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General Considerations
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Classic hyperaldosteronism (with hypokalemia) accounts for about 07% of cases of hypertension Milder hyperaldosteronism, without hypokalemia, is more common, with a prevalence of 5 14% among hypertensives The disorder is more common in women Primary hyperaldosteronism may be due to unilateral adrenocortical adenoma (Conn s syndrome, 73%) or bilateral cortical hyperplasia (27%), which may be corticosteroid suppressible due to an autosomal-dominant genetic defect allowing ACTH stimulation of aldosterone production
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Clinical Findings
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A Symptoms and Signs
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Hypertension, muscular weakness (at times with paralysis simulating periodic paralysis), paresthesias with frank tetany, headache, polyuria, and polydipsia are the main complaints Hypertension is typically moderate Some patients have only diastolic hypertension, without other symptoms and signs Malignant hypertension is rare Edema is rarely seen in primary hyperaldosteronism
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B Laboratory Findings
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For a patient to be properly tested for hyperaldosteronism, all antihypertensive medications must be discontinued Calcium channel blockers can normalize aldosterone secretion, thus interfering with the diagnosis -Blockers suppress plasma renin activity in patients with essential hypertension The patient must have a high sodium intake (> 120 mEq/d) during the entire evaluation period; plasma potassium may be low A 24-hour urine collection is assayed for aldosterone, free cortisol, and creatinine A low plasma renin activity (< 5 mcg/ dL) with 24-hour urine aldosterone over 20 mcg indicates hyperaldosteronism The ratio of plasma aldosterone concentration to plasma renin activity has been used to screen for hyperaldosteronism Unfortunately, this test lacks sensitivity and specificity Once hyperaldosteronism is diagnosed, plasma is assayed for 18-hydroxycorticosterone; a level over 85 ng/dL is seen with adrenal neoplasms, whereas levels under 85 ng/dL are nondiagnostic Additionally, plasma can be assayed for aldosterone at 8 am while the patient is supine after overnight recumbency and again after 4 hours upright Patients with an adrenal adenoma usually have a baseline plasma aldosterone level > 20 ng/dL that does not rise In one study, serum aldosterone levels fell (after 4 hours upright) in 63% of patients with a unilateral aldosteronoma and in no patients with bilateral adrenal hyperplasia Patients with hyperplasia typically have a baseline plasma aldosterone level < 20 ng/dL that rises during upright posture Exceptions occur
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PRIMARY HYPERALDOSTERONISM
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ESSENTIALS OF DIAGNOSIS
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Hypertension, polyuria, polydipsia, muscular weakness Hypokalemia, alkalosis
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C Imaging
If biochemical testing implicates an adrenal aldosteronesecreting adenoma, a thin-section CT scan of the adrenals is
Endocrine Disorders
obtained A discrete adrenal adenoma (> 1 cm in diameter with normal contralateral adrenal) is found is 60 80% of such patients However, about 20% of such adenomas are found to be hyperplasia at surgery A dexamethasone-suppressed 131 I-labeled 6 -iodomethyl-19-norcholesterol scan (adrenal scintigraphy) can identify an aldosteronoma but may yield misleading results Therefore, it is often prudent to supplement CT localization with adrenal vein catheterization for aldosterone
CMDT 2008
Treatment
Conn s syndrome (unilateral adrenal adenoma secreting aldosterone) is treated by laparoscopic adrenalectomy, though lifelong spironolactone therapy is an option Bilateral adrenal hyperplasia is best treated with spironolactone; bilateral adrenalectomy corrects the hypokalemia but not the hypertension and should not be performed Antihypertensive agents may also be necessary Hyperplasia sometimes responds well to dexamethasone suppression
Differential Diagnosis
The differential diagnosis of hyperaldosteronism includes other causes of hypokalemia (see 21) in patients with essential hypertension For example, hypokalemia develops in many hypertensive patients taking diuretics even while taking potassium-sparing diuretics or potassium supplements Chronic depletion of intravascular volume stimulates renin secretion and secondary hyperaldosteronism Thus, it is important to discontinue diuretics and ensure adequate hydration and sodium intake when assessing a patient for primary hyperaldosteronism (see above) Excessive ingestion of real licorice (black and derived from anise) may produce hypertension and hypokalemia caused by a derivative of its glycyrrhizinic acid inhibiting 11 -hydroxysteroid dehydrogenase, thereby enhancing cortisol s mineralocorticoid effect Oral contraceptives may increase aldosterone secretion in some patients Renal vascular disease can cause severe hypertension with hypokalemia; plasma renin activity is high, distinguishing it from primary hyperaldosteronism Excessive adrenal secretion of other corticosteroids (besides aldosterone) may also cause hypertension with hypokalemia This occurs with certain congenital adrenal enzyme disorders such as P450c11 deficiency (increased deoxycorticosterone with virilization and deficient cortisol) or P450c17 deficiency (increased deoxycorticosterone, corticosterone, and progesterone but deficient estradiol and testosterone) P450c17 deficiency results from a defect in the 17-hydroxylase enzyme in both the adrenal and ovarian steroidogenic pathways Presenting signs include hypertension and ambiguous genitalia or primary amenorrhea Urinary aldosterone secretion is less than 20 mcg/24 h and plasma renin is low in both P450c11 and P450c17 deficiencies Primary cortisol resistance can cause hypertension and hypokalemia; renin and aldosterone are suppressed, while plasma levels of cortisol, ACTH, and deoxycorticosterone are high Liddle s syndrome is an autosomal dominant cause of hypertension and hypokalemia resulting from excessive sodium absorption from the renal tubule; renin and aldosterone levels are low Thyrotoxicosis and familial periodic paralysis may also present with hypokalemia Hyperaldosteronism may rarely be due to a malignant ovarian tumor
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