Department of Internal Medicine, Faculty of Medicine, Cairo University, Cairo, Egypt.
J Investig Med. 2011 Dec;59(8):1276-9. doi: 10.2130/JIM.0b013e31823908ca.
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.
肿瘤坏死因子 α(TNF-α)是一种细胞因子,巨噬细胞和其他细胞类型在受到各种刺激后会产生这种细胞因子。许多研究表明,TNF-α 参与了糖尿病的发生。它在慢性丙型肝炎的炎症过程中也起着关键作用。
本研究旨在检验以下假设,即感染丙型肝炎病毒(HCV)且合并糖尿病的患者的 TNF-α 水平升高,而不仅仅是感染 HCV 或合并糖尿病的患者的 TNF-α 水平升高。
将患者分为 5 组:无并发症和无 HCV 感染的糖尿病患者(第 1 组)、有并发症但无 HCV 感染的糖尿病患者(第 2 组)、无糖尿病但有 HCV 感染的患者(第 3 组)、无并发症但有 HCV 感染的糖尿病患者(第 4 组)以及有并发症和 HCV 感染的糖尿病患者(第 5 组)。
与之前研究中埃及健康人的水平相比,所有接受检测的患者的 TNF 轴均被激活。然而,尽管这些组中 TNF 轴的激活呈逐渐上升趋势,但组间差异无统计学意义(P>0.05)。然而,在 HCV 感染合并糖尿病及其并发症的患者中,这一趋势呈上升趋势。本研究的局限性在于患者数量较少。在不同组中,TNF 受体 II 的水平与转氨酶、白蛋白和肌酐的水平之间,或糖尿病并发症患者组中微量白蛋白尿的程度之间均无相关性。此外,TNF 受体 II 的水平与肝脾大小之间也没有关系。
在埃及患者中,HCV 感染合并糖尿病及其并发症的发生不能仅归因于 TNF 系统的激活。