Developmental Trends in Cord and Postpartum Serum Thyroid Hormones in Preterm Infants

Abstract

The purpose of this study was first to clarify postnatal trends in sera T(4), free T(4) (FT(4)), T(4)-binding globulin, TSH, T(3), rT(3), and T(4) sulfate levels in cord and at 7, 14, and 28 d in groups of preterm infants at 23-27 wk (n = 101), 28-30 wk (n = 196), and 31-34 (n = 253) wk gestation, and second to compare these trends to those of term infants and also with cord sera levels of equivalent gestational ages (n = 812; 23-42 wk gestation). In all preterm groups, TSH and rT(3) decrease to below, T(4)-binding globulin increases to within, and T(3) and T(4) sulfate increase to above cord levels of equivalent gestational age. Term infants are hyperthyroxinemic relative to cord and nonpregnant adult levels of T(4). Postnatal T(4) increases are attenuated in 31- to 34-wk infants, absent in 28- to 30-wk infants (although levels are equivalent to gestational age), and crucially reversed in 23- to 27-wk infants. This immature group is hypothyroxinemic relative to other groups and to cord levels of equivalent gestational age. Compared with term infants, postnatal FT(4) increases are lower in 31- to 34-wk infants, attenuated in 28- to 30-wk infants, and absent in 23- to 27-wk infants. The 23- to 27-wk group is distinctive; they are hypothyroxinemic on T(4) levels, yet FT(4) levels are within the cord levels of equivalent gestational age.

Management of neonates born to women with Graves' disease: a cohort study

“…The FT 4 increase and TSH decrease developed gradually, after day 3 but before day 15 in neonates who subsequently developed hyperthyroidism. (Table 1) are consistent with the previously described time-course of FT 4 , FT 3 , and TSH values in neonates, once gestational age at birth is taken into account (25,36,37). When interpreting thyroid function data in neonates, the values must be compared with age-specific normal ranges.…”

Ten-Year Follow-up of Children Born at <30 Weeks’ Gestational Age Supplemented With Thyroxine in the Neonatal Period in a Randomized, Controlled Trial

“…At present, there is more knowledge on FT4 concentrations, which are more important for the biological effect than bound-T4 concentrations. 21 FT4 concentrations are decreased to a much lesser extent than bound-T4 concentrations, [3][4][5] and thyroid-hormone deficiency in preterm infants seems to be a subtle problem that increases in severity in more immature infants. 5,22 In view of the results discussed above, our present results can be of importance for additional studies.…”

“…FT4 concentrations in the more immature infants might indeed be too low [3][4][5] to ensure normal brain development. It could also be caused by thyroid-hormone-dependent maturational processes in the brain, which may especially take place in the window of time before 29 weeks.…”

“…[2][3][4] This is especially true in infants of Ͻ28 weeks' gestation. 5,6 In these infants, like in fetal life, inactivation of T4 is still a dominant metabolic pathway and results in high concentrations of sulfated thyroid hormones and reverse T3. 5,6 Low concentrations of T4, T3, and FT4 in the neonatal period are associated with worse neurodevelopmental outcome up until the age of 9 years.…”

“…5,6 In these infants, like in fetal life, inactivation of T4 is still a dominant metabolic pathway and results in high concentrations of sulfated thyroid hormones and reverse T3. 5,6 Low concentrations of T4, T3, and FT4 in the neonatal period are associated with worse neurodevelopmental outcome up until the age of 9 years. [7][8][9] Therefore, shortage of thyroid hormone could be one of the causes of impaired neurodevelopment that is often found in very preterm infants.…”