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How to assess hypercoagulability in heparin-induced thrombocytopenia? Biomarkers of potential value to support therapeutic intensity of non-heparin anticoagulation
Thrombosis Journal ( IF 3.1 ) Pub Date : 2023-09-19 , DOI: 10.1186/s12959-023-00546-8
Antoine Barocas 1 , Philippe Savard 1 , Audrey Carlo 2 , Thomas Lecompte 1, 3, 4 , Emmanuel de Maistre 1
Affiliation  

In case of heparin-induced thrombocytopenia (HIT), the switch to a non-heparin anticoagulant is mandatory, at a therapeutic dose. Such a treatment has limitations though, especially for patients with renal and/or hepatic failure. Candidate laboratory tests could detect the more coagulable HIT patients, for whom therapeutic anticoagulation would be the more justified. This was a monocentre observational prospective study in which 111 patients with suspected HIT were included. Nineteen were diagnosed with HIT (ELISA and platelet activation assay), among whom 10 were classified as HITT + when a thrombotic event was present at diagnosis or during the first following week. Two plasma prethrombotic biomarkers of in vivo activation of the haemostasis system, procoagulant phospholipids (ProcoagPPL) associated with extracellular vesicles and fibrin monomers (FM test), as well as in vitro thrombin potential (ST Genesia; low picomolar tissue factor) after heparin neutralization (heparinase), were studied. The results were primarily compared between HITT + and HITT- patients. Those HIT + patients with thrombotic events in acute phase or shortly after (referred as HITT+) had a more coagulable phenotype than HIT + patients without thrombotic events since: (i) clotting times related to plasma procoagulant phospholipids tended to be shorter; (ii) fibrin monomers levels were statistically significantly higher (p = 0.0483); (iii) thrombin potential values were statistically significantly higher (p = 0.0404). Of note, among all patients suspected of suffering from HIT, we did not evidence a hypercoagulable phenotype in patients diagnosed with HIT compared to patients for whom the diagnosis of HIT was ruled out. The three tests could help identify those HIT patients the most prone to thrombosis.

中文翻译:

如何评估肝素诱导的血小板减少症的高凝状态?具有支持非肝素抗凝治疗强度潜在价值的生物标志物

如果出现肝素诱导的血小板减少症 (HIT),则必须转用治疗剂量的非肝素抗凝剂。但这种治疗有其局限性,特别是对于肾衰竭和/或肝衰竭的患者。候选实验室测试可以检测出凝血能力更强的 HIT 患者,对他们来说,抗凝治疗更为合理。这是一项单中心观察性前瞻性研究,纳入了 111 名疑似 HIT 患者。19 例被诊断为 HIT(ELISA 和血小板活化测定),其中 10 例在诊断时或随后的第一周内出现血栓事件时被分类为 HITT +。体内止血系统激活的两种血浆血栓前生物标志物、与细胞外囊泡和纤维蛋白单体相关的促凝血磷脂 (ProcoagPPL)(FM 测试),以及肝素中和后的体外凝血酶电位(ST Genesia;低皮摩尔组织因子)(肝素酶),进行了研究。主要比较 HITT + 和 HITT- 患者的结果。那些在急性期或不久后发生血栓事件的 HIT + 患者(称为 HITT +)比没有血栓事件的 HIT + 患者具有更高的凝血表型,因为:(i)与血浆促凝磷脂相关的凝血时间往往更短;(ii) 纤维蛋白单体水平在统计上显着较高 (p = 0.0483);(iii) 凝血酶电位值在统计上显着较高 (p = 0.0404)。值得注意的是,在所有疑似患有 HIT 的患者中,与排除 HIT 诊断的患者相比,我们没有证明诊断为 HIT 的患者存在高凝表型。这三项测试可以帮助识别那些最容易发生血栓的 HIT 患者。
更新日期:2023-09-19
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