This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via Google Scholar Google Scholar Articles by HO, K. Y. Articles by LAZARUS, L. Search for Related Content PubMed PubMed Citation Articles by HO, K. Y. Articles by LAZARUS, L.

Dopamine Infusion Studies in Patients with Pathological Hyperprolactinemia: Evidence of Normal Prolactin Suppressibility but Abnormal Dopamine Metabolism

Garvan Institute of Medical Research St. Vincent's Hospital Sydney 2010, New South Wales, Australia

The cause of pathological hyperprolactinemia (PHP) is not known, although it has beenpostulated that lactotroph refractoriness to dopamine (DA) is an important factor. We, therefore, studied PRL suppressibility in response to iv DA administered in a dose designed to achieve peripheral plasma DA concentrations in the range reported in rat pituitary portal plasma. Nine normal subjects and 14 patients (8 with probable microadenomas and 6 with macroadenomas) with PHP were studied during a 4-h infusion of 0.5 g/kg min DA. Serum PRL levels decreased in normal subjectsto 18 ± 3% (mean ± SEM) of initial basal levels, not significantly different from the fall to 22 ± 2% of basal levels found in patients with PHP. Maximal PRL suppression in patientswith probable microad-enomas (21 ± 2%) was not significantly different from that in those with macroadenomas (22.8 ± 2.0%). Upon cessation of DA infusion, there was a rapid rebound in PRL release, which wassignificantly greater (P < 0.05) in patients (155 ± 15%) than in normal subjects (118 ± 13%).

Plasma DA levels were measured by gas chromatography/ mass spectroscopy and were significantly higher (P < 0.05) in patients than in normal subjects during the infusion. The MCR for DA in normal subjects (12.5 ± 2.8 liters/kg-h) was significantly greater (P < 0.005) than thatinpatients (6.2 ± 0.5 liters/ kg-h).

The data show that the release of PRL in patients with PHP i s not refractory to physiological concentrations of DA, but that there is an abnormality of peripheral DA metabolism in these patients.We conclude that the development of PHP is unlikely to be due to insensitivity of lactotrophs to endogenous DA and that patients with PHP have a systemic disturbance of DA metabolism.

^* To whom requests for reprints should be addressed.

Received May 6, 1983.