ABSTRACT
This study was conducted on 80 patients with type 2 diabetes mellitus and 30 healthy control subjects in order to find out the relationship between HCV infection and diabetes mellitus. All cases and controls were subjected to full history taking, clinical examination, serological study of HCV antibodies by 3[rd] generation ELISA, HBsAg by ELISA, routine. Laboratory investigations, liver function tests, abdominal ultrasonography, diabetic biochemical profile [fasting and two hours postprandial blood glucose], glycosylated HbAIC and serum insulin level, serum anti-insulin antibodies and liver biopsy for 40 patients for histopathological examimition. The study showed that 49 out of 80 diabetic patients [61%] were anti-HCV +ve compared to controls [16.7%]. HBsAg was +ve in 4 cases only [5%]. Easy fatigability, swelling of both legs and abdominal distension were significantly more in anti-HCV +ve group. Shrunken liver, splenomegaly, ascites or lower limb oedema were the clinical signs that were significantly higher in anti-HCV +ve group. The aminotransferases [ALT, AST] showed significant increase, while serum albumin showed significant reduction in anti-HCV +ve group. Ultrasonographic study showed shrunken liver, periportal fibrosis, cirrhosis, portal vein dilatation, splenomegaly and ascites more in anti-HCV +ve group while bright liver was significantly more in anti-HCV -ve group. Liver biopsy showed that all cases of anti-HCV +ve group [23 cases] had chronic active hepatitis, 10 of them also showed cirrhosis while only one case had fatty change. In anti-HCV -ve cases [17 cases], 14 cases had chronic persistent hepatitis, 13 cases had fatty change, 2 cases showed chronic active hepatitis [they were HBsAg +ve] and one case had normal histology. This denotes that HCV infection leads to more severe and progressive pathological changes in diabetics. The biochemical pattern of diabetics showed that the 2 hours postprandial was the only parameter that had a significant difference between the two groups. So there is a delay in glucose consumption in patients with chronic HCV and this may be attributed to a defect in insulin action and this suggests that HCV could play a role in the development of diabetes. Serum insulin level was higher in anti-HCV +ve diabetics but not significant while HbAIC was lower. As regards anti-insulin antibodies there was no significant difference because only one case of anti-HCV +ve diabetics had it. This minimizes the role of auto immunity in the pathogenesis of diabetes in patients with HCV infection. In conclusion, we found a high prevalence of anti-HCV antibodies among diabetic patients. Therefore we suggest an association between them. The exact mechanism is not known, we suggest B-cell dysfunction [due to low insulin level], liver damage [because all anti-HCV +ve diabetics had severe histopathological hepatic changes] or defect in insulin action [because the 2 hours P.P glucose was significantly higher in anti-HCV +ve diabetics]. Further studies are needed to clarify the nature of the association and its exact mechanism