Division of Hematology-Oncology, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA.
Clin Appl Thromb Hemost. 2011 Nov-Dec;17(6):E190-5. doi: 10.1177/1076029610395571. Epub 2011 Mar 14.
Second-generation activated protein C resistance (APC-R) assay was developed to avert interferences from lupus anticoagulant (LA) and warfarin therapy by prediluting the patient sample with factor V (FV)-depleted plasma. We investigated the effect of LA on the second generation APC-R assay in 121 LA-positive patients. Twenty-five APC-R-positive patients were tested for the mutation in FV (Leiden, Hong Kong, and Cambridge). Eleven had FV Leiden and twelve were negative for any mutation (2 were not tested). Of 12, 8 had APC-R suggestive of heterozygous and 4 had APC-R suggestive of homozygous defects. These patients had strong LA activity, compared to those with concurrent FVL. This was associated with a trend toward increased thrombosis risk compared to those with normal APC-R. These findings suggest that LA causes acquired APC-R, reflecting an in vivo pathophysiologic effect of LA rather than merely an in vitro phenomenon even with the second generation APC-R assay.
第二代活化蛋白 C 抵抗（APC-R）检测方法是为了避免狼疮抗凝物（LA）和华法林治疗的干扰而开发的，该方法通过预先用缺乏因子 V（FV）的血浆稀释患者样本。我们研究了 LA 对 121 例 LA 阳性患者第二代 APC-R 检测方法的影响。25 例 APC-R 阳性患者进行了 FV（莱顿、香港和剑桥）突变检测。11 例存在 FV 莱顿突变，12 例不存在任何突变（2 例未进行检测）。在这 12 例患者中，有 8 例 APC-R 结果提示杂合缺陷，4 例 APC-R 结果提示纯合缺陷。与同时存在 FVL 的患者相比，这些患者具有较强的 LA 活性。这与与正常 APC-R 相比，血栓形成风险增加的趋势相关。这些发现表明，LA 引起获得性 APC-R，反映了 LA 的体内病理生理作用，而不仅仅是第二代 APC-R 检测方法中的体外现象。
