Startseite Increased serum concentrations of soluble ST2 predict mortality after burn injury
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Increased serum concentrations of soluble ST2 predict mortality after burn injury

  • Stefan Hacker ORCID logo EMAIL logo , Benjamin Dieplinger , Gregor Werba , Stefanie Nickl , Georg A. Roth , Claus G. Krenn , Thomas Mueller , Hendrik J. Ankersmit und Thomas Haider
Veröffentlicht/Copyright: 27. Juni 2018
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Abstract

Background:

Large burn injuries induce a systemic response in affected patients. Soluble ST2 (sST2) acts as a decoy receptor for interleukin-33 (IL-33) and has immunosuppressive effects. sST2 has been described previously as a prognostic serum marker. Our aim was to evaluate serum concentrations of sST2 and IL-33 after thermal injury and elucidate whether sST2 is associated with mortality in these patients.

Methods:

We included 32 burn patients (total body surface area [TBSA] >10%) admitted to our burn intensive care unit and compared them to eight healthy probands. Serum concentrations of sST2 and IL-33 were measured serially using an enzyme-linked immunosorbent assay (ELISA) technique.

Results:

The mean TBSA was 32.5%±19.6%. Six patients (18.8%) died during the hospital stay. Serum analyses showed significantly increased concentrations of sST2 and reduced concentrations of IL-33 in burn patients compared to healthy controls. In our study cohort, higher serum concentrations of sST2 were a strong independent predictor of mortality.

Conclusions:

Burn injuries cause an increment of sST2 serum concentrations with a concomitant reduction of IL-33. Higher concentrations of sST2 are associated with increased in-hospital mortality in burn patients.


Corresponding author: Stefan Hacker, MD, FEBOPRAS, Division of Plastic and Reconstructive Surgery, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria

  1. Author contributions: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission.

  2. Research funding: This study was partly financed by the Medical University of Vienna (research scholarship to TH), the Surgical Research Laboratory of the Medical University of Vienna, and the Ankersmit Laboratory for Cardiac and Thoracic Diagnosis & Regeneration.

  3. Employment or leadership: None declared.

  4. Honorarium: None declared.

  5. Competing interests: The funding organization(s) played no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.

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Received: 2018-01-11
Accepted: 2018-05-24
Published Online: 2018-06-27
Published in Print: 2018-11-27

©2018 Walter de Gruyter GmbH, Berlin/Boston

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