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Hyperaldosteronism, also aldosteronism,^[1] is a medical condition wherein too much aldosterone is produced by the adrenal glands, which can lead to lowered levels of potassium in the blood (hypokalemia) and increased hydrogen ion excretion (alkalosis).

This cause of mineralocorticoid excess is primary hyperaldosteronism reflecting excess production of aldosterone by adrenal zona glomerulosa. Bilateral micronodular hyperplasia is more common than unilateral adrenal adenoma.

Signs and symptoms

It can be asymptomatic, but these symptoms may be present:

Fatigue
Headache
High blood pressure
Hypokalemia
Hypernatraemia
Hypomagnesemia
Intermittent or temporary paralysis
Muscle spasms
Muscle weakness
Numbness
Polyuria
Polydipsia
Tingling
Metabolic alkalosis^[2]

Cause

The causes of primary hyperaldosteronism are adrenal hyperplasia and adrenal adenoma (Conn's syndrome). These cause hyperplasia of aldosterone-producing cells of the adrenal cortex resulting in primary hyperaldosteronism. The causes of secondary hyperaldosteronism are massive ascites, left ventricular failure, and cor pulmonale. These act either by decreasing circulating fluid volume or by decreasing cardiac output, with resulting increase in renin release leading to secondary hyperaldosteronism.

Diagnosis

When taking a blood test, the aldosterone-to-renin ratio is abnormally increased in primary hyperaldosteronism, and decreased or normal but with high renin in secondary hyperaldosteronism.

Types

In endocrinology, the terms 'primary' and 'secondary' are used to describe the abnormality (e.g., elevated aldosterone) in relation to the defect, i.e., the tumor's location. Hyperaldosteronism can also be caused by plant poisoning, where the patient has been exposed to too much licorice. Licorice is a perennial herb that is used in making candies and in cooking other desserts because of its sweet taste. It contains the chemical glycyrrhizin, which has medicinal uses, but at higher levels it can be toxic. It has the potential for causing problems with sodium and potassium in the body. It also interferes with the enzyme in the kidneys that converts cortisol to cortisone.

Primary

Primary aldosteronism (hyporeninemic hyperaldosteronism) was previously thought to be most commonly caused by an adrenal adenoma, termed Conn's syndrome. However, recent studies have shown that bilateral idiopathic adrenal hyperplasia is the cause in up to 70% of cases. Differentiating between the two is important, as this determines treatment. Also see congenital adrenal hyperplasia. Adrenal carcinoma is an extremely rare cause of primary hyperaldosteronism. Two familial forms have been identified: type I (dexamethasone suppressible), and type II (that has been linked to 7p22.)^[3]

Features

Hypertension
Hypokalemia (e.g., may cause muscle weakness)
Alkalosis

Investigations

High serum aldosterone
Low serum renin
High-resolution CT abdomen

Management

Adrenal adenoma: surgery
Bilateral adrenocortical hyperplasia: aldosterone antagonist, e.g., spironolactone

Secondary

Secondary hyperaldosteronism (also hyperreninism, or hyperreninemic hyperaldosteronism) is due to overactivity of the renin–angiotensin–aldosterone system (RAAS).

Secondary refers to an abnormality that indirectly results in pathology through a predictable physiologic pathway, i.e., a renin-producing tumor leads to increased aldosterone, as the body's aldosterone production is normally regulated by renin levels.

One cause is a juxtaglomerular cell tumor. Another is renal artery stenosis, in which the reduced blood supply across the juxtaglomerular apparatus stimulates the production of renin. Likewise, fibromuscular dysplasia may cause stenosis of the renal artery, and therefore secondary hyperaldosteronism. Other causes can come from the tubules: Hyporeabsorption of sodium (as seen in Bartter and Gitelman syndromes) will lead to hypovolemia/hypotension, which will activate the RAAS.

Treatment

Treatment includes spironolactone, a potassium-sparing diuretic that works by acting as an aldosterone antagonist.

References

^ "aldosteronism" at Dorland's Medical Dictionary
^ "Hyperaldosteronism: eMedicine Pediatrics: General Medicine". Retrieved 2009-06-16.
^ Lafferty AR, Torpy DJ, Stowasser M, et al. (November 2000). "A novel genetic locus for low renin hypertension: familial hyperaldosteronism type II maps to chromosome 7 (7p22)". J. Med. Genet. 37 (11): 831–5. doi:10.1136/jmg.37.11.831. PMC 1734468 . PMID 11073536.

Williams, Cheryll J. 2012. Medicinal Plants in Australia. Sydney: Rosenberg Publishing

External links

UpToDate Contents

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1. Diagnosis of primary aldosteronism
2. 原発性アルドステロン症の病態生理および臨床的特徴 pathophysiology and clinical features of primary aldosteronism
3. 原発性アルドステロン症の治療 treatment of primary aldosteronism
4. 家族性アルドステロン症 familial hyperaldosteronism
5. 見かけの鉱質コルチコイド過剰（AME）症候群（長期甘草摂取を含む） apparent mineralocorticoid excess syndromes including chronic licorice ingestion

English Journal

Measurement of serum aldosterone in picomolar level by LC-MS/MS using charge-tagged technique.

