Karen J Gibbins1, Robert M Silver2, Halit Pinar3, Uma M Reddy4, Corette B Parker5, Vanessa Thorsten5, Marian Willinger4, Donald J Dudley6, Radek Bukowski7, George R Saade8, Matthew A Koch4, Deborah Conway9, Carol J Hogue10, Barbara J Stoll10, Robert L Goldenberg11. 1. The University of Utah School of Medicine, Salt Lake City, UT, United States. Electronic address: Karen.gibbins@hsc.utah.edu. 2. The University of Utah School of Medicine, Salt Lake City, UT, United States. 3. The Warren Alpert Medical School of Brown University, Providence, RI, United States. 4. Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, United States. 5. RTI International, Durham, NC, United States. 6. University of Virginia, United States. 7. Yale-New Haven Hospital, United States. 8. University of Texas Medical Branch, Galveston, TX, United States. 9. University of Texas San Antonio, United States. 10. Emory University, United States. 11. Columbia University School of Medicine, New York, NY, United States.
Abstract
INTRODUCTION: Stillbirth, preeclampsia, and gestational hypertension (PE/GH) have similar clinical risk factors and redundant placental pathology. We aim to discern if stillbirth with PE/GH has a particular phenotype by comparing stillbirths with and without PE/GH. METHODS: Secondary analysis of the Stillbirth Collaborative Research Network, a population-based cohort study of all stillbirths and a sample of live births from 2006 to 2008 in five catchment areas. We compared placental pathology between stillbirths and with and without PE/GH, stratified by term or preterm. We also compared placental pathology between stillbirths and live births with PE/GH. RESULTS: 79/518 stillbirths and 140/1200 live births had PE/GH. Amongst preterm stillbirths, there was higher feto-placental ratio in PE/GH pregnancies (OR 1.24 [1.11, 1.37] per unit increase), and there were more parenchymal infarctions (OR 5.77 [3.18, 10.47]). Among PE/GH pregnancies, stillbirths had increased maternal and fetal vascular lesions, including retroplacental hematoma, parenchymal infarction, fibrin deposition, fetal vascular thrombi, and avascular villi. DISCUSSION: Stillbirth pregnancies are overwhelmingly associated with placental lesions. Parenchymal infarctions are more common in PE/GH preterm stillbirths, but there is significant overlap in lesions found in stillbirths and PE/GH.
INTRODUCTION: Stillbirth, preeclampsia, and gestational hypertension (PE/GH) have similar clinical risk factors and redundant placental pathology. We aim to discern if stillbirth with PE/GH has a particular phenotype by comparing stillbirths with and without PE/GH. METHODS: Secondary analysis of the Stillbirth Collaborative Research Network, a population-based cohort study of all stillbirths and a sample of live births from 2006 to 2008 in five catchment areas. We compared placental pathology between stillbirths and with and without PE/GH, stratified by term or preterm. We also compared placental pathology between stillbirths and live births with PE/GH. RESULTS: 79/518 stillbirths and 140/1200 live births had PE/GH. Amongst preterm stillbirths, there was higher feto-placental ratio in PE/GH pregnancies (OR 1.24 [1.11, 1.37] per unit increase), and there were more parenchymal infarctions (OR 5.77 [3.18, 10.47]). Among PE/GH pregnancies, stillbirths had increased maternal and fetal vascular lesions, including retroplacental hematoma, parenchymal infarction, fibrin deposition, fetal vascular thrombi, and avascular villi. DISCUSSION: Stillbirth pregnancies are overwhelmingly associated with placental lesions. Parenchymal infarctions are more common in PE/GH preterm stillbirths, but there is significant overlap in lesions found in stillbirths and PE/GH.
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