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Tytuł pozycji:

Soluble ICAM-1 is Modulated by Hyperbaric Oxygen Treatment and Correlates with Disease Severity and Mortality in Patients with Necrotizing Soft-tissue Infection.

Tytuł :
Soluble ICAM-1 is Modulated by Hyperbaric Oxygen Treatment and Correlates with Disease Severity and Mortality in Patients with Necrotizing Soft-tissue Infection.
Autorzy :
Hedetoft M; Department of Anaesthesia, Copenhagen University Hospital, Denmark.
Moser C; Department of Clinical Microbiology, Copenhagen University Hospital, Denmark.
Jensen PØ; Department of Clinical Microbiology, Copenhagen University Hospital, Denmark.
Vinkel J; Copenhagen University Hospital, Denmark.
Hyldegaard O; Department of Anaesthesia, Centre of Head and Orthopaedics, Copenhagen University Hospital, Denmark.
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Źródło :
Journal of applied physiology (Bethesda, Md. : 1985) [J Appl Physiol (1985)] 2021 Jan 14. Date of Electronic Publication: 2021 Jan 14.
Publication Model :
Ahead of Print
Typ publikacji :
Journal Article
Język :
English
Imprint Name(s) :
Original Publication: Bethesda, MD : American Physiological Society, c1985-
Grant Information :
R167-A7352-B3897 Copenhagen University Hospital, Rigshospitalet; NNF17OC0025074 Novo Nordisk Fonden (NNF); 8113-00009B Innovation Fund Denmark; 8113-00009B EU Horizon 2020; 8114-00005B Innovation Fund Denmark; 8114-00005B NordForsk
Contributed Indexing :
Keywords: Endothelial shedding; HBO2 treatment; disease severity; necrotizing soft-tissue infection; survival
Entry Date(s) :
Date Created: 20210114 Latest Revision: 20210114
Update Code :
20210210
DOI :
10.1152/japplphysiol.00844.2020
PMID :
33444122
Czasopismo naukowe
The inflammatory response in patients with necrotizing soft-tissue infection (NSTI) is excessive and often causes collateral damage, thereby worsening disease severity and prognosis. Shedding of endothelial adhesion molecules may be a key regulatory mechanism to modulate the inflammatory response in septic NSTI patients. Hyperbaric oxygen (HBO 2 ) treatment has demonstrated an effect on adhesion molecules. However, endothelial shedding and its association with NSTI disease severity and prognosis is not fully understood. We hypothesized that shedding of intercellular adhesion molecule-1, and the resulting release of the soluble isoform sICAM-1, is modified by HBO 2 treatment, and secondly, that sICAM-1 concentrations are associated with severity of disease and mortality in patients with NSTI. We measured sICAM-1 in 80 patients with NSTI immediately before and after first session of HBO 2 treatment as well as on the following day. We found an overall sICAM-1 level of 594 ng/mL (IQR 406-817). HBO 2 significantly (p=0.01) increased sICAM-1 by a median of 45.1 ng/mL, which remained elevated until the following day; this effect was more pronounced in patients with septic shock. Furthermore, sICAM-1 was significantly correlated with disease severity (SAPS II; rho 0.24, p=0.04) and low sICAM-1 was found to be an independent predictor for 90-day mortality in age-sex-SAPS II adjusted analysis (Odds Ratio 14.0, 95% CI 1.82-341.4, p=0.03). These results support the hypothesis that endothelial shedding is an important pathophysiological mechanism in NSTI, and suggest that HBO 2 treatment may induce immunomodulatory effects that potentially decreases collateral damage and mortality.

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