EARLY IDENTIFICATION OF CONGENITAL HYPOTHYROID INFANTS WITH ABNORMALITIES IN PITUITARY SETPOINT FOR T-4-INDUCED TSH RELEASE

It is now clear that early detection and adequate replacement therapy of congenital hypothyroidism (CH) results in normal growth and psychom otor development. However, there is evidence that some of those infant s might have a persistent alteration in the T-4 feedback control of TS H release. To characterize further this phenomenon, 25 treated CH chil dren were divided into two groups: group A consisted of children whose TSH was suppressed as early as 1 month after the onset of therapy, an d group B consisted of children whose TSH suppression occurred much la ter. There were no differences in the etiology of CH, in the mean T-4 and T-3 Serum levels or in the mean LT(4) treatment dosage between the two groups. All children were clinically euthyroid throughout the fol low-up, developed according to expected norms and no deviations were n oted in bone age. However, serum TSH levels remained elevated in group B infants throughout the follow-up period (up to 14 years). Increase of LT(4) 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 T-4 control of TSH secretion and that these infa nts can be detected as early as 1 month after birth. Thus, serum T-4, T-3 levels and clinical progress are better guides to the adequacy of therapy than serum TSH concentrations in this group of CH infants.