title: Aldosterone as a key mediator of the cardiometabolic syndrome in primary aldosteronism: an observational study.
abstract: OBJECTIVE
  Primary aldosteronism (PA) is characterized by the onset of both cardiac and gluco-metabolic alterations. The aim of this study was to evaluate the impact of aldosterone excess on the development of such complications, and the effects of surgical and pharmacological treatment on their long-term outcome.
  
  
  METHODS
  We prospectively re-examined 61 patients: 25 with aldosterone-producing adenoma (APA), after surgery, and 36 patients with idiopathic hyperaldosteronism (IHA) on pharmacological treatment. The lipid, fasting and dynamic glucose profiles and the echocardiographic parameters were evaluated at diagnosis and at follow-up.
  
  
  RESULTS
  After adrenalectomy all patients had normalization of aldosterone levels and were cured of hypokalaemia, and a resolution of hypertension was achieved in 12 of 25 patients. APA patients showed a significant reduction of both plasma glucose (P=0.017) and insulin levels (P=0.001) after 75 g oral glucose tolerance test. Stabilization of glucose metabolism complications was observed in IHA patients. Multiple regression analysis at diagnosis showed a positive correlation between homeostasis model assessment (HOMA) insulin resistance index and HOMA beta cell and serum aldosterone levels in both APA and IHA. Echocardiographic parameters were improved in both APA and IHA at follow-up and the difference was statistically significant for left ventricular mass index (P=0.017) and interventricular septum thickness (P=0.007) in APA patients.
  
  
  CONCLUSIONS
  The removal of aldosterone excess in APA patients induces the regression of both cardiac and gluco-metabolic complications, indicating aldosterone as a main determinant of such alterations. In IHA patients the medical treatment seems to avoid the possible progression of the these alterations that appear to be stable.
authors.affiliation: Division of Endocrinology, Azienda Ospedaliero-Universitaria, Ospedali Riuniti Umberto I- G.M. Lancisi- G. Salesi, Università Politecnica delle Marche, Ancona, Italy. g.giacchetti@ao-umbertoprimo.marche.it
authors.forename: Gilberta
authors.initials: G
authors.lastname: Giacchetti
authors.forename: Vanessa
authors.initials: V
authors.lastname: Ronconi
authors.forename: Federica
authors.initials: F
authors.lastname: Turchi
authors.forename: Laura
authors.initials: L
authors.lastname: Agostinelli
authors.forename: Franco
authors.initials: F
authors.lastname: Mantero
authors.forename: Silvia
authors.initials: S
authors.lastname: Rilli
authors.forename: Marco
authors.initials: M
authors.lastname: Boscaro
mesh_terms: D000236:Adenoma / Q000097:blood / Q000150:complications / Q000601:surgery; D000310:Adrenal Gland Neoplasms / Q000097:blood / Q000150:complications / Q000601:surgery; D000315:Adrenalectomy; D000450:Aldosterone / Q000097:blood*; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001786:Blood Glucose / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D005260:Female; D005500:Follow-Up Studies; D044882:Glucose Metabolism Disorders / Q000097:blood / Q000188:drug therapy / Q000209:etiology*; D006331:Heart Diseases / Q000097:blood / Q000188:drug therapy* / Q000209:etiology* / Q000503:physiopathology; D006801:Humans; D006929:Hyperaldosteronism / Q000097:blood / Q000150:complications* / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D006973:Hypertension / Q000097:blood / Q000188:drug therapy / Q000209:etiology; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D016014:Linear Models; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology / Q000627:therapeutic use*; D011446:Prospective Studies; D012084:Renin-Angiotensin System / Q000187:drug effects; D013997:Time Factors; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D000959:Antihypertensive Agents; D001786:Blood Glucose; D007328:Insulin; D000451:Mineralocorticoid Receptor Antagonists; D000450:Aldosterone