Elevated trefoil factor 3 plasma levels in critically ill patients with abdominal sepsis or non-infectious abdominal illness
MARS Consortium
(2020) Cytokine, volume 133
(Article)
Abstract
Trefoil factor 3 (TFF3) is a small peptide secreted mainly by goblet cells in the gut, where it plays a key role in gastrointestinal defence and repair. Plasma TFF3 has been reported as a biomarker of intestinal injury and as such it has been evaluated as a marker of disease
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activity in colitis. Impaired gut barrier function has been postulated as the "motor" of critical illness. We here sought to determine the temporal dynamics of plasma TFF3 in adult patients admitted to intensive care unit with abdominal sepsis or after major abdominal surgery for a non-infectious condition (post-op GI patients). TFF3 was measured in plasma obtained from 143 patients with abdominal sepsis and 98 post-op GI patients on admission to the intensive care (day 0) and at days 2 and 4 thereafter. Abdominal sepsis patients showed sustained elevated plasma TFF3 levels from day 0 to 4 relative to healthy control values, while in post-op GI patients admission TFF3 levels were not increased, only rising at day 2 and 4. In both patient groups, the presence of shock was associated with higher TFF3 levels. Moreover, patients with 3 or more organs failing had higher plasma TFF3 concentrations. While plasma TFF3 was higher in sepsis patients who did not survive until day 30, TFF3 levels were not independently associated with 30-day mortality in a Cox regression analysis. These results could support the theory that intestinal injury contributes to the pathogenesis of critical illness. Future studies are needed to elucidate whether the proposed gut dysfunction precedes or supersedes organ dysfunction in time.
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Keywords: Biomarker, Critical illness, Infection, Intraabdominal infections, Sepsis, Trefoil factor 3, Molecular Biology, Hematology, Biochemistry, Immunology and Allergy, Immunology, Journal Article
ISSN: 1043-4666
Publisher: Academic Press Inc.
Note: Funding Information: The authors acknowledge all members of the MARS consortium for the participation in data collection and especially acknowledge: J.M. Bonten; J.F. Frencken; K. van de Groep; M.E. Koster-Brouwer; P.M. Klein Klouwenberg; D.S.Y. Ong; D. Verboom (Department of Intensive Care, University Medical Center Utrecht, The Netherlands), F.M. de Beer; L.D. Bos; G.J. Glas; J. Horn; R.T.M. van Hooijdonk; L.R.A. Schouten; M. Straat; E. Witteveen; L. Wieske (Department of Intensive Care, Amsterdam UMC, Academic Medical Center Amsterdam, The Netherlands), A.J. Hoogendijk; M.A. Huson; L.A. van Vught, M.A. Wiewel. This work was supported by the Center for Translational Molecular Medicine (http://www.ctmm.nl), project MARS (grant 04I-201). The sponsor CTMM was not involved in the design or conduction of the study; nor was the sponsor involved in collection, management, analysis or interpretation of the data, or preparation, review or approval of the manuscript. The decision to submit the manuscript was not dependent on the sponsor. Funding Information: This work was supported by the Center for Translational Molecular Medicine ( http://www.ctmm.nl ), project MARS (grant 04I-201 ). The sponsor CTMM was not involved in the design or conduction of the study; nor was the sponsor involved in collection, management, analysis or interpretation of the data, or preparation, review or approval of the manuscript. The decision to submit the manuscript was not dependent on the sponsor. Publisher Copyright: © 2020 Elsevier Ltd
(Peer reviewed)