Poster Only Presentation
Concurrent Session 1B - Placental Fetal Physiology
Introduction: Cigarette smoking during pregnancy is associated with adverse pregnancy outcomes. Paradoxically, women who smoke during pregnancy have a reduced risk of preeclampsia. Preeclampsia is an endothelial disease, associated with elevated anti-angiogenic factors such as soluble endoglin (sEng) and soluble vascular endothelial growth factor receptor-1 (sVEGFR1), and lower placental growth factor (PlGF), an angiogenic factor. Transforming growth factor beta (TGF-beta) is an angiogenic cytokine that binds to endoglin receptors on vascular endothelium and is responsible for many vascular actions. The objective of the study is to determine serum levels of anti-angiogenic factors, PIGF, and TGF-beta in smoking and non-smoking pregnant women.
Methods: Using Enzyme-linked immunosorbent assay we prospectively analyzed serum levels of PIGF, sENG, sVEGFR1, and TGF-beta in normotensive pregnant smokers and non-smokers. Exclusion criteria included hypertension, auto-immune disorders, rupture of membranes, evidence of labour, fever, and any significant medical illness. A two-way student’s t-test or Mann -Whitney U test was used for continuous variables as appropriate, and the ꭓ2 test for categorical variables.
Results: Maternal age was significantly lower in smoking mothers as compared to non-smoking mothers, with no significant difference in other demographic variables. Median TGF-beta levels were significantly higher in the smoking group, and remained significant after adjusting for maternal age, gestation, BMI, parity and ethnicity (P<.001). TGF-beta levels correlated positively with cotinine levels in the smoking group (Spearman coefficient 0.78, P<.001). The levels of anti-angiogenic factors and PIGF were not significantly different between smokers and non-smokers.
Conclusion: We speculate that higher TGF-beta levels in mothers who smoke may explain the lower incidence of preeclampsia. With increased TGF-beta in the serum, it is available for action on endoglin receptors on the maternal endothelium, even after inactivation by the circulating maternal sEng, allowing for normal maternal and placental endothelial function.