Several works have explored the blood concentrations of endocan in sepsis and acute respiratory distress syndrome (ARDS). However, data from the literature seem apparently conflicting, with high endocan levels being associated with either good or poor prognosis according to the different studies. Indeed, endocan levels on intensive care unit (ICU) admission correlate with the severity of sepsis [1]. In septic shock patients without ARDS at admission, high levels of endocan are found predominantly in patients who do not develop ARDS [2]. Ioakeimidou et al. reported that progression to ARDS in septic patients was associated with the increase of blood endocan during follow-up [3]. Furthermore, Orbegozo et al. and Tsangaris et al. reported that higher endocan levels measured at the clinical onset of ARDS were associated with poor respiratory outcomes [4, 5]. The above-stated observations suggest that endocan’s predictive values may sound more complex than a simple association between high plasmatic levels and the development of poor outcomes.
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To better understand the evolution of endocan over the time course of sepsis and ARDS, we conducted a post hoc analysis of the kinetics of blood endocan over 72 h, based on the data from a previously published cohort of 72 septic patients without ARDS on baseline [2]. Among the 72 patients enrolled in this cohort, 11 subjects developed an ARDS at 72 h (8 mild, 3 moderate, 1 severe).
In patients without ARDS, endocan continually decreased during the 72-h time course following enrollment, with median [IQR] values falling from 9.2 [5.6–14.8] ng/mL on enrolment to 3.9 [2.6–7.7] ng/mL 72 h later (Fig. 1a). In patients progressing to mild ARDS, endocan moderately increased from 2.5 [1.3–3.4] ng/mL on enrolment to 4.1 [2.3–7.3] ng/mL at 72 h (Fig. 1b). We observed a higher increase of blood endocan in patients progressing to moderate and severe ARDS, with median [IQR] values rising from 4.7 [2.5–5.4] ng/mL on enrollment to 11 [9.5–12.6] ng/mL at 72 h (Fig. 1c).
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This study highlights the kinetics of endocan in severe sepsis and ARDS, thus helping to understand the apparently conflicting results observed in the literature. However, the interpretability of this work remains limited given the small effectives in each subgroup of ARDS, yet it may be used jointly with other data from the literature to elaborate a model of endocan’s kinetics during severe sepsis and ARDS. Therefore, further explorations are required to comfort these results.
Acknowledgements
Not applicable.
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Funding
This work was supported by BPI France (grant number BPI 2012-05-336). This funding was attributed to D. M, representing Lille University Hospital. There was no role of the funding body in the design of the study and collection, analysis, and interpretation of data and in writing the manuscript.
Availability of data and materials
The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.
Ethics approval and consent to participate
This study has been approved by the ethics committee of Lille University Hospital (approval number CP03/07). All the participants to this study gave their informed consent prior to enrollment.
Consent for publication
Not applicable.
Competing interests
The Endomark H1 and DIYEK C1 ELISA kits used in this study were provided by Lunginnov. P. L. is the cofounder of Lunginnov. N. D. and L. P. are staff members of Lunginnov. The other authors declare that they have no conflicts of interest.
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