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Tuija Männistö, Is There Enough Evidence of Poor Fetal Growth to Merit Narrowing Free T4 Reference Ranges during Pregnancy?, The Journal of Clinical Endocrinology & Metabolism, Volume 98, Issue 1, 1 January 2013, Pages 43–44, https://doi.org/10.1210/jc.2012-4010
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Thyroid function undergoes profound changes during pregnancy, with enlargement of the thyroid gland, up to 50% increase in thyroid hormone production and in iodine requirements, changes in thyroid hormone binding proteins, as well as decreases in TSH due to direct thyroidal stimulation by human chorionic gonadotropin (1). Maternal hypothyroidism and hyperthyroidism during pregnancy are associated with increases in maternal and fetal morbidity, and hypothyroidism and hypothyroxinemia are also associated with adverse cognitive development in offspring (1–3). The American Thyroid Association and The Endocrine Society both recommend measuring serum TSH concentration in women with high risk for or with symptoms of hypothyroidism or hyperthyroidism to diagnose thyroid diseases during pregnancy as well as when adjusting levothyroxine treatment in hypothyroid pregnant patients (1–3). Both guidelines note the importance of measuring free T4 concentrations in distinguishing between overt and subclinical thyroid disease as well as in adjusting antithyroid drug treatment in patients with Graves' disease, but they also note the potential for error when measuring free T4 concentrations by immunoassays in pregnant patients (1–3). The guidelines suggest that each laboratory should establish trimester-specific reference intervals of free T4, use calculations of free T4 index, measure total T4, or preferably use the “gold standard” method of measuring free T4 in the dialysate or ultrafiltrate of serum samples with liquid chromatography-tandem mass spectrometry (1–3). Most studies evaluating pregnant women with thyroid diseases have used laboratory-specific measures of free T4 rather than the gold standard and place a higher emphasis on serum TSH concentrations in the diagnoses of thyroid diseases. This approach clearly limits the quality of evidence regarding the possible adverse effects of changes in free T4 concentrations within the established reference intervals (1–3).
