Maternal hypothyroidism: To screen or not to screen?


The debate over universal screening for maternal hypothyroidism has raged for years. Recent concrete data points to just testing at-risk mothers.

Background: Maternal thyroid function and fetal neurodevelopment

Severe maternal and fetal hypothyroidism due to iodine deficiency has clear and unequivocal neonatal sequelae: cretinism.1 However, early, aggressive replacement therapy for infants born with congenital hypothyroidism due to thyroid dysgenesis or inborn errors of thyroid hormone synthesis results in normal to near-normal IQ.2 This suggests that transplacental passage of maternal thyroid hormones can largely prevent adverse neurodevelopmental consequences in the fetus. In other words, normal maternal thyroid function can blunt the harmful effects of impaired fetal thyroid function on fetal brain development. However, since the fetal thyroid does not begin to function effectively until 12 weeks' gestation, concerns have been raised that impaired maternal thyroid function in the first trimester may exert deleterious effects on embryonic and early fetal neurodevelopment.

In contrast, Henrichs, et al measured both TSH and free T4 levels in 3,659 mothers at 13 weeks and observed that elevated maternal TSH levels were not associated with abnormal cognitive outcomes.4 However, these authors found that levels of free T4 below the 10th and 5th percentiles were associated with expressive language delay (odds ratio [OR], 1.44; 95% Confidence Intervals [CI], 1.09-1.91; and OR, 1.80; 95% CI, 1.24-2.61, respectively). Moreover, severe maternal hypothyroxinemia also predicted an increased risk of nonverbal cognitive delay (OR, 2.03; 95% CI, 1.22-3.39). Pop, et al observed that children whose mothers had free T4 levels below the 5th and 10th percentiles at 12 weeks' gestation had significantly lower Bayley Psychomotor Developmental Index scores at 10 months of age compared with children of euthyroid mothers (mean index score difference, 14.1; 95% CI, 5.9-22; mean index score, 7.4; 95% CI, 1.1-13.9, respectively).5 Taken together, these latter 2 studies suggested that first-trimester maternal hypothyroxinemia, but not subclinical thyroid dysfunction manifested solely by isolated elevated TSH levels, was associated with long-term fetal neurodevelopmental delays.

Further complicating matters were the results of a prospective cohort study by Casey, et al, who tested stored serum samples from 17,298 women enrolled before 20 weeks' gestation for TSH and free T4, and observed that 404 (2.3%) had TSH values at or above the 97.5th percentile and normal free T4 levels (ie, subclinical hypothyroidism).6 The latter pregnancies were more likely to be complicated by placental abruption (relative risk [RR], 3.0; 95% CI, 1.1-8.2) and preterm birth at or before 34 weeks (RR, 1.8, 95% CI, 1.1-2.9). This suggested that perhaps preterm delivery could be confounding the association between maternal subclinical hypothyroidism.

In contrast, data from the First- and Second-Trimester Evaluation of Risk (FASTER) prospective cohort of nearly 11,000 women identified no association between first-trimester subclinical hypothyroidism (ie, high TSH) and preterm birth. Although the data found an association between hypothyroxinemia and preterm labor (adjusted odds ratio [AOR], 1.62; 95% CI, 1.00-2.62), no link was observed with preterm delivery (AOR, 1.15; 95% CI, 0.72-1.84).7 Ironically, maternal hypothyroxinemia was associated with macrosomia (AOR, 1.97; 95% CI, 1.37-2.83). The authors concluded that maternal thyroid hypofunction was not associated with "a consistent pattern of adverse outcomes."

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