Accessibility navigation


Intestinal injury and endotoxemia in children undergoing surgery for congenital heart disease

Pathan, N., Burmester, M., Adamovic, T., Berk, M., Ng, K. W., Betts, H., Macrae, D., Waddell, S., Paul-Clark, M., Nuamah, R., Mein, C., Levin, M., Montana, G. and Mitchell, J. A. (2011) Intestinal injury and endotoxemia in children undergoing surgery for congenital heart disease. American Journal of Respiratory and Critical Care Medicine, 184 (11). pp. 1261-1269. ISSN 1535-4970

Full text not archived in this repository.

To link to this article DOI: 10.1164/rccm.201104-0715OC

Abstract/Summary

RATIONALE: Children with congenital heart disease are at risk of gut barrier dysfunction and translocation of gut bacterial antigens into the bloodstream. This may contribute to inflammatory activation and organ dysfunction postoperatively. OBJECTIVES: To investigate the role of intestinal injury and endotoxemia in the pathogenesis of organ dysfunction after surgery for congenital heart disease. METHODS: We analyzed blood levels of intestinal fatty acid binding protein and endotoxin (endotoxin activity assay) alongside global transcriptomic profiling and assays of monocyte endotoxin receptor expression in children undergoing surgery for congenital heart disease. MEASUREMENTS AND MAIN RESULTS: Levels of intestinal fatty acid binding protein and endotoxin were greater in children with duct-dependent cardiac lesions. Endotoxemia was associated with severity of vital organ dysfunction and intensive care stay. We identified activation of pathogen-sensing, antigen-processing, and immune-suppressing pathways at the genomic level postoperatively and down-regulation of pathogen-sensing receptors on circulating immune cells. CONCLUSIONS: Children undergoing surgery for congenital heart disease are at increased risk of intestinal mucosal injury and endotoxemia. Endotoxin activity correlates with a number of outcome variables in this population, and may be used to guide the use of gut-protective strategies.

Item Type:Article
Refereed:Yes
Divisions:No Reading authors. Back catalogue items
ID Code:28102
Publisher:American Thoracic Society

University Staff: Request a correction | Centaur Editors: Update this record

Page navigation