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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.

Core temperature correlates with expression of selected stress and immunomodulatory genes in febrile patients with sepsis and noninfectious SIRS

“…As noted previously, about 1/6 of the sequences identified in this study correspond to genes that were previously reported to be affected by EHI (Sonna et al 2004). Furthermore, of the 12 sequences for which the expression response to temperature was affected by clinical diagnosis in this study, at least three correspond to proteins that have been found by others to display different levels of expression in serum obtained from patients with sepsis vs. noninfectious SIRS:interleukin 8 (Rodriguez-Gaspar et al 2001), lipopolysaccharide binding protein (Prucha et al 2003), and HSP 70 (Adib-Conquy and Cavaillon 2007). Finally, housekeeping genes reported to show stable expression after exertional hyperthermia in vivo in a prior work (Sonna et al 2004) also showed stable expression with respect to temperature and clinical diagnosis in this study.…”

Serum Lipopolysaccharide Binding Protein Levels Predict Severity of Lung Injury and Mortality in Patients with Severe Sepsis

“…They measured LBP plasma levels in 253 patients with severe sepsis and/or septic shock and reported mean LBP levels in the lower range of those not only in our series but also in other recent reports [13], [22], [29]. They found that LBP levels were less elevated in non-survivors than survivors.…”

“…Prucha et al [13] assessed LBP levels at study entry and at 3- to 5-day intervals for 30 days or until death in a mixed population of 68 patients with systemic inflammatory response, sepsis or septic shock. However, they did not find significant differences in LBP levels between patients with systemic inflammatory response and sepsis or between survivors and non-survivors, since only 9 patients had severe sepsis and/or septic shock.…”

“…LBP is a type I acute phase response protein that is produced by hepatocytes, respiratory epithelial cells and a myriad of other cell types [10], and enhances the recognition of endotoxin and pathogens by the immune system [11]. LBP binds to Gram-negative bacteria via the lipid A part of the lipopolysaccharide (LPS) which mediates its binding to the CD14 cellular receptor molecule presented by monocytes and macrophages [12], [13]. Binding of LPS activates monocyte/macrophage system cells via Toll-like receptors [14], resulting in the production of pro-inflammatory cytokines that aggravate the clinical presentation of sepsis.…”

Dynamics of Systemic Inflammatory Response Markers in Patients With Urgent Conditions Depend-Ing on the Development of Sepsis

“…This allows differentiating infectious and noninfectious inflammation, local or systemic infection, as well as predicting the severity of the course of sepsis and its outcomes [16].…”