Associations Between Maternal Thyroid Function in Pregnancy and Obstetric and Perinatal Outcomes.

CONTEXT: The effects of maternal subclinical hypothyroidism on pregnancy outcomes are not clear.
OBJECTIVE: We aimed to assess potential associations between maternal thyrotropin (thyroid-stimulating hormone [TSH]) levels in pregnancy and obstetric and perinatal outcomes.
DESIGN: Retrospective cohort study.
SETTING: Tertiary academic medical center. PATIENTS: Women aged ≥18 years with a singleton gestation and no known thyroid disease seen for prenatal care at Boston Medical Center from January 1, 2003 through May 22, 2014, and their fetuses and infants were included. MAIN OUTCOME MEASURES: Risk ratios of adverse obstetric and perinatal outcomes.
RESULTS: A total of 8,413 pregnant women (mean age 29.1 years, 15% white, 60% black, 13% Hispanic) and their fetuses and infants (mean gestational age at birth 38.5 weeks, 52% male, mean birth weight 3.2 kg) were included in the analyses. The median (interquartile range) TSH level was 1.06(0.62-1.60) mIU/L, and 130 women (1.6%) had TSH > 4 mIU/L. Maternal TSH levels > 4 mIU/L were associated with increased risks of prematurity (risk ratio [RR] 2.17 [95% confidence interval 1.15-4.07] P = .016) and neonatal respiratory distress syndrome (RDS) (RR 2.83 [95% confidence interval 1.02-7.86] P = .046) compared to TSH levels ≤ 4 mIU/L. Although not statistically significant, TSH levels > 4 mIU/L were also associated with increased RRs for fetal loss, preeclampsia/eclampsia, and low birth weight. TSH levels > 4 mIU/L were not associated with preterm labor, placental abruption, cesarean section, gestational hypertension or diabetes, or neonatal intensive care unit admission.
CONCLUSION: Maternal serum TSH concentration > 4 mIU/L in pregnancy was associated with approximately 2-fold increased risks of prematurity and RDS in offspring. Elevated TSH was also associated with statistically non-significant increases in the risk of fetal loss, preeclampsia/eclampsia, and low birth weight. © Endocrine Society 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.