogenic index and ∆ C-peptide (Tables 11, 12) showed significant decrease in diabetic group and impaired OGTT group when compared to control group or to patients with normal glucose tolerance. The hepatic insulin extraction (Table 13) was not significantly different among the three groups. It could be concluded that there is an association between insulin resistance and chronic HCV infection. Insulin resistance in chronic HCV patients is not related to liver enzymes. It could be demonstrated that both insulin resistance and β-cell dysfunction contribute to glucose intolerance in patients with CHC. Pancreatic β-cell dysfunction may occur early in the disease. The hepatic extraction of insulin has no significant importance in the development of glucose intolerance in these patients. The fact that HCV infection induces insulin resistance through disturbing the insulin signaling pathway may influence the progression of chronic liver disease and open up novel therapeutic approaches Key words: Insulin resistance, chronic hepatitis C