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.

Sepsis is a multifactorial clinical syndrome with an extremely dynamic clinical course and with high diverse clinical phenotype. Early diagnosis is crucial for the final clinical outcome. Previous studies have not identified a biomarker for the diagnosis of sepsis which would have sufficient sensitivity and specificity. Identification of the infectious agents or the use of molecular biology, next gene sequencing, has not brought significant benefit for the patient in terms of early diagnosis. Therefore, we are currently searching for biomarkers, through “omics” technologies with sufficient diagnostic specificity and sensitivity, able to predict the clinical course of the disease and the patient response to therapy. Current progress in the use of systems biology technologies brings us hope that by using big data from clinical trials such biomarkers will be found.

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.

The objectives of this study were to evaluate patients with aortic abdominal aneurysm (AAA) with regard to immunoglobulin (Ig)G4‐related disease (IgG4‐RD). IgG4‐RD represents a recently defined condition comprised of a collection of disorders characterized by IgG4 hypergammaglobulinemia, the presence of IgG4‐positive plasma cells in organs affected with fibrotic or sclerotizing changes and typical histopathological features. It was identified as a possible cause of vasculitis in large vessels. Studies have been published on a possible association between inflammatory aortic or cardiovascular disease and IgG4‐RD. We examined 114 patients with AAA requiring surgery in order to identify findings which are characteristic of IgG4‐RD. Aneurysm samples from seven patients showed histopathological features consistent with IgG4‐RD and the presence of IgG4⁺ plasma cells. Only two of these seven patients showed elevated IgG4 serum levels higher 1·35 g/l. In five of the patients, the concentration of serum IgG4 was lower than 1·20 g/l, with the number of IgG4⁺ plasma cells being higher than 50/high‐power field. These findings were consistent with AAA being a heterogeneous group of inflammatory diseases with different pathogenesis.

We present a retrospective analysis of patients treated in our Department of Clinical Biochemistry, Haematology and Immunology, Na Homolce Hospital, during 1997–2013 for Ormond’s disease. We analyse the clinical history, diagnostic approaches, surgical, and immunosuppressive therapies and their subsequent effect on our patients. 28 patients treated for Ormond’s disease were included. Patients with established disease activity (26 patients) were given immunosuppressive treatment, using corticosteroids in combination with azathioprine. Treatment response was evaluated using clinical symptomatology, inflammatory parameters and imaging methods. In the cohort as a whole, immunosuppressive therapy was applied in 26 patients; in two patients it was not used as no inflammatory activity was found with the disease. In all 26 patients, computed tomography showed that immunosuppressive treatment resulted in partial or complete regression of inflammatory infiltrate. Out of the total number of 26 patients, two patients experienced disease exacerbation 7 and 16 months after the immunosuppressive treatment was discontinued. The longest follow-up period was 16 years; the shortest one was 21 months. Idiopathic retroperitoneal fibrosis – Ormond’s disease – is a disease with serious complications. Standard treatment involves a combination of surgery and immunosuppressive treatment. The combination of corticosteroids and azathioprine represents a potentially safe and useful method of treatment.