The Compensatory Anti-inflammatory Response Syndrome (CARS) in Critically Ill Patients

被引:301
作者
Ward, Nicholas S. [1 ]
Casserly, Brian [1 ]
Ayala, Alfred [2 ]
机构
[1] Brown Univ, Warren Alpert Med Sch, Div Pulm Crit Care & Sleep Med, Providence, RI 02912 USA
[2] Brown Univ, Warren Alpert Med Sch, Dept Surg, Div Surg Res, Providence, RI 02912 USA
关键词
Sepsis; Compensatory anti-inflammatory response syndrome; Anergy; Systemic inflammatory response syndrome; Anti-inflammatory; Human leukocyte antigen;
D O I
10.1016/j.ccm.2008.06.010
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Like the systemic inflammatory response syndrome (SIRS), the compensatory anti-inflammatory response syndrome (CARS) is a complex pattern of immunologic responses to severe infection or injury. The difference is that while SIRS is a proinflammatory response tasked with killing infectious organisms through activation of the immune system, CARS is a global deactivation of the immune system tasked with restoring homeostasis. Much research now suggests that the timing and relative magnitude of this response have a profound impact on patient outcomes.
引用
收藏
页码:617 / +
页数:10
相关论文
共 78 条
[1]  
ABRAHAM E, 1985, CIRC SHOCK, V15, P141
[2]  
Åhlström A, 2004, CLIN NEPHROL, V61, P103
[3]   Early postoperative monocyte deactivation predicts systemic inflammation and prolonged stay in pediatric cardiac intensive care [J].
Allen, ML ;
Peters, MJ ;
Goldman, A ;
Elliott, M ;
James, I ;
Callard, R ;
Klein, NJ .
CRITICAL CARE MEDICINE, 2002, 30 (05) :1140-1145
[4]   Dehydroepiandrosterone -: An inexpensive steroid hormone that decreases the mortality due to sepsis following trauma-induced hemorrhage [J].
Angele, MK ;
Catania, RA ;
Ayala, A ;
Cioffi, WG ;
Bland, KI ;
Chaudry, IH .
ARCHIVES OF SURGERY, 1998, 133 (12) :1281-1287
[5]  
Angele MK, 1997, ARCH SURG-CHICAGO, V132, P1207
[6]  
Asadullah K, 1995, Eur J Emerg Med, V2, P184, DOI 10.1097/00063110-199512000-00003
[7]   Anti-inflammatory response is associated with mortality and severity of infection in sepsis [J].
Ashare, A ;
Powers, LS ;
Butler, NS ;
Doerschug, KC ;
Monick, MM ;
Hunninghake, GW .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2005, 288 (04) :L633-L640
[8]   Monocyte response to bacterial toxins, expression of cell surface receptors, and release of anti-inflammatory cytokines during sepsis [J].
Astiz, M ;
Saha, D ;
Lustbader, D ;
Lin, R ;
Rackow, E .
JOURNAL OF LABORATORY AND CLINICAL MEDICINE, 1996, 128 (06) :594-600
[9]   Increased mucosal B-lymphocyte apoptosis during polymicrobial sepsis is a Fas ligand but not an endotoxin-mediated process [J].
Ayala, A ;
Xu, YX ;
Ayala, CA ;
Sonefeld, DE ;
Karr, SM ;
Evans, TA ;
Chaudry, IH .
BLOOD, 1998, 91 (04) :1362-1372
[10]  
Baker CC, 1998, J TRAUMA, V44, P1045