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

The fetus depends onmaternal thyroid hormone crossing via a placental route in a critical period of development during the first trimester. Untreated maternal hypothyroidism increases risk of adverse pregnancy outcomes including fetal loss, preeclampsia, abruption placenta, and postpartum hemorrhage, as well as adverse perinatal outcomes including premature birth, low birth weight (LBW), and neonatal respiratory distress syndrome (RDS). The American Thyroid Association recommends using trimester-specific, population-based reference ranges for thyroid-stimulating hormone (TSH), or if not available using an upper reference range of 4.0 mIU/L. The association between maternal subclinical hypothyroidism (SCH) and adverse obstetric and perinatal outcomes is less understood. This retrospective cohort study aimed to evaluate the association between maternal thyroid status, measured by TSH, and perinatal and obstetric outcomes. Pregnant women older than 18 years with singleton pregnancies, no known thyroid disease, at least 1 TSH measurement during prenatal period, and seen between 2003 and 2014 at Boston Medical Center were included. In the case of multiple TSH measurements in a pregnant woman, the first measurement of the study pregnancy was used. Normal thyroid function was defined as TSH between 0.1 and 4.0 mIU/L. Obstetric outcomes evaluated included fetal loss, preterm labor, cesarean section, placental abruption, preeclampsia/eclampsia, gestational hypertension, and gestational diabetes. Perinatal outcomes evaluated included prematurity, LBW, admission to NICU, Apgar score at 1 and 5 minutes, neonatal death, and RDS. Log-binomial generalized estimating equation models were used to measure association between perinatal and obstetric outcomes and maternal TSH greater than 4 mIU/L andmultivariable analyses to assess the potential impact of confounders. A total of 8413 women were included in the analysis (mean age of 29.1 years, 15% white, 60% black, 13% Hispanic). The median (interquartile range) maternal TSH value was 1.06 (0.62–1.1.60), with 130 (1.6%) having TSH levels greater than 4.0 mIU/L and 16 (0.2%) with TSH levels greater than 10.0 mIU/L. Maternal TSH level greater than 4 mIU/L was associated with a 2.17-fold increased risk of prematurity (risk ratio [RR], 2.17; P = 0.016; 95% confidence interval, 1.15–4.07) and a 2.83-fold increased risk of RDS (RR 2.83; P = 0.046; 95% confidence interval, 1.02–7.86). Although an increased RR was also observed between a maternal TSH level greater than 4 mIU/L and fetal loss, preeclampsia/eclampsia, and LBW, these associations were not statistically significant. A secondary analysis using trimester-specific reference ranges was completed, with results of multivariable regression showing results similar to those of the primary analysis. When restricted to a subset of women with TSH measured in the first trimester, the RR for prematurity and RDS increased to 2.95 and 8.73, respectively. The results of this study show a greater than 2-fold increase in risk of prematurity and RDS in offspring of women with a TSH measurement of greater than 4.0 mIU/L during pregnancy. Future interventional studies are needed to assess the benefit of treating maternal SCH in pregnancy.