Thyrotropin fetal

The fetal thyroid-pituitary axis functions independently from the mother s axis in most cases. However, if the mother has preexisting Graves disease (see Chapter 52), her autoantibodies can cross the placenta and stimulate the fetal thyroid gland. Thus the fetus can develop hyperthyroidism. Measurement of thyrotropin-binding inhibitory immmioglobu-lins (TBII) is useful for assessing risk of fetal or neonatal Graves disease. 

Thyroid hormones also accelerate fetal lung maturation. Fetal thyroid hormone levels may be increased by antenatal administration of thyrotropin-releasing hormone (TRH), a tripeptide that crosses the placental barrier, stimulates fetal pituitary production of thyroid stimulating hormone (TSH), and which, in turn, increases fetal thyroid hormone production (Chapter 33). This indirect method of enhancement of fetal thyroid hormone production is utilized because thyroid hormones do not readily cross the placental barrier. Insulin delays surfactant synthesis and so fetal hyperinsulinemia in diabetic mothers may increase the incidence of RDS even in the full-term infant. Androgen synthesized in the fetal testis is the probable cause of a slower onset of surfactant production in male fetuses. Prophylactic, or after onset of RDS, administration of synthetic or natural pulmonary surfactants intratracheally to preterm infants improves oxygenation and decreases pulmonary morbidity. 

Use of thyrotropin-releasing hormone (TRH) as an adjunct to antenatal corticosteroids was thought to further accelerate fetal lung maturation. However, the Australian Collaborative Trial of Antenatal Thyrotropin-Releasing Hormone (ACTOBAT) study failed to show additional benefits from TRH 200 meg every 12 hours. The frequencies of RDS (relative risk [RR] 1.17, 95% Cl 1.00-1.36) and need for ventilation (RR 1.15, 95% Cl 1.01-1.31) were not reduced, and treatment was associated with maternal nausea, vomiting, and light-headedness. Of more concern was the 12-month follow-up report in which TRH treatment was associated with motor delays (OR 1.51, 95% Cl 1.11-2.05), sensory impairment (OR 2.00, 95% Cl 1.06-3.74), social delays (OR 1.41, 95% Cl 1.01-1.95), and severe neurodevelopmental impairment (OR 1.75, 95% Cl 1.07-2.87). At this point, antenatal TRH treatment cannot be advised. 

When iodine requirements are not met, TH synthesis is reduced, resulting in enlargement of the thyroid gland to compensate for this reduction. In adults, mild iodine deficiency (ID) is associated with nontoxic nodular goiter and, less often, with toxic nodular goiter, due to increases in the constitutive (thyrotropin-independent) growth and functional potential of some clones of thyroid cells. In pregnancy, this can result in fetal neurodevelopmental deficits and mental retardation. 

Polk, D.H., Reviczky, A.L., Lam, R.W. and Fisher, D.A. (1988) Thyrotropin releasing hormone effect of thyroid status on tissue concentrations in fetal sheep. Clin Res 36 203A. 

Leduque, P., Aratan-Spire, S., Czernichow, P. and Dubois, P.M. (1986) Ontogenesis of thyrotropin releasing hormone in human fetal pancreas. J Clin Invest 78 1028. 

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