Nalbant Selim, Koc Bayram, Top Cihan, Kucukardali Yasar, Baykal Yavuz, Danaci Mehmet, Kocer Ismail Hakki
Department of Internal Medicine, Gata Haydarapasa Training Hospital, 81327 Istanbul, Turkey.
Rheumatol Int. 2002 Nov;22(6):244-8. doi: 10.1007/s00296-002-0235-6. Epub 2002 Sep 6.
Hypersensitivity vasculitis (HSV) is secondary vasculitis due to an immune response to exogenous substances. Because of the relative rarity of the vasculitides there are no reports on the role cytokines. This report evaluates some of cytokines which might be involved in pathophysiological events of HSV.
Patients with HSV ( n=20) were classified as active ( n=12) ornd inactive ( n=8) according to a vasculitis activity index for systemic necrotizing vasculitis (VAI). All the patients were males. A control group was formed from 20 healthy male employees of our department. We performed tests for serum interleukins 6, IL-10, sIL-2 receptor, tumor necrosis factor (TNF) alpha, C-reactive protein (CRP) levels using enzyme-linked immunosorbent assay and erythrocyte sedimentation rate (ESR).
The mean ESR value, CRP, and fibrinogen levels were significantly different in both active and inactive HSV from those in the healthy group; they were also significantly higher in the active than in the inactive group. There was no significant difference between healthy and inactive groups for serum IL-10, IL-6, sIL-2 receptor, and TNFalpha levels. However, it was also significantly higher for in active HSV patients than in the healthy group. Similar results were obtained comparing active and inactive groups, namely, all cytokine levels were significantly higher for all patients. The most striking finding is the high correlation of ESR (also for CRP, fibrinogen) with serum levels of TNFalpha and IL-10, but not with IL-6 and IL2R.
These data show that serum TNFalpha and IL-10 levels can be studied in comparison to traditional markers of inflammation such as sedimentation rate or C-reactive protein. This may lead to new approaches to treating or managing HSV.
超敏性血管炎(HSV)是由对外源性物质的免疫反应引起的继发性血管炎。由于血管炎相对罕见,尚无关于细胞因子作用的报道。本报告评估了一些可能参与HSV病理生理过程的细胞因子。
根据系统性坏死性血管炎的血管炎活动指数(VAI),将20例HSV患者分为活动期(n = 12)和非活动期(n = 8)。所有患者均为男性。对照组由本部门20名健康男性员工组成。我们采用酶联免疫吸附测定法检测血清白细胞介素6、IL-10、可溶性IL-2受体、肿瘤坏死因子(TNF)α、C反应蛋白(CRP)水平以及红细胞沉降率(ESR)。
活动期和非活动期HSV患者的平均ESR值、CRP和纤维蛋白原水平与健康组相比均有显著差异;活动期患者的这些指标也显著高于非活动期患者。健康组和非活动期组的血清IL-10、IL-6、可溶性IL-2受体和TNFα水平无显著差异。然而,活动期HSV患者的这些指标也显著高于健康组。比较活动期和非活动期组也得到了类似结果,即所有患者的所有细胞因子水平均显著升高。最显著的发现是ESR(CRP和纤维蛋白原也是如此)与血清TNFα和IL-10水平高度相关,但与IL-6和IL-2R无关。
这些数据表明,血清TNFα和IL-10水平可与血沉率或C反应蛋白等传统炎症标志物进行比较研究。这可能会为HSV的治疗或管理带来新方法。