Scattered case reports have described patients who have been diagnosed with both primary hyperaldosteronism and prolactinoma. Prolactin receptor (PRLR) is known to be expressed in human adrenal cortex. Furthermore, PRLR mRNA and protein have both been detected in human adrenal tumors. It has also been shown that PRL treatment of adrenal cells is capable of stimulating aldosterone secretion. The contribution of PRL to the development of hyperaldosteronism is unkown. We hypothesize that a subset of adrenal adenomas may be stimulated to produce aldosterone due to elevated PRL sensitivity which occurs via increased PRLR expression. To begin to assess this, we identified a well-defined group of patients with aldosterone-producing adenomas. Tissue samples from adrenal adenomas as well as adjacent normal adrenal tissue were collected from 12 patients (six males and six females). A real-time RT qPCR assay was used to quantify the expression of PRLR mRNA in these samples. We found high PRLR mRNA expression in both tumors and normal adrenal tissue from APA patients. Strikingly, PRLR mRNA expression was higher than the reference gene, hypoxanthineguanine phosphoribosyltransferase. There was no significant difference in PRLR mRNA expression between tumors and healthy adrenal tissue. In conclusion, we have no indication that expression of PRLR mRNA is upregulated in aldosterone-producing adrenal adenomas relative to non-tumoral adrenal tissue in APA patients. Further work is necessary to better understand the interplay between pituitary hormones and adrenal function and disease.
03 - 07 May 2014
European Society of Endocrinology