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Review
. 2018 Oct 26;22(1):280.
doi: 10.1186/s13054-018-2222-7.

Endocan, sepsis, pneumonia, and acute respiratory distress syndrome

Nathalie De Freitas Caires  1   2   3   4   5 , Alexandre Gaudet  6   7   8   9   10 , Lucie Portier  1   2   3   4   5 , Anne Tsicopoulos  1   2   3   4   11 , Daniel Mathieu  1   2   3   4   12 , Philippe Lassalle  1   2   3   4   5
Affiliations
Review

Endocan, sepsis, pneumonia, and acute respiratory distress syndrome

Nathalie De Freitas Caires et al. Crit Care. .

Abstract

Acute respiratory distress syndrome (ARDS) and hospital-acquired pneumonia (HAP) are major problems of public health in intensive care units (ICUs), occurring in 15% of critically ill patients. Among the factors explaining ARDS development, sepsis is known as a frequent cause. Sepsis, ARDS, and HAP increase morbidity, mortality, length of stay in the ICU, and the overall costs of healthcare. The major challenge remains to identify accurately among critically ill patients those at risk of poor outcomes who could benefit from novel therapies. Endocan is released by the pulmonary endothelium in response to local or systemic injury. It inhibits mainly leukocyte diapedesis rather than leukocyte rolling or adhesion to the endothelial cells both in vitro and in vivo. Endocan was evaluated in 25 clinical reports, including 2454 critically ill patients and 452 healthy controls. The diagnostic value of endocan for sepsis or sepsis severity was equal to procalcitonin but its prognostic value was better. A predictive value for postoperative pneumonia was evidenced in two studies, and a predictive value for ARDS in four studies from three independent centers. This review presents an overview of the structure, expression, and functions of endocan. We also hereby summarize the potential applications of endocan in the prediction and prognosis of ARDS and HAP, as well as in the prognosis of sepsis.

Keywords: Acute respiratory distress syndrome; Endocan; Pneumonia; Sepsis.

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Conflict of interest statement

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Not applicable.

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Not applicable.

Competing interests

NDFC and LP are employees of Lunginnov. PL is cofounder of Lunginnov. The remaining authors declare that they have no competing interest.

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Figures

Fig. 1
Fig. 1
Comparative structure and expression of human and mouse endocan
Fig. 2
Fig. 2
Hypothetical model of endocan kinetics in acute systemic and lung inflammatory states. ARDS acute respiratory distress syndrome, ICU intensive care unit, SIRS systemic inflammatory response syndrome
See this image and copyright information in PMC

Comment in

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