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Primary hyperaldosteronism medical therapy

Introduction

Overview

Overview

The optimal therapy for primary hyperaldosteronism depends on the etiology of hyperaldosteronism. Medical therapy is indicated for bilateral adrenal hyperplasia, and all ambiguous causes of primary hyperaldosteronism.

Medical Therapy

Medical Therapy

Indications

Medical therapy is indicated for:

The following agents may be used to medical management of primary hyperaldosteronism:

Drug Class Agents Mechanism of action Dosage Side effects
Mineralocorticoid receptor antagonists Spironolactone
  • 12.5 – 25 mg PO q12h
  • Max of 400 mg PO daily
Potassium canrenoate
  • 200 mg IV daily
  • Max of 800 mg daily
Eplerenone 50 mg PO daily[3]
Potassium-sparing diuretics
Calcium channel blockers
  • 5 mg PO daily
  • Max of 10 mg PO daily[7]
ACE inhibitors
  • 20mg-40mg PO daily[11]
Angiotensin receptor blockers
Dexamethasone therapy(For familial hyperaldosteronism type I) Dexamethasone
  • 0.5mg-0.75mg IV daily
References

References

  1. ↑ Greiner JW, Kramer RE, Jarrell J, Colby HD (1976). “Mechanism of action of spironolactone on adrenocortical function in guinea pigs”. J. Pharmacol. Exp. Ther. 198 (3): 709–15. PMIDΒ 978470.
  2. ↑ “www.accessdata.fda.gov” (PDF).
  3. ↑ Craft J (2004). “Eplerenone (Inspra), a new aldosterone antagonist for the treatment of systemic hypertension and heart failure”. Proc (Bayl Univ Med Cent). 17 (2): 217–20. PMCΒ 1200656. PMIDΒ 16200104.
  4. ↑ Vidt DG (1981). “Mechanism of action, pharmacokinetics, adverse effects, and therapeutic uses of amiloride hydrochloride, a new potassium-sparing diuretic”. Pharmacotherapy. 1 (3): 179–87. PMIDΒ 6927605.
  5. ↑ “Amiloride Dosage Guide with Precautions – Drugs.com”.
  6. ↑ Katz AM (1986). “Pharmacology and mechanisms of action of calcium-channel blockers”. J Clin Hypertens. 2 (3 Suppl): 28S–37S. PMIDΒ 3540226.
  7. ↑ “www.accessdata.fda.gov” (PDF).
  8. ↑ “www.accessdata.fda.gov” (PDF).
  9. ↑ Brown MJ, Hopper RV (1999). “Calcium-channel blockade can mask the diagnosis of Conn’s syndrome”. Postgrad Med J. 75 (882): 235–6. PMCΒ 1741191. PMIDΒ 10715768.
  10. ↑ “www.accessdata.fda.gov” (PDF).
  11. ↑ “www.accessdata.fda.gov” (PDF).
  12. ↑ “www.accessdata.fda.gov” (PDF).
  13. ↑ Burnier M, Brunner HR (2000). “Angiotensin II receptor antagonists”. Lancet. 355 (9204): 637–45. PMIDΒ 10696996.
  14. ↑ Barreras A, Gurk-Turner C (2003). “Angiotensin II receptor blockers”. Proc (Bayl Univ Med Cent). 16 (1): 123–6. PMCΒ 1200815. PMIDΒ 16278727.
  15. ↑ “www.accessdata.fda.gov” (PDF).
  16. ↑ “www.accessdata.fda.gov” (PDF).
  17. ↑ “www.accessdata.fda.gov” (PDF).
  18. ↑ Barreras A, Gurk-Turner C (2003). “Angiotensin II receptor blockers”. Proc (Bayl Univ Med Cent). 16 (1): 123–6. PMCΒ 1200815. PMIDΒ 16278727.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]