Advances in Therapy

, Volume 23, Issue 6, pp 893–901 | Cite as

Circulating complement (C3 and C4) for differentiation of SIRS from sepsis

  • Hülya Sungurtekin
  • Ugur Sungurtekin
  • Canan Balci


The systemic inflammatory response of the body to invading microorganisms, called sepsis, leads to profound activation of the complement (C3 and C4) system. The present study was conducted to compare the use of serum C3 and C4 levels with C-reactive protein (CRP) and thrombocyte and leukocyte counts in differentiating patients with systemic inflammatory response syndrome (SIRS) from those with sepsis. Over a 6-mo period, all patients with SIRS or sepsis who stayed in the intensive care unit for > 24 h were enrolled in the study. At admission, each patient’s clinical status was recorded, and blood was taken for laboratory analysis (complete blood count, CRP, C3, and C4). A total of 58 patients with SIRS and 41 patients with sepsis were admitted to the study. The mean±SD thrombocyte count was found to be significantly lower in septic patients (179,975±95,615) than in those with SIRS (243,165±123,706) (P=.005); no difference in plasma concentrations of CRP and levels of C3 and C4 was noted between groups. The thrombocyte count was determined to be the most reliable parameter for differentiating between SIRS and sepsis (highest area under the curve=0.656).


