Hyperparathyroidism in Patients with Primary Aldosteronism: Cross-Sectional and Interventional Data from the GECOH Study

Author:

Pilz Stefan12,Kienreich Katharina1,Drechsler Christiane3,Ritz Eberhard4,Fahrleitner-Pammer Astrid1,Gaksch Martin1,Meinitzer Andreas5,März Winfried567,Pieber Thomas R.1,Tomaschitz Andreas1

Affiliation:

1. Department of Internal Medicine (S.P., K.K., A.F.-P., M.G., T.R.P., A.T.), 8036 Graz, Austria

2. Department of Epidemiology and Biostatistics and EMGO Institute for Health and Care Research (S.P.), VU University Medical Center, 1081 BT Amsterdam, The Netherlands

3. Department of Medicine (C.D.), Division of Nephrology, University of Würzburg, 97070 Würzburg, Germany

4. Department of Medicine (E.R.), Division of Nephrology, University Hospital Heidelberg, 69115 Heidelberg, Germany

5. Division of Endocrinology and Metabolism, and Clinical Institute of Medical and Chemical Laboratory Diagnostics (A.M., W.M.), Medical University of Graz, 8036 Graz, Austria

6. Synlab-Academy (W.M.), Synlab Services LLC, 69214 Eppelheim, Germany

7. Mannheim Institute of Public Health (W.M.), Medical Faculty Mannheim, Ruperto Carola University Heidelberg, 68167 Mannheim, Germany

Abstract

Context: Experimental studies suggest that aldosterone induces hypercalciuria and might contribute to hyperparathyroidism. Objective: We aimed to test for differences in PTH levels and parameters of calcium and vitamin D metabolism in patients with primary aldosteronism (PA) compared with patients with essential hypertension (EH) and to evaluate the impact of PA treatment on these laboratory values. Design, Setting, and Participants: The Graz Endocrine Causes of Hypertension study includes hypertensive patients referred for screening for endocrine hypertension at a tertiary care center in Graz, Austria. Main Outcome Measures: Differences in PTH levels between patients with PA and EH. Results: Among 192 patients, we identified 10 patients with PA and 182 with EH. PTH levels (mean ± sd in picograms per milliliter) were significantly higher in PA patients compared with EH (67.8 ± 26.9 vs. 46.5 ± 20.9; P = 0.002). After treatment of PA with either adrenal surgery (n = 5) or mineralocorticoid receptor antagonists (n = 5), PTH concentrations decreased to 43.9 ± 14.9 (P = 0.023). Serum 25-hydroxyvitamin D concentrations were similar in both groups. Compared with EH, serum calcium concentrations were significantly lower (2.35 ± 0.10 vs. 2.26 ± 0.10 mmol/liter; P = 0.013), and there was a nonsignificant trend toward an increased spot urine calcium to creatinine ratio in PA [median (interquartile range) 0.19 (0.11–0.31) vs. 0.33 (0.12–0.53); P = 0.094]. Conclusions: Our results suggest that PA contributes to secondary hyperparathyroidism. Further studies are warranted to evaluate whether PTH has implications for PA diagnostics and whether mineralocorticoid receptor antagonists have a general impact on PTH and calcium metabolism.

Publisher

The Endocrine Society

Subject

Biochemistry (medical),Clinical Biochemistry,Endocrinology,Biochemistry,Endocrinology, Diabetes and Metabolism

Reference21 articles.

1. Evidence for an increased rate of cardiovascular events in patients with primary aldosteronism.;Milliez,2005

2. Calcium paradox of aldosteronism and the role of the parathyroid glands.;Vidal;Am J Physiol Heart Circ Physiol,2006

3. Hyperparathyroidism and the calcium paradox of aldosteronism.;Chhokar;Circulation,2005

4. Effect of chronic mineralocorticoid administration on calcium excretion in the rat.;Suki;Am J Physiol,1968

5. Aldosterone and parathyroid hormone: a complex and clinically relevant relationship.;Pilz;Calcif Tissue Int,2010

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