Walther Thomas, Wallukat Gerd, Jank Alexander, Bartel Sabine, Schultheiss Heinz-Peter, Faber Renaldo, Stepan Holger
Department of Cardiology and Pneumology, Charité-Campus Benjamin Franklin, Berlin, Germany.
Hypertension. 2005 Dec;46(6):1275-9. doi: 10.1161/01.HYP.0000190040.66563.04. Epub 2005 Oct 31.
Abnormal uterine perfusion detected by Doppler sonography reflects impaired trophoblast invasion, a factor involved in the pathogenesis of pregnancy complications such as preeclampsia or intrauterine growth retardation. Recent studies have demonstrated an autoantibody against the angiotensin type 1 (AT1) receptor in pregnant women with preeclampsia. Our aim was to determine whether the AT1 autoantibody precedes the clinical symptoms and is thus predictive of preeclampsia. We therefore detected this antibody in serum from second trimester pregnancies with abnormal uterine perfusion because these women show an indirect sign of inadequate trophoblast invasion. Then the AT1 autoantibody distribution/concentration was compared with that of women at term with or without pregnancy pathology. The AT1 autoantibody was already detectable in second trimester pregnant women with abnormal uterine perfusion before the clinical manifestation of preeclampsia (80%). However, it was also found in second trimester pregnant women with abnormal uterine perfusion who later developed intrauterine growth retardation (60%) or even had a normal course of pregnancy (62%). In the third trimester, the AT1 autoantibody was demonstrated in 89% of patients with manifest preeclampsia, 86% of those with manifest intrauterine growth retardation, and even in healthy pregnant women at term with a history of abnormal uterine perfusion in the second trimester. We conclude that the AT1 autoantibody is an early but nonspecific marker for preeclampsia. The generation of this antibody seems to be associated with distinct types of pregnancy disorders resulting from impaired placental development. The AT1 autoantibody may thus be causative for pathological uteroplacental perfusion.
通过多普勒超声检测到的子宫灌注异常反映了滋养层细胞浸润受损，这是子痫前期或宫内生长受限等妊娠并发症发病机制中的一个因素。最近的研究表明，子痫前期孕妇体内存在抗血管紧张素1（AT1）受体自身抗体。我们的目的是确定AT1自身抗体是否先于临床症状出现，从而能否预测子痫前期。因此，我们在妊娠中期子宫灌注异常的孕妇血清中检测这种抗体，因为这些女性表现出滋养层细胞浸润不足的间接迹象。然后将AT1自身抗体的分布/浓度与足月时有或无妊娠病理情况的女性进行比较。在子痫前期临床表现出现之前，妊娠中期子宫灌注异常的孕妇中已可检测到AT1自身抗体（80%）。然而，在妊娠中期子宫灌注异常、后来发生宫内生长受限的孕妇中（60%）甚至妊娠过程正常的孕妇中（62%）也发现了该抗体。在妊娠晚期，89%的子痫前期患者、86%的宫内生长受限患者以及有妊娠中期子宫灌注异常病史的足月健康孕妇中都检测到了AT1自身抗体。我们得出结论，AT1自身抗体是子痫前期的一个早期但非特异性标志物。这种抗体的产生似乎与胎盘发育受损导致的不同类型妊娠疾病有关。因此，AT1自身抗体可能是病理性子宫胎盘灌注的原因。
