429 MATERNAL LIPID PROFILE IN SUBSEQUENT PREGNANCIES DAVID MANKUTA1,MATAN ELAMI-SUZIN1, ASHER ELHAYANI2, SHLOMO VINKER3, 1Hadassah University Hos-pital, Obstetrics and Gynecology, Jerusalem, Israel, 2Ben-Gurion University, De-partment of public health, Beer-Sheva, Israel, 3Tel Aviv University, Family Medi-cine, Tel Aviv, Israel

OBJECTIVE: To describe the lipid profile of women prior, during and afterpregnancy and to assess effect of consecutive pregnancies on plasma lipid profile

STUDY DESIGN: Electronic medical records of 1752 women between the ages20-45 years that have delivered between 1999 and 2005 were retrieved. The lipidprofile included; Total cholesterol, LDL (Low density lipoprotein) HDL-C (Highdensity lipoprotein-C), VLDL (Very low density lipoprotein) and triglycerides. Themeasurements were classified according to the following categories: non pregnantstate (12 month prior to conception), during 3 trimesters of pregnancy, and from 6weeks and up to 12 month after birth.The lipid profile of the women’s subsequentpregnancies (up to 3) was tested. An independent two-sample t-test was used toanalyze the results.

RESULTS: The overall total cholesterol levels show a rise during pregnancy.During the first trimester there is an average decrease of 11.4 mg/dL in total cho-lesterol level (p�0.0001) followed by an average increase of 50.5 mg/dL(p�0.0001), and a further increase of 28.5 mg/d, in the third trimester (p�0.0001).In the year after the pregnancy, the levels return to pre pregnancy levels.LDL andtriglycerides levels show a similar pattern. In contrast, HDL-C levels do not changesignificantly in the first trimester. The second trimester is characterized by an av-erage elevation of 14 mg/dl.(p�0.0001) and a further decrease of 5mg/dL in thethird trimester (p�0.03).

The average HDL-C levels of every period tested were lower on the 2nd and 3rdsubsequent pregnancies. On each consecutive pregnancy, the rise of HDL-C is tolesser extent, and the nadir is lower.

CONCLUSION: A general increase in total cholesterol, LDL and VLDL occursduring pregnancy . We demonstrate a cumulative effect of consecutive pregnancieson lowering HDL cholesterol levels. This effect may have negative implications onfuture cardiovascular health.

0002-9378/$ - see front matterdoi:10.1016/j.ajog.2007.10.448

430 ARE EICOSANOIDS A NEW CLASS OF TOCOLYTICS IN PREGNANT RATMYOMETRIUM? ISABELLE GIRARD1, MARYSE BERTHIAUME2, STÉPHANIE CORRIVEAU3,ERIC ROUSSEAU4, JEAN-CHARLES PASQUIER1, 1Université de Sherbrooke, Obstetricsand gynecology, Sherbrooke, Quebec, Canada, 2Universite de Sherbrooke, Obstet-rics and gynecology, Sherbrooke, Quebec, Canada, 3Université de Sherbrooke,Quebec, Canada, 4Université de Sherbrooke, Physiology and biophysics, Sher-brooke, Quebec, Canada

OBJECTIVE: Eicosanoids have emerged as a novel class of smooth muscle tonemodulators on bronchial and vascular tissues but their mode of action on pregnantmyometrium has never been explored. The purpose of this study was to evaluate theeffect of the exogenous eicosanoids 14,15-EET (14,15-epoxyeicosatrienoic acid)and 20-HETE (20-hydroxyeicosatetraenoic acid) on contractile activity of myome-trial rings of timed pregnant Sprague-Dawley rats. The endogenous production ofthese paracrine mediators in myometrium was assessed using specific enzyme in-hibitors known to modulate the basal level of eicosanoids in other tissues.

STUDY DESIGN: Isometric tension measurements were performed in vitro onfresh myometrial rings (n�84) in isolated organ bath. Contractile activities wereassessed by calculating the area under the curve over 10 minute periods. Changeswere expressed as percentage of the basal activity as a function of drug concentra-tions or time and compared to the effect of the solvant ethanol.

RESULTS: Addition of exogenous 14,15-EET (1nM to 3�M) had no effect oncontractile activity (p� 0.79). Neither 10�M MS-PPOH (p� 0.58), which preventsthe formation of 14,15-EET, nor 1�M AUDA (p�0.81), which prevents EET deg-radation, had an effect on myometrial contractility at both 10 and 20 gestationnaldays. In contrast, we have observed an uterotonic response to exogenous 3�M20-HETE (p�0.02). However, 10�M DDMS, which prevents the production of20-HETE, had no influence on contractile activity (p�0.5).

CONCLUSION: Exogenous 20-HETE induces uterotonic responses while exog-enous 14,15-EET had no net tocolytic effect when compared to control. In addition,there was apparently no endogenous production of 14,15-EET and 20-HETE inisolated pregnant rat myometrial rings, which suggests that the membranes or theplacenta could be other sites of eicosanoid production.

