Endotoxin immunity and the development of the systemic inflammatory response syndrome in critically ill children
- PMID: 16450100
- DOI: 10.1007/s00134-005-0019-z
Endotoxin immunity and the development of the systemic inflammatory response syndrome in critically ill children
Abstract
Background: The systemic inflammatory response syndrome (SIRS) may be triggered by endotoxin. Humans have antibodies directed against the core of endotoxin (endotoxin core antibodies, EndoCAb) that appear to be protective following surgery and in sepsis. We hypothesised that children with elevated antibodies to endotoxin core would be less likely to develop SIRS in their initial period on intensive care. Because of the existing literature we defined two sub-groups according to the primary reason for ICU admission: infection and non-infection.
Methods: We recruited 139 consecutive patients admitted to a paediatric intensive care unit (PICU) with more than one organ failure for longer than 12 h as part of another study. Patients were classified on admission to PICU as having an infectious or a non-infections diagnosis. The occurrence of SIRS within 48 h of admission was recorded along with detailed clinical and demographic data, EndoCAb concentration and the potential confounding variables C-reactive protein and mannose-binding lectin.
Results: In the 71 patients admitted without infection (primarily post-operative and head injured) IgG EndoCAb was significantly lower in patients who developed SIRS than those who did not (72 vs. 131 MU/ml), independent of potential confounding variables. In patients with infection there was no significant difference in IgG EndoCAb between children developing SIRS and those who did not (111 vs. 80 MU/ml).
Conclusion: Head injured and post-operative patients admitted to PICU who develop early SIRS have significantly lower serum IgG EndoCAb levels than those who do not.
Comment in
-
Searching for the etiology of systemic inflammatory response syndrome: is SIRS occult endotoxemia?Intensive Care Med. 2006 Feb;32(2):181-184. doi: 10.1007/s00134-005-0067-4. Epub 2006 Feb 1. Intensive Care Med. 2006. PMID: 16450092 No abstract available.
Similar articles
-
Relationship of antibodies to endotoxin core to mortality in medical patients with sepsis syndrome.Intensive Care Med. 1999 May;25(5):435-44. doi: 10.1007/s001340050877. Intensive Care Med. 1999. PMID: 10401935
-
Low apolipoprotein A-I level at intensive care unit admission and systemic inflammatory response syndrome exacerbation.Crit Care Med. 2004 Mar;32(3):632-7. doi: 10.1097/01.ccm.0000114820.47460.0a. Crit Care Med. 2004. PMID: 15090939
-
Increased incidence and severity of the systemic inflammatory response syndrome in patients deficient in mannose-binding lectin.Intensive Care Med. 2004 Jul;30(7):1438-45. doi: 10.1007/s00134-004-2303-8. Epub 2004 May 4. Intensive Care Med. 2004. PMID: 15127191
-
Endotoxemia in pediatric critical illness--a pilot study.Crit Care. 2011;15(3):R141. doi: 10.1186/cc10264. Epub 2011 Jun 8. Crit Care. 2011. PMID: 21651808 Free PMC article.
-
Endogenous endotoxin-core antibody (EndoCAb) as a marker of endotoxin exposure and a prognostic indicator: a review.Prog Clin Biol Res. 1995;392:263-72. Prog Clin Biol Res. 1995. PMID: 8524931 Review. No abstract available.
Cited by
-
Year in Review in Intensive Care Medicine, 2006. III. Circulation, ethics, cancer, outcome, education, nutrition, and pediatric and neonatal critical care.Intensive Care Med. 2007 Mar;33(3):414-22. doi: 10.1007/s00134-007-0553-y. Epub 2007 Feb 14. Intensive Care Med. 2007. PMID: 17325834 Review. No abstract available.
-
Mannose-Binding Lectin: Biologic Characteristics and Role in the Susceptibility to Infections and Ischemia-Reperfusion Related Injury in Critically Ill Neonates.J Immunol Res. 2017;2017:7045630. doi: 10.1155/2017/7045630. Epub 2017 Jan 26. J Immunol Res. 2017. PMID: 28246614 Free PMC article. Review.
-
Trefoil factor 3 as a marker of intestinal cell damage during sepsis.Open Med (Wars). 2015 Apr 24;10(1):261-266. doi: 10.1515/med-2015-0020. eCollection 2015. Open Med (Wars). 2015. PMID: 28352704 Free PMC article.
-
Differential protection against oxidative stress and nitric oxide overproduction in cardiovascular and pulmonary systems by propofol during endotoxemia.J Biomed Sci. 2009 Jan 15;16(1):8. doi: 10.1186/1423-0127-16-8. J Biomed Sci. 2009. PMID: 19272174 Free PMC article.
-
Lipopolysaccharide exposure is linked to activation of the acute phase response and growth failure in pediatric Crohn's disease and murine colitis.Inflamm Bowel Dis. 2010 May;16(5):856-69. doi: 10.1002/ibd.21132. Inflamm Bowel Dis. 2010. PMID: 19924809 Free PMC article.
References
Publication types
MeSH terms
Grants and funding
LinkOut - more resources
Full Text Sources
Research Materials