Effect of chronic endogenous hypercalcemia on prolactin and thyrotropin responsiveness in man.
To investigate whether chronic endogenous hypercalcemia influences TSH and/or PRL release from pituitary thyrotrophs and lactotrophs in man, 10 patients with endogenous hypercalcemia, due either to cancer or to primary hyperparathyroidism, were injected with 25 micrograms TRH iv. The TSH and PRL responses were compared with those obtained in an age-, sex-, and weight-matched group of patients comprised of 10 normocalcemic individuals with other diseases. The mean maximal TSH response in the hypercalcemic group (3.7 +/- 0.4 microU/ml) was 46% lower than in the normocalcemic group (6.8 +/- 1.2 microU/ml; p less than 0.02). Similarly, the mean maximal PRL response was 45% lower in the hypercalcemic (31 +/- 5 ng/ml) than in the normocalcemic patients (57 +/- 9 ng/ml; p less than 0.05). Feasible mechanisms behind this inhibitory influence of chronic endogenous hypercalcemia on TSH and PRL responsiveness are discussed.
D000328:Adult; D000368:Aged; D005260:Female; D006801:Humans; D006934:Hypercalcemia / Q000097:blood / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011388:Prolactin / Q000097:blood*; D013972:Thyrotropin / Q000097:blood*; D013973:Thyrotropin-Releasing Hormone; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
D014284:Triiodothyronine; D013973:Thyrotropin-Releasing Hormone; D011388:Prolactin; D013972:Thyrotropin; D013974:Thyroxine