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Thirty‐eight congenitally hypothyroid children who were detected in a neonatal screening programme have been treated for a mean period of 3.8 years (range, 0.5 ‐ 8.5 years) by the maintenance of the free thyroxine index in the upper normal range as the main determinant of the dose of thyroxine. Only excessive elevation of, or serial rises in, thyroid stimulating hormone (TSH) level influenced the dose of thyroxine. This treatment strategy, which aims to avoid the potentially adverse effects of thyroxine overdosage, has often resulted in delayed return of TSH levels to normal, especially in athyrotic children (mean TSH ± SD at one year of age in athyrotic children, 72 ± 90 mU/L; in children with ectopic thyroid glands, 24 ± 16 mU/L; normal range, 0‐7 mU/L). The mean thyroxine dose of about 100 μg/m2did not change significantly with age, and is lower than the doses that are sometimes quoted in the literature; athyrotic children require significantly more thyroxine (P<0.05) than those with ectopic thyroid glands. Symptoms and signs of congenital hypothyroidism, although subtle, were significantly more common (P<0.05 for symptoms and P<0.001 for signs) in athyrotic children compared with those with ectopic glands. No physical or developmental abnormality related to congenital hypothyroidism has been demonstrated on follow‐up; mean height and weight percentiles approximate the 50th percentile at ages one to six years and mean developmental scores ± SD at about two years of age by the Griffiths Mental Development Scale and at 4.5‐6.5 years by the Wechsler Preschool and Primary Scale are 102.4 ± 10.4 and 111.2 ± 12.2, respectively. Long‐term follow‐up studies are necessary to exclude more subtle developmental and neurological abnormalities.

In a 12-month study, nine boys, aged 4.8–15.6 years, with bone ages 4.6–13 years, with moderate to severe chronic renal failure and resultant growth failure were treated with daily recombinant human growth hormone (rhGH), in conjunction with a strict low-protein/low-phosphate diet supplemented with keto and amino forms of the essential amino acids, histidine and additional energy. Improved growth had previously been observed with this dietary management over that obtained with conventional treatment for chronic renal failure. Each child had been on this diet for at least 2 years before rhGH was commenced. Mean height velocity increased from 4.6±1.3 to 9.0±1.3 cm/year (P<0.001) in the pre-pubertal group, and in the pubertal group from 5.4±1.4 to 10.4±1.8 cm/year (P<0.01). The mean height velocity standard deviation scores (SDSs) increased from -1.2±0.6 to +2.3±0.9 (P<0.001) in the pre-pubertal group and from -0.4±0.6 to +1.9±1.1 (P<0.01) in the pubertal group. Mean height SDS for chronological age increased from -2.2±0.7 to -1.5±0.5 (P<0.01) in the pre-pubertal group and from -1.9±0.7 to -1.3±0.9 in the pubertal group (P<0.02). There was no significant deterioration in renal function or renal bone disease, and bone age did not advance more than chronological age over the 12-month period.