• Shiho Nomura, Hitoshi Ikegami, Hiroshi Wada, Hiroshi Tamai, Masahisa Funato, and Haruo Shintaku.
• Osaka City Med J. 2014 Jun 1; 60 (1): 29-37.

BackgroundPreterm infants show transient hypothyroxinemia without thyroid-stimulating hormone (TSH) elevation. In addition, the degree of neurodevelopmental delay in preterm infants become severe according to the decreasing gestational age (GA). Because of the crucial role of thyroid hormones in brain development, hypothyroxinemia has the potential to cause developmental delay; however, the effectiveness of thyroxine (T4) supplementation on developmental outcomes remains controversial. To resolve these issues, we evaluated the clinical course of transient hypothyroxinemia and the effects of levothyroxine (LT4) supplementation in extremely low birth weight (ELBW) infants.MethodsSerum levels of free T4 (FT4) and TSH were examined in 36 ELBW infants from 7 days after birth. LT4 (5-10 microg/kg/day) was orally administered to 18 of 36 infants with a low serum FT4 level (< 0.4 ng/dL) or normal serum FT4 levels and a clinical manifestation of hypothyroidism, whereas remaining 18 patients without a low serum FT4 level or clinical hypothyroidism were not given LT4 supplementation as control subjects. Infants were followed-up at a corrected age of 12 months, and clinical outcome was compared between infants that received LT4 and those that did not.ResultsELBW infants showed low serum FT4 levels without TSH elevation. During hospitalization and at follow-up, LT4-administered infants with low serum FT4 levels showed a shorter GA compared with the control group. There were no other statistically significant differences in clinical outcomes at 12 months of corrected age between LT4-administered and control groups.ConclusionsOur results show that shorter GA is associated with lower serum FT4 levels. Shorter GA is known to cause developmental delay, however, LT4 supplementation prevents the developmental delay of ELBW infants with transient hypothyroxinemia.

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