Infectious Diseases: Research and Treatment

Background: Chronic hepatitis C virus (HCV) infection is not a simple viral infection; it has many metabolic and autoimmune complications.

Objective: To investigate the impacts of chronic HCV infection on glucose and lipid metabolism and its correlation-if any-with body mass index (BMI) and hepatosteatosis in chronic HCV patients.

Patients and Methods: One hundred and three (103) chronic HCV patients were involved in this study. After blood sugar testing patients were classified into three groups; Group I: 68 chronic HCV patients with type 2 diabetes. Group II: 35 chronic HCV patients without Type 2 Diabetes and Group III: 25 patients with Type 2 Diabetes as a control group. With informed written consents and approval from Ain Shams medical ethics committee, all groups were subjected to the following: full history taking, thorough clinical examination, calculation of BMI, and measurement of the waist/hip ratio were done. Assessment of fasting plasma insulin level was done by the immune-enzymatic method. Assessment of the insulin resistance state was done by Homeostatic Model Assessment (HOMA-IR). Detection of anti-HCV was done by the 3rd generation ELISA test and confirmed by qualitative polymerase chain reaction (PCR).

Results: Diabetic and non diabetic chronic HCV patients were found to have significantly higher fasting plasma insulin levels and insulin resistance states than the control group. This insulin resistance was not due to increased body mass index as there was a non significant difference in BMI between all the studied groups. Positive correlations were found between plasma insulin level, liver enzymes and steatohepatitis in HCV patients whether they were diabetic or not. No correlation was found between BMI and plasma insulin level in group II patients (HCV only).

Conclusion: Chronic HCV infection may be regarded as an independent risk factor for the development of insulin resistance and type 2 diabetes. HCV induces insulin resistance; the key step for glucose intolerance, and virus C induced steatohepatitis therefore leading to faster progression to cirrhosis. The impacts of chronic HCV infection on glucose and lipid metabolism should be recognized in clinical care centers and addressed in future studies.