Bacterial toxins and enteral feeding of premature infants at risk for necrotizing enterocolitis

✍ Scribed by Linda C. Duffy; Maria A. Zielezny; Vivien Carrion; Elizabeth Griffiths; Diane Dryja; Milo Hilty; James Cummings; Frederick Morin III

• Publisher: John Wiley and Sons
• Year: 1998
• Tongue: English
• Weight: 86 KB
• Volume: 10
• Category: Article
• ISSN: 1042-0533
• DOI: 10.1002/(sici)1520-6300(1998)10:2<211::aid-ajhb6>3.0.co;2-n

✦ Synopsis

Bacterial translocation and enteral feeding are factors implicated in neonatal necrotizing enterocolitis (NEC) in the preterm infant. A cohort of 60 preterm low birth-weight (LBW) infants (600-1,600 g at birth) consecutively admitted to the neonatal intensive care unit (NICU; N = 183) were prospectively followed to evaluate the role of bacterial endotoxins (lipopolysaccharides) and enteral feeding in the development of NEC. Stage I NEC was identified in 14/60 (23%) infants. In all, 15% (9/60) of infants followed, which represented roughly 5% of higher risk, LBW infants admitted to the NICU, progressed to Stage II or III NEC disease. Infants not enterally fed (nothing by mouth [NPO]) were at greatest risk of developing NEC. No infant who was breast milk fed progressed to Stage II or III NEC. The protective effect of breast milk was most evident when compared with the combined group of NPO or formula-feeding infants per person-week at risk (RR = .15, P < .04). Toxin-producing bacteria and endotoxin levels in stool filtrates predicted early and advanced stages of NEC disease. Cytokine concentrations (interleukin-6 [IL-6]) in stool appeared of limited value in reflecting mucosally limited disease in the gastrointestinal tract. Overgrowth of toxin-producing bacteria and their toxin products may adversely affect gut barrier function; monitoring endotoxin concentrations in stool filtrates may be most clinically useful in NPO and formula-fed infants identified at risk of developing NEC. Am. J. Hum. Biol. 10:211-219, 1998. © 1998 Wiley-Liss, Inc.