sepsis complement SIRS 


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Bossink AWJ, Groeneveld ABJ, Hack CE, Thijs LG. The clinical host response to microbial infection in medical patients with fever.Chest. 1999; 116: 380–390.PubMedCrossRefGoogle Scholar
  2. 2.
    Bossink AW, Groeneveld AB, Thijs LG. Prediction of microbial infection and mortality in medical patients with fever: plasma procalcitonin, neutrophilic elastase-alpha1-antitrypsin, and lactoferrin compared with clinical variables.Clin Infect Dis. 1999; 29: 398–407.PubMedCrossRefGoogle Scholar
  3. 3.
    Balci C, Sungurtekin H, Gurses E, Sungurtekin U, Kaptanoglu B. Usefulness of procalcitonin for diagnosis of sepsis in the intensive care unit.Crit Care. 2003; 7: 85–90.PubMedCrossRefGoogle Scholar
  4. 4.
    Katja B, Hartmut K, Pawel M, Stefan B, Kox WJ, Spies CD. The value of immune modulating parameters in predicting the progression from peritonitis to septic shock.Shock. 2001; 15: 95–100.PubMedGoogle Scholar
  5. 5.
    Groeneveld AB, Bossink AW, van Mierlo GJ, Hack CE. Circulating inflammatory mediators in patients with fever: predicting bloodstream infection.Clin Diagn Lab Immun. 2001; 8: 1189–1195.CrossRefGoogle Scholar
  6. 6.
    Casey LC, Balk RA, Bone RC. Plasma cytokine and endotoxin levels correlate with survival in patients with the sepsis syndrome.Ann Intern Med. 1993; 119: 771–778.PubMedGoogle Scholar
  7. 7.
    Hack CE, Nuijens JH, Felt-Bersma RJF, et al. Elevated plasma levels of the anaphylatoxins C3a and C4a are associated with a fatal outcome in sepsis.Am J Med. 1989; 86: 20–26.PubMedCrossRefGoogle Scholar
  8. 8.
    Gardinali M, Padalino P, Vesconi S, et al. Complement activation and polymorphonuclear neutrophil leukocyte elastase in sepsis: correlation with severity of disease.Arch Surg. 1992; 127: 1219–1224.PubMedGoogle Scholar
  9. 9.
    Stove S, Welte T, Wagner TO, et al. Circulating complement proteins in patients with sepsis or systemic inflammatory response syndrome.Clin Diagn Lab Immunol. 1996; 3: 175–183.PubMedGoogle Scholar
  10. 10.
    Damas P, Canivet JL, deGroote D, et al. Sepsis and serum cytokine concentrations.Crit Care Med. 1997; 25: 405–412.PubMedCrossRefGoogle Scholar
  11. 11.
    Selberg O, Hecker H, Martin M, Klos A, Bautsch W, Kohl J. Discrimination of sepsis and systemic inflammatory response syndrome by determination of circulating plasma concentrations of procalcitonin, protein complement 3a, and interleukin-6.Crit Care Med. 2000; 28: 2793–2798.PubMedCrossRefGoogle Scholar
  12. 12.
    Bone RC, Balk RA, Cerra FB, et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis: The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine.Chest. 1992; 101: 1644–1655.PubMedCrossRefGoogle Scholar
  13. 13.
    Oberhoffer M, Karzai W, Meier-Hellmann A, Bogel D, Fassbinder J, Reinhart K. Sensitivity and specificity of various markers of inflammation for the prediction of tumor necrosis factor-alpha and interleukin-6 in patients with sepsis.Crit Care Med. 1999; 27: 1814–1818.PubMedCrossRefGoogle Scholar
  14. 14.
    Ember JA, Hugli TE. Complement factors and their receptors.Immunopharmacology. 1997; 38: 3–15.PubMedCrossRefGoogle Scholar
  15. 15.
    Pinsky MR, Vincent JL, Deviere J, Alegre M, Kahn RJ, Dupont E. Serum cytokine levels in human septic shock: relation to multiple-system organ failure and mortality.Chest. 1993; 103: 565–575.PubMedCrossRefGoogle Scholar
  16. 16.
    Heideman M, Hugli TE. Anaphylatoxin generation in multisystem organ failure.J Trauma. 1984; 24: 1038–1043.PubMedCrossRefGoogle Scholar
  17. 17.
    Groeneveld ABJ, Tacx AN, Bossink AWJ, van Mierlo GJ, Hack CE. Circulating inflammatory mediators predict shock and mortality in febrile patients with microbial infection.Clin Immunol. 2003; 106: 106–115.PubMedCrossRefGoogle Scholar
  18. 18.
    Nakae H, Endo S, Inada K, Yoshida M. Chronological changes in the complement system in sepsis.Surg Today. 1996; 26: 225–229.PubMedCrossRefGoogle Scholar
  19. 19.
    Kang HJ, Kim JH, Lee EH, Lee YK, Hur M, Lee KM. Change of complement system predicts the outcome of patients with severe thermal injury.J Burn Care Rehabil. 2003; 24: 148–153.PubMedCrossRefGoogle Scholar
  20. 20.
    Messias-Reason IJ, Hayashi SY, Nisihara RM, Kirschfink M. Complement activation in infective endocarditis: correlation with extracardiac manifestations and prognosis.Clin Exp Immunol. 2002; 127: 310–315.PubMedCrossRefGoogle Scholar
  21. 21.
    Hecke F, Schmidt U, Kola A, Bautsch W, Klos A, Kohl J. Circulating complement proteins in multiple trauma patients: correlation with injury severity, development of sepsis, and outcome.Crit Care Med. 1997; 25: 2015–2024.PubMedCrossRefGoogle Scholar
  22. 22.
    Vanderschueren S, DeWeerdt A, Malbrain M, et al. Thrombocytopenia and prognosis in intensive care.Crit Care Med. 2000; 28: 1871–1876.PubMedCrossRefGoogle Scholar
  23. 23.
    Boldt J, Menges T, Wollbruck M, Sonneborn S, Hempelmann G. Platelet function in critically ill patients.Chest. 1994; 106: 899–903.PubMedCrossRefGoogle Scholar
  24. 24.
    Stephan F, Montblanc JD, Cheffi A, Bonnet F. Thrombocytopenia in critically ill surgical patients: a case-control study evaluating attributable mortality and transfusion requirements.Crit Care. 1999; 3: 151–158.PubMedCrossRefGoogle Scholar
  25. 25.
    Stephan F, Hollande J, Richard O, Cheffi A, Maier-Redelsperger M, Flahault A. Thrombocytopenia in a surgical ICU.Chest. 1999; 115: 1363–1370.PubMedCrossRefGoogle Scholar
  26. 26.
    Riedler GF, Straub PW, Frick PG. Thrombocytopenia in septicemia: a clinical study for the evaluation of its incidence and diagnostic value.Helv Med Acta. 1971; 36: 23–38.PubMedGoogle Scholar

Copyright information

© Health Communications Inc 2006

Authors and Affiliations

  • Hülya Sungurtekin
    • 1
  • Ugur Sungurtekin
    • 1
  • Canan Balci
    • 1
  1. 1.Department of Anesthesiology and ReanimationPamukkale University School of MedicineDenizliTurkey

Personalised recommendations