We studied the effect of Somatostatin on the pituitary-thyroid axis of 37 volunteer subjects. 17 were euthyroid, 12 hypothyroid, 7 hyperthyroid and one had a TSH secreting pituitary adenoma. We measured by radioimmunoassay plasma iodothyronines T4, T3, rT3, FT4 and FT3, as well as TSH in basal conditions and after TRH stimulation. Somatostatin (as an initial bolus of 250 micrograms i.v. followed by an infusion of 500 micrograms/h) was given in short-term infusion (3 h) or long-term infusion (12 h). The results obtained showed that during short-term infusion Somatostatin: does not influence TSH in normal subjects; reduces significantly basal TSH in hypothyroid patients; reduces significantly the TSH response to TRH both in normal and in hypothyroid subjects as well as in the case with a TSH secreting pituitary adenoma. During long-term infusion Somatostatin: does not change TSH levels in normal or hyperthyroid subjects; does not change the values of T4, FT4, T3, FT3 and rT3 in normal subjects; does not change the values of T4 and FT4 in hyperthyroid subjects but reduces significantly the values of T3 and FT3 and produces a marked rise in rT3 in the same ones. In conclusion, the inhibiting effect of exogenous Somatostatin is evident whenever TSH levels are high for pathological conditions or for drug stimulation. The findings of T3 and FT3 reduction with a marked rise in rT3 in hyperthyroid subjects during the long infusion indicate an extrathyroidal effect of Somatostatin on the peripheral metabolism of iodothyronines.
De Rosa, G., Corsello, S. M., Della Casa, S., De Rosa, E., Raimondo, S., Effect of somatostatin on the pituitary-thyroid axis, <<ANNALES D'ENDOCRINOLOGIE>>, 1983; 44 (6): 355-360 [http://hdl.handle.net/10807/10731]
Effect of somatostatin on the pituitary-thyroid axis
De Rosa, Giovina;Corsello, Salvatore Maria;Della Casa, Silvia;De Rosa, Emilia;
1983
Abstract
We studied the effect of Somatostatin on the pituitary-thyroid axis of 37 volunteer subjects. 17 were euthyroid, 12 hypothyroid, 7 hyperthyroid and one had a TSH secreting pituitary adenoma. We measured by radioimmunoassay plasma iodothyronines T4, T3, rT3, FT4 and FT3, as well as TSH in basal conditions and after TRH stimulation. Somatostatin (as an initial bolus of 250 micrograms i.v. followed by an infusion of 500 micrograms/h) was given in short-term infusion (3 h) or long-term infusion (12 h). The results obtained showed that during short-term infusion Somatostatin: does not influence TSH in normal subjects; reduces significantly basal TSH in hypothyroid patients; reduces significantly the TSH response to TRH both in normal and in hypothyroid subjects as well as in the case with a TSH secreting pituitary adenoma. During long-term infusion Somatostatin: does not change TSH levels in normal or hyperthyroid subjects; does not change the values of T4, FT4, T3, FT3 and rT3 in normal subjects; does not change the values of T4 and FT4 in hyperthyroid subjects but reduces significantly the values of T3 and FT3 and produces a marked rise in rT3 in the same ones. In conclusion, the inhibiting effect of exogenous Somatostatin is evident whenever TSH levels are high for pathological conditions or for drug stimulation. The findings of T3 and FT3 reduction with a marked rise in rT3 in hyperthyroid subjects during the long infusion indicate an extrathyroidal effect of Somatostatin on the peripheral metabolism of iodothyronines.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.