Gut mucosal cell damage in meningococcal sepsis in children: relation with clinical outcome.
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.


METHODS
Retrospective human study.


METHODS
Pediatric intensive care unit at a university hospital.


METHODS
Nineteen consecutive children with meningococcal sepsis were studied during their pediatric intensive care unit stay.


METHODS
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.
Derikx
Joep P M
JP
Department of Surgery, Maastricht University Medical Centre & Nutrition and Toxicology Research Institute, Maastricht, The Netherlands.
Bijker
Else M
EM
Vos
Gijs D
GD
van Bijnen
Annemarie A
AA
Heineman
Erik
E
Buurman
Wim A
WA
van Waardenburg
Dick A
DA
D000293:Adolescent; D000367:Age Factors; D016470:Bacteremia / Q000175:diagnosis* / Q000401:mortality* / Q000628:therapy; D015415:Biomarkers / Q000378:metabolism; D001774:Blood Chemical Analysis; D002648:Child; D002675:Child, Preschool; D015331:Cohort Studies; D016638:Critical Illness / Q000401:mortality; D020895:Enterocytes / Q000473:pathology; D050556:Fatty Acid-Binding Proteins / Q000378:metabolism*; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology; D017052:Hospital Mortality; D006785:Hospitals, University; D006801:Humans; D007223:Infant; D015278:Intensive Care Units, Pediatric; D015850:Interleukin-6 / Q000378:metabolism; D007413:Intestinal Mucosa / Q000473:pathology; D008297:Male; D008589:Meningococcal Infections / Q000175:diagnosis* / Q000401:mortality* / Q000628:therapy; D011237:Predictive Value of Tests; D011336:Probability; D011379:Prognosis; D012189:Retrospective Studies; D012737:Sex Factors; D016019:Survival Analysis
D015415:Biomarkers; C493404:FABP2 protein, human; D050556:Fatty Acid-Binding Proteins; D015850:Interleukin-6