Levels of TNF-α, IL-1β, TGF-β, and IL-6 in patients with chronic hepatitis C virus infection and hyperinsulinemia

Background: Previous evidences support to inflammatory process associated with the IR those important factors in the development of fibrosis and hepatic damage in patients with HCV infection. Objectives: Determine the presence of immunological or histological differentces between hyperinsulinemic and non-hyperinsulinemic chronic HCV-infected patients with at least 10 years of evolution. Material and Methods: The body mass index, Child-Puigh score, liver function tests, and biochemical profile were evaluated in 30 control, 40 chronic HCV-infected patients with hyperinsulinemia, and in 40 normoinsulinemic chronic HCV-infected patients with at least 10 years of evolution. In addition, HCV genotype and viral load were established with the Amplicor System. In addition, nitrites in plasma, and TNF-α, IL-1β, TGF-β, IL-6, and insulin levels were determined. Results: No differences were found in BMI, Child-Pugh “A” scores, ALT, viral load, or genotype between the hyperinsulinemic (>25 IU/ml) and normoinsulinemic (<25 IU/ml) patients. Hyperinsulinemia patients had a higher HOMAIR value (13.6) than normoinsulinemia patients (3.4), and none had a glycemia > 126 mg/dl. Cytokines concentration did not show differences with respect to controls. Nitrites showed a slight increase only in patients with HCV infection. Conclusions: Absence of changes in the proinflammatory cytokines concentration or in some inflammation markers in chronic HCV patients with hyperinsulinemia suggests that long-term insulin levels, in presence of HCV, cannot explain by themselves the hepatic alterations observed in the patient with HCV infection, the presence of others elements (alcoholism, cirrhosis, etc.) is necessary to onset hepatic damage in these patients.