Hindawi Publishing Corporation Journal of Pregnancy Volume 2012, Article ID 435090, 9 pages doi:10.1155/2012/435090 Review Article Prevention of Preeclampsia Sammya Bezerra Maia e Holanda Moura, 1 Laudelino Marques Lopes, 2 Padma Murthi, 3, 4 and Fabricio da Silva Costa 3, 4 1 Department of Public Health, State University of Ceara, 60.740-000 Fortaleza, CE, Brazil 2 Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynaecology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, ON, Canada N6H 5W9 3 Department of Perinatal Medicine, Pregnancy Research Centre, The Royal Women’s Hospital, 7th Floor, 20 Flemington Road, Parkville, Melbourne, VIC 3052, Australia 4 Department of Obstetrics and Gynaecology, University of Melbourne, Melbourne, VIC 3052, Australia Correspondence should be addressed to Fabricio da Silva Costa, fabricio.costa@thewomens.org.au Received 24 September 2012; Accepted 15 November 2012 Academic Editor: Antonio Farina Copyright © 2012 Sammya Bezerra Maia e Holanda Moura et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Preeclampsia (PE) affects around 2–5% of pregnant women. It is a major cause of maternal and perinatal morbidity and mortality. In an attempt to prevent preeclampsia, many strategies based on antenatal care, change in lifestyle, nutritional supplementation, and drugs have been studied. The aim of this paper is to review recent evidence about primary and secondary prevention of preeclampsia. 1. Introduction Preeclampsia (PE) is a multisystem disorder characterized by de novo hypertension and proteinuria or superimposed to maternal hypertension or nephropathy in pregnant women who are usually beyond 20 weeks of gestational age. It affects around 2–5% of pregnancies. The prevalence may range as high as 10 to 18% in some developing countries [1]. PE can be classified into early-onset and late-onset PE and these subtypes may represent different forms of the disease. Early-onset PE is commonly associated with fetal growth restriction (FGR), abnormal uterine and umbilical artery Doppler waveforms, and adverse maternal and neonatal outcomes. In contrast, late-onset PE is mostly associated with milder maternal disease and a lower rate of fetal involvement, with usually favorable perinatal outcomes [2–4]. Screening for PE attempts to identify high-risk pregnan- cies to modify antenatal care and institute preventive treat- ment regimens in order to reduce complications and deaths [2, 5–9]. The SCOPE group developed a predictive model for PE based on clinical risk factors for nulliparous women and concluded that screening for PE using maternal history alone is an unreliable method. MAP (mean arterial pressure, defined as “twice the diastolic plus the systolic blood pressure divided by three”) when studied alone in the second trimester of 90 mmHg or above presents a positive likelihood ratio of 3.5 (95% CI 2–5) and a negative likelihood ratio of 0.46 (95% CI 0.16–0.75) to predict PE onset [10]. Howewer, a study combined maternal factors to uterine artery Doppler PI. The detection rate of early PE at a 10% false-positive rate increased from 47% in screening by maternal factors alone to 81% in screening by maternal factors and the lowest UtA- PI. The respective detection rates for late PE increased from 41% to 45% [11]. The concentration of many biomarkers including pregnancy-associated plasma protein A (PAPP-A) and placental growth factor (PIGF) in the maternal serum are known to be altered during the first trimester of pregnancies destined to develop PE [12, 13]. Furthermore, numerous studies have examined the effectiveness of uterine artery Doppler in the second trimester prediction of PE and fetal growth restriction (FGR). This technique has been shown to have controversial effectiveness in terms of such prediction, because the effectiveness is dependent of which outcome would be predicted (early-onset PE, late-onset PE, or FGR)