Association of race-ethnicity and placental lesions in stillbirth cases
Jessica Page, MD (1,2); Greg Stoddard, MPH, MBA (1), Michelle Debbink, MD, PhD (1,2), Karen Gibbins, MD, MSCI (3), Robert Silver, MD (1,2)
(1) University of Utah Health, Salt Lake City, UT, USA; (2) Intermountain Healthcare, Salt Lake City, UT, USA; (3) Oregon Health and Science University, Portland, OR, USA
There is racial and ethnic disparity in stillbirth but mechanisms are uncertain. Our objective was to compare placental lesions between race/ethnicity groups, stratifying by stillbirths and live births.
Secondary analysis utilizing Stillbirth Collaborative Research Network data, collected in a prospective case-control fashion from five geographic catchment areas in the Unites States. Pathologic placental findings in singleton, non-anomalous stillbirths and live births were compared between race/ethnicity groups, stratifying on gestational age. Multivariable logistic regression was used to account for maternal age, education, insurance and income with non-Hispanic white as the referent group.
Placental pathology results from 456 stillbirths and 1160 live births were analyzed. In term pregnancies, non-Hispanic black women were more likely to have terminal villous immaturity or hypoplasia in live births (aOR 3.72 (95% CI 1.56-8.89)). Non-Hispanic black women with a live birth at term were also more likely to have placental evidence of maternal inflammation with chorioamnionitis (aOR 2.61 (95% CI 1.29-5.26)). In non-Hispanic black women with preterm stillbirths, both maternal and fetal inflammatory lesions were more common (aOR 5.51 (95% CI 2.60-11.70) and aOR 4.18 (95% CI 1.42-12.32) respectively). At term, Hispanic women with stillbirths were more likely to have parenchymal infarction (aOR 3.72 (95% CI 1.12-12.37). Developmental umbilical cord abnormalities (aOR 2.69 (95% CI 1.06-6.83) and fetal vascular thrombi (aOR 2.46 (95% CI 1.11-5.41) were more common in term live births in Hispanic women. Among preterm stillbirths in Hispanics, maternal inflammation was more likely (aOR 2.14 (95% CI 1.05-4.35). Terminal villous immaturity/hypoplasia (aOR 52.24 (95% CI 1.69-1618.87) and fetal vascular thrombi (aOR 15.99 (95% CI 2.67-95.73) were more prevalent in Hispanic preterm live births. We had too few women of other race/ethnicity to comment on placental lesions.
Inflammatory and circulatory placental lesions are more common among non-Hispanic black and Hispanic women in both live births and stillbirths. These data suggest targeting inflammation and placental function may help reduce disparity in stillbirth.
All participants gave written informed consent as part of the original study and the study was approved by the institutional review boards of each clinical site and the data coordinating and analysis center.