Mapping the theories of preeclampsia and the role of angiogenic factors: a systematic review.

Nuffield Department of Obstetrics and Gynecology, University of Oxford, John Radcliffe Hospital, Oxford, UK.
Obstetrics and Gynecology (Impact Factor: 4.8). 02/2007; 109(1):168-80. DOI: 10.1097/01.AOG.0000249609.04831.7c
Source: PubMed

ABSTRACT To evaluate claims that elevated soluble fms-like tyrosine kinase-1 receptor (sFlt-1) and decreased placental growth factor predict preeclampsia.
MEDLINE (1966-March 2006), EMBASE (1980-June 2006), POPLINE (1980-June 2006), CINAHL (1982-June 2006), and LILACS (1982-June 2006) were searched, and experts contacted.
Studies identified and included were those reporting blood and urine levels of sFlt-1 or placental growth factor obtained before gestational week 30 or overt preeclampsia.
Ten of 184 available studies analyzing sFlt-1 and 14 of 319 studies analyzing placental growth factor were included in this review. There was considerable interreport heterogeneity in methodology and results for sFlt-1 measured before gestational week 25. After week 25 placental growth factor and sFlt-1 levels varied consistently between the normal pregnancy group and women destined to develop preeclampsia, achieving significance in women who developed severe preeclampsia.
Third-trimester increases in sFlt-1 and decreases in placental growth factor levels are associated with preeclampsia, specifically severe disease, based on retrospective data. The evidence is insufficient to recommend these markers to be used for screening, and prospective studies employing rigorous laboratory and study design criteria are needed to determine the clinical usefulness of these tests.

1 Bookmark
  • [Show abstract] [Hide abstract]
    ABSTRACT: There is general agreement that a generalized vascular dysfunction, an abnormal interaction between trophoblast and decidua and an exaggerated inflammatory response are involved in the pathogenesis of preeclampsia. We speculate that each of the above described pathogenetic aspects could be elicited or enhanced by an infection occurring before or during pregnancy. Here, we review the existing evidence of an association between infections and preeclampsia and propose hypotheses regarding their role in the development of the disease. Further prospective, well-designed trials are needed to confirm the evidence currently available. The ultimate demonstration of the role of infection in the etiology and pathogenesis of preeclampsia will open up new possibilities for its prevention and treatment.
    Expert Review of Obstetrics &amp Gynecology 11/2007; 2(6):735.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Preeclampsia is characterized by the onset of high blood pressure and proteinuria in pregnancy, leading to substantial maternal and neonatal morbidity and mortality. It involves abnormal remodeling of the placental bed vasculature, placental ischemia and endothelial cell dysfunction. Defective placental development might reflect alterations in the levels of various biological markers. Affected patients show remarkable imbalances of angiogenic factors, including PlGF, soluble FMS-like tyrosine kinase 1, soluble endoglin and angiopoietin-2; these factors could therefore be potential markers for predicting preeclampsia with or without uterine artery Doppler ultrasonography. However, use of these markers to predict preeclampsia has yet to achieve the positive and negative likelihood ratios necessary if they are to be used in clinical practice. Large-scale studies using known markers are likely to identify suitable candidates that will enable greatly improved perinatal care, including prevention and better outcomes for patients with preeclampsia.
    Expert Review of Obstetrics &amp Gynecology 01/2014; 5(6).
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Preeclampsia (PE) is an often fatal pathology characterized by hypertension and proteinuria at the 20th week of gestation that affects 5-10% of the pregnancies. The problem is particularly important in developing countries in where the incidence of hypertensive disorders of pregnancy is higher and maternal mortality rates are 20 times higher than those reported in developed countries. Risk factors for the development of PE include obesity, insulin resistance and hyperlipidemia that stimulate inflammatory cytokine release and oxidative stress leading to endothelial dysfunction (ED). However, how all these clinical manifestations concur to develop PE is still not very well understood. The related poor trophoblast invasion and uteroplacental artery remodeling described in PE, increases reactive oxygen species (ROS), hypoxia and ED. Here we aim to review current literature from research showing the interplay between oxidative stress, ED and PE to the outcomes of current clinical trials aiming to prevent PE with antioxidant supplementation.
    Frontiers in physiology. 01/2014; 5:372.

Full-text (2 Sources)

Available from
Jun 11, 2014