O espectro das síndromes de hipertensão esteróide na infância e adolescência
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...
| Autores: | , |
|---|---|
| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2001 |
| País: | Brasil |
| Institución: | Universidade Federal de São Paulo (UNIFESP) |
| Repositorio: | Repositório Institucional da UNIFESP |
| Idioma: | portugués |
| OAI Identifier: | oai:repositorio.unifesp.br:11600/1102 |
| Acceso en línea: | http://dx.doi.org/10.1590/S0004-27302001000100011 http://repositorio.unifesp.br/handle/11600/1102 |
| Access Level: | acceso abierto |
| Palabra clave: | Hypertension Adrenal cortex Childhood Mineralocorticoid Aldosterone Cortisol Hipertensão Córtex adrenal Infância Mineralocorticóide Aldosterona |
| Sumario: | 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. |
|---|