Han Yue, Lu Xiao-Xu, Wu De-Pei, Sun Ai-Ning, Zhang Wei, Hu Xiao-Hui, Gao Hai-Li, Wang Zhao-Yue, Ruan Chang-Geng
Key Laboratory of Thrombosis and Haemostasis, Ministry of Health, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Zhonghua Xue Ye Xue Za Zhi. 2009 Nov;30(11):731-4.
To illustrate the early alteration of plasminogen activator inhibitor-1 (PAI-1) in the recipients of hematopoietic stem cell transplantation (HSCT) and explore its clinical significance in transplantation-associated thrombotic complications.
Ninety-five patients undergoing HSCT were enrolled in this study. PAI-1 level and other hemostatic parameters were measured by enzyme linked immunosorbent assay (ELISA) in platelet poor plasma samples from patients on conditioning therapy and then weekly until four weeks after HSCT.
Significant increase in PAI-1 was detected after conditioning treatment, followed by a diminution in the very week on transplantation (week 0), then increased with in time after transplantation. According to the occurrence of transplant-associated complications, patients were classified into four groups: thrombus group [veno-occlusive disease (VOD) (n = 5), thrombotic microangiopathy (TMA) n = 1], aGVHD group (n = 29), infection group (n = 19) and non-complication group (n = 41). One of 30 patients (3.3%) was diagnosed as thrombus in the auto-HSCT group, while five of 65 patients (7.7%) did in the allo-HSCT group. PAI-1 level of thrombotic patients was significantly increased compared with non-thrombotic subjects, and the patients without thrombotic complications have higher PAI-1 level in the allo-HSCT group than in auto-HSCT group. All the patients with complications presented with significantly increased PAI-1 compared with those with no complications (P < 0.05). The six patients with thrombotic complications showed extremely elevated PAI-1 [(62.8 +/- 7.5) microg/L] compared with that of aGVHD patients [(45.1 +/- 9.1) microg/L] or infection patients [(50.0 +/- 11.2) microg/L] post-HSCT (P < 0.05).
The increase in plasma PAI-1 may be a specific mark for transplantation-associated thrombotic complications. Increased PAI-1 reflects the development of thrombotic complications. Extreme elevation of PAI-1 contributes to the early diagonsis of VOD and TMA after HSCT.
阐述造血干细胞移植(HSCT)受者纤溶酶原激活物抑制剂-1(PAI-1)的早期变化,并探讨其在移植相关血栓并发症中的临床意义。
95例行HSCT的患者纳入本研究。通过酶联免疫吸附测定(ELISA)检测预处理治疗时患者乏血小板血浆样本中的PAI-1水平及其他止血参数,此后每周检测一次,直至HSCT后四周。
预处理治疗后检测到PAI-1显著升高,随后在移植当周(第0周)下降,然后在移植后随时间增加。根据移植相关并发症的发生情况,患者分为四组:血栓组[肝静脉闭塞病(VOD)(n = 5),血栓性微血管病(TMA)n = 1],急性移植物抗宿主病(aGVHD)组(n = 29),感染组(n = 19)和无并发症组(n = 41)。自体HSCT组30例患者中有1例(3.3%)被诊断为血栓形成,而异基因HSCT组65例患者中有5例(7.7%)发生血栓形成。与非血栓形成患者相比,血栓形成患者的PAI-1水平显著升高,且异基因HSCT组中无血栓形成并发症的患者PAI-1水平高于自体HSCT组。所有有并发症的患者与无并发症的患者相比,PAI-1均显著升高(P < 0.05)。与HSCT后aGVHD患者[(45.1 ± 9.1)μg/L]或感染患者[(50.0 ± 11.2)μg/L]相比,6例有血栓形成并发症的患者PAI-1极度升高[(62.8 ± 7.5)μg/L](P < 0.05)。
血浆PAI-1升高可能是移植相关血栓并发症的一个特异性标志。PAI-1升高反映了血栓形成并发症的发生。PAI-1极度升高有助于HSCT后VOD和TMA的早期诊断。