The introduction of neonatal screening programmes for congenital hypothyroidism in the 1970s is now regarded as a highly cost effective strategy to detect the commonest congenital metabolic disorder seen in the newborn (1 in around 4000 births).¹ There is no doubt that early diagnosis and treatment of the condition has led to the disappearance of mental retardation, which was the most dramatic long term sequel of congenital hypothyroidism.² However, it has been clearly recognised that persistent selective impairments may still occur in these children, such as language delays, minor motor problems, visuospatial defects, and attention problems.³ Also, postnatal somatic abnormalities including an accelerated cranial growth⁴ and delayed bone age⁵ to 3 years have been observed, especially in children given high starting doses of levothyroxine. Initially, starting doses of thyroxine were in the range of 8–10 μg/kg/day,⁶ but the dose was later revised upwards to 10–16 μg/kg/day.⁷ There is clearly a need to define the optimal dose of T4 to initiate therapy as well as the desirable levels of serum T4 to be achieved during long term therapy.

This subject was recently discussed by Rovet, …