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目的:探讨晚期妊娠母体血清中可溶性Fas水平与妊娠期高血压疾病的关系。方法:采用ELISA测定方法测定63例晚期妊娠母体血清可溶性Fas水平,其中正常晚孕组18例,轻度子痫前期组21例,重度子痫前期组24例;同时测定15例育龄期健康非孕妇女血清作为对照组。结果:孕妇组的血清游离Fas水平比较,轻度子痫前期组血清游离Fas水平高于正常晚孕组(P<0.05),重度子痫前期组也高于正常晚孕组(P<0.01),两者差异均有统计学意义,健康未孕组妇女血清游离Fas水平明显低于正常晚孕组(P<0.01)。结论:子痫前期患者外周血清中高水平的sFas可结合激活的淋巴细胞及胎盘滋养细胞中的FasL,抑制Fas/FasL系统介导激活淋巴细胞的AICD,破坏母胎界面的免疫豁免机制,导致母体对胎儿的免疫排斥作用增加,这可能是妊娠期高血压疾病发病的又一重要原因。
Objective: To investigate the relationship between soluble Fas level in maternal serum of late pregnancy and hypertensive disorder complicating pregnancy. Methods: Serum levels of soluble Fas in 63 pregnant women with late pregnancy were measured by ELISA. Among them, 18 cases were normal pregnant group, 21 cases were mild preeclampsia group and 24 cases were severe preeclampsia group. Pregnant women serum as a control group. Results: Serum free Fas level in pregnant women group was higher than that in normal pregnant women (P <0.05), severe preeclampsia group (P <0.01) (P <0.01). The level of serum free Fas in healthy non-pregnant group was significantly lower than that in normal pregnant group (P <0.01). Conclusion: High levels of sFas in peripheral blood of preeclampsia can bind FasL in activated lymphocytes and placental trophoblasts, inhibit Fas / FasL-mediated AICD of activated lymphocytes, destroy the immune immunity mechanism of maternal-fetal interface, Fetal immune rejection increased, which may be another important cause of pregnancy-induced hypertension.