Paradoxical stimulation of prolactin secretion by L-dopa in metastatic prostate cancer and its possible role in prostate-cancer-related hyperprolactinemia

• Published in: European urology Vol. 37; no. 5; p. 569
• Main Authors: Lissoni, P, Mandalà, M, Rovelli, F, Casu, M, Rocco, F, Tancini, G, Scardino, E
• Format: Journal Article
• Language: English
• Published: Switzerland 01-05-2000
• Subjects: Aged; Humans; Hyperprolactinemia - etiology; Levodopa - pharmacology; Male; Metoclopramide - pharmacology; Middle Aged; Neoplasm Metastasis; Prolactin - drug effects; Prolactin - secretion; Prostatic Neoplasms - complications
• ISSN: 0302-2838
• DOI: 10.1159/000020194

In addition to sex steroids, prolactin (PRL) may also stimulate prostate cancer growth. Abnormally high blood levels of PRL have been noted in metastatic prostate cancer patients. However, most studies have been limited to the evaluation of basal levels of PRL rather than to investigate its secretion in response to classical endocrine dynamic tests. This study was carried out to analyze PRL secretion in metastatic prostate cancer patients both at basal conditions and in response to L-Dopa and metoclopramide, which represents the most classical inhibitory and stimulatory tests for PRL secretion, respectively.
The study included 12 patients with metastatic prostate cancer. On separate occasions, PRL secretion was evaluated in response to L-Dopa (500 mg orally) and to metoclopramide (10 mg i.v. as a bolus). Serum levels of PRL were measured by RIA.
Mean PRL concentrations significantly increased after metoclopramide administration, even though no PRL response occurred in 6 of 12 patients. L-Dopa was unable to reduce PRL levels, which, in contrast, paradoxically significantly increased in response to L-Dopa, with mean values comparable to those achieved after metoclopramide injection.
By showing a paradoxical stimulatory effect of L-Dopa on PRL secretion and a lack of response to metoclopramide in some patients, this study would suggest the existence of evident alterations in the neuroendocrine regulation of PRL release in advanced prostate cancer.