ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2019) 63 P111 | DOI: 10.1530/endoabs.63.P111

The coincidence of primary hyperparathyroidism and primary hyperaldosteronism is not infrequent: a retrospective case analysis

Elvira Barrio1, Elvira Ramos1, Irene Crespo2, Raquel Pallarés1, Mario Pazos1, Paz de Miguel1, Martín Cuesta1, María José Torrejón1, Alfonso Calle1 & Isabelle Runkle1


1Hospital Clínico San Carlos, Madrid, Spain; 2Hospital Central de la Defensa Gómez Ulla, Madrid, Spain.


Introduction: Primary hyperparathyroidism (PHP) has been postulated to be a cause of primary hyperaldosteronism (PHA). In fact, PTH receptors have been detected in aldosteronoma tissue. Hyperaldosteronism can also induce elevation of PTH levels, as increased circulating volume increases calciuria, with secondary elevation of PTH levels as serum calcium levels rise. We studied the prevalence of PHP in a group of patients diagnosed with PHA either following or simultaneously with diagnosis of PHP.

Methods: A retrospective study was performed. In a single Endocrine outpatient clinic of a general hospital, 46 patients were diagnosed as having PHA over a 6-year period (2010–2016), with strict application of the Endocrine Society 2008/2016 guidelines. The 25 mg captopril test was considered diagnostic when either the 2-hour aldosterone level was ≥130 pg/ml and/or the 2-hour aldosterone/renin ratio (ARR) was ≥50. Patient histories were reviewed to detect cases in which PHP had been diagnosed prior to or simultaneously with PHA. We describe the characteristics of the patients presenting PHP. Direct renin and serum aldosterone were measured by RIA and expressed in pg/ml.

Results: 10/46 (21.7%) patients were diagnosed as having both PHA and PHP. 7/10 were females. The mean age was 64.3 (SD 14.3). PHP was secondary to a parathyroid adenoma in 4/10 patients and secondary to hyperplasia in 3/10. In another 3/10 patients PHP responded to vitamin D therapy and localization tests were not undertaken. Adrenal vein sampling (AVS) was performed in 7/10 patients. 2/7 presented unilateral aldosterone secretion, whereas 5/7 presented bilateral secretion (Table 1). No correlation was found between maximum calcium levels and corresponding PTH values on the one hand, and basal or 2-hour post-captopril aldosteronemias on the other hand.

Table 1 Calcium, PTH, vitamin D, and serum aldosterone values in patients with PHP and PHA.
Maximum calcium (mg/dl)PTH (pg/ml)25-OH Vitamin D (ng/ml)Basal (pre-captopril) serum aldosterone (pg/mL)2-hour post-captopril serum aldosterone (pg/mL)
11,39 (SD 0.74)122 [IQR 74-197]21.4 (SD 13.2)197.5 [IQR 169-293]211 [IQR 201-352]

Conclusions: The coincidence of primary hyperparathyroidism and primary hyperaldosteronism is not infrequent, affecting over 20% of our primary hyperaldosteronism patients. Although hyperparathyroidism has been postulated to induce an aldosterone-secreting adrenal adenoma, in our small series of patients with primary hyperparathyroidism, primary hyperaldosteronism was found to be due more often to bilateral aldosterone secretion, as indicated by AVS. The relationship between the two entities has yet to be elucidated.