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N Engl J Med. 2017 Mar 30;376(13):1245-1255. doi: 10.1056/NEJMoa1611942.

Docosahexaenoic Acid and Bronchopulmonary Dysplasia in Preterm Infants.

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From Healthy Mothers, Babies, and Children, South Australian Health and Medical Research Institute (C.T.C., M.M., A.J.M., R.A.G.), the Schools of Medicine (C.T.C., M.M., A.J.M., M.J.S.), Public Health (T.R.S.), and Agriculture, Food, and Wine (R.A.G.) and the Robinson Research Institute (M.J.S.), University of Adelaide, the Department of Neonatal Medicine, Women's and Children's Hospital (A.J.M., M.J.S.), and the School of Medicine (S.A.M.), Flinders University, Adelaide, SA, the Newborn Research Centre, Royal Women's Hospital (P.G.D., M.T.), University of Melbourne (P.G.D., M.T.), Murdoch Children's Research Institute (M.T.), the Department of Paediatrics, Mercy Hospital for Women (G.F.O., J.H.), the Department of Paediatrics, Monash University and Monash Newborn, Monash Children's Hospital (K.T.), Melbourne, VIC, the Clinical Trials Centre, University of Sydney (K.S.), School of Women's and Children's Health, University of New South Wales (K.L., J.S.), and Newborn Care, Royal Hospital for Women (S.B.), Sydney, the Neonatal Intensive Care Unit, John Hunter Children's Hospital and School of Medicine and Public Health, University of Newcastle, Newcastle, NSW (J.T.), the Neonatal Intensive Care Unit, Liverpool Hospital, Liverpool, NSW (J.S., I.R.C.), the Department of Newborn Medicine, Centre for Neonatal Research and Education, University of Western Australia, Perth (K.S.), and Newborn Services, Mater Misericordiae, and Mater Research Institute, University of Queensland, Brisbane (H.G.L.) - all in Australia; the Department of Paediatrics and Child Health, University of Otago, Wellington (M.J.B.), the Newborn Intensive Care Unit, Waikato Hospital, Hamilton (D.L.H.), and Liggins Institute, University of Auckland, Auckland (D.L.H.) - all in New Zealand; and the Department of Neonatology, KK Women's and Children's Hospital (V.S.R., M.-C.C., P.A.J.), Yong Loo Lin School of Medicine, National University of Singapore (V.S.R., M.-C.C.), and Duke-National University of Singapore Medical School (V.S.R., M.-C.C.) - all in Singapore.



Studies in animals and in humans have suggested that docosahexaenoic acid (DHA), an n-3 long-chain polyunsaturated fatty acid, might reduce the risk of bronchopulmonary dysplasia, but appropriately designed trials are lacking.


We randomly assigned 1273 infants born before 29 weeks of gestation (stratified according to sex, gestational age [<27 weeks or 27 to <29 weeks], and center) within 3 days after their first enteral feeding to receive either an enteral emulsion providing DHA at a dose of 60 mg per kilogram of body weight per day or a control (soy) emulsion without DHA until 36 weeks of postmenstrual age. The primary outcome was bronchopulmonary dysplasia, defined on a physiological basis (with the use of oxygen-saturation monitoring in selected infants), at 36 weeks of postmenstrual age or discharge home, whichever occurred first.


A total of 1205 infants survived to the primary outcome assessment. Of the 592 infants assigned to the DHA group, 291 (49.1% by multiple imputation) were classified as having physiological bronchopulmonary dysplasia, as compared with 269 (43.9%) of the 613 infants assigned to the control group (relative risk adjusted for randomization strata, 1.13; 95% confidence interval [CI], 1.02 to 1.25; P=0.02). The composite outcome of physiological bronchopulmonary dysplasia or death before 36 weeks of postmenstrual age occurred in 52.3% of the infants in the DHA group and in 46.4% of the infants in the control group (adjusted relative risk, 1.11; 95% CI, 1.00 to 1.23; P=0.045). There were no significant differences between the two groups in the rates of death or any other neonatal illnesses. Bronchopulmonary dysplasia based on a clinical definition occurred in 53.2% of the infants in the DHA group and in 49.7% of the infants in the control group (P=0.06).


Enteral DHA supplementation at a dose of 60 mg per kilogram per day did not result in a lower risk of physiological bronchopulmonary dysplasia than a control emulsion among preterm infants born before 29 weeks of gestation and may have resulted in a greater risk. (Funded by the Australian National Health and Medical Research Council and others; Australian New Zealand Clinical Trials Registry number, ACTRN12612000503820 .).

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