Original Paper Horm Res 2003;59:85–90 DOI: 10.1159/000068576 Suppression of TSH in Congenital Hypothyroidism Is Significantly Related to Serum Levels and Dosage of Thyroxine J.J. Brown a V. Datta a A.J. Sutton b P.G.F. Sw ift a a Children’s Hospital, Leicester Royal Infirmary, Leicester, and b Department of Epidemiology and Public Health, University of Leicester, Leicester, UK Received: June 28, 2002 Accepted after revision: October 25, 2002 Dr. P.G.F. Swift Children’s Hospital Leicester Royal Infirmary Leicester LE1 5WW (UK) Tel. +44 116 254 1414, Fax +44 116 258 7637, E-Mail peterswift@webleicester.co.uk ABC Fax + 41 61 306 12 34 E-Mail karger@karger.ch www.karger.com © 2003 S. Karger AG, Basel 0301–0163/03/0592–0085$19.50/0 Accessible online at: www.karger.com/hre Key Words Congenital hypothyroidism, infants W Thyroxine serum levels W Thyrotropin suppression Abstract Aim: To assess thyrotropin (thyroid-stimulating hor- mone; TSH) suppression and serum thyroxine (T 4 ) con- centrations in infants with congenital hypothyroidism in relation to T 4 dose and pretreatment parameters. Meth- od: A retrospective study of all cases treated in a single centre since neonatal screening began was performed. Results: In 54 infants treated with a mean daily T 4 dose of 9.8 Ìg/kg, the TSH concentration was suppressed (! 6mU/l) in 65% of the cases by 6 months with the serum T 4 level at the upper end of the infant reference range. Infants who suppressed their TSH later did not dif- fer in pretreatment serum TSH or T 4 concentration. T 4 dose and serum T 4 level were lower in infants whose TSH was not suppressed. Conclusions: TSH suppression in congenital hypothyroidism is significantly related to serum levels and dosage of T 4 . We suggest that a delay in TSH suppression is mainly due to undertreatment. Copyright © 2003 S. Karger AG, Basel Introduction Thyroxine (T 4 ) plays an important role in brain devel- opment, the critical period being from fetal life to 36 months of age. Congenital hypothyroidism (CH) is a major cause of preventable mental handicap. Universal neonatal screening was introduced with the aim of detect- ing CH early, initiating treatment during the presymp- tomatic phase, obtaining a euthyroid state as soon as pos- sible, and normalizing intellectual and developmental outcomes. Many reports have confirmed improvement in outcome since the introduction of CH screening [1, 2]. However, aspects of treatment for CH remain contro- versial in the absence of evidence from randomized con- trolled trials [3–5]. There is a debate regarding what con- stitutes optimum treatment and whether optimum treat- ment can produce a normal developmental outcome. There is lack of agreement about the appropriate replace- ment dose of T 4 , levels of T 4 achieved, and how to best monitor the biochemical response. Relatively recent stud- ies [6, 7] have shown that early treatment (by 2 weeks of age) with higher doses of T 4 (10–15 vs. 6–8 Ìg/kg/day) may result in a normal developmental outcome. In monitoring the effects of T 4 replacement, a delay in thyrotropin (thyroid-stimulating hormone; TSH) suppres-