Publications

Abstract

Recent studies have suggested that patients with prolactinomas have a defect in the central regulation of prolactin (Prl) release but it is not clear whether the defect results from a true loss of hypothalamic dopamine activity or from a functional inability of inherent dopaminergic inhibition to be mediated effectively. We have studied this question by the use of monoiodtyrosine (MIT, 1 g orally), a specific inhibitor of central dopamine synthesis to remove dopaminergic inhibitory control of Prl release in 10 normal ovulating women, 8 women on oral contraceptive steroids (OC) and 8 patients with pathological hyperprolactinaemia (PHP). LH, TSH and GH were also measured during the study in view of recent reports suggesting that dopaminergic mechanisms may be involved in modulating their secretion. Subjects on OC had a significantly higher (P less than 0.05) mean basal Prl (353 +/- 34 vs 280 +/- 26 mIU/l) and a significantly greater (P less than 0.05) peak response (incremental change 2270 +/- 300 mIU/l to MIT than normal controls (1320 +/- 220 mIU/l). Patients with PHP had a highly significantly blunted (P less than 0.001). Prl response (incremental chane 290 +/- 95 mIU/l) compared to controls. MIT administration caused a significant increase in LH (P less than 0.05), TSH (P less than 0.01) and GH (P less than 0.01) in patients with PHP but not in normal or OC-treated subjects. The augmented Prl response of subjects on OC is consistent with an increase in dopaminergic inhibitory control of Prl release. The lack of Prl response in subjects with PHP is indicative of a functional loss of dopaminergic control.(ABSTRACT TRUNCATED AT 250 WORDS)