Hyperaldosteronism hypertension

Bilateral adrenal hyperplasia Secondary hyperaldosteronism Hyperreninemic hyperaldosteronism (hypertension) Congenital adrenal hyperplasia (due to adrenal enzyme deficiencies in cortisol production [11 3- or 17a-hydroxylase])... 

Mulatero P, Schiavone D, Fallo F, Rabbia F, Pi-Ion C, Chiandussi L, Pascoe L, Veglio F (2000) CYP11B2 gene polymorphisms in idiopathic hyperaldosteronism. Hypertension 35 694-698... 

Hyperaldosteronism is a syndrome caused by excessive secretion of aldosterone. It is characterized by renal loss of potassium. Sodium reabsorption in the kidney is increased and accompanied by an increase in extracellular fluid. Clinically, an increased blood pressure (hypertension) is observed. Primary hyperaldosteronism is caused by aldosterone-producing, benign adrenal tumors (Conn s syndrome). Secondary hyperaldosteronism is caused by activation of the renin-angiotensin-aldosterone system. Various dtugs, in particular diuretics, cause or exaggerate secondary peadosteronism. 

ACE inhibitors do not completely block aldosterone synthesis. Since this steroid hormone is a potent inducer of fibrosis in the heart, specific antagonists, such as spironolactone and eplerenone, have recently been very successfully used in clinical trials in addition to ACE inhibitors to treat congestive heart failure [5]. Formerly, these drugs have only been applied as potassium-saving diuretics in oedematous diseases, hypertension, and hypokalemia as well as in primary hyperaldosteronism. Possible side effects of aldosterone antagonists include hyperkalemia and, in case of spironolactone, which is less specific for the mineralocorticoid receptor than eplerenone, also antiandrogenic and progestational actions. 

Potassium-sparing diuretics are often coadministered with thiazide or loop diuretics in the treatment of edema and hypertension. In this way, edema fluid is lost to the urine while K+ ion balance is better maintained. The aldosterone antagonists are particularly useful in the treatment of primary hyperaldosteronism. 

Long test-400 mg/day for 3 to 4 weeks. Correction of hypokalemia and hypertension provides presumptive evidence for diagnosis of primary hyperaldosteronism. 

When used for diagnosis of primary hyperaldosteronism, positive results are (long test) correction of hyperkalemia and hypertension (short test) serum potassium increases during administration, but falls upon discontinuation... 

Like all diuretics, the thiazides can cause electrolyte abnormalities, such as hypokalemia and hyponatremia, and dehydration. These complications are uncommon in patients with uncomplicated hypertension, but are more common in patients with heart failure or decompensated hepatic cirrhosis with secondary hyperaldosteronism. Until a patient is accustomed to the effect of a diuretic, dizziness may be experienced. Serum lipid concentrations are slightly raised acutely and hyperglycemia can occur during long-term therapy. Rare effects are thrombocytopenia, rashes, drug fever, cholestatic jaundice, pancreatitis, and precipitation of hepatic... 

Indications Hyperaldosteronism, hirsutism, hypertension Category Aldosterone antagonist Diuretic Half-life 78-84 minutes... 

Fardella CE, Mosso L, Gomez-Sanchez C, et al. Primary hyperaldosteronism in essential hypertensives Prevalence, biochemical profile, and molecular biology. J Clin Endocrinol Metab 2000 85 1863-1867. 

Primary hyperaldosteronism (Conn s syndrome) is rare. In most cases, the disease is due to a single adrenocortical adenoma. Patients may present with polydipsia and polyuria, symptoms of neuromuscular abnormalities such as weakness, paraeslhesiae and tetany, and hypertension. All symptoms other than hyjjcrtcnsion are attributable to potassium depletion. 

As with other K+-sparing diuretics, spironolactone often is coadministered with thiazide or loop diuretics in the treatment of edema and hypertension. Such combinations result in increased mobilization of edema fluid while causing lesser perturbations of K+ homeostasis. Spironolactone is particularly useful in the treatment of primary hyperaldosteronism (adrenal adenomas or bilateral adrenal hyperplasia) and of refractory edema associated with secondary aldosteronism (cardiac failure, hepatic cirrhosis, nephrotic syndrome, and severe ascites). Spironolactone is considered the diuretic of choice in patients with hepatic cirrhosis. Added to standard therapy, spironolactone substantially reduces morbidity and mortality and ventricular arrhythmias in patients with heart failure. 

These actions on electrolyte transport, in the kidney and in other tissues e.g., colon, salivary glands, and sweat glands), appear to account for the physiological and pharmacological activities that are characteristic of mineralocorticoids. Thus, the primary features of hyperaldosteronism are positive Na balance with consequent expansion of extracellular fluid volume, normal or slight increases in plasma Na+ concentration, hypokalemia, and alkalosis. Mineralocorticoid deficiency, in contrast, leads to Na+ wasting and contraction of the extracellular fluid volume, hyponatremia, hyperkalemia, and acidosis. Chronically, hyperaldosteronism can cause hypertension, whereas aldosterone deficiency can lead to hypotension and vascular collapse. 

Primary Hyperaldosteronism Caused by adrenal adenoma which secretes aldosterone. Results in hypertension, hypokalemia, metabolic alkalosis, suppressed renin. 

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