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Hyperaldosteronism

What is Hyperaldosteronism?

In hyperaldosteronism, hypersecretion of the mineralocorticoid aldosterone by the adrenal cortex causes excessive reabsorption of sodium and water and excessive renal excretion of potassium.

The disorder may be classified as primary, resulting from a stimulus inside the adrenal gland, or secondary, resulting from an extra-adrenal stimulus. Incidence of hyperaldosteronism is two times greater in women than in men and highest between ages 30 and 50.

Causes of Hyperaldosteronism

Primary hyperaldosteronism (Conn's syndrome) is uncommon. In 70% of patients, it results from a small, unilateral aldosterone-producing adrenal adenoma. In the remaining 30%, the cause is either unclear, adrenocortical hyperplasia (in children), or carcinoma. Excessive ingestion of English black licorice or a similar substance can produce a syndrome similar to primary hyperaldosteronism due to the mineralocorticoid action of a type of acid found in licorice.

Secondary hyperaldosteronism results from extra-adrenal pathology. which stimulates the adrenal gland to increase production of aldosterone. For example, conditions that reduce renal blood flow (renal artery stenosis) and extracellular fluid volume or that produce a sodium deficit activate the renin-angiotensin system and, subsequently, increase aldosterone secretion. Thus, secondary hyperaldosteronism may result from conditions that induce hypertension through increased renin production (such as Wilms' tumor), from ingestion of oral contraceptives, and from pregnancy. Secondary hyperaldosteronism may also result from disorders unrelated to hypertension that may or may not cause edema. For example, nephrotic syndrome, hepatic cirrhosis with ascites, and heart failure commonly induce edema; Bartter's syndrome and salt-losing nephritis don't.

Signs & Symptoms of Hyperaldosteronism

Symptoms can be very non specific and subtle. In many cases mild to moderate high blood pressure may be the only Signs of Conn's syndrome.

  • High blood pressure
  • fatigue
  • numbness
  • headache
  • Mild hypertension
  • intermittent paralysis
  • Absence of edema
  • Muscular weakness due to low potassium
  • Polyuria and polydipsia
  • Minimal retinal vascular changes

Diagnostic tests

A persistently low serum potassium level in a nonedamatous patient who isn't taking diuretics, who doesn't have obvious GI losses (from diarrhea), and who has a normal sodium intake suggests hyperaldosteronism. If hypokalemia develops in a hypertensive patient shortly after starting treatment with potassium-wasting diuretics (such as thiazides) and it persists after the diuretic has been discontinued and potassium replacement therapy has been instituted, evaluation for hyperaldosteronism is necessary. The following test results confirm hyperaldosteronism:

  • A low plasma renin level after volume depletion by diuretic administration when the patient is sitting or standing and a high plasma aldosterone level after volume expansion by salt loading confirm primary hyperaldosteronism in a hypertensive patient without edema.
  • Elevated serum bicarbonate levels with ensuing alkalosis commonly results from hydrogen and potassium ion loss in the distal renal tubules.
  • Other test findings show markedly increased urine aldosterone levels, increased plasma aldosterone levels, and increased plasma renin levels (in secondary hyperaldosteronism).
  • A suppression test is used to differentiate between primary and secondary hyperaldosteronism. The patient receives oral desoxycorticosterone acetate for 3 days while plasma aldosterone levels and urine metabolites are continuously measured. These levels decrease in secondary hyperaldosteronism but remain the same in primary hyperaldosteronism. Simultaneously, renin levels are low in primary hyperaldosteronism and high in secondary hyperaldosteronism.
  • Other helpful diagnostic evidence includes increased plasma volume of 30% to 50% above normal; electrocardiogram Signs of hypokalemia (ST-segment depression and U waves); chest X-ray showing left ventricular hypertrophy from chronic hypertension; and location of tumor shown on computed tomography scan, ultrasonography, or magnetic resonance imaging.

Treatment

Treatment for primary hyperaldosteronism may include unilateral adrenalectomy, but hyperaldosteronism may be controlled without surgery through administration of the potassium-sparing diuretic spironolactone and sodium restriction. Bilateral adrenalectomy reduces blood pressure for most patients with idiopathic primary hyperaldosteronism. However, some degree of hypertension usually persists, requiring treatment with spironolactone or other antihypertensive drug. Such patients also require lifelong adrenal hormone replacement.

Treatment of secondary hyperaldosteronism must include correction of the underlying cause.

Prevention Tips

There is no known prevention for most causes of hyperaldosteronism.


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