Dekker G A, Sibai B M
Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynaecology, Free University Hospital, Amsterdam, The Netherlands.
Am J Obstet Gynecol. 1998 Nov;179(5):1359-75. doi: 10.1016/s0002-9378(98)70160-7.
The etiology of preeclampsia is unknown. At present, 4 hypotheses are the subject of extensive investigation, as follows: (1) Placental ischemia-Increased trophoblast deportation, as a consequence of ischemia, may inflict endothelial cell dysfunction. (2) Very low-density lipoprotein versus toxicity-preventing activity-In compensation for increased energy demand during pregnancy, nonesterified fatty acids are mobilized. In women with low albumin concentrations, transporting extra nonesterified fatty acids from adipose tissues to the liver is likely to reduce albumin's antitoxic activity to a point at which very-low density lipoprotein toxicity is expressed. (3) Immune maladaptation-Interaction between decidual leukocytes and invading cytotrophoblast cells is essential for normal trophoblast invasion and development. Immune maladaptation may cause shallow invasion of spiral arteries by endovascular cytotrophoblast cells and endothelial cell dysfunction mediated by an increased decidual release of cytokines, proteolytic enzymes, and free radical species. (4) Genetic imprinting-Development of preeclampsia-eclampsia may be based on a single recessive gene or a dominant gene with incomplete penetrance. Penetrance may be dependent on fetal genotype. The possibility of genetic imprinting should be considered in future genetic investigations of preeclampsia.
子痫前期的病因尚不清楚。目前，有4种假说正在广泛研究中，具体如下：（1）胎盘缺血——由于缺血导致滋养层细胞排出增加，可能会引起内皮细胞功能障碍。（2）极低密度脂蛋白与毒性-预防活性——为了补偿孕期增加的能量需求，非酯化脂肪酸被动员起来。在白蛋白浓度低的女性中，将额外的非酯化脂肪酸从脂肪组织转运至肝脏可能会使白蛋白的抗毒性活性降低到表达极低密度脂蛋白毒性的程度。（3）免疫适应不良——蜕膜白细胞与侵入的细胞滋养层细胞之间的相互作用对于正常的滋养层细胞侵入和发育至关重要。免疫适应不良可能会导致血管内细胞滋养层细胞对螺旋动脉的侵入较浅，并由蜕膜释放的细胞因子、蛋白水解酶和自由基介导内皮细胞功能障碍。（4）基因印记——子痫前期-子痫的发生可能基于单个隐性基因或一个具有不完全外显率的显性基因。外显率可能取决于胎儿基因型。在未来子痫前期的基因研究中应考虑基因印记的可能性。
