The Rate of Bloodstream Infection Is High in Infants with Short Bowel Syndrome: Relationship with Small Bowel Bacterial Overgrowth, Enteral Feeding, and Inflammatory and Immune Responses
Objective
This pilot study in parenteral nutrition–dependent infants with short bowel syndrome (SBS) evaluated the impact of feeding route and intestinal permeability on bloodstream infection (BSI), small bowel bacterial overgrowth (SBBO), and systemic immune responses, as well as fecal calprotectin as a biomarker for SBBO.
Study design
Ten infants (ages 4.2-15.4 months) with SBS caused by necrotizing enterocolitis were evaluated. Nutritional assessment, breath hydrogen testing, intestinal permeability, fecal calprotectin, serum flagellin- and lipopolysaccharide-specific antibody titers, and proinflammatory cytokine concentrations (tumor necrosis factor–α [TNF-α], interleukin-1 β, -6, and -8) were performed at baseline and at 60 and 120 days. Healthy, age-matched control subjects (n = 5) were recruited.
Results
BSI incidence was high (80%), and SBBO was common (50%). SBBO increased the odds for BSI (>7-fold; P = .009). Calprotectin levels were higher in children with SBS and SBBO versus those without SBBO and healthy control subjects (P < .05). Serum TNF-α, was elevated at baseline versus controls. Serum TNF-α and interleukin-1 β, -6, and -8 levels diminished with increased enteral nutrition. Anti-flagellin and anti-lipopolysaccharide immunoglobulin G levels in children with SBS were lower versus control subjects and rose over time.
Conclusion
In children with SBS, SBBO increases the risk for BSI, and systemic proinflammatory response decreases with increasing enteral feeding and weaning parenteral nutrition.
BSI, Bloodstream infection, GCRC, General Clinical Research Center, IgG, Immunoglobulin G, L/M, Lactulose:mannitol, NEC, Necrotizing enterocolitis, PN, Parenteral nutrition, SBS, Short bowel syndrome, SBBO, Small bowel bacterial overgrowth, TNF-α, Tumor necrosis factor-α
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Supported in part by National Institutes of Health grants K12 RR017643 and KL2 RR025009 (to CRC), R01 DK55850 and K24 RR023356 (to T.Z.), UL1 RR025008 from the Clinical and Translational Science Award program and M01 RR0039 from the General Clinical Research Center program, National Center for Research Resources. The authors declare no conflicts of interest.
PII: S0022-3476(09)01236-0
doi:10.1016/j.jpeds.2009.12.008
© 2010 Mosby, Inc. All rights reserved.
