Tailoring Human Milk Oligosaccharides to Prevent Necrotising Enterocolitis Among Preterm Infants.

Necrotising enterocolitis (NEC) is a devastating disease affecting preterm infants, with little improvement in mortality rates and treatment strategies in the last 30 years. Human milk oligosaccharides (HMOs) are emerging as a potential preventive therapy, with multiple protective functions postulated. Our aim is to summarise the evidence concerning the role of HMOs in NEC development and emerging strategies to tailor the delivery of HMOs to preterm infants. Most research efforts to date have focused on supplementing preterm infants with simple oligosaccharides, which are structurally different to HMOs and derived mainly from plants. Clinical trials demonstrate limited benefits for NEC prevention arising from the use of these supplements. Alternative strategies under investigation include optimising HMOs for infants receiving donor human milk, concentrating oligosaccharides from donor human milk and from animal milks, as well as more sophisticated synthetic oligosaccharide production strategies. Critically, high quality evidence to support implementation of any of these approaches in the neonatal unit is lacking. Whether it is a specific HMO alone or a combination of HMOs that exert protective effects remains to be elucidated. Further challenges include how best to manufacture and administer oligosaccharides whilst retaining bioactivity and safety, including evaluation of the long-term effects of altering the balance of HMOs and gut microbiota in preterm infants. While several human clinical trials are underway, further research is needed to understand whether a tailored approach to oligosaccharide supplementation is beneficial for preterm infants.

In preterm infants, does fluid restriction, as opposed to liberal fluid prescription, reduce the risk of important morbidities and mortality?

AIM: To answer the clinical question: 'In preterm infants, does fluid restriction, as opposed to liberal fluid prescription, reduce the risk of important morbidities (namely, intraventricular haemorrhage, necrotising enterocolitis, bronchopulmonary dysplasia and patent ductus arteriosus) and mortality?' METHODS: Literature searches were conducted of Medline, Embase and Cochrane Library. Results were limited to human clinical trials on infants and those published in English. The reference lists of relevant articles were screened for further articles. Studies that examined measures which inform diagnostic criteria of morbidities of interest (such as echocardiographic changes) but did not go further to confirm or exclude presence of said morbidities in study populations were excluded. RESULTS: A total of 110 articles were found and screened by title and abstract. The final analysis included five randomised controlled trials and five case control studies. Among the randomised controlled trials, there is some suggestion (though not unanimous) that liberal fluid regimens are associated with an increased risk of patent ductus arteriosus, necrotising enterocolitis and mortality. Case control studies focused on patent ductus arteriosus and bronchopulmonary dysplasia or chronic lung disease, with all but one study suggesting an increased risk of these complications with liberal fluid regimens. CONCLUSION: Further investigation is needed to clarify the optimal fluid regimen for preterm infants to ensure adequate hydration and nutrition without contributing to serious complications.