Fong BM1, Siu TS1, Tam S2.
Analytical and bioanalytical chemistry.Anal Bioanal Chem.2015 Oct;407(25):7765-74. doi: 10.1007/s00216-015-8944-3. Epub 2015 Sep 15.
Aldosterone is a mineralocorticoid steroid hormone, the measurement of which in the clinical laboratory is principally performed for the investigation of primary hyperaldosteronism. Primary hyperaldosteronism is a specifically treatable and potentially curable form of hypertension, which typically p
PMID 26374566

Is there a role for segmental adrenal venous sampling and adrenal sparing surgery in patients with primary aldosteronism?

Satoh F1, Morimoto R2, Seiji K2, Satani N2, Ota H2, Iwakura Y2, Ono Y2, Kudo M2, Nezu M2, Omata K3, Tezuka Y3, Kawasaki Y2, Ishidoya S2, Arai Y2, Takase K2, Nakamura Y2, McNamara K2, Sasano H2, Ito S2.
European journal of endocrinology / European Federation of Endocrine Societies.Eur J Endocrinol.2015 Oct;173(4):465-77. doi: 10.1530/EJE-14-1161. Epub 2015 Jul 20.
OBJECTIVE AND DESIGN: Adrenal venous sampling (AVS) is critical to determine the subtype of primary aldosteronism (PA). Central AVS (C-AVS) - that is, the collection of effluents from bilateral adrenal central veins (CV) - sometimes does not allow differentiation between bilateral aldosterone-produc
PMID 26194502

Galectin-3 Blockade Inhibits Cardiac Inflammation and Fibrosis in Experimental Hyperaldosteronism and Hypertension.

Martínez-Martínez E1, Calvier L1, Fernández-Celis A1, Rousseau E1, Jurado-López R1, Rossoni LV1, Jaisser F1, Zannad F1, Rossignol P1, Cachofeiro V1, López-Andrés N2.
Hypertension.Hypertension.2015 Oct;66(4):767-75. doi: 10.1161/HYPERTENSIONAHA.115.05876. Epub 2015 Aug 3.
Hypertensive cardiac remodeling is accompanied by molecular inflammation and fibrosis, 2 mechanisms that finally affect cardiac function. At cardiac level, aldosterone promotes inflammation and fibrosis, although the precise mechanisms are still unclear. Galectin-3 (Gal-3), a β-galactoside-binding
PMID 26238446

Japanese Journal

Outcomes analysis of surgical and medical treatments for patients with primary aldosteronism

Endocrine Journal, 2017
NAID 130005628148

ACTH stimulation test and computed tomography are useful for differentiating the subtype of primary aldosteronism

Endocrine Journal 64(1), 65-73, 2017
NAID 130005305972

若年発症した急性大動脈解離を契機に診断に至った原発性アルドステロン症の1 例

脈管学 56(5), 65-69, 2016
NAID 130005156675

Related Pictures

Hyperaldosteronism | Endocrinology | Which Disease Hyperaldosteronism; Aldosteronism Adrenal Gland Emad Raddaoui, MD, FCAP, FASC - ppt video online download Primary Hyperaldosteronism or Primary Aldosteronism|Treatment|Complications|Risk Factors Adrenal gland diseases and tumors Chapter 21 Endocrine Problems- Hyperaldosteronism - primary and secondary - Pictures

★リンクテーブル★

リンク元	「アルドステロン」「アルドステロン症」「高アルドステロン症」
拡張検索	「glucocorticoid remediable hyperaldosteronism」「glucocorticoid suppressible hyperaldosteronism」「dexamethasone suppressible hyperaldosteronism」

「アルドステロン」

Classification	D ICD-10: E26; ICD-9-CM: 255.1; OMIM: 103900 605635; MeSH: D006929; DiseasesDB: 6187;
External resources	MedlinePlus: 000330; eMedicine: radio/354; Patient UK: Hyperaldosteronism;

Hyperaldosteronism
	Aldosterone
Classification and external resources
Specialty	endocrinology
Patient UK	Hyperaldosteronism
	[edit on Wikidata]

　　[★]

英: aldosterone
関: 尿細管

基準値

血漿濃度は35-240 pg/ml, EDTA加血漿安静臥位　30-160 pg/ml
30-160 pg/ml (LAB.715)
35.7-240 pg/ml (随時), 29.9-159pg/ml (臥位), 38.9-307pg/ml (立位) (SRL)

分類

副腎皮質ホルモン

電解質コルチコイド

性状

ステロイド

産生組織

副腎皮質球状層

標的組織

主に集合管(SP.792)

