Hyperprolactinemia Is Associated with Reproducible Rise in Serum DHEA-S Levels: The Important Role of Intact HPA Function

Presentation Number: SAT 407
Date of Presentation: April 1st, 2017

Yosra Moria*, Ribal Alaridi, Nadine El Asmar and Baha M Arafah
UH Cleveland Medical Center/Case Western Reserve University, Cleveland, OH

Abstract

Introduction: DHEA and its sulfated ester DHEA-S are ACTH-dependent adrenal androgens that are increasingly utilized as markers of HPA functional integrity1. In patients with adrenal insufficiency, loss of adrenal androgens precede the decrease in glucocorticoid secretion1,2 and hence, it has been stated that a normal serum DHEA-S makes the diagnosis of adrenal insufficiency unlikely. Published data suggest that PRL modulates DHEA/DHEA-S secretion.

IN this study, we examined changes in serum DHEA-S in patients with prolactinomas who had normal HPA function and others with impaired function before and after medical therapy with dopamine agonist.

Methods: We included 30 patients (20-60 years of age; 34±10.2) with prolactinomas who had normal HPA function (23F / 7M) as well as 5 males (51 ± 15.1 years of age) with prolactinomas and impaired HPA function (Am cortisol of 2.3 ±1.9 ug/dL). Serum levels of cortisol, PRL and DHEA-S were measured repeatedly after dopamine agonist therapy. None of the 30 patients were known to have other illnesses or were taking medications known to influence PRL levels or adrenal function. Patients with impaired HPA function had other pituitary hormone deficits whereas those with normal HPA function had only gonadal dysfunction.

Results:  In all patients with normal HPA function serum PRL levels decreased gradually from a baseline of 421.8±859 to 30.8±40.3 at 3-6 months (P<0.01) and to 12.2±12.8 ug/L at 12 months (P<0.01). Concurrently, their serum DHEA-S levels decreased from 231.8±191.9 to 170.2±137 at 3-6 months (P<0.001) and to 119.1±61 ug/dL at 12 months (P<0.001). Even though the decline in mean PRL concentration between 3-6 and 12 months was modest (from 30.8 to 12. 2 ug/L) and of borderline significance (P=0.06) it was still associated with significant (P<0.04) decrease in respective DHEA-S levels. Discontinuation of therapy in some patients was associated with a rise in serum PRL and a parallel increase in DHEA-S levels. Although younger patients had higher serum DHEA-S levels, the aforementioned parallel changes in PRL and DHEA-S levels were observed in all patients irrespective of their age. However, despite marked elevation in serum PRL 374±196 ug/L in patients with impaired HPA function, the respective serum DHEA-S levels remained very low (28.4±24 ug/dL).

Conclusion: The data indicate that hyperprolactinemia results in elevation of serum DHEA-S levels that decrease with medical therapy. However, despite markedly elevated serum PRL levels, patients with impaired HPA function had low serum DHEA-S concentrations that remained as low when PRL levels were lowered with dopamine agonists. This indicates that the modulating influence of PRL on serum DHEA-S levels requires normal ACTH secretion. Thus, a normal age and gender adjusted serum DHEA-S level implies normal HPA function even in patients with hyperprolactinemia.

 

Nothing to Disclose: YM, RA, NE, BMA