Carol Lynn Berseth1. 1. Director Medical Affairs North America, Mead Johnson and Company, Evansville, Indiana 47721, USA. carol.berseth@bms.com
Abstract
PURPOSE OF REVIEW: To update clinical trials concerning feeding strategies or feeding interventions to prevent necrotizing enterocolitis (NEC). RECENT FINDINGS: The overall incidence of NEC remains unchanged. Several studies have shown that it is safe to use small feeding volumes early in life even in selected circumstances, such as feeding during the use of indomethacin to treat symptomatic patent ductus arteriosus. Although descriptive case reports have linked some feeding interventions such as thickened feedings to NEC, there is no evidence to establish a causal relation. Interestingly, one report showed that neither the presence of-nor characteristics of-gastric residuals was helpful to identify those infants who subsequently develop NEC. Numerous studies in animals show that vascular and host defense responses are not adequate in the immature gut. A few small clinical trials showed that various feeding strategies may alter these responses in preterm infants. However, larger clinical trials around these issues await further characterization of the mechanisms that regulate these two aspects of gastrointestinal function with respect to feeding. SUMMARY: Studies continue to demonstrate how fragile the immature gut is, but further work directed to understanding the mechanisms that regulate gastrointestinal responses to feeding is needed to design meaningful interventions for large prospective trials.
PURPOSE OF REVIEW: To update clinical trials concerning feeding strategies or feeding interventions to prevent necrotizing enterocolitis (NEC). RECENT FINDINGS: The overall incidence of NEC remains unchanged. Several studies have shown that it is safe to use small feeding volumes early in life even in selected circumstances, such as feeding during the use of indomethacin to treat symptomatic patent ductus arteriosus. Although descriptive case reports have linked some feeding interventions such as thickened feedings to NEC, there is no evidence to establish a causal relation. Interestingly, one report showed that neither the presence of-nor characteristics of-gastric residuals was helpful to identify those infants who subsequently develop NEC. Numerous studies in animals show that vascular and host defense responses are not adequate in the immature gut. A few small clinical trials showed that various feeding strategies may alter these responses in preterm infants. However, larger clinical trials around these issues await further characterization of the mechanisms that regulate these two aspects of gastrointestinal function with respect to feeding. SUMMARY: Studies continue to demonstrate how fragile the immature gut is, but further work directed to understanding the mechanisms that regulate gastrointestinal responses to feeding is needed to design meaningful interventions for large prospective trials.
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