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Inicio Endocrinología y Nutrición Cambios hormonales en las enfermedades críticas
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Vol. 48. Núm. 1.
Páginas 6-20 (enero 2001)
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Vol. 48. Núm. 1.
Páginas 6-20 (enero 2001)
Acceso a texto completo
Cambios hormonales en las enfermedades críticas
Normal changes in critical illness
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4783
M. Albaredaa,**, R. Corcoyb
a Serveis d'Endocrinología i Nutrició. Hospital de la Creu Roja. Barcelona
b Hospital de la Santa Creu i Sant Pau. UAB. Barcelona
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Bibliografía
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Una enfermedad critica conlleva respuestas endocrinas que difieren segun la duracion del estres. En las situaciones agudas, se produce un aumento de secrecion de prolactina, cortisol, glucagon, catecolaminas y hormona de crecimiento (GH) con valores disminuidos de factor de crecimiento similar a la insulina tipo 1 (IGF-1) y descenso de la actividad β pancreatica, tiroidea y gonadal. Se considera que estos cambios son adaptativos y no especificos del tipo de estres, y van dirigidos a adecuar el volumen intravascular, la presion de perfusion y la disponibilidad de sustratos. Si el proceso critico se prolonga, se produce un estado de hipercatabolismo proteico que se acompana de hiperglucemia, hiperinsulinemia, insulinorresistencia, hipoproteinemia y deplecion de agua y potasio intracelular. Esta respuesta se ha valorado como inadecuada y puede dificultar la recuperacion de los sistemas, contribuyendo, ademas, a una mayor necesidad de cuidados intensivos.

Palabras clave:
Catabolismo
Estrés
Eje hipotálamo-hipófiso-adrenal
Eje hipotálamo-hipófiso-tiroideo
Eje somatotrópico
Metabolismo hidrocarbonado
Metabolismo fosfocálcico
Catecolaminas
Sistema renina-angiotensina-aldosterona

Criticall illness results in endocrine responses which depend on the duration of the stress. The initial endocrine response includes hypersecretion of prolactin, cortisol, catecholamines, glucagon and growth hormone (GH) with low insulin-like growth factor (IGF-1) and a reduced of the â cell and thyroid and gonadal axis. These changes have been considered adaptative and non-specific and provide optimal intravascular volume, pressure perfussion and substrate availability. If the stress is prolonged, protein hypercatabolism becomes important and it is accompained by hyperglycemia, hypertriglyceridemia, insulin resistance, hypoproteinemia and intracellular water and potassium depletion. This response is considered inappropiate does not assist to the recovery of the dysfunctioning systems, and can contribute to prolong the intensive care dependency.

Key words:
Catabolism
Stress
Hypothalamic-pituitary-adrenocortical axis
Hypothalamicpituitary-thyroid axis
Somatotropic axis
Carbohydrate metabolism
Calcium metabolism
Catecholamines
Renin-angiotensin-aldosterone axis
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