Study of diabetes mellitus among patients with hepatitis C virus

Abstract

Introduction Hepatitis C virus (HCV) infection and type 2 diabetes are two common disorders with high impact on health worldwide. There is growing evidence to support the concept that HCV is associated with type 2 diabetes. Purpose This work aimed to study the clinical phenotype of type 2 diabetes in HCV patients. Patients and methods Our study was conducted upon 100 nonobese, noncirrhotic hepatitis C positive patients who were classified into two groups according to homeostatic model assessment (HOMA) test for insulin resistance (HOMA IR). This study also included 15 nonobese type 2 diabetic patients negative for HCV and hepatitis B virus infection classified as control groups. We excluded alcoholics and drug addicts and patients with conditions that affect blood glucose such as endocrine diseases associated with disordered glucose metabolism and use of drugs. All participants were subjected to full history taking and complete clinical examination including BMI and the following investigations: complete blood count, fasting blood sugar, 2 h postprandial blood sugar, glycosylated hemoglobin, fasting insulin level, cholesterol level, HDL, LDL, triglyceride, serum urea, creatinine, complete urine analysis, liver function tests: total bilirubin, alkaline phosphatase, albumin, prothrombin time, INR, SGOT, SGPT, quantitative PCR for determination of HCV-RNA, surface antigen (HbsAg), abdominal ultrasonography, liver biopsy when needed and possible for HCV patients, and ECG. Results In this study, we found that the prevalence of type 2 diabetes in group I is 24%. HCV can independently contribute to IR with viral genotypes 1 or 4. We noticed significant positive correlation between fasting insulin and HOMA IR in hepatitis C +ve patients. IR in HCV-infected patients is high irrespective of the degree of liver injury even before a minimal fibrosis is present. Both IR and diabetes can adversely affect the course of chronic hepatitis C, leading to enhanced steatosis and liver fibrosis, and even increase the risk of hepatocellular carcinoma. A significant correlation between HOMA IR and steatosis, a significant positive correlation between fasting insulin and steatosis and a negative correlation between steatosis and BMI in HCV patients was found. No correlation was found between HOMA IR and the viral load (quantitative HCV RNA). Conclusion We can concluded that diabetic HCV patients had intermediate clinical phenotype lower BMI and LDL than control and development of type 2 diabetes mellitus in HCV patients was significantly higher in nontreated patients than treated patients. Antiviral therapy and clearance of HCV improves IR, β-cell function, the blood glucose abnormalities.