Endocrinological study of the dopaminergic regulation of prolactin releasein metastatic breast cancer

Citation
M. Mandala et al., Endocrinological study of the dopaminergic regulation of prolactin releasein metastatic breast cancer, TUMORI, 85(6), 1999, pp. 494-497
Citations number
12
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
TUMORI
ISSN journal
03008916 → ACNP
Volume
85
Issue
6
Year of publication
1999
Pages
494 - 497
Database
ISI
SICI code
0300-8916(199911/12)85:6<494:ESOTDR>2.0.ZU;2-N
Abstract
Aims and background: Prolactin (PRL) may be a growth factor for breast canc er. Abnormally high levels of PRL have been proven to be associated with a poor prognosis in metastatic breast cancer. However, most studies have been limited to the evaluation of basal levels of PRL rather than its response to the classical endocrine dynamic tests. This study was performed to analy se the dynamic secretion of PRL under stimulatory and inhibitory tests in m etastatic breast cancer. Methods: The study included 10 untreated metastatic breast cancer women, wh o were evaluated after the classical stimulatory and inhibitory tests for P RL secretion with the antidopaminergic agent Metoclopramide (10 mg iv as a bolus) and with L-dopa, respectively. Serum levels of PRL were measured by RIA before and at subsequent intervals after drug administration. PRL level s were considered to be elevated when they were higher than 25 ng/ml. Results: Abnormally high basal levels of PRL were seen in 6/10 patients. L- dopa was unable to inhibit PRL secretion, whose mean concentrations paradox ically significantly increased in response to L-dopa, with values comparabl e to those observed after the classical stimulatory test with metoclopramid e. Conclusions: This study confirm the existence of hyperprolactinemia associa ted with metastatic breast cancer. In addition, by showing a paradoxical ri se of PRL in response to L-dopa, which inhibits PRL secretion in physiologi cal conditions, this study would suggest that breast cancer-related hyperpr olactinemia may depend at least in part on endogenous disease-related neuro endocrine alterations.