血小板激活抗体在肝素诱导的血小板减少症的最早发病时即可检测到，这对 5-羟色胺释放试验的操作特征有影响。
Platelet-Activating Antibodies Are Detectable at the Earliest Onset of Heparin-Induced Thrombocytopenia, With Implications for the Operating Characteristics of the Serotonin-Release Assay.
机构信息
Department of Pathology and Molecular Medicine, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, ON, Canada; Department of Medicine, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, ON, Canada; McMaster Centre for Transfusion Research, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, ON, Canada.
Department of Medicine, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, ON, Canada; McMaster Centre for Transfusion Research, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, ON, Canada; Canadian Blood Services, Hamilton, ON, Canada.
出版信息
Chest. 2018 Jun;153(6):1396-1404. doi: 10.1016/j.chest.2018.01.001. Epub 2018 Jan 8.
BACKGROUND
Heparin-induced thrombocytopenia (HIT) is a prothrombotic drug reaction caused by platelet-activating antibodies that recognize platelet factor 4 (PF4)/heparin complexes. It is unknown whether platelet-activating antibodies are detectable at the onset of the HIT-related platelet count fall.
METHODS
Available blood samples from 18 patients obtained at onset of HIT were tested using the serotonin-release assay (SRA), a test for platelet-activating antibodies, and a PF4-dependent enzyme-linked immunosorbent assay (ELISA). Patient samples showing a delay of > 2 days between ELISA and SRA seroconversion were tested for subthreshold levels of platelet-activating antibodies using two modifications of the SRA that amplify detection of HIT antibodies. We also estimated SRA sensitivity and specificity in two postorthopedic surgery clinical trials (633 samples), including assessing whether a positive SRA influenced platelet count recovery in the absence of thrombocytopenia.
RESULTS
Platelet-activating HIT antibodies were detected in all 18 patients at the beginning of the HIT-related platelet count fall. Although ELISA seroconversion usually preceded SRA seroconversion by only 1 day (median), subthreshold levels of platelet-activating antibodies were detected in both patients who exhibited a lag between ELISA and SRA seroconversion. SRA sensitivity was 100% (18/18), and its specificity was 97% (597/615). Nonthrombocytopenic SRA-positive patients with ongoing heparin treatment exhibited blunted platelet count recovery vs control subjects, suggesting even higher SRA specificity for detecting abnormal platelet count profiles.
CONCLUSIONS
Platelet-activating HIT antibodies are detectable at the onset of the HIT-related platelet count fall. The SRA has high sensitivity and specificity for HIT, and indicates that presence of HIT antibodies can blunt postoperative platelet count recovery.
背景
肝素诱导的血小板减少症（HIT）是一种由血小板激活抗体引起的促血栓形成药物反应，这些抗体可识别血小板因子 4（PF4）/肝素复合物。目前尚不清楚在 HIT 相关血小板计数下降开始时是否可以检测到血小板激活抗体。
方法
使用血小板激活抗体检测的血清素释放试验（SRA）和 PF4 依赖性酶联免疫吸附试验（ELISA）检测了 18 名 HIT 发病时获得的可用血液样本。对 ELISA 和 SRA 血清转化之间延迟> 2 天的患者样本，使用两种可放大检测 HIT 抗体的 SRA 改良方法，检测亚阈值水平的血小板激活抗体。我们还在两项矫形手术后临床试验（633 例样本）中评估了 SRA 的敏感性和特异性，包括评估在没有血小板减少症的情况下，SRA 阳性是否会影响血小板计数恢复。
结果
在 HIT 相关血小板计数下降开始时，18 例患者均检测到血小板激活的 HIT 抗体。尽管 ELISA 血清转化通常仅比 SRA 血清转化提前 1 天（中位数），但在 ELISA 和 SRA 血清转化之间存在延迟的两名患者中均检测到亚阈值水平的血小板激活抗体。SRA 的敏感性为 100%（18/18），特异性为 97%（597/615）。正在接受肝素治疗且非血小板减少性的 SRA 阳性患者与对照组相比，血小板计数恢复减弱，这表明 SRA 对检测异常血小板计数谱具有更高的特异性。
结论
在 HIT 相关血小板计数下降开始时可以检测到血小板激活的 HIT 抗体。SRA 对 HIT 具有高敏感性和特异性，表明存在 HIT 抗体可以减弱术后血小板计数恢复。
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