Pre-eclampsia

被引:181
作者
Sibai, B
Dekker, G
Kupferminc, M
机构
[1] Univ Cincinnati, Coll Med, Dept Obstet & Gynecol, Cincinnati, OH 45267 USA
[2] Univ Adelaide, Med Sch N, Lyell McEwin Hlth Serv, Womens & Childrens Div, Adelaide, SA 5005, Australia
[3] Tel Aviv Univ, Sackler Fac Med, Tel Aviv Sourasky Med Ctr, Lis Matern Hosp,Dept Obstet & Gynecol, IL-69978 Tel Aviv, Israel
关键词
D O I
10.1016/S0140-6736(05)17987-2
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Pre-eclampsia is a major cause of maternal mortality (15-20% in developed countries) and morbidities (acute and long-term), perinatal deaths, preterm birth, and intrauterine growth restriction. Key findings support a causal or pathogenetic model of superficial placentation driven by immune maladaptation, with subsequently reduced concentrations of angiogenic growth factors and increased placental debris in the maternal circulation resulting in a (mainly hypertensive) maternal inflammatory response. The final phenotype, maternal pre-eclamptic syndrome, is further modulated by pre-existing maternal cardiovascular or metabolic fitness. Currently, women at risk are identified on the basis of epidemiological and clinical risk factors, but the diagnostic criteria of pre-eclampsia remain unclear, with no known biomarkers. Treatment is still prenatal care, timely diagnosis, proper management, and timely delivery. Many interventions to lengthen pregnancy (eg, treatment for mild hypertension, plasma-volume expansion, and corticosteroid use) have a poor evidence base. We review findings on the diagnosis, risk factors, and pathogenesis of pre-eclampsia and the present status of its prediction, prevention, and management.
引用
收藏
页码:785 / 799
页数:15
相关论文
共 143 条
[1]  
Abalos E, 2001, COCHRANE DB SYST REV, V1
[2]   Random urine protein-creatinine ratio to predict proteinuria in new-onset mild hypertension in late pregnancy [J].
Al, RA ;
Baykal, C ;
Karacay, O ;
Geyik, PO ;
Altun, S .
OBSTETRICS AND GYNECOLOGY, 2004, 104 (02) :367-371
[3]   How strong is the association between maternal thrombophilia and adverse pregnancy outcome? A systematic review [J].
Alfirevic, Z ;
Roberts, D ;
Martlew, V .
EUROPEAN JOURNAL OF OBSTETRICS & GYNECOLOGY AND REPRODUCTIVE BIOLOGY, 2002, 101 (01) :6-14
[4]   Neutrophils are stimulated by syncytiotrophoblast microvillous membranes to generate superoxide radicals in women with preeclampsia [J].
Aly, AS ;
Khandelwal, M ;
Zhao, J ;
Mehmet, AH ;
Sammel, MD ;
Parry, S .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 2004, 190 (01) :252-258
[5]   Corticosteroid therapy for prevention of respiratory distress syndrome in severe preeclampsia [J].
Amorim, MMR ;
Santos, LC ;
Faúndes, A .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1999, 180 (05) :1283-1288
[6]  
[Anonymous], COCHRANE DATABASE SY
[7]  
[Anonymous], COCHRANE DA IN PRESS
[8]  
[Anonymous], BMJ
[9]   Fetal inherited thrombophilias influence the severity of preeclampsia, IUGR and placental abruption [J].
Anteby, EY ;
Musalam, B ;
Milwidsky, A ;
Blumenfeld, A ;
Gilis, S ;
Valsky, D ;
Hamani, Y .
EUROPEAN JOURNAL OF OBSTETRICS GYNECOLOGY AND REPRODUCTIVE BIOLOGY, 2004, 113 (01) :31-35
[10]   Uterine spiral artery remodeling involves endothelial apoptosis induced by extravillous trophoblasts through Fas/FasL interactions [J].
Ashton, SV ;
Whitley, GSJ ;
Dash, PR ;
Wareing, M ;
Crocker, IP ;
Baker, PN ;
Cartwright, JE .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2005, 25 (01) :102-108