Abstract
Background: 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. Methods: 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. Results: 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). Conclusions: 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.
| Original language | English |
|---|---|
| Pages (from-to) | 1245-1255 |
| Number of pages | 11 |
| Journal | New England Journal of Medicine |
| Volume | 376 |
| Issue number | 13 |
| DOIs | |
| Publication status | Published - 30 Mar 2017 |
Cite this
}
Docosahexaenoic acid and bronchopulmonary dysplasia in preterm infants. / Collins, Carmel T.; Makrides, Maria; McPhee, Andrew J.; Sullivan, Thomas R.; Davis, Peter G.; Thio, Marta; Simmer, Karen; Rajadurai, Victor S.; Travadi, Javeed; Berry, Mary J.; Liley, Helen G.; Opie, Gillian F.; Tan, Kenneth; Lui, Kei; Morris, Scott A.; Stack, Jacqueline; Stark, Michael J.; Chua, Mei Chien; Jayagobi, Pooja A.; Holberton, James; Bolisetty, Srinivas; Callander, Ian R.; Harris, Deborah L.; Gibson, Robert A.
In: New England Journal of Medicine, Vol. 376, No. 13, 30.03.2017, p. 1245-1255.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - Docosahexaenoic acid and bronchopulmonary dysplasia in preterm infants
AU - Collins, Carmel T.
AU - Makrides, Maria
AU - McPhee, Andrew J.
AU - Sullivan, Thomas R.
AU - Davis, Peter G.
AU - Thio, Marta
AU - Simmer, Karen
AU - Rajadurai, Victor S.
AU - Travadi, Javeed
AU - Berry, Mary J.
AU - Liley, Helen G.
AU - Opie, Gillian F.
AU - Tan, Kenneth
AU - Lui, Kei
AU - Morris, Scott A.
AU - Stack, Jacqueline
AU - Stark, Michael J.
AU - Chua, Mei Chien
AU - Jayagobi, Pooja A.
AU - Holberton, James
AU - Bolisetty, Srinivas
AU - Callander, Ian R.
AU - Harris, Deborah L.
AU - Gibson, Robert A.
PY - 2017/3/30
Y1 - 2017/3/30
N2 - Background: 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. Methods: 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. Results: 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). Conclusions: 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.
AB - Background: 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. Methods: 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. Results: 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). Conclusions: 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.
UR - http://www.scopus.com/inward/record.url?scp=85016964266&partnerID=8YFLogxK
U2 - 10.1056/NEJMoa1611942
DO - 10.1056/NEJMoa1611942
M3 - Article
VL - 376
SP - 1245
EP - 1255
JO - New England Journal of Medicine
JF - New England Journal of Medicine
SN - 0028-4793
IS - 13
ER -