Associations between Maternal and Fetal Inherited Thrombophilias, Placental Characteristics Associated with Vascular Malperfusion, and Fetal Growth

Pregnancy results in alterations in coagulation processes, which may increase the risk of thrombosis. Inherited thrombophilia mutations may further increase this risk, possibly through alterations in the placenta, which may result in pregnancy complications such as poor fetal growth. The purpose of...

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Main Authors: Alexa A. Freedman, Carol J. Hogue, Donald J. Dudley, Robert M. Silver, Barbara J. Stoll, Halit Pinar, Robert L. Goldenberg, Carolyn Drews-Botsch
Format: Article
Language:English
Published: Georg Thieme Verlag KG 2017-06-01
Series:TH Open
Subjects:
Online Access:http://www.thieme-connect.de/DOI/DOI?10.1055/s-0037-1603925
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spelling doaj-fab827ed5354444e9ee848938de8c9bc2020-11-25T02:38:20ZengGeorg Thieme Verlag KGTH Open2512-94652017-06-010101e43e5510.1055/s-0037-1603925Associations between Maternal and Fetal Inherited Thrombophilias, Placental Characteristics Associated with Vascular Malperfusion, and Fetal GrowthAlexa A. Freedman0Carol J. Hogue1Donald J. Dudley2Robert M. Silver3Barbara J. Stoll4Halit Pinar5Robert L. Goldenberg6Carolyn Drews-Botsch7Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia, United StatesDepartment of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia, United StatesDepartment of Obstetrics and Gynecology, School of Medicine, University of Virginia, Charlottesville, Virginia, United StatesDepartment of Obstetrics and Gynecology, School of Medicine, University of Utah, Salt Lake City, Utah, United StatesMcGovern Medical School, University of Texas Health Science Center, Houston, Texas, United StatesDepartment of Pathology and Laboratory Medicine, Alpert Medical School, Brown University, Providence, Rhode Island, United StatesDepartment of Obstetrics and Gynecology, Columbia University Medical Center, New York, New York, United StatesDepartment of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia, United StatesPregnancy results in alterations in coagulation processes, which may increase the risk of thrombosis. Inherited thrombophilia mutations may further increase this risk, possibly through alterations in the placenta, which may result in pregnancy complications such as poor fetal growth. The purpose of our study is to evaluate the association of fetal growth, approximated by birth weight for gestational age percentile, with genetic markers of thrombophilia and placental characteristics related to vascular malperfusion. We analyzed data from the Stillbirth Collaborative Research Network's population-based case–control study conducted in 2006–2008. Study recruitment occurred in five states: Rhode Island and counties in Massachusetts, Georgia, Texas, and Utah. The analysis was restricted to singleton, nonanomalous live births ≤42 weeks' gestation with a complete placental examination and successful testing for ≥1 thrombophilia marker (858 mothers, 902 infants). Data were weighted to account for oversampling, differential consent, and availability of placental examination. We evaluated five thrombophilia markers: factor V Leiden, factor II prothrombin, methylenetetrahydrofolate reductase A1298C and C677T, and plasminogen activator inhibitor type 1 in both maternal blood and placenta/cord blood. We modeled maternal and fetal thrombophilia markers separately using linear regression. Maternal factor V Leiden mutation was associated with a 13.16-point decrease in adjusted birth weight percentile (95% confidence interval: −25.50, −0.82). Adjustment for placental abnormalities related to vascular malperfusion did not affect the observed association. No other maternal or fetal thrombophilia markers were significantly associated with birth weight percentile. Maternal factor V Leiden may be associated with fetal growth independent of placental characteristics.http://www.thieme-connect.de/DOI/DOI?10.1055/s-0037-1603925pregnancyinherited thrombophiliasperinatal hemostasis
collection DOAJ
language English
format Article
sources DOAJ
author Alexa A. Freedman
Carol J. Hogue
Donald J. Dudley
Robert M. Silver
Barbara J. Stoll
Halit Pinar
Robert L. Goldenberg
Carolyn Drews-Botsch
spellingShingle Alexa A. Freedman
Carol J. Hogue
Donald J. Dudley
Robert M. Silver
Barbara J. Stoll
Halit Pinar
Robert L. Goldenberg
Carolyn Drews-Botsch
Associations between Maternal and Fetal Inherited Thrombophilias, Placental Characteristics Associated with Vascular Malperfusion, and Fetal Growth
TH Open
pregnancy
inherited thrombophilias
perinatal hemostasis
author_facet Alexa A. Freedman
Carol J. Hogue
Donald J. Dudley
Robert M. Silver
Barbara J. Stoll
Halit Pinar
Robert L. Goldenberg
Carolyn Drews-Botsch
author_sort Alexa A. Freedman
title Associations between Maternal and Fetal Inherited Thrombophilias, Placental Characteristics Associated with Vascular Malperfusion, and Fetal Growth
title_short Associations between Maternal and Fetal Inherited Thrombophilias, Placental Characteristics Associated with Vascular Malperfusion, and Fetal Growth
title_full Associations between Maternal and Fetal Inherited Thrombophilias, Placental Characteristics Associated with Vascular Malperfusion, and Fetal Growth
title_fullStr Associations between Maternal and Fetal Inherited Thrombophilias, Placental Characteristics Associated with Vascular Malperfusion, and Fetal Growth
title_full_unstemmed Associations between Maternal and Fetal Inherited Thrombophilias, Placental Characteristics Associated with Vascular Malperfusion, and Fetal Growth
title_sort associations between maternal and fetal inherited thrombophilias, placental characteristics associated with vascular malperfusion, and fetal growth
publisher Georg Thieme Verlag KG
series TH Open
issn 2512-9465
publishDate 2017-06-01
description Pregnancy results in alterations in coagulation processes, which may increase the risk of thrombosis. Inherited thrombophilia mutations may further increase this risk, possibly through alterations in the placenta, which may result in pregnancy complications such as poor fetal growth. The purpose of our study is to evaluate the association of fetal growth, approximated by birth weight for gestational age percentile, with genetic markers of thrombophilia and placental characteristics related to vascular malperfusion. We analyzed data from the Stillbirth Collaborative Research Network's population-based case–control study conducted in 2006–2008. Study recruitment occurred in five states: Rhode Island and counties in Massachusetts, Georgia, Texas, and Utah. The analysis was restricted to singleton, nonanomalous live births ≤42 weeks' gestation with a complete placental examination and successful testing for ≥1 thrombophilia marker (858 mothers, 902 infants). Data were weighted to account for oversampling, differential consent, and availability of placental examination. We evaluated five thrombophilia markers: factor V Leiden, factor II prothrombin, methylenetetrahydrofolate reductase A1298C and C677T, and plasminogen activator inhibitor type 1 in both maternal blood and placenta/cord blood. We modeled maternal and fetal thrombophilia markers separately using linear regression. Maternal factor V Leiden mutation was associated with a 13.16-point decrease in adjusted birth weight percentile (95% confidence interval: −25.50, −0.82). Adjustment for placental abnormalities related to vascular malperfusion did not affect the observed association. No other maternal or fetal thrombophilia markers were significantly associated with birth weight percentile. Maternal factor V Leiden may be associated with fetal growth independent of placental characteristics.
topic pregnancy
inherited thrombophilias
perinatal hemostasis
url http://www.thieme-connect.de/DOI/DOI?10.1055/s-0037-1603925
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