title: Mild hyperparathyroidism:  a novel surgically correctable feature of primary aldosteronism.
abstract: BACKGROUND
  The parathyroid hormone (PTH) stimulates aldosterone secretion and cell proliferation in human adrenocortical cells; moreover, in rats hyperaldosteronism was associated with hyperparathyroidism. Hence, PTH could drive aldosterone excess in human primary aldosteronism.
  
  
  METHODS
  To test this hypothesis, we recruited 105 consecutive hypertensive patients, of whom 44 had primary aldosteronism due to an aldosterone-producing adenoma (APA) and 61 had primary (essential) hypertension. We measured the plasma levels of (1-84)-PTH, 25(OH)D, 1,25(OH)2D, and serum Ca (total and ionized), inorganic P, Mg, K, and the 24-h urinary excretion of Ca, P, and deoxypyridinoline. In primary aldosteronism patients, these measurements were repeated after adrenalectomy or mineralocorticoid receptor blockade. We also sought for PTH receptor (PTHR-1) mRNA and protein in APA tissue.
  
  
  RESULTS
  Compared with primary (essential) hypertension patients, those with primary aldosteronism showed significantly higher plasma PTH (+31%), despite comparable urinary Ca excretion and similarly deficient 25(OH) vitamin D levels. In APA patients, who showed the PTHR-1 transcript and protein in tumor tissue, adrenalectomy normalized PTH levels (from 118 ± 13 to 76 ± 12 ng/l; P = 0.002) and increased ionized Ca(from 1.17 ± 0.04 to 1.22 ± 0.03 mmol/l; P < 0.001). The slope of the inverse PTH/ionized Ca relationship was steeper in primary aldosteronism than in primary (essential) hypertension, but normalized after adrenalectomy.
  
  
  CONCLUSIONS
  Hence, in primary aldosteronism an increased sensitivity of parathyroid cells to Ca lowering leads to an increase of PTH. This subtle hyperparathyroidism by acting on PTHR-1 in APA might contribute to maintaining hyperaldosteronism despite suppression of angiotensin II formation.
authors.affiliation: Department of Medicine-Internal Medicine 4 , The University of Padua School of Medicine, I-35121 Padua, Italy.
authors.forename: Carmela
authors.initials: C
authors.lastname: Maniero
authors.forename: Ambrogio
authors.initials: A
authors.lastname: Fassina
authors.forename: Teresa M
authors.initials: TM
authors.lastname: Seccia
authors.forename: Antonio
authors.initials: A
authors.lastname: Toniato
authors.forename: Maurizio
authors.initials: M
authors.lastname: Iacobone
authors.forename: Mario
authors.initials: M
authors.lastname: Plebani
authors.forename: Raffaele
authors.initials: R
authors.lastname: De Caro
authors.forename: Lorenzo A
authors.initials: LA
authors.lastname: Calò
authors.forename: Achille C
authors.initials: AC
authors.lastname: Pessina
authors.forename: Gian P
authors.initials: GP
authors.lastname: Rossi
mesh_terms: D000315:Adrenalectomy; D000328:Adult; D001794:Blood Pressure; D002118:Calcium / Q000378:metabolism; D005260:Female; D006801:Humans; D006929:Hyperaldosteronism / Q000150:complications*; D006961:Hyperparathyroidism / Q000209:etiology / Q000601:surgery*; D008297:Male; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000097:blood
chemical_list: D010281:Parathyroid Hormone; D002118:Calcium