title: Comparison of oxidative stress & leukocyte activation in patients with severe sepsis & burn injury.
abstract: OBJECTIVE
  We evaluated pro- and anti-oxidant disturbances in sepsis and non-sepsis burn patients with systemic inflammatory response syndrome (SIRS). Adhesion molecules and inflammation markers on leukocytes were also analyzed. We hypothesized that oxidative stress and leukocyte activation markers can lead to the severity of sepsis.
  
  
  METHODS
  In 28 severe sepsis and 27 acute burn injury patients blood samples were collected at admission and 4 days consecutively. Oxidative stress markers: production of reactive oxygen species (ROS), myeloperoxidase, malondialdehyde and endogenous antioxidants: plasma protein sulphydryl groups, reduced glutathione, superoxide dismutase and catalase were measured. Flow cytometry was used to determine CD11a, CD14, CD18, CD49d and CD97 adhesion molecules on leukocytes. Procalcitonin, C-reactive protein, fibrinogen, platelet count and lactate were also analyzed.
  
  
  RESULTS
  Pro-oxidant parameters were significantly elevated in sepsis patients at admission, ROS intensity increased in burn patients until the 5th day. Endogenous antioxidant levels except catalase showed increased levels after burn trauma compared to sepsis. Elevated granulocyte activation and suppressed lymphocyte function were found at admission and early activation of granulocytes caused by increasing activation/migration markers in sepsis. Leukocyte adhesion molecule expression confirmed the suppressed lymphocyte and monocyte function in sepsis.
  
  
  CONCLUSIONS
  Severe sepsis is accompanied by oxidative stress and pathological leukocyte endothelial cell interactions. The laboratory parameters used for the evaluation of sepsis and several markers of pro- and antioxidant status were different between sepsis and non-sepsis burn patients. The tendency of changes in these parameters may refer to major oxidative stress in sepsis and developing SIRS in burns.
authors.affiliation: Department of Anaesthesia & Intensive Therapy, University of Pécs, Faculty of Medicine, Pécs, Hungary. drdianamuhl@gmail.com
authors.forename: Diana
authors.initials: D
authors.lastname: Mühl
authors.forename: Gábor
authors.initials: G
authors.lastname: Woth
authors.forename: Livia
authors.initials: L
authors.lastname: Drenkovics
authors.forename: Adrienn
authors.initials: A
authors.lastname: Varga
authors.forename: Subhamay
authors.initials: S
authors.lastname: Ghosh
authors.forename: Csaba
authors.initials: C
authors.lastname: Csontos
authors.forename: Lajos
authors.initials: L
authors.lastname: Bogár
authors.forename: György
authors.initials: G
authors.lastname: Wéber
authors.forename: János
authors.initials: J
authors.lastname: Lantos
mesh_terms: D000368:Aged; D002056:Burns / Q000503:physiopathology*; D002374:Catalase / Q000097:blood; D015815:Cell Adhesion Molecules / Q000097:blood*; D005260:Female; D005978:Glutathione / Q000097:blood; D006098:Granulocytes / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007962:Leukocytes / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D018384:Oxidative Stress; D009195:Peroxidase / Q000097:blood; D017382:Reactive Oxygen Species / Q000097:blood*; D018805:Sepsis / Q000503:physiopathology*; D013482:Superoxide Dismutase / Q000097:blood; D018746:Systemic Inflammatory Response Syndrome / Q000503:physiopathology*
chemical_list: D015815:Cell Adhesion Molecules; D017382:Reactive Oxygen Species; D008315:Malondialdehyde; D002374:Catalase; D009195:Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione