The trusted source for
healthcare information and
Two hundred premature infants (< 30 weeks of gestation) were randomized to receive thyroxin supplementation (8 mcg/kg of birth weight) or placebo from 12-24 hours to 6 weeks of age. Plasma-free thyroxin levels were consistently higher in the treatment group. At six, 12, and 24 months, neurological outcome and scores on the Bayley Mental and Psychomotor Development Indexes were assessed. There were no statistically significant differences between the thyroxine supplemental and placebo group at any time.
Six months ago, I reviewed a report hypothesizing that severe hypothyroxinemia might be an independent cause of long-term neurodevelopmental deficits in premature infants.1,2 In my comment, I described the results of this retrospective analysis that identified a "potentially treatable cause of poor neurodevelopmental outcome of premature infants" as "exciting." I also called for appropriately designed, prospective therapeutic studies to investigate this further.
Van Wassenaer et al, from Amsterdam, conducted a placebo-controlled, double-blind trial of 200 infants born at less than 30 weeks who were randomized to receive either thyroid supplementation or placebo. The infants were studied with the Bayley Mental Development Index at six, 12, and 24 months. No differences were noted between treated and placebo groups.
This kind of study is being repeated by other groups in the United States, but this study suggests that thyroid supplementation does little more than increase the level of serum thyroxin in premature infants.
1. Ehrenkranz RA. Transient hypothyroxinemia in preterm infants associated with neurological defects at age two? Pediatr Adolesc Med Rep 1996;1:45-46.
2. Rucks ML, et al. The relation of transient hypothyroxinemia in preterm infants to neurological development at two years of age. N Engl J Med 1996;334:821-827.