title: The innate immune response in HIV/AIDS septic shock patients: a comparative study.
abstract: BACKGROUND
  In recent years, the incidence of sepsis has increased in critically ill HIV/AIDS patients, and the presence of severe sepsis emerged as a major determinant of outcomes in this population. The inflammatory response and deregulated cytokine production play key roles in the pathophysiology of sepsis; however, these mechanisms have not been fully characterized in HIV/AIDS septic patients.
  
  
  METHODS
  We conducted a prospective cohort study that included HIV/AIDS and non-HIV patients with septic shock. We measured clinical parameters and biomarkers (C-reactive protein and cytokine levels) on the first day of septic shock and compared these parameters between HIV/AIDS and non-HIV patients.
  
  
  RESULTS
  We included 30 HIV/AIDS septic shock patients and 30 non-HIV septic shock patients. The HIV/AIDS patients presented low CD4 cell counts (72 [7-268] cells/mm(3)), and 17 (57%) patients were on HAART before hospital admission. Both groups were similar according to the acute severity scores and hospital mortality. The IL-6, IL-10 and G-CSF levels were associated with hospital mortality in the HIV/AIDS septic group; however, the CRP levels and the surrogates of innate immune activation (cytokines) were similar among HIV/AIDS and non-HIV septic patients. Age (odds ratio 1.05, CI 95% 1.02-1.09, p=0.002) and the IL-6 levels (odds ratio 1.00, CI 95% 1.00-1.01, p=0.05) were independent risk factors for hospital mortality.
  
  
  CONCLUSIONS
  IL-6, IL-10 and G-CSF are biomarkers that can be used to predict prognosis and outcomes in HIV/AIDS septic patients. Although HIV/AIDS patients are immunocompromised, an innate immune response can be activated in these patients, which is similar to that in the non-HIV septic population. In addition, age and the IL-6 levels are independent risk factors for hospital mortality irrespective of HIV/AIDS disease.
authors.affiliation: Laboratório de Medicina Intensiva, Instituto de Pesquisa Clinica Evandro Chagas (IPEC), Rio de Janeiro, RJ, Brazil.
authors.forename: Rodrigo T
authors.initials: RT
authors.lastname: Amancio
authors.forename: Andre M
authors.initials: AM
authors.lastname: Japiassu
authors.forename: Rachel N
authors.initials: RN
authors.lastname: Gomes
authors.forename: Emersom C
authors.initials: EC
authors.lastname: Mesquita
authors.forename: Edson F
authors.initials: EF
authors.lastname: Assis
authors.forename: Denise M
authors.initials: DM
authors.lastname: Medeiros
authors.forename: Beatriz
authors.initials: B
authors.lastname: Grinsztejn
authors.forename: Patrícia T
authors.initials: PT
authors.lastname: Bozza
authors.forename: Hugo C
authors.initials: HC
authors.lastname: Castro-Faria Neto
authors.forename: Fernando A
authors.initials: FA
authors.lastname: Bozza
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000276:immunology*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000378:metabolism; D002097:C-Reactive Protein / Q000276:immunology / Q000378:metabolism; D018791:CD4 Lymphocyte Count / Q000379:methods; D015331:Cohort Studies; D016638:Critical Illness; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D005260:Female; D016179:Granulocyte Colony-Stimulating Factor / Q000276:immunology / Q000378:metabolism; D015658:HIV Infections / Q000276:immunology*; D017052:Hospital Mortality; D006801:Humans; D007113:Immunity, Innate; D016753:Interleukin-10 / Q000276:immunology / Q000378:metabolism; D015850:Interleukin-6 / Q000276:immunology / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D018805:Sepsis / Q000276:immunology*; D012772:Shock, Septic / Q000276:immunology*
chemical_list: D015415:Biomarkers; D016207:Cytokines; D015850:Interleukin-6; D016753:Interleukin-10; D016179:Granulocyte Colony-Stimulating Factor; D002097:C-Reactive Protein