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393 THE NATURE OF HYPOTHYROXINEMIA IN SICK PRETERM INFANTS

To evaluate the nature of hypothyroxinemia in small sick preterm infants, the hypothalamic-pituitary-thyroid axis was evaluated by determining the thyrotropin-response to TRH. Preterm infants of gestational ages 26-28 weeks, with T4<4μg/dl on two occasions and low TSH (<20μu/m1) were included in a double blind study. Following a TRH test, 20 μg/kg IV babies were assigned to a therapeutic regimen of either T4 (10μg/kg) or placebo. Nine babies were tested prior to therapy, 3 from T4 group and 6 from placebo group. Four babies, 2 from each group were tested 1-2 wks post therapy and 4 were not tested. In untreated babies the baseline TSH of 7.25±1.4 rose to 23.7±4.1μu/m1 at 30′. This response was slightly, but not significantly greater than that in full term babies, 23.7±4.1 vs 16.6±0.97, P>0.05. In 2 babies treated with T4, TSH response was completely suppressed. Serial T4 assay showed normalization of T4 in both groups at about the same time interval, 22.9±4.1 vs 23.8±4.9 days, P>0.5. There was no beneficial effect of T4 therapy on head growth 23.0±0.5 vs 31.2±0.6cm, P>0.05, length 42.5±0.6 vs 42.0±0.7cm, P>0.05, weight 1987±100 vs 1951±105gms, P>0.05, or duration of hospitalization 98.8±8.5 vs 110±8.3 day, P>0.05.In conclusion: hypothroxinemia in sick preterm infants is not caused by hypothyroidism. The physiological pituitary responses to stimulatory effect of TRH and suppressive action of T4 negate such a possibility. Based on these observations routine supplemental T4 therapy in preterm infants with low T4 is unwarranted.