title: Nosocomial infections after severe trauma are associated with lower apolipoproteins B and AII.
abstract: BACKGROUND
  Infection after severe trauma is a significant cause of morbidity and mortality days to weeks after the initial injury. Apolipoproteins play important roles in host defense and circulating concentrations are altered by the acute inflammatory response. The purpose of this study was to determine if patients who acquire infection after severe trauma have significantly lower apolipoprotein levels than trauma patients who do not become infected.
  
  
  METHODS
  We conducted a case-control study on a prospectively identified cohort of adult patients admitted to our intensive care unit after severe trauma (Injury Severity Score ≥ 16). We compared plasma apolipoprotein levels between patients who acquired an infection within 30 days after trauma (cases) and those that remained infection free (controls).
  
  
  RESULTS
  Of 40 patients experiencing severe trauma, we identified 22 cases that developed an infection within 30 days after injury. Cases had significantly lower posttrauma plasma levels of apolipoprotein B (p = 0.02) and apolipoprotein AII (p = 0.02) compared with controls. Consistent with previous studies, cases also received greater volumes of crystalloid infusions (p < 0.01) and blood transfusions (p < 0.01). Cases also had a more profound inflammatory response as measured by interleukin 6 levels (p = 0.02).
  
  
  CONCLUSIONS
  Infection after severe trauma is associated with decreased circulating apolipoproteins as compared with uninfected controls. Profoundly decreased plasma apolipoproteins B and AII could potentially contribute to the impaired immunity after severe trauma. Apolipoproteins are potential targets for identifying those patients at risk of infection after trauma and for interventions aimed at preventing nosocomial infections.
  
  
  METHODS
  Prognostic study, level III.
authors.affiliation: Department of Emergency Medicine, University of New Mexico Health Sciences Center, Albuquerque, New Mexico, USA. jfemling@salud.unm.edu
authors.forename: Jon K
authors.initials: JK
authors.lastname: Femling
authors.forename: Sonlee D
authors.initials: SD
authors.lastname: West
authors.forename: Erik K
authors.initials: EK
authors.lastname: Hauswald
authors.forename: Hattie D
authors.initials: HD
authors.lastname: Gresham
authors.forename: Pamela R
authors.initials: PR
authors.lastname: Hall
mesh_terms: D000328:Adult; D016633:Apolipoprotein A-II / Q000097:blood* / Q000172:deficiency; D001055:Apolipoproteins B / Q000097:blood* / Q000172:deficiency; D003428:Cross Infection / Q000097:blood* / Q000453:epidemiology / Q000209:etiology; D005260:Female; D017052:Hospital Mortality / Q000639:trends; D006801:Humans; D015994:Incidence; D015601:Injury Severity Score; D008297:Male; D008875:Middle Aged; D009516:New Mexico / Q000453:epidemiology; D011379:Prognosis; D012189:Retrospective Studies; D015996:Survival Rate / Q000639:trends; D014193:Trauma Centers; D014947:Wounds and Injuries / Q000097:blood / Q000150:complications* / Q000401:mortality; D055815:Young Adult
chemical_list: D016633:Apolipoprotein A-II; D001055:Apolipoproteins B