0002-9378/$ - see front matterdoi:10.1016/j.ajog.2007.10.449

431 DURATION OF LACTATION AND MATERNAL METABOLISM AT 3 YEARSPOSTPARTUM ALISON STUEBE1, MATTHEW GILLMAN2, KEN KLEINMAN3, SHERYLRIFAS-SHIMAN3, JANET RICH-EDWARDS4, 1Society for Maternal-Fetal Medicine, Bos-ton, Massachusetts, 2Harvard University, Boston, Massachusetts, 3Harvard Uni-versity, Massachusetts, 4Brigham and Women’s Hospital, Boston, Massachusetts

OBJECTIVE: Lactation has been associated with reduced risk of type 2 diabetesin mothers. We examined the relation between breastfeeding duration and meta-bolic markers at 3 years postpartum.

STUDY DESIGN: Project Viva is a longitudinal prospective cohort study of 2128mother-infant dyads enrolled in early pregnancy. We used linear regression torelate duration of lactation to maternal glucose and lipid metabolism at 3 yearspostpartum.

RESULTS: 3-year postpartum blood samples were available for 578 womenwithout a birth since the index pregnancy, including 177 who were fasting. 85.8%had initiated breastfeeding, and 26.5% had breastfed ��12 months. In multivar-iate analyses we observed no consistent trends relating duration of lactation tomaternal metabolism at 3 years postpartum. In an unexpected finding, women whobreastfed for 3 to 6 months appeared to have the most favorable metabolic profile(Table).

CONCLUSION: In this prospective cohort study, we did not observe a consistentrelationship between duration of lactation and metabolic risk at 3 years postpar-tum.

Adjusted differences† from 12� mobreastfeeding

Outcome Mean (sd) 0 �0 to �3 3 to �6 6 to �12

N (all) 82 90 113 140HbA1c (%) 5.1 (0.3) �0.01 0.01 �0.07 0.01N (fasting) 17 30 40 39HOMA-IR 1.9 (2.1) 0.49 0.08 �0.55 �0.10Insulin (u/ml)* 10.3 (9.7) 4.4 �0.4 �2.8 �0.2Glucose (mg/dl) 74 (15) �5.1 �1.8 �2.1 0.7Total chol (mg/dl) 178 (31) �6.1 0.2 �1.0 1.3LDL-chol (mg/dl) 107 (28) �5.5 �2.2 �7.5 0.6HDL-chol (mg/dl)* 54 (12) 3.4 4.5 9.1 2.0Trig (mg/dl) 86 (46) �18.4 �8.9 �15.6 0.3

*Adjusted for age, race/ethnicity, parity, prepregnancy BMI, gestational weight gain,GDM status and family history of diabetes†Partial F test p � 0.05.

0002-9378/$ - see front matterdoi:10.1016/j.ajog.2007.10.450

432 CHORIOAMNIONITIS AND ACTIVIN A IN HUMAN CORD BLOOD AND UMBILICALENDOTHELIAL CELLS SERENA WU1, EILEEN WANG2, 1University of Chicago, Chicago,Illinois, 2University of Pennsylvania, Philadelphia, Pennsylvania

OBJECTIVE: Since increases in activin have been associated with inflammatorystates, such as sepsis, with evidence for endothelial activin production, we sought todetermine if activin in human cord blood and umbilical vein cord endothelial cellsis altered by chorioamnionitis.

STUDY DESIGN: This is a prospective study of term pregnancies with and with-out chorioamnionitis. Strict exclusion criteria include IUGR, aneuploidy, hyper-tension, diabetes, preeclampsia, PPROM, preterm labor, and multiple gestations.Chorioamnionitis was defined clinically and confirmed histologically by pathology.At delivery, umbilical cord and cord blood were obtained. Activin concentrations incord blood were measured by ELISA [R&D, Minneapolis, MN]. Tissue sections ofumbilical cord were analyzed by immunohistochemistry using an activin subunitantibody. Cytoplasmic staining for the activin subunit was quantified using Auto-mated Cellular Imaging System [Clarient, San Juan Capistrano, CA] to assess stain-ing intensity using integrated optical density (IOD) normalized by standard area.Two-sample Wilcoxon rank-sum test and two-sample mean comparison were usedto calculate p-values with 95% confidence intervals.

RESULTS: Data on 15 pregnancies with chorioamnionitis and 19 pregnancieswithout choriomanionitis were collected. Mean activin concentrations (�/- SD)with and without chorioamnionitis were 1669.8 �/- 1419.6 pg/ml and 3095.9 �/-3618.4 pg/ml, respectively (p-value�0.377). Greater activin staining intensity wasnoted with a mean IOD score of 314 �/- 151.5 from infected pregnancies and amean IOD score of 157.1 �/- 123.5 from uninfected pregnancies [p-value�0.003,95% CI (168.589, 278.7105)]. There was also evidence of activin staining in umbil-ical arterial smooth muscle.

CONCLUSION: In this pilot study, the local presence of activin in umbilical veinendothelial cells was increased with chorioamnionitis, while activin concentrationsin cord blood were not significantly different. This suggests that infection does alteractivin expression in umbilical cord though further study is warranted.

0002-9378/$ - see front matterdoi:10.1016/j.ajog.2007.10.451

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S128 American Journal of Obstetrics & Gynecology Supplement to DECEMBER 2007