Silveri F, De Angelis R, Poggi A, Muti S, Bonapace G, Argentati F, Cervini C
Department of Rheumatology, Ancona University, Ospedale A. Murri, Jesi, Italy.
Scand J Rheumatol. 2001;30(5):290-6. doi: 10.1080/030097401753180372.
To evaluate the relative roles of endothelium and platelets in the pathogenesis of primary RP and RP secondary to SSc.
Endothelial derived ET-1, t-PA, PAI-1, and platelet derived beta-TG, PDGF, TGF-beta were measured in 36 patients with primary RP, 14 patients with RP secondary to SSc and 30 age and sex matched controls.
A significative increase of ET-1, t-PA, PAI-1, TGF-beta, and beta-TG were the most relevant changes in patients with RP secondary to SSc with respect to the controls. Less relevant increases of t-PA, PAI-1, PDGF, and beta-TG levels were observed in patients with primary RP vs controls.
These data seem to confirm the involvement of endothelial cells and platelets in the pathogenesis of RP, with mild changes in primary RP and more relevant changes in RP secondary to SSc.
评估内皮细胞和血小板在原发性雷诺现象(RP)及系统性硬化症(SSc)继发的RP发病机制中的相对作用。
检测了36例原发性RP患者、14例SSc继发RP患者以及30例年龄和性别匹配的对照者的内皮细胞源性内皮素-1(ET-1)、组织型纤溶酶原激活物(t-PA)、纤溶酶原激活物抑制剂-1(PAI-1),以及血小板源性β-血小板球蛋白(β-TG)、血小板衍生生长因子(PDGF)、转化生长因子-β(TGF-β)。
与对照组相比,ET-1、t-PA、PAI-1、TGF-β以及β-TG显著升高是SSc继发RP患者最相关的变化。与对照组相比,原发性RP患者中t-PA、PAI-1、PDGF和β-TG水平升高程度较小。
这些数据似乎证实了内皮细胞和血小板参与了RP的发病机制,原发性RP变化较轻,而SSc继发RP变化更显著。