ArticleJournal of burn care & research : official publication of the American Burn Association
Noninvasive measurement of intestinal inflammation after burn injury.
Article in Journal of burn care & research : official publication of the American Burn Association. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- Article
- The Artificial Sweetener Splenda Promotes Gut Proteobacteria, Dysbiosis, and Myeloperoxidase Reactivity in Crohn's Disease-Like Ileitis.Inflammatory bowel diseases · 2018Article
- Intraluminal Flagellin Differentially Contributes to Gut Dysbiosis and Systemic Inflammation following Burn Injury.PloS one · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Intestinal inflammation has been linked with multiorgan failure in patients with burn and other traumatic injuries. We hypothesized that markers of intestinal inflammation are detectible noninvasively. Fecal samples were collected from seven severely burned patients and 15 control patients for the measurement of inflammatory cytokines using a multiplex assay kit. In addition, fecal levels of myeloperoxidase (MPO) and elastase were measured using standard procedures. Compared with a control group, levels of inflammatory cytokines were significantly increased in the burn group. Interleukin (IL)-6 increased to a mean (± SEM) of 2.16 ± 0.61 to 3.81 ± 0.49 pg/mg (P < .05), as did IL-8 (3.32 ± 0.76 to 20.51 ± 6.65 pg/mg; P < .05), IL-12 (6.23±0.98 to 8.11±0.95pg/mg; P=0.01), IL-13 (3.86 ± 0.32 to 11.83 ± 1.47 pg/mg; P < .05), monocyte chemoattractant protein-1 (2.78 ± 2.61 to 6.5 ± 3.97 pg/mg; P < .05), MPO (13.41 ± 1.40 to 24.52 ± 4.31 units/mg protein; P < .05), and elastase (2.46 ± 0.38 to 5.08 ± 0.72 pg/mL; P < .05). Our results suggest that markers of intestinal inflammation are measurable by noninvasive means and are increased after burn injury compared with controls. Of note, increased IL-8 correlated with increased MPO and elastase activity, suggesting a role for neutrophil activation in burn-mediated intestinal inflammation. Thus, these inflammatory cytokine profiles may be valuable biomarkers of intestinal inflammation after burn injury.
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Registered trials
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