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PubMed1996

[Aldosterone precursors and hypertension with hypokalemia and adrenal module non caused by primary hyperaldosteronism].

The purpose of the study was to evaluate the interest of aldosterone precursors assays in arterial hypertension with hypokaliemia and adrenal nodules non due to aldosterone. Seven hypertensive patients, 3 men and 4 women, aged 59.5 +/- 10.1 years were included in the study. After drug withdrawal, kaliemia was 3.1 +/- 0.3 mmol/l (2.7-3.6), active renin 2.9 +/- 1.4 ng/l, plasma aldosterone (aldo) 108 +/- 49.4 pg/ml, cortisol 13 +/- 3.1 micrograms/100 ml, and [S] 0.47 +/- 0.5 micrograms/100 ml. Adrenal CT scan showed an adenoma in 3 patients (30.5 +/- 5 mm) and an unilateral nodular hyperplasia in 4 patients. In all patients, the plasma levels (RIA, chomatographic step) of the following steroids in the mineralocorticoid (MC) pathway were determined: DOC, 18 OH-DOC, B, 18 OH-B and aldosterone. Two from 7 (28%) exerted aldosterone precursors excess, 1 with DOC-producing adenoma (DOC-PA) (table), and 1 with a partial 11 beta hydroxylase deficiency (DOC: 211 pg/ml; S: 1 mu/100 ml). Aldosterone/DOC + 18 OH-DOC ratio proposed as a malignancy index was decreased in the patient with DOC-PA (8.1). No dysfunction in the MC pathway was identified in the 5 other patients. [table: see text] The study suggests the relevance of aldosterone precursors assays in low renin hypertension non due to aldosterone and in incidentally discovered adrenal masses.

Adenoma↗
PubMed1998

[Primary hyperaldosteronism and adenoma of the adrenal cortex. Suppression of aldosterone with dexamethasone].

The aim of the study was to evaluate dexamethazone test in a patient with primary aldosteronism caused by an adrenocortical adenoma. We observed a 50% decrease of plasma aldosterone as in glucocorticoid suppressible aldosteronism (GSA) but absolute value of aldosterone remained higher than 40 pg/ml. Basal plasma and urinary values of 18 OXO and 18 OH cortisol were not significantly elevated as in GSA. Inversely, the evaluation of 11 beta-hydroxylase activity of mineralocorticoids was in favor of a benign adrenal tumor.

Adenoma↗
PubMed1993

Hyperrenin-hyperaldosterone-dependent malignant hypertension in polyarteritis nodosa.

We have described a patient, subsequently found to have polyarteritis, whose renin activity was 60 times normal, a level associated with malignant hypertension and severe renal artery stenosis. The severe hypertension and its resistance to multiple medications in the face of a dramatic response to low-dose enalapril imply the renin-angiotensin system was the primary pathophysiologic mechanism. We believe renin activity should be measured in hypertensive patients with polyarteritis. Furthermore, PAN should be in the differential diagnosis of hyperreninemic hypertension. ACE inhibitors should be strongly considered in the management of classical PAN-induced hypertension.

Adult↗
PubMedDate not supplied

Primary hyperaldosteronism.

OBJECTIVE: To characterize the syndrome of primary aldosteronism and summarize diagnostic and therapeutic strategies. METHODS: We review the mechanisms of action of aldosterone and outline features that distinguish the major subtypes of aldosteronism. RESULTS: The state of aldosterone excess should be suspected in every patient manifesting hypertension and hypokalemia. The documentation of low renin activity and high plasma aldosterone concentration in such patients suggests the presence of primary aldosteronism. Lack of appropriate suppression of plasma aldosterone after saline infusion is thought to be the best maneuver for confirming primary aldosteronism. Nonetheless, a similar lack of aldosterone suppressibility after either oral salt loading for 3 days or oral administration of a single 25-mg dose of captopril may help achieve the same purpose. Once primary aldosteronism has been diagnosed, the distinction between two major subtypes--unilateral adrenal adenoma or Conn's syndrome and bilateral idiopathic adrenal hyperplasia--is important because of the difference in management. Certain physiologic maneuvers, such as change of posture from supine to upright, oral administration of cyproheptadine, and radiologic localization with several techniques including iodocholesterol scanning and adrenal venous sampling, will almost always help distinguish unilateral adenoma from bilateral hyperplasia. CONCLUSION: The distinction between adrenal adenoma and adrenal hyperplasia is critical because of the varied approach to treatment. Most patients with bilateral adrenal hyperplasia are managed medically with an aldosterone antagonist such as spironolactone, whereas most unilateral adenomas are resected after correction of hypertension and hypokalemia with appropriate medical therapy.

Journal Article↗