Effect of ticlopidine on platelet-derived microparticles in patients with connective tissue diseases.

Haemostasis Pub Date : 1999-01-01 DOI:10.1159/000022510
H Kagawa, S Nomura, M Nagahama, Y Ozaki, S Fukuhara
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引用次数: 15

Abstract

We evaluated the plasma concentrations of platelet activation markers and platelet-derived microparticles (PMP) in patients with connective tissue diseases complaining of peripheral circulation disorders (n = 16) and studied the effect of ticlopidine hydrochloride (ticlopidine) on PMP generation. There were significant differences in the levels of PMP and a platelet activation marker between before and after treatment with ticlopidine (PMP: 695 +/- 393 vs. 354 +/- 206/10(4) platelets, p < 0. 01; platelet CD63: 9.13 +/- 5.64 vs. 5.22 +/- 2.74%, p < 0.05). On the other hand, markers of vascular endothelium, such as vascular endothelium-derived small vesicles and serum thrombomodulin levels, were not affected by the administration of ticlopidine. Levels of cytokines and soluble adhesion molecules remained unchanged by ticlopidine administration. These findings suggest that ticlopidine may be useful for the inhibition of PMP-dependent vascular damage in patients with connective tissue diseases complaining of peripheral circulation disorders.

噻氯匹定对结缔组织病患者血小板源性微粒的影响。
我们评估了16例伴有外周循环障碍的结缔组织病患者血浆中血小板活化标志物和血小板衍生微粒(PMP)的浓度,并研究了盐酸噻氯匹定(噻氯匹定)对PMP生成的影响。噻氯匹定治疗前后PMP和血小板活化标志物水平(PMP: 695 +/- 393 vs 354 +/- 206/10(4)个血小板,p < 0。01;血小板CD63: 9.13 + / - 5.64和5.22 + / - 2.74%,p < 0.05)。另一方面,血管内皮标志物,如血管内皮源性小泡和血清血栓调节蛋白水平,不受噻氯匹定的影响。细胞因子和可溶性粘附分子水平在噻氯匹定给药后保持不变。这些发现表明噻氯匹定可能有助于抑制以外周循环障碍为主因的结缔组织疾病患者的pmp依赖性血管损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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