Response of the Maternal, Fetal, and Neonatal Pituitary-Thyroid Axis to Thyrotropin-Releasing Hormone

Abstract

ABSTRACT. Thyrotropin releasing hormone (TRH) readily crosses the placenta and stimulates the fetal pituitary. We studied the response of the maternal and fetal pituitarythyroid axes to TRH and the influence of prenatal exposure to TRH on the physiological postnatal increase in thyrotropin (TSH) and triiodothyronine (T 3 ) in the neonate. Twenty-six pregnant women received TRH (400 or 600 ILg) intravenous or saline (controls) either 2 or 12 h before elective cesarean section at term. Administration of 400 ILg of TRH resulted in significant elevations of maternal TSH (15.7 ± 2.9 versus 3.2 ± O.4ILU/ml,p < 0.01) and prolactin (416 ± 94 versus 223 ± 41 nglml, p < 0.05) 2 h later.Maternal T 3 remained unchanged. A higher dose of TRH (600 ILg) produced comparable results. Maternal administration of TRH (400 ILg) 2 h before delivery resulted in significant increases in fetal TSH and T 3 over controls (21.1 ± 3.7 versus 4.8 ± 1.0 ILU/ml, and 132 ± 12 versus 64 ± 9 ngldl, p < 0.01, respectively). Cord blood hormone levels 12 hours after TRH administration were similar to controls. Higher doses of TRH did not produce further increases in fetal TSH or T 3 • Control and treated neonates demonstrated similar physiological postnatal increases in TSH and T3, suggesting that prior exposure to TRH did not blunt this response. These data suggest that maternal administration of TRH is an effective way of increasing fetal T 3 levels, and that this treatment does not inhibit the postnatal surge in TSH and T 3 • (Pediatr Res 20: 982-986, 1986)

Antenatal Thyrotropin-Releasing Hormone to Prevent Lung Disease in Preterm Infants

“…This hormone does cross the placenta and stimulates fetal secretion of thyrotropin, triiodothyronine, thyroxine, and prolactin. [18][19][20][21] Antenatal glucocorticoid therapy reduces the incidence and severity of respiratory distress syndrome in premature infants but has no effect on the occurrence of chronic lung disease. 4,6 In most but not all trials of antenatal thyrotropin-releasing hormone in combination with glucocorticoid, the incidence and severity of respiratory distress syndrome, chronic lung disease, or an adverse outcome, defined as chronic lung disease or death by 28 days' postnatal age, were reduced.…”

Effects of Maternal Administration of Dexamethasone and Thyrotropin-Releasing Hormone on Fetal Rat Pulmonary Surfactant Synthesis

“…Glucocorticoid hormones have been shown to accelerate several aspects of this pro cess and thyroid hormone, insulin, prolactin and several other hormones and growth fac tors may also be involved in surfactant pro tein regulation. TRH is a tripeptide that crosses the placenta readily and stimulates the fetal pituitary to produce both TSH and pro lactin [23,24], Recently, administration of TRH and a glucocorticoid in combination was reported to accelerate fetal lung matura tion more than glucocorticoid therapy alone [13][14][15]. Our study was carried out to evaluate the effects of maternal administration of DEX and TRH and to determine whether they had a synergistic effect on the mRNA levels of pul monary surfactant in the fetal rat lung.…”

Effects of Betamethasone and Thyroid Hormone on Fetal Rat Lung Maturation in vivo

“…Uncontrolled studies in humans are not strongly suggestive of marked or rapid effects of thyroid hormones on fetal lung maturation [26,27]. Recent studies in humans suggest that combined hormonal therapy with beta methasone plus thyrotropin-releasing hor mone (TRH), a tripeptide that crosses the pla centa and increases fetal thyroid hormones, ameliorates respiratory distress syndrome and its consequences [28][29][30]. Our findings would suggest that the additional benefit in fetal lung maturation derived from adding TRH to betamethasone may not derive from the mild elevations of thyroid hormones ob served in premature fetuses with TRH [31 ].…”