Departments of Laboratory Medicine, Jai Prakash Narayan Apex Trauma Centre, AIIMS, New Delhi, India.
Department of Haematology and Pathology AIIMS, New Delhi, India.
Neurol India. 2024 Mar 1;72(2):285-291. doi: 10.4103/ni.ni_1159_21. Epub 2024 Apr 30.
Microparticles (MPs) have been implicated in thrombosis and endothelial dysfunction. Their involvement in early coagulopathy and in worsening of outcomes in isolated severe traumatic brain injury (sTBI) patients remains ill defined.
We sought to quantify the circulatory MP subtypes derived from platelets (PMPs; CD42), endothelial cells (EMPs; CD62E), and those bearing tissue factor (TFMP; CD142) and analyze their correlation with early coagulopathy, thrombin generation, and in-hospital mortality.
Prospective screening of sTBI patients was done. Blood samples were collected before blood and fluid transfusion. MP enumeration and characterization were performed using flow cytometry, and thrombin-antithrombin complex (TAT) levels were determined using enzyme-linked immunosorbent assay (ELISA). Circulating levels of procoagulant MPs were compared between isolated sTBI patients and age- and gender-matched healthy controls (HC). Patients were stratified according to their PMP, EMP, and TFMP levels, respectively (high ≥HC median and low < HC median).
Isolated sTBI resulted in an increased generation of PMPs (456.6 [228-919] vs. 249.1 [198.9-404.5]; P = 0.01) and EMPs (301.5 [118.8-586.7] vs. 140.9 [124.9-286]; P = 0.09) compared to HCs. Also, 5.3% of MPs expressed TF (380 [301-710]) in HCs, compared to 6.6% MPs (484 [159-484]; P = 0.87) in isolated sTBI patients. Early TBI-associated coagulopathy (TBI-AC) was seen in 50 (41.6%) patients. PMP (380 [139-779] vs. 523.9 [334-927]; P = 0.19) and EMP (242 [86-483] vs. 344 [168-605]; P = 0.81) counts were low in patients with TBI-AC, compared to patients without TBI-AC.
Our results suggest that enhanced cellular activation and procoagulant MP generation are predominant after isolated sTBI. TBI-AC was associated with low plasma PMPs count compared to the count in patients without TBI-AC. Low PMPs may be involved with the development of TBI-AC.
微粒（MPs）已被牵涉到血栓形成和内皮功能障碍中。其在孤立性严重创伤性脑损伤（sTBI）患者早期凝血异常和预后恶化中的作用仍未明确。
我们旨在定量检测源自血小板（PMPs；CD42）、内皮细胞（EMPs；CD62E）和携带组织因子（TFMP；CD142）的循环 MP 亚型，并分析其与早期凝血异常、凝血酶生成和院内死亡率的相关性。
对 sTBI 患者进行前瞻性筛选。在输血和输液前采集血液样本。使用流式细胞术进行 MP 计数和特征分析，并使用酶联免疫吸附试验（ELISA）测定凝血酶-抗凝血酶复合物（TAT）水平。将孤立性 sTBI 患者与年龄和性别匹配的健康对照者（HC）的循环促凝 MP 水平进行比较。根据患者的 PMP、EMP 和 TFMP 水平进行分层（高：≥HC 中位数和低：<HC 中位数）。
与 HC 相比，孤立性 sTBI 导致 PMPs（456.6 [228-919] vs. 249.1 [198.9-404.5]；P = 0.01）和 EMPs（301.5 [118.8-586.7] vs. 140.9 [124.9-286]；P = 0.09）的生成增加。HC 中 5.3%的 MPs 表达 TF（380 [301-710]），而孤立性 sTBI 患者中 6.6%的 MPs（484 [159-484]；P = 0.87）。50 名（41.6%）患者发生早期创伤性脑损伤相关凝血异常（TBI-AC）。TBI-AC 患者的 PMP（380 [139-779] vs. 523.9 [334-927]；P = 0.19）和 EMP（242 [86-483] vs. 344 [168-605]；P = 0.81）计数较低，与无 TBI-AC 的患者相比。
我们的结果表明，孤立性 sTBI 后细胞激活和促凝 MP 生成增强为主。与无 TBI-AC 的患者相比，TBI-AC 患者的血浆 PMP 计数较低。低 PMPs 可能与 TBI-AC 的发生有关。
Zotero 插件