Research

Significance of lipopolysaccharide-binding protein (an acute phase protein) in monitoring critically ill patients

Miroslav Prucha¹ , Ivan Herold², Roman Zazula³, Ladislava Dubska¹, Miroslav Dostal¹, Thomas Hildebrand¹ and Josef Hyanek⁴

¹Staff, Department of Clinical Biochemistry, Hematology and Immunology, Hospital Na Homolce, Czech Republic

²Head, Department of Anesthesiology and Intensive Care Medicine, Klaudian's Hospital – Mlada Boleslav, Czech Republic

³Head, Department of Anesthesiology and Intensive Care, Thomayer's Hospital, Prague, Czech Republic

⁴Head, Department of Clinical Biochemistry, Hematology and Immunology, Hospital Na Homolce, Czech Republic

author email corresponding author email

Critical Care 2003, 7:R154-R159doi:10.1186/cc2386

Published:	1 October 2003

Abstract

Introduction

The present study was conducted to assess the value of serum concentration of lipopolysaccharide-binding protein (LBP) in patients with systemic inflammatory response syndrome (SIRS), sepsis and septic shock with respect to its ability to differentiate between infectious and noninfectious etiologies in SIRS and to predict prognosis.

Methods

This prospective cohort study was conducted in a multidisciplinary intensive care unit. Sixty-eight patients, admitted consecutively to the intensive care unit and who met criteria for SIRS, sepsis or septic shock were included. Serum LBP was measured using an immunochemiluminiscence assay.

Results

Serum levels of LBP were significantly increased in patients with SIRS (n = 40; median 30.6 μg/ml, range 9.2–79.5 μg/ml), sepsis (n = 19; median 37.1 μg/ml, range 11.8–76.2 μg/ml) and septic shock (n = 9; median 59.7 μg/ml, range 31.1–105 μg/ml), as compared with levels in the healthy volunteers (5.1 ± 2.2 μg/ml; P < 0.0001). Serum LBP at study entry was statistically significantly lower in patients with SIRS than in those with septic shock (P < 0.014); no statistically significant difference existed between patients with SIRS and those with sepsis (P = 0.61). Specificity and sensitivity of an LBP concentration of 29.8 μg/ml to distinguish between infectious and noninfectious etiologies for SIRS were 50% and 74.2%, respectively. There was no statistically significant difference in LBP concentration between survivors and nonsurvivors in both groups of patients. Furthermore, in septic patients the LBP response appeared to exhibit a decreased magnitude.

Conclusion

LBP is a nonspecific marker of the acute phase response and cannot be used as a diagnostic tool for differentiating between infectious and noninfectious etiologies of SIRS.