Randomized Controlled Trial of Early Docosahexaenoic Acid and Arachidonic Acid Enteral Supplementation in Very Low Birth Weight Infants.

Objective: To determine feasibility of providing a concentrated emulsified long-chain polyunsaturated fatty acids (LCPUFA) supplement to very low birth weight infants, and to evaluate blood LCPUFA concentrations at 2 and 8 weeks of study supplementation.

Study Design: This prospective, randomized, double-blind, placebo-controlled trial randomized infants to receive (1) LCPUFA-120 (a supplement of 40 mg/kg/day docosahexaenoic acid [DHA] and 80 mg/kg/day arachidonic acid [ARA]; DHA:ARA at 1:2 ratio), (2) LCPUFA-360 (a supplement of 120 mg/kg/day DHA and 240 mg/kg/day ARA), or (3) sunflower oil (placebo control). Infants received supplement daily for 8 weeks or until discharge, whichever came first.

Can Fish Oil Reduce the Incidence of Necrotizing Enterocolitis by Altering the Inflammatory Response?

Necrotizing enterocolitis (NEC) is a devastating bowel necrosis that predominantly affects preterm infants and is characterized by an imbalance toward a proinflammatory state. Fish oil or omega-3 long-chain polyunsaturated fatty acids have the potential to modulate inflammation. In this article, the authors examine the evidence in support of fish oil supplementation to alter the inflammatory response and potentially reduce the risk of NEC.

New Medical and Surgical Insights Into Neonatal Necrotizing Enterocolitis: A Review.

Importance: Necrotizing enterocolitis (NEC) has long remained a significant cause of morbidity and mortality in neonatal intensive care units. While the mainstay of treatment for this devastating condition remains largely supportive, research efforts continue to be directed toward understanding pathophysiology as well as how best to approach surgical management when indicated.

Observations: In this review, we first examine recent medical observations, including overviews on the microbiome and a brief review of the use of probiotics.

Transforming growth factor-β2 is sequestered in preterm human milk by chondroitin sulfate proteoglycans.

Human milk contains biologically important amounts of transforming growth factor-β2 isoform (TGF-β2), which is presumed to protect against inflammatory gut mucosal injury in the neonate. In preclinical models, enterally administered TGF-β2 can protect against experimental necrotizing enterocolitis, an inflammatory bowel necrosis of premature infants. In this study, we investigated whether TGF-β bioactivity in human preterm milk could be enhanced for therapeutic purposes by adding recombinant TGF-β2 (rTGF-β2) to milk prior to feeding.

Maternal breast milk transforming growth factor-beta and feeding intolerance in preterm infants.

Background: Feeding intolerance (FI) occurs commonly in the neonatal intensive care unit. Breast milk contains a large pool of transforming growth factor-beta (TGF-β). Few studies describe TGF-β levels in preterm milk, and the relationship to FI remains unexplored.

Necrotizing enterocolitis: pathophysiology, platelet-activating factor, and probiotics.

Although smaller and younger preterm neonates can now survive long term due to advances in neonatal medicine, necrotizing enterocolitis (NEC) continues to plague the clinicians caring for these tiny patients. Research studies have contributed to our understanding of this complex disease, including the role of platelet-activating factor (PAF), but preventative and treatment strategies remain limited. One promising preventative measure in recent years has been enteral supplementation of probiotics, but concerns remain regarding the optimal use of these organisms, and safe administration must be assured.

Preterm human milk contains a large pool of latent TGF-β, which can be activated by exogenous neuraminidase.

Human milk contains substantial amounts of transforming growth factor (TGF)-β, particularly the isoform TGF-β2. We previously showed in preclinical models that enterally administered TGF-β2 can protect against necrotizing enterocolitis (NEC), an inflammatory bowel necrosis of premature infants. In this study we hypothesized that premature infants remain at higher risk of NEC than full-term infants, even when they receive their own mother's milk, because preterm human milk contains less bioactive TGF-β than full-term milk.

Probiotics and prevention of neonatal necrotizing enterocolitis.

Purpose Of Review: This review will summarize the clinical trials evaluating the role of prophylactic probiotic supplementation in preterm infants in order to reduce the incidence of necrotizing enterocolitis (NEC).

Recent Findings: Evidence suggests that probiotic supplementation in preterm infants reduces the incidence of NEC. In fact, recent meta-analyses have called for the use of probiotics as preventive therapy in subsets of this population.

The importance of pro-inflammatory signaling in neonatal necrotizing enterocolitis.

Despite modern medical advances, necrotizing enterocolitis (NEC) remains a significant cause of morbidity and mortality in neonatal intensive care units, affecting 10% of premature neonates born weighing less than 1500 g. Although many advances have been made in the understanding of NEC, the etiology and pathophysiology remain incompletely understood, and treatment is limited to supportive care. In recent years, many studies have evaluated the inflammatory cascade that is central to the disease process, and research is ongoing into strategies to prevent and/or ameliorate neonatal NEC.