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. 2017 Oct;36(10):1749-1756.
doi: 10.1007/s10096-017-2988-6. Epub 2017 Apr 28.

Increase of circulating endocan over sepsis follow-up is associated with progression into organ dysfunction

Affiliations

Increase of circulating endocan over sepsis follow-up is associated with progression into organ dysfunction

A Ioakeimidou et al. Eur J Clin Microbiol Infect Dis. 2017 Oct.

Abstract

How circulating inflammatory mediators change upon sepsis progression has not been studied. We studied the follow-up changes of circulating vasoactive peptides and cytokines until the improvement or the worsening of a patient and progression into specific organ dysfunctions. In a prospective study, concentrations of tumor necrosis factor-alpha (TNFα), interleukin (IL)-6, IL-8, IL-10, interferon-gamma (IFNγ), endocan and angiopoietin-2 (Ang-2) were measured in serum by an enzyme immunoassay in 175 patients at baseline; this was repeated within 24 h upon progression into new organ dysfunction (n = 141) or improvement (n = 34). Endocan and Ang-2 were the only parameters that were significantly increased among patients who worsened. Any increase of endocan was associated with worsening with odds ratio 16.65 (p < 0.0001). This increase was independently associated with progression into acute respiratory distress syndrome (ARDS) as shown after logistic regression analysis (odds ratio 2.91, p: 0.002). Changes of circulating cytokines do not mediate worsening of the critically ill patients. Instead endocan and Ang2 are increased and this may be interpreted as a key-playing role in the pathogenesis of ARDS and septic shock. Any increase of endocan is a surrogate of worsening of the clinical course.

Keywords: Acute Kidney Injury; Acute Lung Injury; Organ Dysfunction; Septic Shock; Systemic Inflammatory Response Syndrome.

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Conflict of interest statement

None of the authors has any conflict of interest related to this submission.

Figures

Fig. 1
Fig. 1
Study flow chart. SOFA sequential organ failure assessment
Fig. 2
Fig. 2
Comparative concentrations of endocan, angiopoietin-2 (Ang-2) and cytokines on initial presentation of sepsis (baseline) and on follow-up. Patients are divided into those with worsening of their clinical course with a new organ dysfunction (n = 141) and into those with improving clinical course (n = 34). Only the p values of comparisons that provided statistical significance are provided. IFNγ interferon-gamma, IL interleukin, TNFα tumor necrosis factor-alpha
Fig. 3
Fig. 3
Change of endocan from baseline as prognostic of the clinical course of sepsis. a ROC curve of the % change of baseline endocan for worsening of the clinical course. b Distribution of patients into worsening and improvement of their clinical course in relation to an absolute increase or decrease of baseline endocan on follow-up. AUC area under curve, CIs: confidence intervals, NPV negative predictive value, PPV positive predictive value, Sens sensitivity, Spec specificity
Fig. 4
Fig. 4
Concentrations of endocan and of angiopoietin-2 (Ang-2) at sepsis baseline and on progression to the indicated organ dysfunction. P values of the indicated comparisons are provided. ARDS acute respiratory distress syndrome, AKI acute kidney injury

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