Primary hyperaldosteronism causes: Difference between revisions
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==Overview== | ==Overview== | ||
Common causes of primary hyperaldosteronism | Common causes of primary hyperaldosteronism are [[aldosterone]]-secreting [[adenoma]], bilateral [[hyperplasia]] of the [[Adrenal gland|adrenal glands]], and [[ectopic]] secretion of [[aldosterone]] from [[ovaries]] and [[kidneys]]. Less common causes of primary hyperaldosteronism are familial hyperaldosteronism types I-III, pure [[aldosterone]]-producing [[Adrenal carcinoma|adrenocortical carcinomas]], and unilateral [[hyperplasia]] of the [[adrenal gland]]. | ||
==Causes== | ==Causes== | ||
=== Common Causes === | === Common Causes === | ||
Common causes of | Common causes of primary hyperaldosteronism (PA) may be divided into:<ref name="urlPrimary aldosteronism: renaissance of a syndrome - Young - 2007 - Clinical Endocrinology - Wiley Online Library">{{cite web |url=http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2265.2007.02775.x/full |title=Primary aldosteronism: renaissance of a syndrome - Young - 2007 - Clinical Endocrinology - Wiley Online Library |author= |authorlink= |coauthors= |date= |format= |work= |publisher= |pages= |language= |archiveurl= |archivedate= |quote= |accessdate=}}</ref><ref name="pmid24944753">{{cite journal |vauthors=Aronova A, Iii TJ, Zarnegar R |title=Management of hypertension in primary aldosteronism |journal=World J Cardiol |volume=6 |issue=5 |pages=227–33 |year=2014 |pmid=24944753 |pmc=4062125 |doi=10.4330/wjc.v6.i5.227 |url= |issn=}}</ref> | ||
*Adrenal causes: | *[[Adrenal gland|Adrenal]] causes: | ||
**Aldosterone-secreting adrenal adenoma (APA-benign tumor, 50-60%) | **[[Aldosterone]]-secreting [[Adrenal gland|adrenal]] [[adenoma]] (APA-[[benign tumor]], 50-60%) | ||
**Idiopathic hyperaldosteronism (IHA-Bilateral hyperplasia of the adrenal gland, 40-50%) | **Idiopathic hyperaldosteronism (IHA-Bilateral [[hyperplasia]] of the [[adrenal gland]], 40-50%) | ||
*Extra-adrenal causes | *Extra-adrenal causes | ||
**Ectopic secretion of aldosterone ( | **[[Ectopic]] secretion of [[aldosterone]] ([[ovaries]] and [[kidneys]]) | ||
===Less Common Causes=== | ===Less Common Causes=== | ||
Less common causes of primary hyperladosteronism include:<ref name="urlPrimary aldosteronism: renaissance of a syndrome - Young - 2007 - Clinical Endocrinology - Wiley Online Library2">{{cite web |url=http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2265.2007.02775.x/full |title=Primary aldosteronism: renaissance of a syndrome - Young - 2007 - Clinical Endocrinology - Wiley Online Library |author= |authorlink= |coauthors= |date= |format= |work= |publisher= |pages= |language= |archiveurl= |archivedate= |quote= |accessdate=}}</ref><ref name="pmid16003173">{{cite journal |vauthors=So A, Duffy DL, Gordon RD, Jeske YW, Lin-Su K, New MI, Stowasser M |title=Familial hyperaldosteronism type II is linked to the chromosome 7p22 region but also shows predicted heterogeneity |journal=J. Hypertens. |volume=23 |issue=8 |pages=1477–84 |year=2005 |pmid=16003173 |doi= |url= |issn=}}</ref> | Less common causes of primary hyperladosteronism include:<ref name="urlPrimary aldosteronism: renaissance of a syndrome - Young - 2007 - Clinical Endocrinology - Wiley Online Library2">{{cite web |url=http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2265.2007.02775.x/full |title=Primary aldosteronism: renaissance of a syndrome - Young - 2007 - Clinical Endocrinology - Wiley Online Library |author= |authorlink= |coauthors= |date= |format= |work= |publisher= |pages= |language= |archiveurl= |archivedate= |quote= |accessdate=}}</ref><ref name="pmid16003173">{{cite journal |vauthors=So A, Duffy DL, Gordon RD, Jeske YW, Lin-Su K, New MI, Stowasser M |title=Familial hyperaldosteronism type II is linked to the chromosome 7p22 region but also shows predicted heterogeneity |journal=J. Hypertens. |volume=23 |issue=8 |pages=1477–84 |year=2005 |pmid=16003173 |doi= |url= |issn=}}</ref><ref name="pmid22707896">{{cite journal |vauthors=Song MS, Seo SW, Bae SB, Kim YJ, Kim SJ |title=Aldosterone-producing adrenocortical carcinoma without hypertension |journal=Korean J. Intern. Med. |volume=27 |issue=2 |pages=221–3 |year=2012 |pmid=22707896 |pmc=3372808 |doi=10.3904/kjim.2012.27.2.221 |url= |issn=}}</ref> | ||
*Familial hyperaldosteronism type I (glucocorticoid-remediable aldosteronism [GRA]) | *Familial hyperaldosteronism type I ([[glucocorticoid]]-remediable aldosteronism [GRA]) | ||
*Familial hyperaldosteronism II (the familial occurrence of APA or bilateral idiopathic hyperplasia or both) | *Familial hyperaldosteronism type II (the familial occurrence of APA or bilateral idiopathic hyperplasia or both) | ||
*Familial hyperaldosteronism type III (associated with the germline mutation in the KCNJ5 potassium channel) | *Familial hyperaldosteronism type III (associated with the [[germline mutation]] in the [[KCNJ5]] [[potassium channel]]) | ||
*Pure aldosterone-producing adrenocortical carcinomas | *Pure [[aldosterone]]-producing [[Adrenal carcinoma|adrenocortical carcinomas]] | ||
*Unilateral adrenal hyperplasia | *Unilateral [[Adrenal gland|adrenal]] [[hyperplasia]] | ||
Latest revision as of 16:48, 18 October 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]
Overview
Common causes of primary hyperaldosteronism are aldosterone-secreting adenoma, bilateral hyperplasia of the adrenal glands, and ectopic secretion of aldosterone from ovaries and kidneys. Less common causes of primary hyperaldosteronism are familial hyperaldosteronism types I-III, pure aldosterone-producing adrenocortical carcinomas, and unilateral hyperplasia of the adrenal gland.
Causes
Common Causes
Common causes of primary hyperaldosteronism (PA) may be divided into:[1][2]
- Adrenal causes:
- Aldosterone-secreting adrenal adenoma (APA-benign tumor, 50-60%)
- Idiopathic hyperaldosteronism (IHA-Bilateral hyperplasia of the adrenal gland, 40-50%)
- Extra-adrenal causes
- Ectopic secretion of aldosterone (ovaries and kidneys)
Less Common Causes
Less common causes of primary hyperladosteronism include:[3][4][5]
- Familial hyperaldosteronism type I (glucocorticoid-remediable aldosteronism [GRA])
- Familial hyperaldosteronism type II (the familial occurrence of APA or bilateral idiopathic hyperplasia or both)
- Familial hyperaldosteronism type III (associated with the germline mutation in the KCNJ5 potassium channel)
- Pure aldosterone-producing adrenocortical carcinomas
- Unilateral adrenal hyperplasia
References
- ↑ "Primary aldosteronism: renaissance of a syndrome - Young - 2007 - Clinical Endocrinology - Wiley Online Library".
- ↑ Aronova A, Iii TJ, Zarnegar R (2014). "Management of hypertension in primary aldosteronism". World J Cardiol. 6 (5): 227–33. doi:10.4330/wjc.v6.i5.227. PMC 4062125. PMID 24944753.
- ↑ "Primary aldosteronism: renaissance of a syndrome - Young - 2007 - Clinical Endocrinology - Wiley Online Library".
- ↑ So A, Duffy DL, Gordon RD, Jeske YW, Lin-Su K, New MI, Stowasser M (2005). "Familial hyperaldosteronism type II is linked to the chromosome 7p22 region but also shows predicted heterogeneity". J. Hypertens. 23 (8): 1477–84. PMID 16003173.
- ↑ Song MS, Seo SW, Bae SB, Kim YJ, Kim SJ (2012). "Aldosterone-producing adrenocortical carcinoma without hypertension". Korean J. Intern. Med. 27 (2): 221–3. doi:10.3904/kjim.2012.27.2.221. PMC 3372808. PMID 22707896.