Abstract
Although prenatal corticosteroid therapy is efficacious and safe it does not always prevent RDS, and infants of low birth weight often develop chronic lung disease. To study effects of thyroid hormone, we performed a blinded, randomized trial in which 404 women with threatened preterm delivery at <32 wk gestation received betamethasone plus TRH (4 doses of 400 μg at 8-h intervals) or betamethasone plus placebo. 103 fully treated infants of <1500 g birth weight were evaluated for outcome. TRH therapy did not affect total RDS (47.3% vs 58.3% in control) or occurrence of severe disease (12.7% vs 25% in control, p=0.11). Significantly fewer TRH-treated infants developed chronic lung disease (requirement for supplemental O2 at 28 days of age), 17.6% vs 43.9% in control (p<0.01). TRH increased maternal plasma TSH by 100% at 2-4 h after treatment and decreased levels by 28-34% at 5-36 h. In cord blood of treated infants delivered at 2-6 h, TSH, T3 and PRL were all increased about 2-fold vs control and free T4 was increased 19%. In infants delivering at 7-36 h, cord TSH and T3 were decreased 62 and 54%, respectively, and all thyroid hormones were lower at 2 h of age. Conclusion: Prenatal TRH therapy produces a sustained elevation of fetal thyroid hormones and reduces the occurrence of chronic lung disease in premature infants. Pituitary-thyroid function is transiently suppressed after treatment, to a greater extent in fetus than mother.
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