生理作用

1. 腎の接合尿細管と集合管、唾液腺、乳腺、汗腺等に働いてNa⁺の再吸収を促進し、K⁺の排出(分泌)を促進する (SP.791,792 によれば、腎接合尿細管を含む)
2. 腎集合管でH⁺の排出(分泌)を促進する。

Na+/K+-ATPase活性↑＠遠位尿細管・皮質集合管　→　管腔側K↑　→　K再吸収/H+分泌 (QB CBT vol2 p.360)　←　成書での裏付けがないが、確かにアルドステロン↑によりK+分泌が↑となれば、管腔側にK+があふれるのでα間在細胞上の管腔側にあるK+/H+交換輸送体担体によりH+管腔側にくみ出されるな。

作用機序

アルドステロンは何らかの経路を経て、ある遺伝子(アルドステロン誘導タンパク質 AIP)の転写・発現を促進する。これにより、以下の作用を及ぼす (2007年度後期生理学授業プリント)

(1)Na⁺-K⁺ATPaseの発現
(2)基底膜面積の増加
(3)Na⁺チャネルの活性化
(4)K⁺チャネルの活性化

管腔側細胞膜のNaチャネルが増加(SP.792)

これが最も重要

Na⁺-K⁺ ATPase活性を上昇させる(SP.792)
ミトコンドリアのエネルギー産生系が活性化される(SP.792)

分泌調節

1. 体液↓、血圧↓→レニン-アンジオテンシン-アルドステロン系でアンジオテンシンIIが生成→P450scc↑、P450aldo↑

アンジオテンシンIIによるCYP11B2(18-hydroxylase, 18-hydroxydehydrogenase; aldosterone synthase)のup-regulationによる
アンギオテンシンIIとアンギオテンシンIIIはアルドステロン分泌能をもつ(NEL.2351)。

→レニン-アンギオテンシン-アルドステロン系

2. 血漿K+↑→アルドステロン分泌↑　　←　direct action on the adrenal cortical cells.
3. ドパミン、ソマトスタチン→アルドステロン分泌↓　(出典不明)
4. ACTH

アルドステロン分泌作用は弱い。only a short-term effect(NEL.2351).

分子機構

生合成

アルドステロン合成酵素によって18-ヒドロキシコルチコステロンから産生される。
最も強い電解質コルチコイド活性

臨床関連

1. アルドステロン症　←　アルドステロン過剰症高アルドステロン症 hyperaldosteronism

原発アルドステロン症

2. アルドステロン減少症：低アルドステロン症：hypoaldosteronism

「アルドステロン症」

　　[★]

英: aldosteronism
同: アルドステロン過剰症高アルドステロン症 hyperaldosteronism
関

広義のアルドステロン症

アルドステロン過剰症：高アルドステロン症：hyperaldosteronism
アルドステロン減少症：低アルドステロン症：hypoaldosteronism

狭義のアルドステロン症

アルドステロン過剰症：高アルドステロン症：hyperaldosteronism

原発性アルドステロン症 primary aldosteronism 　：レニン上昇せず　←　循環血液量の増加によりネガティブフィードバックによりレニン分泌が抑制される一方で、高血圧となる

コン症候群 (アルドステロン産生腺腫)　80-90%
特発性アルドステロン主要　副腎皮質球状層の過形成　10%程度

続発性アルドステロン症

二次性アルドステロン症　：レニン上昇

レニン-アンジオテンシン系の亢進(腎虚血など)、

「高アルドステロン症」

　　[★]

英: hyperaldosteronism
関: アルドステロン症

[show details]

アルドステロン過剰症 : 53 件
高アルドステロン症 : 約 44,900 件

アルドステロン過剰症 hyperaldosteronism : 33 件
高アルドステロン症 hyperaldosteronism : 38 件

「glucocorticoid remediable hyperaldosteronism」

　　[★] グルココルチコイド奏効性アルドステロン症

「glucocorticoid suppressible hyperaldosteronism」

　　[★] 糖質コルチコイド抑制性高アルドステロン症

「dexamethasone suppressible hyperaldosteronism」

　　[★] デキサメタゾン抑制性高アルドステロン症

[1] "aldosteronism" at Dorland's Medical Dictionary

[urlHyperaldosteronism:_eMedicine_Pediatrics:_General_Medicine-2] "Hyperaldosteronism: eMedicine Pediatrics: General Medicine". Retrieved 2009-06-16.

[pmid11073536-3] Lafferty AR, Torpy DJ, Stowasser M, et al. (November 2000). "A novel genetic locus for low renin hypertension: familial hyperaldosteronism type II maps to chromosome 7 (7p22)". J. Med. Genet. 37 (11): 831–5. doi:10.1136/jmg.37.11.831. PMC 1734468 . PMID 11073536.

Classification	D ICD-10: E26 ICD-9-CM: 255.1 OMIM: 103900 605635 MeSH: D006929 DiseasesDB: 6187
External resources	MedlinePlus: 000330 eMedicine: radio/354 Patient UK: Hyperaldosteronism

匿名

検索

案内

hyperaldosteronism