Document Detail

Gut mucosal cell damage in meningococcal sepsis in children: relation with clinical outcome.
MedLine Citation:
PMID:  19730255     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: The pathophysiological sequelae of meningococcal sepsis are mainly caused by deregulated microvasculature function, leading to impaired tissue blood flow. Because mature enterocytes are known to be susceptible to altered perfusion, we aimed to investigate: (1) the development of enterocyte damage; and (2) the relation between enterocyte damage and severity of disease and outcome in children with meningococcal sepsis. DESIGN: Retrospective human study. SETTING: Pediatric intensive care unit at a university hospital. PATIENTS: Nineteen consecutive children with meningococcal sepsis were studied during their pediatric intensive care unit stay. INTERVENTIONS: None. MEASUREMENT AND MAIN RESULTS Circulating levels of intestinal fatty acid binding protein, a small cytosolic protein constitutively present in mature enterocytes and released on cell injury, were assessed. Severity of disease was represented by meningococcal-specific Rotterdam Score, generic Pediatric Risk of Mortality II score, and circulating interleukin-6. Clinical outcome was measured by length of pediatric intensive care unit stay and number of ventilator days. Highest plasma intestinal fatty acid binding protein values were measured on pediatric intensive care unit stay admission. At the time of admission, eight of 19 patients had higher intestinal fatty acid binding protein plasma levels than the upper reference limit of 30 healthy volunteers. In all survivors, intestinal fatty acid binding protein levels declined to normal values within 12 hrs after starting intensive treatment, whereas the three nonsurvivors maintained elevated intestinal fatty acid binding protein plasma levels. A significant correlation was found among intestinal fatty acid binding protein and Rotterdam Score, Pediatric Risk of Mortality II, interleukin-6 at admission (Spearman's r = 0.402, p = .006; r = 0.243, p = .045; r = 0.687, p < .001, respectively). Next, a significant correlation was found between intestinal fatty acid binding protein and clinical outcome. CONCLUSIONS: Elevated plasma intestinal fatty acid binding protein is found in eight of 19 children with severe pediatric intensive care unit stay at the time of clinical presentation, suggesting the presence of enterocyte damage. Furthermore, prolonged enterocyte damage is found in nonsurvivors. Further studies are needed to clarify the potential role for assessment of plasma intestinal fatty acid binding protein in monitoring treatment of pediatric intensive care unit stay.
Joep P M Derikx; Else M Bijker; Gijs D Vos; Annemarie A van Bijnen; Erik Heineman; Wim A Buurman; Dick A van Waardenburg
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Critical care medicine     Volume:  38     ISSN:  1530-0293     ISO Abbreviation:  Crit. Care Med.     Publication Date:  2010 Jan 
Date Detail:
Created Date:  2009-12-22     Completed Date:  2010-01-15     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0355501     Medline TA:  Crit Care Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  133-7     Citation Subset:  AIM; IM    
Department of Surgery, Maastricht University Medical Centre & Nutrition and Toxicology Research Institute, Maastricht, The Netherlands.
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MeSH Terms
Age Factors
Bacteremia / diagnosis*,  mortality*,  therapy
Biological Markers / metabolism
Blood Chemical Analysis
Child, Preschool
Cohort Studies
Critical Illness / mortality
Enterocytes / pathology
Fatty Acid-Binding Proteins / metabolism*
Gastric Mucosa / pathology
Hospital Mortality
Hospitals, University
Intensive Care Units, Pediatric
Interleukin-6 / metabolism
Intestinal Mucosa / pathology
Meningococcal Infections / diagnosis*,  mortality*,  therapy
Predictive Value of Tests
Retrospective Studies
Sex Factors
Survival Analysis
Reg. No./Substance:
0/Biological Markers; 0/FABP2 protein, human; 0/Fatty Acid-Binding Proteins; 0/Interleukin-6
Comment In:
Crit Care Med. 2010 Jan;38(1):316-7   [PMID:  20023480 ]

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