Lipopolysaccharide Binding Protein, Soluble-Intercellular Adhesion Molecule-1, Procalcitonin, and Protein C Activity and Clinical Outcome in Systemic Inflammatory Response Syndrome (SIRS) or Sepsis Patients
Abstract
BACKGROUND: Biochemical markers may be used in diagnosis, prognostic and monitoring treatment and therapy for sepsis patients. In this study we used Lipopolysacharide Binding Protein (LBP), serum-Intercellular Adhesion Molecule-1 (ICAM-1), Procalcitonin (PCT) and protein C activity. LBP is related to lipopolysachharide or gram-negative bacterial endotoxin which bound to LBP and induced inflammatory response. ICAM-1 is associated with endothelial dysfunction in response to systemic inflammatory and septic condition. PCT increased in bacterial infection and in severe systemic inflammatory. Role of Protein C is protecting the intravascular system to systemic inflammation, sepsis and the concomitant intravascular coagulopathy. The aim of this study was to examine the associations between levels of serum LBP, sICAM-1, PCT, and protein C activity with the clinical outcome of SIRS or sepsis patients.
METHODS: We included 19 post surgery patients with SIRS criteria from intensive care unit (ICU) and evaluated the level of LBP serum with Chemiliuminescent Enzyme Immunoassay (Diagnostic Product Co.), ICAM-1 with ELISA (R&D System), PCT with immunochromatography (BRAHMS), protein C activity with chromogenic method (Dade Behring). We performed the samples serially at the first admission of patients and after 72 hours. Data were analysed by non-parametric with Wilcoxon test and Mann-Whitney test. Correlation study between biomarkers calculated by Kendall’s tau and Spearman’s rho.
RESULTS: Of 19 patients, 9 (47,4%) died and 10 (52,6%) surviving. The level of LBP serum decreased after 72 hours in surviving-sepsis patients, and increased in nonsurviving sepsis patients with significant different levels at 72 hours examination (P<0.05). The level of soluble-ICAM-1 which was high in the first admission showed in non-surviving sepsis patients, but the difference levels was not significant between surviving and non-surviving patients (P>0.05). In all patients were found high level of PCT serum since the first admission examination, decreasing levels were occurred significantly in surviving patients after 72 hours (P<0.05) where high PCT levels were found in non-surviving patients after 72 hours. The median level of plasma protein C activity was low at the first admission especially in non-surviving sepsis patients, the decreasing level was not significantly different after 72 hours (P>0.05) both in surviving and non-surviving patients.
CONCLUSIONS: Increasing level of LBP and PCT in sepsis patients showed that those biomarkers useful for predict the clinical outcome in sepsis patients. Decreasing protein C activity level was not a good predictor in worsening clinical outcomes. Soluble ICAM-1 level was not a good marker for predict risk of sepsis severity. LBP and PCT tests were more useful in serially testing from the first admission of sepsis patients, those tests are more faster than bacterial culture.
KEYWORDS: Sepsis, SIRS, Lipopolysachharide Binding Protein, soluble- Intercellular Adhesion Molecule-1, Procalcitonin, Protein C
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Martin GS, Mannino DM, Eaton S, Moss M. The epidemiology of sepsis in the United States from 1979 through 2000. N Engl J Med. 2003; 348: 1546-54, CrossRef.
Carrigan SD, Scott G, Tabrizian M. Toward resolving the challenges of sepsis diagnosis. Clin Chem. 2004; 50: 1301-14, CrossRef.
Takala A, Nupponen I, Kylanpaa-Back ML, Repo H. Markers of inflammation in sepsis. Ann Med. 2002; 34: 614-23, CrossRef.
Silverman MH, Ostro MJ. Bacterial endotoxin in human disease. DPC Industry Workshop AACC. 2000.
Gallin JI, Ognibene FP. Principles and practice of clinical research. 2nd ed.Boston : Elsever; 2007, NLMID.
Whicher J, Bienvenu J, Monneret G. Procalcitonin as an acute phase marker. Ann Clin Biochem. 2001; 38: 483-93, CrossRef.
