Judith A Voynow1,2, Kimberley Fisher3, Mary E Sunday4, Charles M Cotten3, Aaron Hamvas5,6, Karen D Hendricks-Muñoz7, Brenda B Poindexter8,9, Gloria S Pryhuber10, Clement L Ren11,12, Rita M Ryan13,14, Jack K Sharp1,15,16, Sarah P Young17, Haoyue Zhang17, Rachel G Greenberg18, Amy H Herring19, Stephanie D Davis12,20. 1. Division of Pediatric Pulmonology, Duke University, Durham, North Carolina. 2. Division of Pediatric Pulmonology, Children's Hospital of Richmond, Richmond, Virginia. 3. Division of Neonatology, Duke University, Durham, North Carolina. 4. Department of Pathology, Duke University, Durham, North Carolina. 5. Division of Neonatology, Washington University, St Louis, Missouri. 6. Division of Neonatology, Northwestern University, Chicago, Illinois. 7. Division of Neonatology, Children's Hospital of Richmond, Richmond, Virginia. 8. Division of Neonatology, Indiana University, Indianapolis, Indiana. 9. Division of Neonatology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio. 10. University of Rochester, Rochester, New York. 11. Division of Pediatric Pulmonology, University of Rochester, Rochester, New York. 12. Division of Pediatric Pulmonology, Indiana University, Indianapolis, Indiana. 13. Division of Neonatology, State University of New York at Buffalo, Buffalo, New York. 14. Department of Pediatrics, Medical University of South Carolina, Charleston, South Carolina. 15. Division of Pediatric Pulmonology, State University of New York at Buffalo, Buffalo, New York. 16. Division of Pediatric Pulmonology, Baylor College of Medicine, Houston, Texas. 17. Division of Medical Genetics, Duke University, Durham, North Carolina. 18. Division of Neonatology and The Duke Clinical Research Institute, Duke University, Durham, North Carolina. 19. Duke Global Health Institute, Duke University, Durham, North Carolina. 20. Department of Pediatrics, University of North Carolina, Chapel Hill, North Carolina.
Abstract
RATIONALE: Bronchopulmonary dysplasia (BPD) is associated with post-prematurity respiratory disease (PRD) in survivors of extreme preterm birth. Identifying early biomarkers that correlate with later development of BPD and PRD may provide insights for intervention. In a preterm baboon model, elevated gastrin-releasing peptide (GRP) is associated with BPD, and GRP inhibition mitigates BPD occurrence. OBJECTIVE: We performed a prospective cohort study to investigate whether urine GRP levels obtained in the first postnatal week were associated with BPD, PRD, and other urinary biomarkers of oxidative stress. METHODS: Extremely low gestational age infants (23-28 completed weeks) were enrolled in a US multicenter observational study, The Prematurity and Respiratory Outcomes Program (http://clinicaltrials.gov/ct2/show/NCT01435187). We used multivariable logistic regression to examine the association between urine GRP in the first postnatal week and multiple respiratory outcomes: BPD, defined as supplemental oxygen use at 36 + 0 weeks postmenstrual age, and post-PRD, defined by positive quarterly surveys for increased medical utilization over the first year (PRD score). RESULTS: A total of 109 of 257 (42%) infants had BPD, and 120 of 217 (55%) had PRD. On adjusted analysis, GRP level more than 80 was associated with BPD (adjusted odds ratio [aOR], 1.83; 95% confidence interval [CI], 1.03-3.25) and positive PRD score (aOR, 2.46; 95% CI, 1.35-4.48). Urine GRP levels correlated with duration of NICU ventilatory and oxygen support and with biomarkers of oxidative stress: allantoin and 8-hydroxydeoxyguanosine. CONCLUSIONS: Urine GRP in the first postnatal week was associated with concurrent urine biomarkers of oxidative stress and with later diagnoses of BPD and PRD.
RATIONALE: Bronchopulmonary dysplasia (BPD) is associated with post-prematurity respiratory disease (PRD) in survivors of extreme preterm birth. Identifying early biomarkers that correlate with later development of BPD and PRD may provide insights for intervention. In a preterm baboon model, elevated gastrin-releasing peptide (GRP) is associated with BPD, and GRP inhibition mitigates BPD occurrence. OBJECTIVE: We performed a prospective cohort study to investigate whether urine GRP levels obtained in the first postnatal week were associated with BPD, PRD, and other urinary biomarkers of oxidative stress. METHODS: Extremely low gestational age infants (23-28 completed weeks) were enrolled in a US multicenter observational study, The Prematurity and Respiratory Outcomes Program (http://clinicaltrials.gov/ct2/show/NCT01435187). We used multivariable logistic regression to examine the association between urine GRP in the first postnatal week and multiple respiratory outcomes: BPD, defined as supplemental oxygen use at 36 + 0 weeks postmenstrual age, and post-PRD, defined by positive quarterly surveys for increased medical utilization over the first year (PRD score). RESULTS: A total of 109 of 257 (42%) infants had BPD, and 120 of 217 (55%) had PRD. On adjusted analysis, GRP level more than 80 was associated with BPD (adjusted odds ratio [aOR], 1.83; 95% confidence interval [CI], 1.03-3.25) and positive PRD score (aOR, 2.46; 95% CI, 1.35-4.48). Urine GRP levels correlated with duration of NICU ventilatory and oxygen support and with biomarkers of oxidative stress: allantoin and 8-hydroxydeoxyguanosine. CONCLUSIONS: Urine GRP in the first postnatal week was associated with concurrent urine biomarkers of oxidative stress and with later diagnoses of BPD and PRD.
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