Evaluation of serum level of tumor necrosis factor receptor II in hepatitis C virus (genotype 4)-infected middle-aged men with and without diabetes and its complications in Egypt: a pilot study.

Abstract

Tumor necrosis factor α (TNF-α) is a type of cytokine produced by macrophages and other cell types in response to various stimuli. Many studies have shown that TNF-α is involved in the development of diabetes. It also has a pivotal role in the inflammatory process of chronic hepatitis C. This study aimed to examine the hypothesis that TNF is increased in patients infected with hepatitis C virus (HCV) and with diabetes rather than in patients infected with HCV or with diabetes alone. Patients were divided into 5 groups: patients with diabetes without complications and without HCV infection (group 1), patients with diabetes and complications but without HCV infection (group 2), patients without diabetes but with HCV infection (group 3), patients with diabetes without complications but with HCV infection (group 4), and patients with diabetes and complications and with HCV infection (group 5). Results revealed an activation of the TNF axis in all tested patients when compared with the level of healthy Egyptians done in previous studies. However, although there was a gradual escalation in the activation of the TNF axis in these groups, the increase did not amount to a statistical difference between them (P > 0.05). However, the trend was toward the higher values in HCV infection with diabetes and its complications. The number of studied patients may be a limitation of this research. There was no correlation between the level of TNF receptor II and the levels of transaminases, albumin, and creatinine in the different groups or the degree of microalbuminuria in the groups of patients with diabetic complications. Also, there was no relation between the hepatic or splenic size and the level of TNF receptor II. The presence of diabetes and its complications in patients with HCV infection could not be attributed only to the activation of the TNF system at least in Egyptian patients.