Von Andrian UH, Mackay CR. T-Cell function and migration: two sides of the same coin. N Engl J Med. 2000. 343: 1020-34, CrossRef.
Bernard GR, Vincent JL, Laterre PR, Dhainaut JF, Lopez-Rodriguez A, et al. Efficacy and safety of recombinant human activated protein C for severe sepsis. N Engl J Med. 2001; 344: 699-709, CrossRef.
Matthay MA. Severe sepsis – A new treatment with both anticoagulant and antiinflammatory properties. N Engl J Med. 2001; 344: 759-62, CrossRef.
Rivers E, Nguyen B, Havstad S, Ressler J, Muzzib A, Knoblich B, et al. Early goal directed therapy in the treatment of severe Sepsis and Septic Chock. N Engl J Med. 2001; 345: 1368-77, CrossRef.
Bone RC, Balk RA, Cerra FB, Dellinger RP, Fein AM, Knaus WA, et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The AACP/SSCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Chest. 1992; 101: 1644-55, CrossRef.
Carroll SF, Dedrick RL, White ML. Plasma levels of lipopolysaccharide binding protein (LBP) correlate with outcome in sepsis and other patients. Shock. 1997; 8: 101.
Opal SM, Scannon PJ, Vincent JL, White M, Carroll SF, Palardy JE, et al. Relationship between plasma levels of lipopolysaccharide (LPS) and LPS-binding protein in patients with severe sepsis and septic shock. J Infect Dis. 1999; 180: 1584-89, CrossRef.
Hurley JC. Endotxemia: methods detection and clinical correlates. Clin Microbiol Rev. 1995; 8: 268-92, PMID.
Harbarth S, Holeckova K, Froidevaux C, Pittet D, Ricou B, Grau GE, et al. Diagnostic value of procalcitonin, interleukin-6, and interleukin-8 in critically ill patients admitted with suspected sepsis. Am J Respir Crit Care Med. 2001; 164: 396-402, CrossRef.
Dandona P, Nix D, Wilson MF, Aljada A, Love J, Assicot M, et al. Procalcitonin increase after endotoxin injection in normal subjects. J Clin Endocrinol Metab. 1994; 79: 1605-8, CrossRef.
Fourrier F, Chopin C, Goudemand J. Septic shock, multiple organ failure, and disseminated intravascular coagulation: compared patterns of antithrombin III, protein C, and protein S deficiencies. Chest. 1992; 101: 816-23, CrossRef.
Lorente JA, Garcia-Frade LJ, Landin L. Time course of hemostatic abnormalities isn sepsis and its relation to outcome. Chest. 1993; 103: 1536-42, CrossRef.
Boldt J, Papsdorf M, Rothe A, Kumle B. Changes of the hemostatic network in critically ill patients – is there a difference between sepsis, trauma, and neurosurgery patients. Crit Care Med. 2000; 28: 445-50, CrossRef.
Powars D, Larsen R, Johnson J. Epidemic meningococcemia and purpura fulminans with induced protein C deficiency. Clin Infect Dis. 1993; 17: 254-61, CrossRef.
Rintala EM, Aittoniemi J, Nevalainen TJ, Nikoskelainen J. Early identification of bacteremia by biochemical markers of systemic inflammation. Scan J Clin Lab Invest. 2001; 61: 523-30, CrossRef.
Pettila V, Pentti J, Pettila M, Takkunen O, Jousela I. Predictive value of antithrombin III and C-reactive protein concentration in critically ill patients with suspected sepsis. Crit Care Med. 2002; 30: 271-5, CrossRef.
Al-Nawas B, Krammer I, Shah PM. Procalcitonin in diagnosis of severe infection. Eur J Med Res. 1996; 1: 331-3, PMID.
Claeys R, Vinken S, Spapen H, ver Elst K, Decochez K, Huyghens L, et al. Plasma procalcitonin and C-reactive protein in acute septic shock: clinical and biological correlates. Crit Care Med. 2002; 30: 757-62, CrossRef.
DOI: https://doi.org/10.18585/inabj.v1i1.87
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