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Published on: April 1, 2014
Gut mucosal cell damage in meningococcal sepsis in children: relation with clinical outcome
Joep P M Derikx1, Else M Bijker, Gijs D Vos
1Department of Surgery, Maastricht University Medical Centre & Nutrition and Toxicology Research Institute, Maastricht, The Netherlands.
Insights
Meningococcal sepsis in children can cause enterocyte damage, indicated by elevated intestinal fatty acid binding protein (IFABP) levels. Non-survivors showed prolonged IFABP elevation, suggesting its role in disease severity and outcome.
Area of Science:
- Pediatric critical care medicine
- Gastroenterology
- Infectious diseases
Background:
- Meningococcal sepsis pathophysiology involves microvascular dysfunction and impaired tissue perfusion.
- Mature enterocytes are vulnerable to compromised blood flow, potentially leading to damage.
- Understanding enterocyte injury in pediatric sepsis is crucial for improving patient outcomes.
Purpose of the Study:
- To investigate the development of enterocyte damage in children with meningococcal sepsis.
- To determine the relationship between enterocyte damage and disease severity.
- To explore the association between enterocyte damage and clinical outcomes in pediatric meningococcal sepsis.
Main Methods:
- Retrospective study of 19 children admitted to a pediatric intensive care unit with meningococcal sepsis.
- Measurement of circulating intestinal fatty acid binding protein (IFABP) levels upon admission.
- Assessment of disease severity using the Rotterdam Score, Pediatric Risk of Mortality II, and interleukin-6 levels.
- Correlation analysis between IFABP levels and clinical outcomes, including length of ICU stay and ventilator days.
Main Results:
- Eight of 19 patients presented with elevated plasma IFABP levels at admission, indicating enterocyte damage.
- IFABP levels correlated significantly with disease severity scores (Rotterdam Score, PRISM II) and interleukin-6.
- Survivors showed declining IFABP levels within 12 hours of treatment, while non-survivors maintained elevated levels.
- A significant correlation was observed between IFABP levels and clinical outcomes.
Conclusions:
- Elevated plasma IFABP suggests enterocyte damage in children with severe meningococcal sepsis at presentation.
- Persistent enterocyte damage, indicated by prolonged IFABP elevation, is associated with non-survival.
- Plasma IFABP may serve as a potential biomarker for monitoring treatment efficacy in pediatric sepsis.
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.
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