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Shock induced endotheliopathy (SHINE) in acute critical illness - a unifying pathophysiologic mechanism

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dc.contributor Háskóli Íslands
dc.contributor University of Iceland
dc.contributor.author Johansson, Pär Ingemar
dc.contributor.author Stensballe, Jakob
dc.contributor.author Ostrowski, SisseRye
dc.date.accessioned 2017-07-18T15:48:26Z
dc.date.available 2017-07-18T15:48:26Z
dc.date.issued 2017-02-09
dc.identifier.citation Johansson, P., Stensballe, J., & Ostrowski, S. (2017). Shock induced endotheliopathy (SHINE) in acute critical illness - a unifying pathophysiologic mechanism. Critical Care, 21(1), 25. doi:10.1186/s13054-017-1605-5
dc.identifier.issn 1364-8535
dc.identifier.issn 1466-609X (eISSN)
dc.identifier.uri https://hdl.handle.net/20.500.11815/339
dc.description The Erratum to this article has been published in Critical Care 2017 21:187 Unfortunately this article [1] was published with an error. The first and last author names are presented incorrectly. The first author name should be Pär Ingemar Johansson, or alternatively Johansson PI. The last author name should be Sisse Rye Ostrowski, or alternatively Ostrowski SR.
dc.description.abstract One quarter of patients suffering from acute critical illness such as severe trauma, sepsis, myocardial infarction (MI) or post cardiac arrest syndrome (PCAS) develop severe hemostatic aberrations and coagulopathy, which are associated with excess mortality. Despite the different types of injurious “hit”, acutely critically ill patients share several phenotypic features that may be driven by the shock. This response, mounted by the body to various life-threatening conditions, is relatively homogenous and most likely evolutionarily adapted. We propose that shock-induced sympatho-adrenal hyperactivation is a critical driver of endothelial cell and glycocalyx damage (endotheliopathy) in acute critical illness, with the overall aim of ensuring organ perfusion through an injured microvasculature. We have investigated more than 3000 patients suffering from different types of acute critical illness (severe trauma, sepsis, MI and PCAS) and have found a potential unifying pathologic link between sympatho-adrenal hyperactivation, endotheliopathy, and poor outcome. We entitled this proposed disease entity, shock-induced endotheliopathy (SHINE). Here we review the literature and discuss the pathophysiology of SHINE.
dc.format.extent 25
dc.language.iso en
dc.publisher Springer Nature
dc.relation.ispartofseries Critical Care;21(1)
dc.rights info:eu-repo/semantics/openAccess
dc.subject Sjúkdómar
dc.subject Slys
dc.title Shock induced endotheliopathy (SHINE) in acute critical illness - a unifying pathophysiologic mechanism
dc.type info:eu-repo/semantics/article
dcterms.license This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
dc.description.version Peer Reviewed
dc.identifier.journal Critical Care
dc.identifier.doi 10.1186/s13054-017-1605-5
dc.relation.url https://ccforum.biomedcentral.com/articles/10.1186/s13054-017-1756-4
dc.contributor.department Rannsóknarsetur í kerfislíffræði (HÍ)
dc.contributor.department Center for Systems Biology (UI)
dc.contributor.school Verkfræði- og náttúruvísindasvið (HÍ)
dc.contributor.school School of Engineering and Natural Sciences (UI)


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