Hyperaldosteronism
| Hyperaldosteronism | |
|---|---|
| Other names: Aldosteronism[1] | |
 | |
| Aldosterone | |
 | |
| Specialty | Endocrinology |
| Symptoms | None, headaches, tiredness, muscle weakness, muscle cramps[2] |
| Complications | Heart arrhythmias, heart disease[2] |
| Types | Primary, secondary[2] |
| Causes | Primary: Bilateral adrenal hyperplasia, adrenal adenoma[2] Secondary: Renin-producing tumor, renal artery stenosis, heart failure, pregnancy, cirrhosis[2] |
| Diagnostic method | Suspected based on blood tests, confirmed by urine aldosterone[2] |
| Differential diagnosis | Essential hypertension, Liddle syndrome, syndrome of apparent mineralocorticoid excess[2] |
| Treatment | Lifestyle changes, medications, surgery[2] |
| Medication | Spironolactone, eplerenone, ACE inhibitors[2] |
| Frequency | 10% of people with high blood pressure[2] |
Hyperaldosteronism is the condition of too much aldosterone production.[2] Symptoms may vary from none, to high blood pressure and low potassium.[2] The blood pressure is often difficult to treat and can results in tiredness, headaches, and increased urination.[2] The low potassium can result in muscle weakness, muscle cramps, numbness, and heart arrhythmias.[2] Complications can include heart disease.[2]
It is divided into two types primary and secondary.[2] Primary cases occur due to excess production by the adrenal gland such as with bilateral adrenal hyperplasia or an adrenal adenoma (Conn's syndrome).[2] Secondary cases occur due to excessive activation of the renin-angiotensin-aldosterone system (RAAS) such as with renin-producing tumors, renal artery stenosis, heart failure, pregnancy, or cirrhosis.[2] High aldosterone levels result in increased sodium reabsorption by the kidneys.[2] Diagnosis is suspected based on blood tests and confirmed by urine aldosterone.[2]
In primary disease resulting from one adrenal gland, surgical removal is the treatment of choice.[2] In primary disease were both adrenal glands are involved spironolactone or eplerenone together with life style changes, including a low salt diet, is recommended.[2] For secondary disease treatment is directed at the underlying cause.[2] ACE inhibitors are often used to treat high blood pressure and protect the kidneys.[2]
Primary hyperaldosteronism is present in about 10% of cases of high blood pressure while secondary causes are less common.[2] Women are more often affected than men.[2] Primary hyperaldosteronism was first described in 1955 by Jerome W. Conn, an American endocrinologist.[3]
Signs and symptoms
It can be asymptomatic, but these symptoms may be present:
- Tiredness
- Headache
- High blood pressure
- Low potassium
- High sodium
- Low magnesium
- Intermittent or temporary paralysis
- Muscle spasms
- Muscle weakness
- Numbness
- Polyuria
- Polydipsia
- Tingling
- Metabolic alkalosis[4]
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. Secondary hyperaldosteronism can also be caused by Proximal renal tubular acidosis
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
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. Through inhibition of 11-beta-hydroxysteroid dehydrogenase type 2 (11-beta-HSD2), glycyrrhizin allows cortisol to activate mineralocorticoid receptors (MR) in the kidney. This severely potentiates mineralocorticoid receptor mediated renal sodium reabsorbtion, due to much higher circulating concentrations of cortisol compared to aldosterone. This, in turn, expands the extracellular volume, increases total peripheral resistance and increases arterial blood pressure. The condition is termed pseudohyperaldosteronism.
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, which has been linked to the 7p22 gene.[5]
The diagnosis may be supported by high serum aldosterone and low serum renin. A CT scan of the abdomen may detect an adenoma.
Treatment of an adrenal adenoma is by surgery while treatment of bilateral adrenocortical hyperplasia is with aldosterone antagonist such as 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 Renin–angiotensin system (RAAS).
Treatment
Treatment includes spironolactone, a potassium-sparing diuretic that works by acting as an aldosterone antagonist.
See also
References
- ↑ "aldosteronism" at Dorland's Medical Dictionary
- ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 2.18 2.19 2.20 2.21 2.22 2.23 2.24 2.25 Dominguez, A; Muppidi, V; Gupta, S (January 2020). "Hyperaldosteronism". PMID 29763159.
{{cite journal}}: Cite journal requires|journal=(help) - ↑ Clinic, Cleveland (2010). Current Clinical Medicine E-Book: Expert Consult - Online. Elsevier Health Sciences. p. 341. ISBN 978-1-4377-3571-0. Archived from the original on 2021-08-28. Retrieved 2021-02-16.
- ↑ "Hyperaldosteronism: eMedicine Pediatrics: General Medicine". Archived from the original on 2021-02-11. 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. Archived from the original on 2021-08-28. Retrieved 2009-01-03.
External links
| Classification | |
|---|---|
| External resources |