Bai Chun-mei, Ma Shui-qing, Gai Ming-ying, Fan Lian-kai, Ren Feng-yan, Fan Guang-sheng
Department of Hematology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730.
Chin Med Sci J. 2004 Dec;19(4):290-2.
To investigate the mechanism of anticoagulation protein defect in the pathogenesis of unexplained recurrent miscarriage.
Fifty-seven patients with a history of unexplained abortion were enrolled as the investigation group for tests of protein C, protein S, antithrombin III (AT-III), as well as activated protein C resistance (APC-R). The control group consisted of fifty healthy women with a history of normal pregnancy and delivery. Blood samples were obtained for, measuring serum activity of protein C, protein S, AT-III, and APC-R. Patients with positive APC-R were tested for factor V (FV) Leiden gene mutation by PCR-RFLP method.
Of the 57 patients, 12 (21.1%), 1 (1.8%), and 5 (8.8%) cases were found with protein S, protein C, and AT-III deficiency respectively, and 13 (22.8%) cases with positive results of APC-R. Of the control group, no protein C or AT-III deficiency was ever found, whereas 2 (4.0%) volunteers were presented with protein S deficiency and 3 (6.0%) with positive results of APC-R. No FV Leiden gene mutation was identified in all the patients with positive APC-R results. Late spontaneous abortion cases had higher incidence of anticoagulation protein defect than the early cases.
Anticoagulation protein defect may play a role in the pathogenesis of fetal loss, especially for those occurring in late stage of pregnancy.
探讨抗凝蛋白缺陷在不明原因复发性流产发病机制中的作用。
选取57例有不明原因流产史的患者作为研究组,检测其蛋白C、蛋白S、抗凝血酶III(AT-III)以及活化蛋白C抵抗(APC-R)。对照组由50例有正常妊娠和分娩史的健康女性组成。采集血样检测蛋白C、蛋白S、AT-III的血清活性以及APC-R。对APC-R阳性的患者采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法检测凝血因子V(FV)Leiden基因突变。
57例患者中,分别有12例(21.1%)、1例(1.8%)和5例(8.8%)存在蛋白S、蛋白C和AT-III缺乏,13例(22.8%)APC-R检测结果为阳性。对照组中未发现蛋白C或AT-III缺乏,2例(4.0%)志愿者存在蛋白S缺乏,3例(6.0%)APC-R检测结果为阳性。所有APC-R检测结果阳性的患者均未检测到FV Leiden基因突变。晚期自然流产患者抗凝蛋白缺陷的发生率高于早期患者。
抗凝蛋白缺陷可能在胎儿丢失的发病机制中起作用,尤其是在妊娠晚期发生的胎儿丢失。