The impact of isolated maternal hypothyroxinemia on perinatal morbidity

To determine whether maternal hypothyroxinemia during early pregnancy is associated with adverse perinatal outcomes.

Serum samples of a prospective cohort of 879 women collected at 15-16 weeks of pregnancy were analyzed for thyroid-stimulating hormone (TSH) and free thyroxine (T4) concentrations. Women with TSH levels within the normal reference range (0.15-4.0 mU/L) and free T4 levels below the 10th percentile of the sample (8.5 pmol/L) were classified as hypothyroxinemic and were compared with euthyroid women (who had normal TSH and free T4 levels). Thyroid hormone measures were linked to pregnancy outcomes, including small for gestational age (SGA), standardized birth weight z-score, preterm delivery, and Apgar score used as a measure of early neonatal morbidity.

Among 89 hypothyroxinemic women, there was no evidence of an increased risk for fetal growth restriction, preterm birth, or low Apgar score. The relative risk of delivering an SGA infant was 0.38 (95% CI 0.11 to 1.33), the mean difference in birth weight z-score was 0.035 (95% CI -0.17 to 0.24), and the risk of preterm delivery was 0.79 (95% CI 0.38 to 1.67). None of the hypothyroxinemic women gave birth to an infant with a five-minute Apgar score <7. When free T4 levels were substituted for categories of thyroid hormone function, the pattern of results remained unaltered.

Isolated maternal hypothyroxinemia was not observed to have any adverse effect on fetal growth or pregnancy outcome. This study does not provide evidence to support treatment of this condition to prevent fetal growth restriction or neonatal morbidity.