Primary hyperaldosteronism medical therapy: Difference between revisions

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Latest revision as of 19:12, 3 November 2017

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

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

Indications

Medical therapy is indicated for:

Bilateral adrenal hyperplasia
All ambiguous causes of primary hyperaldosteronism.

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	Competitive binding of receptors at the aldosterone-dependent sodium-potassium exchange site in the distal convoluted renal tubule^[1]	12.5 – 25 mg PO q12h Max of 400 mg PO daily	Digestive: Gastric bleeding, ulceration, gastritis, diarrhea and cramping, nausea, vomiting Endocrine: Gynecomastia, irregular menses or amenorrhea, postmenopausal bleeding, carcinoma of the breast Hematologic: Agranulocytosis Hypersensitivity: Fever, urticaria, maculopapular or erythematous cutaneous eruptions, anaphylactic reactions, vasculitis Hyperkalemia Nervous system/psychiatric: Mental confusion, ataxia, headache, drowsiness, lethargy Liver / biliary: Cholestatic/hepatocellular toxicity Renal: Renal dysfunction (including renal failure)^[2]
	Potassium canrenoate	Aldosterone antagonist	Parenetral administration 200 mg IV daily Max of 800 mg daily	Hoarseness Deepening of voice Hyperkalemia Nausea Vomiting
	Eplerenone	Selective aldosterone antagonist	50 mg PO daily^[3]	Hyperkalaemia Hypotension Dizziness Altered renal function Increased creatinine concentration
Potassium-sparing diuretics	Amiloride Triamterene	Acts on distal renal tubule where it selectively blocks sodium transport, leading to inhibition of sodium-potassium exchange^[4]	Initial dose: 5 mg PO daily Maintenance dose: 5-10 mg PO daily^[5]	Nausea Vomiting Stomach or abdominal pain Anorexia Bloating Diarrhea Headache Dizziness Skin rash Weakness Fatigue Constipation Muscle cramps Cough Dyspnea
Calcium channel blockers	Amlodipine Nifedipine	Prevent calcium from entering cells of the blood vessel walls, resulting in lower blood pressure^[6]	5 mg PO daily Max of 10 mg PO daily^[7]	Edema Flushing Diziness Palpitations Headache Abdominal pain Somnolence^[8] May mask diagnosis of Conn's syndrome^[9]
ACE inhibitors	Lisinopril Captopril	Inhibits angiotensin-converting enzyme (ACE) thereby decreasing levels of angiotensin II and blocking the release of aldosterone^[10]	20mg-40mg PO daily^[11]	Cough Increased creatinine concentration Angioedema Hyperkalemia Renal impairment if given in bilateral renal artery stenosis Agranulocytosis^[12]
Angiotensin receptor blockers	Losartan Candesartan Valsartan	Angiotensin II inhibition by interacting selectively with the receptor site and blocking it^[13] ^[14]	Losartan 50 mg PO daily^[15] Candesartan16 mg PO daily^[16] Valsartan 80mg-160mg PO daily^[17]	Dizziness Fatigue Diarrhea Dyspepsia Abdominal pain Arthralgia Sinusitis^[18]
Dexamethasone therapy(For familial hyperaldosteronism type I)	Dexamethasone		0.5mg-0.75mg IV daily

References

↑ 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. PMID 978470.
↑ "www.accessdata.fda.gov" (PDF).
↑ 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. PMC 1200656. PMID 16200104.
↑ 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. PMID 6927605.
↑ "Amiloride Dosage Guide with Precautions - Drugs.com".
↑ Katz AM (1986). "Pharmacology and mechanisms of action of calcium-channel blockers". J Clin Hypertens. 2 (3 Suppl): 28S–37S. PMID 3540226.
↑ "www.accessdata.fda.gov" (PDF).
↑ "www.accessdata.fda.gov" (PDF).
↑ Brown MJ, Hopper RV (1999). "Calcium-channel blockade can mask the diagnosis of Conn's syndrome". Postgrad Med J. 75 (882): 235–6. PMC 1741191. PMID 10715768.
↑ "www.accessdata.fda.gov" (PDF).
↑ "www.accessdata.fda.gov" (PDF).
↑ "www.accessdata.fda.gov" (PDF).
↑ Burnier M, Brunner HR (2000). "Angiotensin II receptor antagonists". Lancet. 355 (9204): 637–45. PMID 10696996.
↑ Barreras A, Gurk-Turner C (2003). "Angiotensin II receptor blockers". Proc (Bayl Univ Med Cent). 16 (1): 123–6. PMC 1200815. PMID 16278727.
↑ "www.accessdata.fda.gov" (PDF).
↑ "www.accessdata.fda.gov" (PDF).
↑ "www.accessdata.fda.gov" (PDF).
↑ Barreras A, Gurk-Turner C (2003). "Angiotensin II receptor blockers". Proc (Bayl Univ Med Cent). 16 (1): 123–6. PMC 1200815. PMID 16278727.

