Abstract
ContextPrimary aldosteronism (PA) is the most frequent form of endocrine hypertension. Besides its deleterious impact on cardiovascular target organ damage, PA is considered to cause osteoporosis.Patients and methodsWe assessed bone turnover in a subset of 36 postmenopausal women with PA. 18 patients had unilateral PA and were treated by adrenalectomy, whereas 18 patients had bilateral PA and received mineralocorticoid receptor antagonist (MRA) therapy respectively. 18 age- and BMI-matched females served as controls. To estimate bone remodeling, we measured the bone turnover markers intact procollagen 1 N-terminal propeptide, bone alkaline phosphatase, osteocalcin and tartrate resistant acid phosphatase 5b in plasma by chemiluminescent immunoassays at time of diagnosis and one year after initiation of treatment.Study designObservational longitudinal cohort study.SettingTertiary care hospital.ResultsCompared with controls, patients with PA had mildly elevated osteocalcin at baseline (p = 0.013), while the other bone markers were comparable between both groups. There were no differences between the unilateral and the bilateral PA subgroup. One year after initiation of MRA treatment with spironolactone bone resorption and bone formation markers had significantly decreased in patients with bilateral PA. In contrast, patients adrenalectomized because of unilateral PA showed no significant change of bone turnover markers.ConclusionThis study shows that aldosterone excess in postmenopausal women with PA is not associated with a relevant increase of bone turnover markers at baseline. However, we observed a significant decrease of bone markers in patients treated with spironolactone, but not in patients treated by adrenalectomy.
Highlights
Supplementary information The online version of this article contains supplementary material, which is available to authorized users.Primary aldosteronism (PA) represents the most common cause of endocrine arterial hypertension and affects about 5–10% of hypertensives [1, 2]
These changes are linked to the development of secondary hyperparathyroidism resulting in a loss of bone mineral density, which could be attenuated by administration of spironolactone in the rodent model [7, 8]
The focus was laid on postmenopausal females to study a collective with endogenously increased bone turnover which might be more sensitive to aldosterone effects than premenopausal females or males. 18 age- and Body mass index (BMI)-matched female controls were recruited in parallel and included in our analysis after exclusion of Cushing syndrome and other endocrinopathies
Summary
PA has frequently been shown to induce target organ damage independent of blood pressure levels and is associated with metabolic changes including type II diabetes mellitus and osteoporosis [3,4,5,6]. From rodent studies we know that aldosterone/salt treatment generates an increase in calciuresis resulting in a decline in plasma calcium concentration. These changes are linked to the development of secondary hyperparathyroidism resulting in a loss of bone mineral density, which could be attenuated by administration of spironolactone in the rodent model [7, 8].
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