Prolactin and TSH response to TRH and metoclopramide before and after l-thyroxine therapy in subclinical hypothyroidism.
The effects of the dopamine (DA) receptor antagonist metoclopramide on the plasma thyroid stimulating hormone (TSH) and prolactin (PRL) levels were studied in 8 patients with subclinical hypothyroidism (defined as absence of clinical signs of hypothyroidism with normal thyroid hormone levels, normal or slightly increased basal plasma TSH levels and increased and long-lasting TSH response to TRH) before and after l-thyroxine replacement therapy. Metoclopramide induced a significant (p less than 0.01) TSH release in the subclinical hypothyroid patients. Two weeks after l-thyroxine replacement therapy (50 micrograms/day), the TSH response to metoclopramide was completely blunted in subclinical hypothyroidism. In these patients a significant (p less than 0.01) inhibition of TSH response to intravenous thyrotropin-releasing hormone (TRH) was also observed after treatment with thyroid hormone. In analogy to the TSH behavior, plasma PRL secretion in response to metoclopramide and TRH administration was significantly (p less than 0.05) inhibited in the subclinical hypothyroid patients after l-thyroxine replacement therapy.
D000328:Adult; D005260:Female; D006801:Humans; D007037:Hypothyroidism / Q000097:blood* / Q000188:drug therapy; D008297:Male; D008787:Metoclopramide; D008875:Middle Aged; D011388:Prolactin / Q000097:blood*; D013972:Thyrotropin / Q000097:blood*; D013973:Thyrotropin-Releasing Hormone; D013974:Thyroxine / Q000627:therapeutic use*
D013973:Thyrotropin-Releasing Hormone; D011388:Prolactin; D013972:Thyrotropin; D008787:Metoclopramide; D013974:Thyroxine