title: Elevated growth-arrest-specific protein 6 plasma levels in patients with severe sepsis.
abstract: OBJECTIVE
  Growth-arrest-specific protein 6 (Gas6), an intracellular protein released by apoptotic cells, has been detected in normal plasma. As the Gas6 system has been implicated in mouse susceptibility to sepsis, and as leukocyte apoptosis is thought to play a major role in the physiopathology of human severe sepsis, we studied Gas6 plasma levels and possibly related variables in patients with severe sepsis.
  
  
  METHODS
  Matched case-control study.
  
  
  METHODS
  Adult intensive care unit in a university hospital.
  
  
  METHODS
  Thirty patients with severe sepsis, 30 patients with organ failure not related to infection, and 30 healthy subjects matched for age and gender.
  
  
  METHODS
  Blood draw.
  
  
  RESULTS
  Gas6 plasma levels were quantified using enzyme-linked immunosorbent assay. Whole-blood gas6 messenger RNA levels were measured by quantitative real-time polymerase chain reaction. Gas6 plasma levels were elevated (110 ng/mL [75, 139]; median values [interquartile range]) in severe sepsis patients compared with organ failure patients (85 ng/mL [56, 101]) and healthy subjects (54 ng/mL [49, 68]). In patients with severe sepsis, this increase correlated with the Acute Physiology and Chronic Health Evaluation II severity score, the organ failure Organ Dysfunction and Infection (ODIN) score, and the existence of a septic shock. Gas6 messenger RNA levels were increased in patients with severe sepsis and correlated specifically with the monocyte count.
  
  
  CONCLUSIONS
  In severe sepsis, the recently described anti-apoptotic protein Gas6 was found at high levels in plasma and correlated well with the degree of organ dysfunction.
authors.affiliation: Inserm U428, Service d'Hématologie Biologique A, Hôpital Européen Georges Pompidou, Paris, France. delphine.borgel@univ-paris5.fr
authors.forename: Delphine
authors.initials: D
authors.lastname: Borgel
authors.forename: Sylvain
authors.initials: S
authors.lastname: Clauser
authors.forename: Caroline
authors.initials: C
authors.lastname: Bornstain
authors.forename: Ivan
authors.initials: I
authors.lastname: Bièche
authors.forename: Alvine
authors.initials: A
authors.lastname: Bissery
authors.forename: Véronique
authors.initials: V
authors.lastname: Remones
authors.forename: Jean-Yves
authors.initials: JY
authors.lastname: Fagon
authors.forename: Martine
authors.initials: M
authors.lastname: Aiach
authors.forename: Jean-Luc
authors.initials: JL
authors.lastname: Diehl
mesh_terms: D018806:APACHE; D000368:Aged; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D003422:Critical Care / Q000379:methods; D016638:Critical Illness; D018450:Disease Progression; D005260:Female; D006785:Hospitals, University; D006801:Humans; D007362:Intensive Care Units; D036341:Intercellular Signaling Peptides and Proteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009102:Multiple Organ Failure / Q000097:blood* / Q000175:diagnosis / Q000401:mortality* / Q000628:therapy; D011336:Probability; D011379:Prognosis; D012016:Reference Values; D018570:Risk Assessment; D012680:Sensitivity and Specificity; D012772:Shock, Septic / Q000097:blood / Q000175:diagnosis / Q000401:mortality / Q000628:therapy; D016019:Survival Analysis; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood* / Q000175:diagnosis / Q000401:mortality* / Q000628:therapy; D000099255:Growth Arrest-Specific Protein 6
chemical_list: D015415:Biomarkers; D036341:Intercellular Signaling Peptides and Proteins; D000099255:Growth Arrest-Specific Protein 6