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痛风患者血浆糖蛋白 VI 水平升高与血小板反应性增强相关。

Increased platelet reactivity as measured by plasma glycoprotein VI in gout.

机构信息

a Department of Rheumatology , Mater Misericordiae University Hospital, Dublin Academic Medical Centre , Dublin , Ireland.

b CARD Newman Research Fellow, University College Dublin , Dublin , Ireland.

出版信息

Platelets. 2018 Dec;29(8):821-826. doi: 10.1080/09537104.2017.1366974. Epub 2017 Nov 1.

DOI:10.1080/09537104.2017.1366974
PMID:29090618
Abstract

Patients with gout have an increased risk of cardiovascular events. The glycoprotein VI (GPVI) receptor is found exclusively on platelets and megakaryocytes, is proteolytically cleaved upon platelet activation, and detectable in plasma as soluble GPVI (sGPVI). Therefore, elevated sGPVI is a marker of platelet activation and a risk marker for cardiovascular events. The aim of this study was to assess platelet activation, as measured by plasma sGPVI level in gout. Blood samples were taken from patients with gout or osteoarthritis, and from healthy volunteers. Demographic and clinical data were collected for all participants. Blood samples were processed as double-spun platelet-poor plasma. Plasma sGPVI levels were measured using enzyme-linked immunosorbent assay. Mann-Whitney U test was used to compare groups. In total, 91 patients were included, 27 during gout flare, 41 with intercritical gout, 23 with osteoarthritis, and 53 healthy controls. Median (interquartile range) sGPVI levels were 6.51 ng/mL (4.52, 8.41) in gout flare, 3.58 ng/mL (2.11, 5.55) in intercritical gout, 2.73 ng/mL (2.17, 3.72) in osteoarthritis, and 2.19 ng/mL (1.72, 3.31) in healthy controls. Plasma sGPVI levels in both gout groups were significantly increased compared to healthy controls (p < 0.005 for each), in gout flare compared to osteoarthritis (p < 0.005), and in gout flare compared to intercritical gout (p = 0.001). There was no significant difference in sGPVI levels in gout patients with and without tophi or in those prescribed colchicine. We conclude that patients with gout exhibit platelet hyperactivity as demonstrated by elevated sGPVI levels. Platelet activation is exacerbated in gout, especially during gout flares.

摘要

痛风患者发生心血管事件的风险增加。糖蛋白 VI(GPVI)受体仅存在于血小板和巨核细胞上,在血小板激活时被蛋白水解切割,并可作为可溶性 GPVI(sGPVI)检测到血浆中。因此,升高的 sGPVI 是血小板激活的标志物,也是心血管事件的风险标志物。本研究旨在评估痛风患者血浆 sGPVI 水平所反映的血小板激活情况。采集痛风或骨关节炎患者以及健康志愿者的血液样本。为所有参与者收集人口统计学和临床数据。将血液样本处理为双离心血小板贫血浆。使用酶联免疫吸附试验测量血浆 sGPVI 水平。使用 Mann-Whitney U 检验比较组间差异。共纳入 91 例患者,其中 27 例痛风发作,41 例间歇期痛风,23 例骨关节炎,53 例健康对照。痛风发作时 sGPVI 中位数(四分位距)为 6.51ng/ml(4.52,8.41),间歇期痛风时为 3.58ng/ml(2.11,5.55),骨关节炎时为 2.73ng/ml(2.17,3.72),健康对照组为 2.19ng/ml(1.72,3.31)。两组痛风患者的血浆 sGPVI 水平均明显高于健康对照组(p<0.005),痛风发作时高于骨关节炎(p<0.005),痛风发作时高于间歇期痛风(p=0.001)。有或无痛风石以及服用秋水仙碱的痛风患者的 sGPVI 水平无显著差异。我们的结论是,痛风患者表现出血小板活性亢进,表现为 sGPVI 水平升高。痛风患者的血小板激活加剧,尤其是在痛风发作时。

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