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Abstract:
Context: Coexisting prolactinoma-primary aldosteronism (PA) is
infrequently reported.
Objective: The objective of the study was to identify patients with
prolactinoma-PA and test the hypothesis that elevated prolactin (PRL)
concentrations play a role in PA pathogenesis.
Setting and Design: Hyperprolactinemia/prolactinoma was diagnosed in PA
patients from two referral centers (Munich, Germany, and Turin, Italy)
and in essential hypertensive (EH) patients from one center (Turin). PRL
receptor (PRLR) gene expression was determined by microarrays on
aldosterone-producing adenomas and normal adrenals and validated by
real-time PCR. H295R adrenal cells were incubated with 100 nM PRL, and
gene expression levels were determined by real-time PCR and aldosterone
production was quantified.
Results: Seven patients with prolacti noma-PA were identified: four of
584 and three of 442 patients from the Munich and Turin PA cohorts,
respectively. A disproportionate number presented with
macroprolactinomas (five of seven). There were five cases of
hyperprolactinemia with no cases of macroprolactinoma of 14 790 patients
in a general EH cohort. In a population of PA patients case-control
matched 1:3 with EH patients there were two cases of hyperprolactinemia
of 270 PA patients and no cases in the EH cohort (n = 810). PRLR gene
expression was significantly upregulated in the aldosterone-producing
adenomas compared with normal adrenals (1.7-fold and 1.5-fold by
microarray and real-time PCR, respectively). In H295R cells, PRL
treatment resulted in 1.3-fold increases in CYP11.82 expression and
aldosterone production.
Conclusion: Elevated PRL caused by systemic hyperprolactinemia may
contribute to the development of PA in those cases in which the two
entities coexist.
