الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Hepatitis C virus (HCV) infection is a frequent cause of acute and chronic hepatitis, and leads to the development of cirrhosis and hepatocellular carcinoma. It is estimated that about 150 to 200 million people have been in contact with HCV worldwide, and approximately 85% are chronically infected. The spectrum of severity of liver disease associated with HCV varies widely, as does the rate of progression towards the cirrhotic stage. The latter seems to depend on several, mostly host-related cofactors, such as age, sex, level of alcohol consumption, overweight, immune status and co-infections. One of these cofactors is type 2 diabetes (T2D), which has been recognized to modify the course of hepatitis C even at the stage of insulin resistance (IR), a condition that precedes the development of T2D. Although individuals may develop IR independently of HCV, a considerable amount of clinical and experimental data suggest that HCV contributes to its pathogenesis. This aspect is important, because IR seems not only to accelerate the course of chronic hepatitis C, but also to influence the response to antiviral therapy. The aim of this work was to study the virological and biochemical response to antiviral therapy ( pegylated INF & ribavirin) in diabetic versus non-diabetic patients with HCV infection. Summary and Conclusions 104 The study included 100 patients, 50 of them were diabetic and the other 50 were non-diabetic All patients were subjected to the following: A. History taking and complete clinical examination. B. CBC. C. Fasting and two hours post prandial blood glucose. D. Liver function tests (bilirubin, albumin, PT, AST, ALT). E. HbA1c before, 3 months, 6 months and at the end of treatment. F. HCV RNA with commercial PCR-based assays. G. Liver biopsy under sonography. Follow up of patients who respond to treatment was done after 6 months by HCV RNA with commercial PCRbased assays to asses sustained virological response (SVR). The following results were found: • BMI was lower in non-diabetic group with mean of 19.47 ± 0.82 while diabetic group mean was 21.76± 0.91 with highly significant statistical difference (t=7.74;p < 0.01). • Albumin was higher in non-diabetic group (mean 3.98± 0.13) than diabetic group (mean 3.92±0.10) with significant statistical difference (t=-0.65;p<0.05). Summary and Conclusions 105 • Fasting and two hours post prandial blood glucose were lower in non diabetic group (mean 81.86 ± 10.36 and 107± 12.11 respectively) than diabetic group (mean 172.54± 24.64 and 242.62± 37.25 respectively) with highly significant statistical difference (t=23.98;p=<0.01) (t=24.32;p=<0.01) • HbA1c before treatment was lower in non-diabetic group with a mean of 5.35±0.52%, while diabetic group’s mean was 6.91±0.936% with highly significant statistical difference (t=-10.23; p<0.01). HbA1c 3 months after treatment was lower in non-diabetic group with a mean of 5.39±0.53% while diabetic group’s mean was 7.13±1.46% with highly significant statistical difference (t= -7.92; p< 0.01). HbA1c 6 months after treatment was lower in non-diabetic group with a mean of 5.46±0.52%, while diabetic group’s mean was 6.95±1.36% with highly significant statistical difference (t=-6.97; p< 0.01). • Response to treatment was higher in non-diabetic group (33 patients (66%)) than diabetic group (25 patients (50%)) with insignificant statistical difference (X2 = 2.011; p- value > 0.05). • SVR was higher in non-diabetic group (26 patients (52%)) than diabetic group (18 patients (36%)) with insignificant statistical difference (X2 =2.978; p-value > 0.05)). Summary and Conclusions 106 • HbA1c in those who achieved SVR in the diabetic group decreased at the end of treatment with a mean of 6.39±0.80. It can be concluded that the response to HCV therapy is affected by the presence of T2D as the response was found to be higher in non-diabetic patients compared to diabetic patients. It was noticed that well control of T2D leads to higher response to anti-viral therapy.