Early identification of congenital hypothyroid infants with abnormalities in pituitary setpoint for T₄-induced TSH release

It is now clear that early detection and adequate replacement therapy of congenital hypothyroidism (CH) results in normal growth and psychomotor development. However, there is evidence that some of those infants might have a persistent alteration in the T₄ feedback control of TSH release. To characterize further this phenomenon, 25 treated CH children were divided into two groups: group A consisted of children whose TSH was suppressed as early as 1 month after the onset of therapy, and group B consisted of children whose TSH suppression occurred much later. There were no differences in the etiology of CH, in the mean T₄ and T₃ serum levels or in the mean LT₄ treatment dosage between the two groups. All children were clinically euthyroid throughout the follow-up, developed according to expected norms and no deviations were noted in bone age. However, serum TSH levels remained elevated in group B infants throughout the follow-up period (up to 14 years). Increase of LT₄ treatment dosage resulted in TSH suppression in both groups. However, the TSH levels obtained in group B were still higher compared to group A. These results suggest that some CH infants might have an abnormal setpoint for T₄ control of TSH secretion and that these infants can be detected as early as 1 month after birth. Thus, serum T₄, T₃ levels and clinical progress are better guides to the adequacy of therapy than serum TSH concentrations in this group of CH infants.