Effect of acute hypercalcemia on thyrotropin (TSH) and triiodothyronine responses to TSH-releasing hormone in man.

In chronic hypercalcemia, basal TSH has been found to be low, with normal serum circulating concentrations of T3 and T4. This observation suggested a potentiation by hypercalcemia of the thyroid secretory response to TSH. The present study was undertaken to assess the possible influence of hypercalcemia on the T3 secretory response to TSH. Since T3 secretion was studied after stimulation of endogenous TSH by TRH, it was first necessary to find a protocol enabling us to study the effect of calcium on T3 release without affecting TSH secretion. Eighteen subjects underwent two TRH tests, with and without simultaneous calcium infusion, at 2-week interval and in a randomized order. In group A (five subjects) calcium infusion started 1 min after TRH, in group B (five subjects) 10 min after TRH, and in group C (eight subjects) 20 min after TRH. In groups A and B, TSH secretion was markedly blunted by hypercalcemia. In contrast, when calcium infusion was started 20 min after TRH (group C), the TSH secretion profile was no longer different from that in the control study. However, in this situation the increments of T3 and free T3 120 and 180 min after TRH were significantly higher when the subjects were rendered hypercalcemic than in the control study. These findings suggest that calcium might act at two different levels, to enhance the thyroid secretory response to TSH and decrease TSH secretion by acting directly on the pituitary gland. Both effects would produce the association of low serum TSH and normal levels of T3 and T4 observed in chronic hypercalcemia.