633: Maternal inflammatory mediators are increased as early as the first trimester in low risk pregnancies

Existing data are conflicting regarding the changes in inflammatory mediators that occur in normal pregnancy. The objective of this study is to describe the changes in vaginal and systemic immunity among low risk first trimester pregnant women. A prospective cohort of pregnant and non-pregnant women was conducted. Pregnant women were enrolled if less than 14 weeks gestation. Non-pregnant women not using hormonal contraception were enrolled as a control group. Women were included if they had no medical or previous pregnancy complications, had no vaginal infections, and did not use tobacco or other substances. Cervical swabs were collected for measurement of pro- and anti- inflammatory cytokines. Vaginal swabs were collected for determination of secretory leukocyte protease inhibitor (SLPI). Serum was collected for measurement of C-reactive protein (CRP). Concentrations of various markers were converted to multiples of the median (MOM) to standardize values. Values were compared and adjustment for potential confounders was performed. 44 pregnant and 14 non-pregnant women were enrolled. The median gestational age of pregnant women was 12 weeks (8-14). After adjusting for race and body mass index, concentrations of the pro-inflammatory cytokine IL-1β were increased in pregnancy, median values 536 versus 31.5 pg/mL (MOM 2.88 versus 0.17), p=0.01. There were no significant differences in concentrations of pro-inflammatory markers IL-6, IFN-γ, or TNF-α, anti-inflammatory markers IL-4 or IL-10, chemokines GM-CSF or MIP-1α, or in the protective mediator SLPI. The systemic marker of inflammation, hsCRP was increased in the pregnancy, median values 6.24 versus 1.13 mg/L (MOM 1.32 versus 0.24), p=0.008. This is among the largest cohorts of low risk pregnant women to date for determination of normal values of inflammatory mediators in the first trimester. Our data confirms previous data suggesting increases in IL-1β and CRP attributable to pregnancy, evident as early as the first trimester.