Endocrine changes in sepsis.
The hormonal changes associated with sepsis appear to be important compensatory responses directed toward (1) increasing the availability of fuel (glucose, fatty acids, and amino acids) for the greatly accelerated needs of the cellular metabolic machinery and (2) maintaining an adequate blood volume, blood pressure, and tissue perfusion. Unrecognized or inadequately treated sepsis with subsequent prolonged trophic hormone stimulation depletes the patient of fuels necessary for the maintenance of the increased metabolic demands. This leads to eventual deleterious effects with muscle wasting, increased susceptibility to infection, and impaired wound healing. Manipulation of some of the hormones in sepsis, particularly insulin, glucagon, and growth hormone, with an adequate caloric intake to promote a more favorable anabolic response, holds exciting promise.
D000302:Adrenal Cortex / Q000378:metabolism; D000313:Adrenal Medulla / Q000378:metabolism; D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D004702:Endocrine Glands / Q000503:physiopathology*; D005934:Glucagon / Q000378:metabolism; D013006:Growth Hormone / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D010179:Pancreas / Q000378:metabolism; D010902:Pituitary Gland / Q000378:metabolism; D018805:Sepsis / Q000503:physiopathology*; D013961:Thyroid Gland / Q000378:metabolism; D013972:Thyrotropin / Q000378:metabolism; D013974:Thyroxine / Q000378:metabolism
D007328:Insulin; D000324:Adrenocorticotropic Hormone; D013972:Thyrotropin; D013006:Growth Hormone; D005934:Glucagon; D013974:Thyroxine