Soluble GPVI is elevated in injured patients: shedding is mediated by fibrin activation of GPVI.

Montague, Samantha J and Delierneux, Céline and Lecut, Christelle and Layios, Nathalie and Dinsdale, Robert J and Lee, Christine S-M and Poulter, Natalie S and Andrews, Robert K and Hampson, Peter and Wearn, Christopher M and Maes, Nathalie and Bishop, Jonathan and Bamford, Amy and Gardiner, Chris and Lee, Woei Ming and Iqbal, Tariq and Moiemen, Naiem and Watson, Steve P and Oury, Cécile and Harrison, Paul and Gardiner, Elizabeth E (2018) Soluble GPVI is elevated in injured patients: shedding is mediated by fibrin activation of GPVI. Blood advances, 2 (3). pp. 240-251. ISSN 2473-9537. This article is available to all UHB staff and students via ASK Discovery tool http://tinyurl.com/z795c8c (HGS Staff) or the Library Intranet Pages (QE Staff) by using their UHB Athens login IDs.

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Official URL: http://www.bloodadvances.org/content/2/3/240

Abstract

Soluble glycoprotein VI (sGPVI) is shed from the platelet surface and is a marker of platelet activation in thrombotic conditions. We assessed sGPVI levels together with patient and clinical parameters in acute and chronic inflammatory conditions, including patients with thermal injury and inflammatory bowel disease and patients admitted to the intensive care unit (ICU) for elective cardiac surgery, trauma, acute brain injury, or prolonged ventilation. Plasma sGPVI was measured by enzyme-linked immunosorbent assay and was elevated on day 14 after thermal injury, and was higher in patients who developed sepsis. sGPVI levels were associated with sepsis, and the value for predicting sepsis was increased in combination with platelet count and Abbreviated Burn Severity Index. sGPVI levels positively correlated with levels of D-dimer (a fibrin degradation product) in ICU patients and patients with thermal injury. sGPVI levels in ICU patients at admission were significantly associated with 28- and 90-day mortality independent of platelet count. sGPVI levels in patients with thermal injury were associated with 28-day mortality at days 1, 14, and 21 when adjusting for platelet count. In both cohorts, sGPVI associations with mortality were stronger than D-dimer levels. Mechanistically, release of GPVI was triggered by exposure of platelets to polymerized fibrin, but not by engagement of G protein-coupled receptors by thrombin, adenosine 5'-diphosphate, or thromboxane mimetics. Enhanced fibrin production in these patients may therefore contribute to the observed elevated sGPVI levels. sGPVI is an important platelet-specific marker for platelet activation that predicts sepsis progression and mortality in injured patients.

Item Type: Article
Additional Information: This article is available to all UHB staff and students via ASK Discovery tool http://tinyurl.com/z795c8c (HGS Staff) or the Library Intranet Pages (QE Staff) by using their UHB Athens login IDs.
Subjects: QW Microbiology. Immunology
WD Diseases and disorders of systemic, metabolic or environmental origin > WD400 Emergency medicine
Divisions: Planned IP Care > Gastroentrology
Related URLs:
Depositing User: Miss Emily Johnson
Date Deposited: 24 Jan 2019 16:32
Last Modified: 24 Jan 2019 16:32
URI: http://www.repository.heartofengland.nhs.uk/id/eprint/1818

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