Arterial hypertension is not a privilege of adults. Besides renal and vascular causes, adrenocortical and correlated diseases must be considered when investigating a hypertensive child or adolescent. The mineralocorticoid (MC) receptor can be activated by typical MC as well as by cortisol, and even run autonomously, as a result of disturbances in the sodium channel. Thus, MC hyperactivity (hypertension, hypokalemia and renin suppression) may result from excess of: (1) aldosterone, (2) deoxycorticosterone (DOC), and (3) cortisol. The first group, called primary hyperaldosteronism (PHA), includes aldosterone-producing adenoma, carcinoma and hyperplasia, in addition to familial causes: dexamethasone suppressible HA (or type I) and type II familial PAH. The second group encompasses DOC-producing, as well as androgen- and estrogen-producing tumors, and ACTH-dependent DOC hypersecretion (Cushing’s syndrome, congenital adrenal hyperplasia due to 11beta- and 17alpha-hydroxylase deficiencies and the syndrome of peripheral cortisol resistance). In the syndrome of apparent MC excess, cortisol acts as the operating MC, due to congenital deficiency or licorice-induced enzymatic inhibition of 11beta-hydroxysteroid dehydrogenase, responsible for cortisol to cortisone oxidation. Sodium and fluids are inappropriately absorbed at the renal tubule, both in Liddle’s syndrome (activating mutations in the epithelial Na+ channel gene) and Arnold-Healy-Gordon’s syndrome (in which excess tubular chloride and sodium resorption impairs H+ and K+ excretion, producing hypertension with acidosis and hyperkalemia). Although not much prevalent, this wide spectrum of hypertensive adrenal diseases should be considered as the potential cause of childhood and adolescence hypertension.
Hypertension; Adrenal cortex; Childhood; Mineralocorticoid; Aldosterone; Cortisol
