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LONG‐TERM BROMOCRIPTINE THERAPY MAY RESTORE THE INHIBITORY CONTROL OF PROLACTIN RELEASE IN SOME PATIENTS WITH PATHOLOGICAL HYPERPROLACTINEMIA
Author(s) -
HO K. Y.,
SMYTHE G. A.,
COMPTON P. J.,
LAZARUS L.
Publication year - 1985
Publication title -
australian and new zealand journal of medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.596
H-Index - 70
eISSN - 1445-5994
pISSN - 0004-8291
DOI - 10.1111/j.1445-5994.1985.tb04009.x
Subject(s) - bromocriptine , metoclopramide , medicine , prolactin , basal (medicine) , thyrotropin releasing hormone , stimulation , endocrinology , pathological , hormone , insulin , vomiting
While bromocriptine is effective in controlling hyperprolactinemia, it is not known if bromocriptine therapy can restore the abnormal regulation of prolactin (PRL) release found in patients with pathological hyperprolactinemia. We report 15 hyperprolactinemic patients treated for a mean duration of 5.5 ± 0.6 years (mean ± SE) in whom stimulation tests to assess PRL control mechanisms [thyrotropin releasing hormone (TRH) and metoclopramide] were performed before and at least one month after withdrawal of bromocriptine therapy. The basal PRL level after withdrawal of bromocriptine therapy was significantly lower (p< 0.001) than that before therapy. All patients had blunted PRL stimulatory responses to TRH and metoclopramide (%D́16.0±5.6%) before treatment. After withdrawal of bromocriptine, PRL responses to stimulatory tests were significantly improved in seven patients (termed ‘responders’, %D́ 376 ±55%) but remained unchanged in eight patients (termed ‘non‐responders’, %D́ 9.2 ± 3.0%). Basal PRL levels were significantly lower (p<0.01) in responders (290 ±35 mlU/l) than in non‐responders (10360 ± 6790 mlU/l). Four of the responders have maintained normoprolactinemia and normal stimulated PRL responses for 15 months to three years following cessation of bromocriptine therapy and appear to be in remission. Favourable factors amongst the responders were the female sex, absence of a macroadenoma, and a pre‐treatment PRL level below 3000 mlU/l. PRL stimulation tests performed before therapy could not predict which patients would respond. No relationship was found between duration of therapy, or age at presentation, and improvement after bromocriptine. Our data demonstrate that the inhibitory control of PRL release can be restored in some patients with pathological hyperprolactinemia and suggest that the underlying hypothalamic‐pituitary defect responsible for the pathogenesis of pathological hyperprolactinemia may be corrected by bromocriptine therapy.