Template:WH Template:WS

[pmid978470-1] 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. PMID 978470.

[urlwww.accessdata.fda.gov-2] "www.accessdata.fda.gov" (PDF).

[pmid16200104-3] 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. PMC 1200656. PMID 16200104.

[pmid6927605-4] 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. PMID 6927605.

[urlAmiloride_Dosage_Guide_with_Precautions_-_Drugs.com-5] "Amiloride Dosage Guide with Precautions - Drugs.com".

[pmid3540226-6] Katz AM (1986). "Pharmacology and mechanisms of action of calcium-channel blockers". J Clin Hypertens. 2 (3 Suppl): 28S–37S. PMID 3540226.

[urlwww.accessdata.fda.gov2-7] "www.accessdata.fda.gov" (PDF).

[urlwww.accessdata.fda.gov3-8] "www.accessdata.fda.gov" (PDF).

[pmid10715768-9] Brown MJ, Hopper RV (1999). "Calcium-channel blockade can mask the diagnosis of Conn's syndrome". Postgrad Med J. 75 (882): 235–6. PMC 1741191. PMID 10715768.

[urlwww.accessdata.fda.gov6-10] "www.accessdata.fda.gov" (PDF).

[urlwww.accessdata.fda.gov4-11] "www.accessdata.fda.gov" (PDF).

[urlwww.accessdata.fda.gov5-12] "www.accessdata.fda.gov" (PDF).

[pmid10696996-13] Burnier M, Brunner HR (2000). "Angiotensin II receptor antagonists". Lancet. 355 (9204): 637–45. PMID 10696996.

[pmid162787272-14] Barreras A, Gurk-Turner C (2003). "Angiotensin II receptor blockers". Proc (Bayl Univ Med Cent). 16 (1): 123–6. PMC 1200815. PMID 16278727.

[urlwww.accessdata.fda.gov7-15] "www.accessdata.fda.gov" (PDF).

[urlwww.accessdata.fda.gov8-16] "www.accessdata.fda.gov" (PDF).

[urlwww.accessdata.fda.gov9-17] "www.accessdata.fda.gov" (PDF).

[pmid16278727-18] Barreras A, Gurk-Turner C (2003). "Angiotensin II receptor blockers". Proc (Bayl Univ Med Cent). 16 (1): 123–6. PMC 1200815. PMID 16278727.

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@@ Line 5: / Line 5: @@
 ==Overview==
-The optimal therapy for primary hyperladosteronism depends on the [[etiology]] of hyperaldosteronism. Medical therapy is indicated for bilateral [[Adrenal gland|adrenal]] [[hyperplasia]], and all ambiguous causes of primary hyperaldosteronism.
+The optimal therapy for primary hyperaldosteronism depends on the [[etiology]] of hyperaldosteronism. Medical therapy is indicated for bilateral [[Adrenal gland|adrenal]] [[hyperplasia]], and all ambiguous causes of primary hyperaldosteronism.
 ==Medical Therapy==
@@ Line 94: / Line 94: @@
 * [[Nifedipine]]
 |
-* Prevent '''[[calcium]]''' from entering cells of the blood [[Blood vessel|vesse]]<nowiki/>l walls, resulting in lower [[blood pressure]]<ref name="pmid3540226">{{cite journal |vauthors=Katz AM |title=Pharmacology and mechanisms of action of calcium-channel blockers |journal=J Clin Hypertens |volume=2 |issue=3 Suppl |pages=28S–37S |year=1986 |pmid=3540226 |doi= |url= |issn=}}</ref>
+* Prevent '''[[calcium]]''' from entering cells of the blood [[Blood vessel|vessel]]<nowiki/> walls, resulting in lower [[blood pressure]]<ref name="pmid3540226">{{cite journal |vauthors=Katz AM |title=Pharmacology and mechanisms of action of calcium-channel blockers |journal=J Clin Hypertens |volume=2 |issue=3 Suppl |pages=28S–37S |year=1986 |pmid=3540226 |doi= |url= |issn=}}</ref>
 |
 * 5 mg PO daily