Characterization of Platelet Biologic Markers in the Early Pathogenesis of Postoperative Acute Respiratory Distress Syndrome.
Characterization of Platelet Biologic Markers in the Early Pathogenesis of Postoperative Acute Respiratory Distress Syndrome.
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血小板生物学标志物在术后急性呼吸窘迫综合征早期发病机制中的作用
DOI：
10.1097/cce.0000000000000728
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发表时间：
2022-07
影响因子：
--
通讯作者：
Kor, Daryl J.
中科院分区：
文献类型：
--
作者：
Yadav, Hemang;Meade, Laurie A.;Carter, Rickey E.;Knutson, Keith;Gajic, Ognjen;Kor, Daryl J.
关键词：
动物模型和有限的人类研究表明，血小板在急性呼吸窘迫综合征(ARDS)的发病机制和解决中可能起着重要作用。然而，关于血小板在ARDS发生中的作用的数据很少。本研究的目的是通过分析两种血小板特异性生物标志物：血栓素A2(TXA2)和可溶性CD-40配体(SCD40L)来表征血小板在术后ARDS模型中的作用。这是一项针对ARDS病例和非ARDS对照病例的嵌套病例对照研究。血液样本采集自500名接受胸部、主动脉血管或心脏手术的患者，这些患者将他们置于术后ARDS的高危状态。在基线(手术切开前)以及术中关键事件发生后2小时和6小时分析TXA2和sCD40L，这些事件被认为与术后ARDS风险增加有关。在入选的500名患者中，根据年龄、性别、手术方式和外科肺损伤预测评分，20例ARDS患者与非ARDS对照组进行了1：2的匹配。患有ARDS的患者手术时间更长，输液更多，最大吸气压更高。TXA2和sCD40L水平在基线、2小时和6小时无显著差异。在基线与2小时或基线与6小时之间，生物标志物浓度的变化也没有差异。在术后ARDS模型中发生ARDS的患者中，两个新的血小板相关生物标志物(TXA2和sCD40L)没有升高。尽管受到相对较小的研究规模的限制，这些结果并不支持血小板在术后ARDS的早期发病机制中的明确作用。
Animal models and limited human studies have suggested a plausible role for platelets in the pathogenesis and resolution of acute respiratory distress syndrome (ARDS). However, there are little data regarding the role of platelets in ARDS development. The objective of this study was to characterize the role of platelets in a postoperative ARDS model through an analysis of two platelet-specific biologic markers: thromboxane A2 (TxA2) and soluble CD-40-ligand (sCD40L). This was a nested case-control study of ARDS cases matched to non-ARDS controls. Blood samples were collected from a cohort of 500 patients undergoing thoracic, aortic vascular, or cardiac surgery that placed them at high-risk of developing postoperative ARDS. TxA2 and sCD40L were analyzed at baseline (prior to surgical incision) as well as 2 hours and 6 hours after the key intraoperative events believed to be associated with increased risk of postoperative ARDS. Of 500 patients enrolled, 20 ARDS cases were matched 1:2 to non-ARDS controls based on age, sex, surgical procedure, and surgical lung injury prediction score. Those who developed ARDS had longer surgeries, greater fluid administration, and higher peak inspiratory pressures. There were no significant differences in levels of TxA2 or sCD40L at baseline, at 2 hours, or at 6 hours. There was also no difference in the change in biomarker concentration between baseline and 2 hours or baseline and 6 hours. Two novel platelet-associated biologic markers (TxA2 and sCD40L) were not elevated in patients who developed ARDS in a postoperative ARDS model. Although limited by the relatively small study size, these results do not support a clear role for platelets in the early pathogenesis of postoperative ARDS.