Furmańczyk-Zawiska A, Tronina O, Baczkowska T, Chmura A, Durlik M
Department of Transplantation Medicine and Nephrology, Transplantation Institute, Medical University of Warsaw, Warsaw, Poland.
Transplant Proc. 2013 Jun;45(5):1983-9. doi: 10.1016/j.transproceed.2013.01.024.
The presence of antiphospholipid antibodies (APLAs) may be associated with increased thrombotic risk. Liver graft thrombosis may necessitate retransplantation.
To determine the prevalence of APLAs among liver recipients and to investigate the relationship between APLAs and liver graft thrombosis.
We included 33 Caucasian patients aged 22 to 75 years who displayed stable liver graft function (21 women and 12 men). The patients were divided into 2 subgroups: high thrombotic risk subgroup T(-) and at low risk T(+) subgroups. The T(-) included 25 patients, T(+) included 8 recipients with a history of severe thrombosis. We investigated: lupus anticoagulant, anticardiolipin antibodies (aCL), anti-β2-glycoprotein I antibodies (anti-β2GPI), antiprothrombin antibodies (immunoglobulin (Ig)G and IgM isotype), protein C and S activities, factor VIII, antithrombin, ADAMTS-13 and anti-ADAMTS-13. The 2 determinations were performed at an interval of 6 months. The mean follow-up was 19.5 ± 4.6 months.
The most commonly detected antibodies were anti-β2GPI IgM (25%) and aCL IgG (15.63%). Comparing the prevalence of APLAs between T(-) and T(+), we observed a significant difference only for aCL IgM (P = .0183), which was not confirmed on a second determination after 6 months. We noted correlations between aCL IgM and number of thrombotic episodes (P = .0040) and between aCL IgM and anti-β2GPI IgM (P = .0074; rho 0.45). Despite receiving low-molecular-weight heparin or aspirin recurrence of thrombosis occurred in 4 T(+) patients: 3 hepatic artery thrombosis and 1 splenic artery thrombosis. Only 1 patient had APLAs; the other 2, protein C or S deficiency and the fourth, a normal test.
The prevalence of APLAs in liver recipients is greater than that in the general population. The usefulness of APLAs as a marker of thrombosis was not demonstrated suggesting multifactorial etiologies of liver graft thrombosis.
抗磷脂抗体（APLA）的存在可能与血栓形成风险增加有关。肝移植血栓形成可能需要再次移植。
确定肝移植受者中APLA的患病率，并研究APLA与肝移植血栓形成之间的关系。
我们纳入了33例年龄在22至75岁之间、肝移植功能稳定的白种人患者（21名女性和12名男性）。患者分为2个亚组：高血栓形成风险亚组T(-)和低风险亚组T(+)。T(-)组包括25例患者，T(+)组包括8例有严重血栓形成病史的受者。我们检测了：狼疮抗凝物、抗心磷脂抗体（aCL）、抗β2糖蛋白I抗体（抗β2GPI）、抗凝血酶原抗体（免疫球蛋白（Ig）G和IgM亚型）、蛋白C和S活性、因子VIII、抗凝血酶、ADAMTS-13和抗ADAMTS-13。两次检测间隔6个月。平均随访时间为19.5±4.6个月。
最常检测到的抗体是抗β2GPI IgM（25%）和aCL IgG（15.63%）。比较T(-)和T(+)组中APLA的患病率，我们仅观察到aCL IgM有显著差异（P = 0.0183），6个月后的第二次检测未证实该差异。我们注意到aCL IgM与血栓形成发作次数之间存在相关性（P = 0.0040），以及aCL IgM与抗β2GPI IgM之间存在相关性（P = 0.0074；rho 0.45）。尽管接受了低分子量肝素或阿司匹林治疗，4例T(+)患者仍发生了血栓复发：3例肝动脉血栓形成和1例脾动脉血栓形成。只有1例患者有APLA；另外2例是蛋白C或S缺乏，第4例检测结果正常。
肝移植受者中APLA的患病率高于普通人群。未证明APLA作为血栓形成标志物的有效性，提示肝移植血栓形成的病因是多因素的。
