Introduction
	The history of congenital hypothyroidism includes a variety of nosologic terms including cretinism, endemic cretinism, goitrous cretinism, and sporadic cretinism. Iodine deficiency was found to be the major etiologic factor in endemic goiter, and the term endemic cretinism refers to the goitrous cretin in regions of endemic goiter. The first description of sporadic cretinism is attributed to Thomas Curling in 1850 to distinguish this entity from endemic cretinism. 1 The term congenital hypothyroidism (CH) now is used to classify any case of hypothyroidism present at birth. In industrialized nations without endemic iodine deficiency these infants represent sporadic CH. Until the 1970’s the prevalence, based on clinical phenotype data, was estimated at 1 in 5000 to 1 in 10,000 births. Untreated CH leads to growth deficiency, mental impairment, and metabolic alterations during childhood and adolescence. Normal brain and intellectual development are critically dependent on thyroid hormones during fetal development and the first 2–3 years of life, and any delay in treatment compromises eventual IQ. In 1957, Smith et al, in a review of treatment outcome in 51 children with more severe CH, reported that 10 of 22 patients treated before 7 months of age had a mean IQ over 90 whereas only 2 of 29 children treated later had an IQ above 90.2 Several subsequent reports confirmed the impact of delayed treatment and severity of hypothyroidism on eventual IQ. In 1972, Klein et al reported that 80% of children treated before 3 months had eventual IQ’s above 90 whereas only 45% of infants treated after 3 months had IQ’s above 90.3 Clearly, an approach to early diagnosis and treatment was needed.