The high response of TSH to the TRH is the first sign that is described in the impaired of the thyroid function, which is present with normal levels of thyroidal hormones (TH) and that is defined as subclinic hypothyroidism (ScH). There are some controversies about their ethiopathogenic mechanism, their related clinical aspects, response limit values of TSH to TRH, evolution and therapeutic conduct to be adopted. In order to try to bring some answers to these questions it was evaluated the behavior of 33 infants (CA 01·1.5y) 9 males and 24 females, hyperresponsives to the TRH test (30' cut-off level: 35 μUI/ml). Those patients were treated with LT4 (mean dose: 3.10 μg/kg/daily) in a variable period until obtaining the minimal age of 2 years old. The therapeutical support was stopped in 18 of 33 patients (54%) in order to evaluate persistence of ScH.

Material and Method: The patients analyzed where term infants and normal birth weight in 94% of the cases. It was registered the mother's background of thyroid pathology. It was determined at the beginning and in the intratreatment controls the SSD of Height (H) and growth velocity(GV) (Tanner), the relationship weigh/height (WFH%), bone age (Grewlich and Pyle), ecography and/or thyroidal scintigram with Tc99. Serum level of T4, T3, free T4 were measured by standard RIA: TSH by IRMA, TSH-TRH test (0, 30, 60 and 90' post 7 μg/kg of TRH IV). TSH-TRAB by inhibition of the linkage of125 I-TSH, and TPOAb and TGAb by direct radio assay. Evaluation of thyroid function and anti thydoideal antibodies in the mothers were made in subgroup of patients. The results were evaluated through descriptive statistics and tests t for paired samples.

Results: Two age groups, ≤0.5 year (n=15) and >0.5 years(n=18) were considered. In the first group 33% of the mothers registered background of thyroid pathology and 28% in the second group. Positive antithyroid antibodies were found (> 0.5 U/ml) in 18% of the infants. Comparing the variables considered in this study among the pre-treatment and the intratreatment last control we can point out: a significant increase of H(0.56 SSD, p= 0.00051), a significant lowering of TSH level (p= 0.0001), a significant increase of T4 (p= 0.0001) and free T4 (p= 0.005), without modification in T3 level.

After analyzing 18 patients who suspended medication, it was found a significant increase of TSH (p=0.00008), a significant lowering of T4(p=0.001) and of free T4 (p=0.0005) with respect to the intratreatment levels. Eleven children (61%) presented again a pathological response of TSH to the TRH test. Comparing this last group with the normal responsive children differences were not found in the set of analyzed variables that could predict their responses. However a significant difference was observed in the mean value of SSD of GV in the pre treatment control (p< 0.05).

Conclusions: Our results with a persistent hyperresponse of TSH to the TRH in 61% of the children as a probable expression of a ScH, although they do not allow to predict their subsequent evolution, are compared to those of the literature, suggesting a first stage of deficiency of TH, more than the consequence of maturity factors of hipothalamic hypofisary thyroid axis.

Although in this group of patients it was not measured oxygen consumption that permitted to establish their hypomethabolic condition and thus to determine on the potential benefits of the treatment, it was assumed a preventive therapeutic conduct with lower doses than those used in the clinical hypothyroidism. This conduct did not show adverse effects, modifying significantly clinical and laboratory parameters.