Does Human Milk Fortifier Affect Intestinal Inflammation in Preterm Infants?

Breastfeed Med

Division of Neonatal-Perinatal Medicine, Cohen Children's Medical Center, Lilling Family Neonatal Research Lab, Feinstein Institutes for Medical Research, Zucker School of Medicine at Hofstra/Northwell, New Hyde Park, New York, USA.

Published: December 2020


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Article Abstract

Fecal calprotectin, a recognized marker of intestinal inflammation, is derived from neutrophil migration to a site of inflammation. Introduction of bovine-based human milk fortifier containing intact protein in preterm infants is associated with an increase in fecal calprotectin suggestive of intestinal inflammation. Newer fortifiers contain protein hydrolysates in place of intact protein. To measure fecal calprotectin in human milk-fed preterm infants before and after human milk fortification using a fortifier containing hydrolyzed protein. Serial stool samples were collected from 24 infants beginning at the first week to 60 days postnatal age. To compare the effect of human milk fortification, samples collected before and after fortification were compared. Infant demographics, diet, postnatal morbidities, and maternal characteristics were recorded. A total of 401 stool samples were collected from 24 study infants who had a birth weight of 993 ± 277 g (mean ± standard deviation), gestational age 27.5 ± 2.8 weeks, and fortifier initiation at 14 days. Median fecal calprotectin before and after fortification were similar. Calprotectin levels were not correlated with birth weight or gestational age but were inversely correlated with postnatal age ( = 0.005), use of fortifier ( < 0.001), receipt of antibiotics antenatally ( = 0.007) and postnatally ( = 0.008). After adjusting for postnatal age, calprotectin levels were significantly lower following receipt of fortifier ( < 0.001) and postnatal antibiotics ( < 0.001). The feeding of protein hydrolysate-containing human milk fortifiers does not appear to be associated with increases in a marker of intestinal inflammation.

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http://dx.doi.org/10.1089/bfm.2020.0205DOI Listing

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