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.

Hospital-acquired pneumonia (HAP) is associated with high mortality. In Central Europe, there is a dearth of information on the prevalence and treatment of HAP. This project was aimed at collecting multicenter epidemiological data on patients with HAP in the Czech Republic and comparing them with supraregional data. This prospective, multicenter, observational study processed data from a database supported by a Czech Ministry of Health grant project. Included were all consecutive patients aged 18 and over who were admitted to participating intensive care units (ICUs) between 1 May 2013 and 31 December 2014 and met the inclusion criterion of having HAP. The primary endpoint was to analyze the relationships between 30-day mortality (during the stay in or after discharge from ICUs) and the microbiological etiological agent and adequacy of initial empirical antibiotic therapy in HAP patients. The group dataset contained data on 330 enrolled patients. The final validated dataset involved 214 patients, 168 males (78.5%) and 46 females (21.5%), from whom 278 valid lower airway samples were obtained. The mean patient age was 59.9 years. The mean APACHE II score at admission was 21. Community-acquired pneumonia was identified in 13 patients and HAP in 201 patients, of whom 26 (12.1%) had early-onset and 175 (81.8%) had late-onset HAP. Twenty-two bacterial species were identified as etiologic agents but only six of them exceeded a frequency of detection of 5% (Klebsiella pneumoniae 20.4%, Pseudomonas aeruginosa 20.0%, Escherichia coli 10.8%, Enterobacter spp. 8.1%, Staphylococcus aureus 6.2% and Burkholderia cepacia complex 5.8%). Patients infected with Staphylococcus aureus had significantly higher rates of early-onset HAP than those with other etiologic agents. The overall 30-day mortality rate for HAP was 29.9%, with 19.2% mortality for early-onset HAP and 31.4% mortality for late-onset HAP. Patients with late-onset HAP receiving adequate initial empirical antibiotic therapy had statistically significantly lower 30-day mortality than those receiving inadequate initial antibiotic therapy (23.8% vs 42.9%). Patients with ventilator-associated pneumonia (VAP) had significantly higher mortality than those who developed HAP with no association with mechanical ventilation (34.6% vs 12.7%). Patients having VAP treated with adequate initial antibiotic therapy had lower 30-day mortality than those receiving inadequate therapy (27.2% vs 44.8%). The present study was the first to collect multicenter data on the epidemiology of HAP in the Central European Region, with respect to the incidence of etiologic agents causing HAP. It was concerned with relationships between 30-day patient mortality and the type of HAP, etiologic agent and adequacy of initial empirical antibiotic therapy.

Sepsis is a common and serious health problem whereby improvements in diagnosis are crucial in increasing survival rates. To test whether profiling transcription is applicable to sepsis diagnosis, we analyzed whole blood using a microarray containing probes for 340 genes relevant to inflammation. The patient’s gene expression pattern was highly homogenous, resulting in 69% of differentially expressed genes. With a positive predictive value of 98%, a list of 50 differentially expressed genes was compiled, and randomly chosen transcripts were confirmed by PCR. Here, we present the first evidence that microarrays can identify typical gene expression profiles in the blood of patients with severe sepsis. Regardless of the heterogeneity of the patients, we observed a striking correlation between the conventional diagnostic classification and our approach. The unity of responses suggests that the principle of this multiparameter approach can be adapted to early stage sepsis diagnosis.

Introduction: The aim of this study was to compare the early postoperative kinetics of procalcitonin (PCT) and C-reactive protein (CRP) serum levels in patients undergoing orthotopic liver transplantation (OLTx) with different immunosuppressive regimens. Methods: PCT and CRP serum concentrations were measured in a group of 28 OLTx recipients before induction of anesthesia, at 4 and 8 hours following graft reperfusion, and daily until postoperative day 4. The same parameters were determined in 12 patients undergoing liver resection without conjunctive immunosuppressive therapy. Summary data are expressed as medians and ranges. Two-tailed nonparametric tests were performed and considered significant at p values of less than 0.05. Results: The highest serum levels of PCT (median 3.0 ng/mL, minimum 1.4 ng/mL, maximum 13.9 ng/mL) were found in patients after OLTx without ATG therapy, on postoperative day 1. In patients with ATG administration, PCT levels were highly increased on postoperative day 1 (median 53.0 ng/mL, minimum 7.9 ng/mL, maximum 249.1 ng/mL). Thereafter, PCT values continuously decreased independently of further ATG administration in both groups of patients. No evidence of infection was present in either group. In 12 patients undergoing liver resection, peak serum PCT levels did not exceed 3.6 ng/mL. CRP serum levels in a group of patients with and without ATG therapy increased significantly on postoperative day 1, followed by a decrease. The highest levels of CRP were found in patients after liver resection on postoperative day 2 and decreased thereafter. Conclusion: ATG administration to patients with OLTx is associated with an increase in serum PCT levels, with peak values on postoperative day 1, and this was in the absence of any evidence of infection. The results of this study indicate that ATG immunosuppressive therapy is a stimulus for the synthesis of PCT.

Sepsis is the most frequent cause of death in noncoronary intensive care units. In the past 10 years, progress has been made in the early identification of septic patients and their treatment. These improvements in support and therapy mean that mortality is gradually decreasing, however, the rate of death from sepsis remains unacceptably high. Immunotherapy is not currently part of the routine treatment of sepsis. Despite experimental successes, the administration of agents to block the effect of sepsis mediators failed to show evidence for improved outcome in a multitude of clinical trials. The following survey summarizes the current knowledge and results of clinical trials on the immunotherapy of sepsis and describes the limitations of our knowledge of the pathogenesis of sepsis. Administration of immunomodulatory drugs should be linked to the current immune status assessed by both clinical and molecular patterns. Thus, a careful daily review of the patient’s immune status needs to be introduced into routine clinical practice giving the opportunity for effective and tailored use of immunomodulatory therapy.