RESUMEN
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.
RESUMEN
Aprotinin (Trasylol; Bayer AG, Leverkusen, Germany), a protease inhibitor resembling or identical with Kunitz' pancreatic trypsin inhibitor, is said to have anticoagulant properties, but these are not clearly defined. The present study provides evidence that one action of aprotinin is inhibition of the activation of Hageman factor (factor XII).