Increased platelet reactivity as measured by plasma glycoprotein VI in gout
Increased platelet reactivity as measured by plasma glycoprotein VI in gout
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DOI：
10.1080/09537104.2017.1366974
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发表时间：
2018-01-01
期刊：
影响因子：
3.3
通讯作者：
McCarthy, Geraldine M.
中科院分区：
文献类型：
--
作者：
Conway, Richard;Murphy, Claire-Louise;McCarthy, Geraldine M.
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裂解，并且在血浆中可检测为可溶性 GPVI (sGPVI)。因此，sGPVI升高是血小板活化的标志物，也是心血管事件的风险标志物。本研究的目的是通过痛风患者血浆 sGPVI 水平来评估血小板活化情况。血液样本取自痛风或骨关节炎患者以及健康志愿者。收集所有参与者的人口统计和临床数据。血样被处理为双旋贫血小板血浆。使用酶联免疫吸附测定法测量血浆 sGPVI 水平。采用曼-惠特尼 U 检验进行组间比较。总共纳入 91 名患者，其中 27 名处于痛风发作期间，41 名患有间期痛风，23 名患有骨关节炎，以及 53 名健康对照。痛风发作时的中位（四分位距）sGPVI 水平为 6.51 ng/mL（4.52，8.41），间期痛风为 3.58 ng/mL（2.11，5.55），骨关节炎为 2.73 ng/mL（2.17，3.72），慢性痛风为 2.19 ng/mL（1.72，3.31）。健康的控制。与健康对照组相比，两个痛风组的血浆 sGPVI 水平均显着升高（p < 0.005），与骨关节炎相比，痛风发作组的血浆 sGPVI 水平显着升高（p < 0.005），与临界间痛风相比，痛风发作组的血浆 sGPVI 水平显着升高（p = 0.001）。有或没有痛风石的痛风患者或服用秋水仙碱的痛风患者的 sGPVI 水平没有显着差异。我们得出的结论是，痛风患者表现出血小板过度活跃，如 sGPVI 水平升高所证明的那样。痛风时，尤其是痛风发作时，血小板活化会加剧。
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.