Insulin Resistance in Patients with Chronic Hepatitis C Infection,HODA ABDELSATAR, MAHMOUD MAHFOUZ, LAYLA RASHED and DALIA AHMAD
Abstract
Chronic HCV infection has emerged as a complex multi-faceted disease with manifestations extending beyond the liver. Hepatic steatosis, insulin resistance (IR) and type II diabetes have been observed to occur more frequently in association with HCV infection than other chronic inflamma-tory liver disease. Most of the studies indicate an independent higher prevalence of diabetes mellitus type II and/or insulin resistance in chronic HCV patients compared to control groups while in others this association was only confirmed in the presence of confounding factors. Antiviral treatment may lead to an improvement of insulin resistance is a strong argument in favor of a causal relationship between HCV infections and the presence of diabetes mellitus II.
Insulin resistance (IR) promotes liver fibrosis as hyperin-sulinemia per se stimulates the proliferation of stellate cells enhancing the secretion of extracellular matrix. Moreover, hyperinsulinemia stimulate the expression of connective tissue growth factor. On the other hand, HCV is directly associated with IR in a dose-dependent manner as viral eradication after antiviral treatment may lead to an improvement of insulin resistance. The aim of this work is to study the relation between patients with CHC infection and insulin resistance. The study was conducted on 50 non diabetic patients with CHC, not to have liver cirrhosis and 10 age, sex, BMI matched group as a control group. Complete history taking and clinical exami-nation specially examination of blood pressure, jaundice vascular spiders, liver flaps, BMI, acanthosis nigricans, clinically detectable organomegaly, laboratory investigations including fasting serum glucose, fasting serum insulin, serum alanine aminotransferase, serum bilirubin, prothrombin time and concentration.
Results: Showed that the means of fasting serum insulin, fasting serum glucose, serum AIT and AST were statistically higher in patients with HCV compared to the control. HOMA IR was found to be higher in patients with HCV than control with value of 4.9±1.6 and 0.99±0.28 respectively. HOMA is found to be statistically related to BMI and serum glucose and nearly significant to HCV (correlation coefficient 0.23 p-value 0.09). HCV was found to be significantly related to serum glucose, and HOMA. Linear regression analysis revealed that BMI and HCV infection were significant predictors for high HOMA level p 0.001, r 0.617 which means that the regression model is significant and could explain 61.7% of change in HOMA level.
Conclusion and Recommendations: Insulin resistance is common in patients with HCV. Monitoring and follow-up of serum glucose is important in euglycemic CHC patients. Study of vascular risk in CHC patients with metabolic IR is important and needed to be clarified.