Abstract
BackgroundIntestinal bile salts (BSs) may be implicated in NEC development. We hypothesized that fecal BS levels are higher in preterm infants at risk for NEC.MethodsWe compared the composition and concentration of fecal BSs in ten preterm infants who developed NEC (Bell’s Stage ≥ II) with twenty matched control infants without NEC. Conjugated and unconjugated fecal BSs were measured after birth (T1) and twice prior to NEC (T2, T3). Data are presented as medians and interquartile ranges.ResultsGA and BW were similar in all preterms: ~27+4 weeks and ~1010 g. Age of NEC onset was day 10 (8–24). T1 was collected 2 (1–3) days after birth. T2 and T3 were collected 5 (5–6) days and 1 (0–2) day before NEC or at corresponding postnatal ages in controls. The composition of conjugated BSs did not differ between the two groups. Total unconjugated BSs were 3-fold higher before NEC compared to controls at corresponding ages (0.41 μmol/g feces (0.21–0.74) versus 0.14 μmol/g feces (0.06–0.46), p < 0.05).ConclusionFecal BS concentrations are higher in preterm infants who develop NEC compared to infants without NEC. Further study is needed to determine the predictive value of fecal BSs in the development of NEC.
Highlights
It remains unpredictable whether or not a preterm infant will develop NEC, despite well-characterized epidemiological and clinical risk factors such as low gestational age (GA), low birth weight (LBW), formula feeding, and antibiotic treatment [1]
GA and BW were similar in all preterms: ~27+4 weeks and ~1010 g
The composition of conjugated bile salts (BSs) did not differ between the two groups
Summary
It remains unpredictable whether or not a preterm infant will develop NEC, despite well-characterized epidemiological and clinical risk factors such as low gestational age (GA), low birth weight (LBW), formula feeding, and antibiotic treatment [1]. Finding parameters that could identify preterm infants at risk of NEC is of great clinical importance. It is thought that the accumulation of intestinal bile salts (BSs) is implicated in the development of NEC. Intestinal BS re-uptake occurs mainly in the distal ileum, i.e. the intestinal segment predominantly affected in NEC. Intraluminal accumulation of hydrophobic BSs can result in intestinal epithelial damage similar to the histopathological findings in NEC [5]. The essential role of intestinal BS transport in the development of NEC has been convincingly demonstrated: NEC is attenuated in mice deficient in apical sodium-dependent bile salt transporter (ASBT), a protein involved in intestinal BS uptake, and in rats treated with an ASBT inhibitor [6]. Intestinal bile salts (BSs) may be implicated in NEC development. We hypothesized that fecal BS levels are higher in preterm infants at risk for NEC
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