子痫前期:从病因到器官功能障碍

Nissar Shaikh, S. Nahid, Firdous Ummunnisa, Ifrah Fatima, Mohamad Hilani, Asma Gul, A. Al Basha, W. Yahia, F. Al Hail, H. Elfil, E. Abdalla, M. Nainthramveetil, M.A Imraan, M. Zubair, Sibghatullah M Khan, N. Korichi, S. AlKhawaga, H. Ismail, S. Yaqoob, Mashael Abdulrahman M. S. Al Khelaifi
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引用次数: 1

摘要

子痫前期是一种妊娠期高血压疾病,影响6-12%的人口。子痫前期的发病有多种风险因素,从高龄产妇到遗传因素。先兆子痫的病因包括胎盘异常、免疫不耐受、内皮损伤和遗传。其发病机制包括内皮细胞激活和功能障碍导致血管痉挛。子痫前期分为两个阶段:无症状期和有症状期。子痫前期可累及多脏器,即中枢神经系统、呼吸系统、心血管系统、血液学功能障碍、HELLP(溶血肝酶升高、血小板低)综合征、内分泌、肾、肝、子宫胎盘功能障碍。这些器官功能障碍增加了子痫前期妊娠患者的发病率和死亡率。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Preeclampsia: From Etiopathology to Organ Dysfunction
Preeclampsia is a hypertensive disorder of pregnancy affecting 6–12% of the population. There are various risk factors for the development of preeclampsia, ranging from advanced maternal age to genetics. The proposed etiologies for preeclampsia are abnormal placentation, immunological intolerance, endothelial damage, and genetic inheritance. The pathogenesis includes endothelial activation and dysfunction leading to vasospasm. Preeclampsia is divided into two stages: asymptomatic and symptomatic stages. Preeclampsia causes multiple organ involvement, namely central nervous system, respiratory, cardiovascular, hematological dysfunction, HELLP (hemolysis elevated liver enzymes, low platelets) syndrome, endocrine, renal, hepatic, and uteroplacental dysfunction. These organ dysfunctions increase morbidity and mortality in preeclamptic pregnant patients.
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