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The TSH response to domperidone reflects the biological activity of prolactin in macroprolactinaemia and hyperprolactinaemia
Author(s) -
Pinto L. P.,
Hanna F. W. F.,
Evans L. M.,
Davies J. S.,
John R.,
Scanlon M. F.
Publication year - 2003
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1046/j.1365-2265.2003.01887.x
Subject(s) - hyperprolactinaemia , domperidone , medicine , endocrinology , dopaminergic , prolactin , dopamine , prolactinoma , hormone
Summary objective To test the hypothesis that patients with hyperprolactinaemia due to biologically inactive macroprolactin will not show the characteristically increased dopaminergic inhibition of TSH release seen in patients with microprolactinomas secreting biologically active monomeric PRL. design Comparison of the TSH and PRL responses to dopamine antagonism with domperidone (10 mg i.v.) in patients with hyperprolactinaemia due to macroprolactinaemia or microprolactinomas. patients Twenty‐two patients referred for the investigation of their hyperprolactinaemia were studied: 11 patients with macroprolactinaemia and 11 patients with hyperprolactinaemia due to microprolactinoma. measurements TSH and PRL levels were measured at baseline and 30 min following domperidone in both groups. results Patients with macroprolactinaemia showed normal TSH and PRL responses to dopamine antagonism whereas patients with microprolactinomas showed exaggerated TSH responses and reduced PRL responses. Although there was considerable overlap between the PRL responses in the two groups, there was very clear separation between the PRL/TSH response ratios (normal > 1·0) of 4·0 ± 1·8 for the macroprolactinaemia group and 0·4 ± 0·2 for the microprolactinoma group ( P < 0·0001). conclusions These data support the hypothesis that elevated circulating levels of macroprolactin, as opposed to biologically active monomeric PRL, do not exert increased positive feedback on the hypothalamic dopaminergic inhibition of TSH release.