RESULTS: 607 women were recruited. Final diagnoses are shown inTable 1. In women presenting under 35 weeks’ gestation, the test per-formance statistics for predicting pre-eclampsia requiring deliverywithin 14 days were: sensitivity 0.95 (0.86-0.98); specificity 0.56 (0.49-0.63); NPV 0.97 (0.92-0.99); PPV 0.42 (0.35 -0.51). Adjusted hazardratio for time-to-delivery (controlling for gestational age at enrolmentand final diagnosis) was 2.31 (1.68-3.18) for PlGF medium and 10.61(7.09-15.89) for PlGF low. Positive likelihood ratio (LR): 2.15; nega-tive LR: 0.10. Pre-test probability: 26%. If test positive: post-test prob-ability 43%. If test negative: post-test probability 3.3%.CONCLUSION: In women presenting under 35 weeks’ gestation withsuspected pre-eclampsia, low PlGF level rules in women requiringpreterm delivery and high PlGF rules out preterm delivery within 14days. PlGF can be used to assist in diagnosis and identify womenrequiring increased care.

637 Is midtrimester folate deficiency associated withpreterm preeclampsia, and is there a modification byvitamin D?Luisa Wetta1, Suzanne Cliver1, Adi Abramovici1, RodneyEdwards1, Joseph Biggio1, Alan Tita1

1University of Alabama at Birmingham, Obstetrics & Gynecology,Birmingham, ALOBJECTIVE: The impact of maternal folate or vitamin D deficiency onpreeclampsia (PE) and other adverse pregnancy outcomes remainscontroversial. Few studies have examined the joint impact of thesemicronutrients which are often co-deficient. We reported a lack ofassociation of midtrimester vitamin D status with preterm PE. Herein,we evaluate whether maternal serum folate is associated with pretermPE and whether vitamin D status modifies the relationship.STUDY DESIGN: We conducted a nested case-control study of 100women with preterm PE (�37 weeks (w)) (cases) and 200 healthywomen who delivered at 39-40 w (controls). Stored serum specimens(midtrimester sample drawn between 15-21 w for multiple markerscreening) were tested for total serum folate using a commerciallyavailable immunoassay. We compared mean folate levels as well asprevalence of folate deficiency (�6ng/mL). Vitamin D was measuredusing a validated liquid chromatography-mass spectrometry method.Logistic regression was used for multivariable adjustments and toevaluate folate-vitamin D interaction.RESULTS: A total of 86 PE cases (mean 33.5 w) and 177 controls (mean39.7 w) had specimens with valid measurements. Cases were morelikely to be nulliparous (p�0.009) and heavier (p�0.025) than con-trols but were similar in regard to maternal age and ethnicity. Meanmidtrimester folate levels werer similar between cases and controls, aswas the prevalence of folate deficiency (Table). After multivariableadjustments, folate deficiency was not associated with preterm PE(aOR 1.19; 95% confidence interval (CI) 0.47-3.01). There was nosignificant interaction between folate and vitamin D status as contin-uous variables (p�0.71). The OR for PE in women who were deficientin both vitamin D (�30ng/mL) and folate compared to those whowere deficient in neither was 1.15 (95% CI 0.43-3.11).CONCLUSION: Midtrimester folate deficiency is not associated withpreterm PE, and the relationship is not modified by vitamin D status.

638 More evidence suggestive of preeclampsia as a state ofprogesterone deficiency: progesterone suppresses hypoxia-stimulated production of TNF-�, IL-6, IL-17, and sFlt-1Luissa Kiprono1, Krystal Frazier1, Kedra Wallace1, JanaeMoseley1, Margaret Wester1, Jeremy Scott1, James Martin1,Babette Lamarca1

1University of Mississippi Medical Center, Maternal-Fetal Medicine, Jackson,MSOBJECTIVE: Placental ischemia plays a role in the pathogenesis of pre-eclampsia (PE). A chronic state of inflammation with PE results inactivated immune cells and the release of inflammatory cytokinessuch as tumor necrosis factor alpha (TNF-�), interleukin-6 (IL-6),interleukin-17 (IL-17), and anti-angiogenic factors such as solublefms-like tyrosine kinase 1(sFlt-1). We have demonstrated previouslythat women with PE have significantly lower circulating progesterone(P) than normal pregnant women (NP). We hypothesize that P sup-presses hypoxia-stimulated TNF-�, IL-6, IL-17, and sFlt-1. Our ob-jective in this study is to determine if anti-inflammatory actions of Psuppress placental production of TNF-�, IL-6, IL-17, and sFlt-1 stim-ulated in response to placental ischemia/hypoxia.STUDY DESIGN: Placentas were obtained from NP subjects at Cesareandelivery in our IRB approved clinical study. Placental explants(0.6mg) were plated on matrigel-coated six-well inserts and culturedwith or without 1uM P-supplemented media in hypoxic (1% O2)conditions for 24hrs. Cell culture supernatants were analyzed byELISA for placental TNF-�, IL-6, IL-17, and sFlt-1 and normalized tototal cell protein.RESULTS: In placental explants from NP subjects under hypoxic con-ditions, all measurements increased two to five-fold. In contrast, un-der hypoxic conditions supplemented by 1uM P, the increase in allmeasurements was blunted (Table). Although we did not achieve astatistical significance, there is clearly a tendency for 1uM P to de-crease hypoxia stimulated cytokines and sFlt-1.CONCLUSION: Supplementation of exogenous P to hypoxic placentalexplants inhibits the release of IL-6, IL-17, TNF-� and sFlt-1. Wehypothesize that the addition of exogenous P to human patients withPE could be beneficial therapeutically by decreasing hypoxia-stimu-lated production of anti-angiogenic factors and inflammatory cyto-kines, thereby lessening disease severity.

639 Down-regulation of placental glucosetransporter 1 in preeclampsiaBenjamin Lüscher1, Marc Baumann2, Marianne Messerli1, DanielSurbek2, Camilla Marini1, Ruth Sager1, Christiane Albrecht3,Matthias Hediger3

1University of Bern, Departement of Clinical Research, Bern, Switzerland,2University Women’s Hospital Bern, Obstetrics & Feto-Maternal Medicine,Bern, Switzerland, 3University of Bern, Institut of Biochemistry andMoleculare Medicine, Bern, SwitzerlandOBJECTIVE: Preeclampsia is a pregnancy-specific disease affecting upto 5% of all pregnancies worldwide associated with hypoxia as well asintrauterine growth restriction. It is a major cause of maternal andfetal morbidity and mortality. Materno-fetal glucose transport is cru-

Final diagnoses in women presenting withsuspected pre-eclampsia

*SGA: small for gestational age by customised birthweight centile.

Folate status between cases and controls

Data are expressed as mean � standard deviation or n (%).

All values are in pg/ml.

H, hypoxic; H�P, hypoxic�progesterone; N, normoxic.

Poster Session IV Academic Issues, Antepartum Fetal, Clinical Ob, Fetus, Genetics, Hypertension, Med-Surg-Diseases, Operative Ob, U/S www.AJOG.org

S270 American Journal of Obstetrics & Gynecology Supplement to JANUARY 2013