Chloe A Zera1, Ellen W Seely2, Louise E Wilkins-Haug3, Kee-Hak Lim4, Samuel I Parry5, Thomas F McElrath3. 1. Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Brigham and Women's Hospital, Boston, MA; Harvard Medical School, Boston, MA. Electronic address: czera@partners.org. 2. Division of Endocrinology, Diabetes, and Hypertension, Department of Medicine, Brigham and Women's Hospital, Boston, MA; Harvard Medical School, Boston, MA. 3. Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Brigham and Women's Hospital, Boston, MA; Harvard Medical School, Boston, MA. 4. Harvard Medical School, Boston, MA; Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Beth Israel-Deaconess Medical Center, Boston, MA. 5. Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Pennsylvania Medical Center, Philadelphia, PA.
Abstract
OBJECTIVE: Because obesity is a risk factor for placental dysfunction, we hypothesized that maternal body mass index (BMI) would be associated with alterations in serum angiogenic markers. STUDY DESIGN: We included 2399 singleton pregnancies with and without placental dysfunction in a prospective longitudinal cohort study of angiogenic markers. We modeled the relationship between categorical and continuous BMI, soluble fms-like tyrosine kinase-1 (sFlt-1), and placental growth factor (PlGF) over gestation, stratified by pregnancy outcome. RESULTS: In women with normal pregnancies, a higher BMI was associated with lower sFlt-1 values across gestation (P < .0001), lower PlGF in the second and third trimesters (P < .0001), and lower rate of change in PlGF (P < .0001). Similar relationships were seen between maternal BMI, sFlt-1 (P < .0001), and PlGF (P = .0005) in women with clinically evident placental dysfunction. CONCLUSION: The sFlt-1 value is inversely associated with maternal BMI. The pattern of change in PlGF is also dependent on maternal BMI, indicating that obese women may have abnormalities in angiogenesis near term.
OBJECTIVE: Because obesity is a risk factor for placental dysfunction, we hypothesized that maternal body mass index (BMI) would be associated with alterations in serum angiogenic markers. STUDY DESIGN: We included 2399 singleton pregnancies with and without placental dysfunction in a prospective longitudinal cohort study of angiogenic markers. We modeled the relationship between categorical and continuous BMI, soluble fms-like tyrosine kinase-1 (sFlt-1), and placental growth factor (PlGF) over gestation, stratified by pregnancy outcome. RESULTS: In women with normal pregnancies, a higher BMI was associated with lower sFlt-1 values across gestation (P < .0001), lower PlGF in the second and third trimesters (P < .0001), and lower rate of change in PlGF (P < .0001). Similar relationships were seen between maternal BMI, sFlt-1 (P < .0001), and PlGF (P = .0005) in women with clinically evident placental dysfunction. CONCLUSION: The sFlt-1 value is inversely associated with maternal BMI. The pattern of change in PlGF is also dependent on maternal BMI, indicating that obesewomen may have abnormalities in angiogenesis near term.
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