Science review Mechanisms of impaired adrenal function in sepsis and molecular actions of glucocorticoids 英文参考文献.docVIP

Available online /content/8/4/243 Review Science review: Mechanisms of impaired adrenal function in sepsis and molecular actions of glucocorticoids Hélène Prigent1, Virginie Maxime1 and Djillali Annane2 1Senior Resident, Service de Réanimation Médicale, H?pital Raymond Poincaré (Assistance Publique H?pitaux de Paris), Faculté de Médecine Paris Ile de France Ouest (Université de Versailles Saint-Quentin en Yvelines), Garches, France 2Director of the ICU, Service de Réanimation Médicale, H?pital Raymond Poincaré (Assistance Publique H?pitaux de Paris), Faculté de Médecine Paris Ile de France Ouest (Université de Versailles Saint-Quentin en Yvelines), Garches, France Corresponding author: Professor Djillali Annane, djillali.annane@rpc.ap-hop-paris.fr Published online: 25 May 2004 Critical Care 2004, 8:243-252 (DOI 10.1186/cc2878) This article is online at /content/8/4/243 ? 2004 BioMed Central Ltd Abstract This review describes current knowledge on the mechanisms that underlie glucocorticoid insufficiency in sepsis and the molecular action of glucocorticoids. In patients with severe sepsis, numerous factors predispose to glucocorticoid insufficiency, including drugs, coagulation disorders and inflammatory mediators. These factors may compromise the hypothalamic–pituitary axis (i.e. secondary adrenal insufficiency) or the adrenal glands (i.e. primary adrenal failure), or may impair glucocorticoid access to target cells (i.e. peripheral tissue resistance). Irreversible anatomical damages to the hypothalamus, pituitary, or adrenal glands rarely occur. Conversely, transient functional impairment in hormone synthesis may be a common complication of severe sepsis. Glucocorticoids interact with a specific cytosolic glucocorticoid receptor, which undergoes conformational changes, sheds heat shock proteins and translocates to the nucleus. Glucocorticoids may also interact