Decreased prolactin responsiveness to thyrotrophin-releasing hormone and metoclopramide in hyperthyroidism
Abstract. To investigate whether prolactin (Prl) responsiveness to thyrotrophin-releasing hormone (TRH) differs in thyrotoxic and normal individuals, serum Prl was determined before and after iv injection of 200 μg TRH in 10 patients with untreated thyrotoxicosis and also in 9 normal subjects. Both the maximal Prl increment after TRH and the total Prl response, represented by the Prl incremental area, were significantly larger in the normal subjects compared with the thyrotoxic (max Prl increment 56 ± 11 vs 15 ± 3 ng/ml, P< 0.001; Prl incremental area 3071 ± 522 vs 579 ± 171, P <0.001; mean ± sem). The maximal Prl increase after 15 mg oral metoclopramide (MET) was also significantly larger in the normal (125 ± 13 ng/ml) than in the thyrotoxic subjects (60 ± 13 ng/ml, P < 0.01). When 200 μg TRH was injected iv 90 min after oral administration of 15 mg MET, an additional Prl increase was observed in normal individuals (21 ±6 ng/ml, P < 0.01). In thyrotoxic patients, however, iv TRH failed to induce a significant increase in Prl after oral priming with MET (0 ± 3 ng/ml). When 7 thyrotoxic patients, made euthyroid by 125I-treatment, were investigated according to the same protocol as the one mentioned above, they displayed normal Prl responses to iv TRH and to oral MET. Furthermore, they showed a significant Prl response to iv TRH after oral priming with MET (20 ± 8 ng/ml, P < 0.05). These findings imply that pituitary lactotrophs of untreated thyrotoxic patients might have cytoplasmic membranes with decreased permeability to Prl and/or reduced stores of releasable Prl which return to normal after oral 125I-therapy.