title: Angiogenic factors and the risk of adverse outcomes in women with suspected preeclampsia.
abstract: BACKGROUND
  An imbalance in circulating angiogenic factors plays a central role in the pathogenesis of preeclampsia.
  
  
  RESULTS
  We prospectively studied 616 women who were evaluated for suspected preeclampsia. We measured plasma levels of antiangiogenic soluble fms-like tyrosine kinase 1 (sFlt1) and proangiogenic placental growth factor (PlGF) at presentation and examined for an association between the sFlt1/PlGF ratio and subsequent adverse maternal and perinatal outcomes within 2 weeks. The median sFlt1/PlGF ratio at presentation was elevated in participants who experienced any adverse outcome compared with those who did not (47.0 [25th-75th percentile, 15.5-112.2] versus 10.8 [25th-75th percentile, 4.1-28.6]; P<0.0001). Among those presenting at <34 weeks (n=167), the results were more striking (226.6 [25th-75th percentile, 50.4-547.3] versus 4.5 [25th-75th percentile, 2.0-13.5]; P<0.0001), and the risk was markedly elevated when the highest sFlt1/PlGF ratio tertile was compared with the lowest (odds ratio, 47.8; 95% confidence interval, 14.6-156.6). Among participants presenting at <34 weeks, the addition of sFlt1/PlGF ratio to hypertension and proteinuria significantly improved the prediction for subsequent adverse outcomes (area under the curve, 0.93 for hypertension, proteinuria, and sFlt1/PlGF versus 0.84 for hypertension and proteinuria alone; P=0.001). Delivery occurred within 2 weeks of presentation in 86.0% of women with an sFlt1/PlGF ratio ≥85 compared with 15.8% of women with an sFlt1/PlGF ratio <85 (hazard ratio, 15.2; 95% confidence interval, 8.0-28.7).
  
  
  CONCLUSIONS
  In women with suspected preeclampsia presenting at <34 weeks, circulating sFlt1/PlGF ratio predicts adverse outcomes occurring within 2 weeks. The accuracy of this test is substantially better than that of current approaches and may be useful in risk stratification and management. Additional studies are warranted to validate these findings.
authors.affiliation: Division of Maternal Fetal Medicine, Department of Obstetrics and Gynecology, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Kirstein 382, Boston, MA 02215, USA.
authors.forename: Sarosh
authors.initials: S
authors.lastname: Rana
authors.forename: Camille E
authors.initials: CE
authors.lastname: Powe
authors.forename: Saira
authors.initials: S
authors.lastname: Salahuddin
authors.forename: Stefan
authors.initials: S
authors.lastname: Verlohren
authors.forename: Frank H
authors.initials: FH
authors.lastname: Perschel
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Levine
authors.forename: Kee-Hak
authors.initials: KH
authors.lastname: Lim
authors.forename: Julia B
authors.initials: JB
authors.lastname: Wenger
authors.forename: Ravi
authors.initials: R
authors.lastname: Thadhani
authors.forename: S Ananth
authors.initials: SA
authors.lastname: Karumanchi
mesh_terms: D000328:Adult; D005260:Female; D006801:Humans; D016015:Logistic Models; D000072483:Placenta Growth Factor; D011225:Pre-Eclampsia / Q000097:blood*; D011247:Pregnancy; D011257:Pregnancy Proteins / Q000097:blood*; D011446:Prospective Studies; D012372:ROC Curve; D012306:Risk; D013599:Systole; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000097:blood*
chemical_list: C000608036:PGF protein, human; D011257:Pregnancy Proteins; D000072483:Placenta Growth Factor; C501162:FLT1 protein, human; D040281:Vascular Endothelial Growth Factor Receptor-1