Hypersensitivity vasculitis and cytokines
Koçer, İsmail Hakkı
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CitationNalbant, S., Koç, B., Top, C., Küçükardalı, Y., Baykal, Y., Danacı, M. ve Koçer, İ. H. (2002). Hypersensitivity vasculitis and cytokines. Rheumatology International, PubMed. 22(6), s. 244-248.
Objective 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. Material and methods 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) a, C-reactive protein (CRP) levels using enzyme-linked immunosorbent assay and erythrocyte sedimentation rate (ESR). Results 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 TNFa 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 TNFa and IL-10, but not with IL-6 and IL2R. Conclusions These data show that serum TNFa 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.
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