title: Bone health and aldosterone excess.
abstract: A picture of hyperparathyroidism secondary to increased urinary calcium excretion was found in 116 patients with primary aldosteronism (PA), compared with 110 essential hypertensives. After medical or surgical treatment in 40 PA patients, parathyroid hormone (PTH) levels were significantly reduced and bone mineral density (BMD) significantly increased at the lumbar spine, femoral neck, and total hip.
  
  
  BACKGROUND
  Recent studies have shown that aldosterone induces urinary calcium excretion leading to a reduction of calcemia with consequent secondary hyperparathyroidism and BMD loss. In patients with PA, this picture of hyperparathyroidism is significantly improved by treatment with adrenal surgery or with mineralocorticoid receptor antagonists. On these premises, the aim of the present study was to evaluate calcium and phosphate metabolism parameters in PA patients, compared with patients with essential hypertension (EH) and the effect of treatment of aldosterone excess on bone health in PA patients.
  
  
  METHODS
  We studied 226 patients: 116 with PA (46 with an aldosterone-producing adenoma and 70 with bilateral adrenal hyperplasia) and 110 patients with EH. In 40 patients with PA, we evaluated biochemical parameters and bone mass, using the dual-energy X-ray absorptiometry, at baseline and after a mean follow-up of 24 months from treatment.
  
  
  RESULTS
  In PA patients, compared with EH, PTH levels and urinary calcium excretion significantly increased while serum calcium significantly decreased with comparable vitamin D levels. At follow-up in PA patients, PTH levels were significantly reduced compared with basal evaluation, despite similar vitamin D amounts. At follow-up, we observed a significant improvement of the Z-score at the lumbar spine, femoral neck, and at total hip sites.
  
  
  CONCLUSIONS
  Our results support previous data showing secondary hyperparathyroidism in PA patients, which is reversible after treatment. Moreover, this targeted treatment appears to be able to determine a significant improvement of BMD both at the spine and hip sites.
authors.affiliation: Division of Endocrinology, Polytechnic University of Marche, Ospedali Riuniti "Umberto I-G.M. Lancisi-G. Salesi", Ancona, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Ceccoli
authors.forename: V
authors.initials: V
authors.lastname: Ronconi
authors.forename: L
authors.initials: L
authors.lastname: Giovannini
authors.forename: M
authors.initials: M
authors.lastname: Marcheggiani
authors.forename: F
authors.initials: F
authors.lastname: Turchi
authors.forename: M
authors.initials: M
authors.lastname: Boscaro
authors.forename: G
authors.initials: G
authors.lastname: Giacchetti
mesh_terms: D015502:Absorptiometry, Photon; D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood; D015519:Bone Density / Q000502:physiology*; D002118:Calcium / Q000378:metabolism; D000075222:Essential Hypertension; D005260:Female; D005272:Femur Neck / Q000503:physiopathology; D005500:Follow-Up Studies; D006621:Hip Joint / Q000503:physiopathology; D006801:Humans; D006929:Hyperaldosteronism / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D006962:Hyperparathyroidism, Secondary / Q000209:etiology / Q000378:metabolism; D006973:Hypertension / Q000150:complications / Q000503:physiopathology; D008159:Lumbar Vertebrae / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000097:blood; D011446:Prospective Studies
chemical_list: D010281:Parathyroid Hormone; D000450:Aldosterone; D002118:Calcium