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Antioxidants and Biomarkers of Oxidative Stress in Preterm Infants with Symptomatic Patent Ductus Arteriosus
Musaddaq Inayat1, Fayez Bany-Mohammed1, Arwin Valencia2
1Division of Neonatal-Perinatal Medicine, Department of Pediatrics, University of California, Irvine, California.
Insights
Preterm infants at risk for patent ductus arteriosus (PDA) have low antioxidant activity at birth. Superoxide dismutase (SOD) may be crucial for ductus arteriosus closure, and low levels might contribute to PDA persistence.
Area of Science:
- Neonatal physiology
- Cardiovascular research
- Antioxidant biochemistry
Background:
- Immature antioxidant and oxygen-sensing mechanisms are implicated in the development of patent ductus arteriosus (PDA).
- Symptomatic PDA is a common complication in preterm infants, necessitating intervention.
Purpose of the Study:
- To test the hypothesis that antioxidant activity is diminished at birth in preterm infants susceptible to symptomatic PDA.
- To investigate the role of antioxidant status in the pathogenesis of PDA.
Main Methods:
- Prospective observational pilot study involving 53 preterm infants (≤32 weeks' gestation) and 30 term controls.
- Collection of blood and urine samples within 48 hours of birth and post-treatment for preterm infants with hemodynamically significant PDA (hsPDA).
- Analysis of biomarkers for antioxidant activity, oxidative stress, and lipid peroxidation.
Main Results:
- Preterm infants who developed hsPDA exhibited significantly lower plasma superoxide dismutase (SOD) and urinary catalase levels at birth.
- Plasma and urinary 8-isoPGF2α, a marker of oxidative stress, were also reduced in preterm infants with hsPDA.
- Post-treatment, plasma 8-isoPGF2α levels increased, while other markers like urinary prostaglandin E2 and plasma SOD decreased.
Conclusions:
- Preterm infants at risk for hsPDA demonstrate a compromised antioxidant status.
- Reduced SOD levels may impair functional ductus arteriosus closure, potentially leading to persistent hsPDA.
- Antioxidant support could be a potential therapeutic strategy for managing PDA in preterm neonates.
Objective:
Immature antioxidant and oxygen-sensing mechanisms are involved in the pathogenesis of the patent ductus arteriosus (PDA). We conducted a prospective, observational, pilot study to test the hypothesis that antioxidant activity is low at birth in preterm infants at risk for symptomatic PDA.
Study Design:
Blood and urine samples were collected within 24 to 48 hours of life in 53 preterm infants (≤32 weeks' gestation) who developed early PDA symptoms and in 30 term (≥37 weeks' gestation) control infants. Thirty preterm infants developed hemodynamically significant PDA (hsPDA) and required pharmacologic treatment and/or PDA ligation. For these infants, blood and urine samples were also collected at 24 hours posttreatment. Samples were analyzed for biomarkers of antioxidant activity, oxidative stress, and lipid peroxidation.
Results:
At 24 to 48 hours after birth, plasma superoxide dismutase (SOD), urinary catalase, and plasma and urinary 8-isoPGF2α were significantly lower in preterm infants who developed hsPDA. Plasma 8-isoPGF2α levels rebounded post-PDA treatment, while urinary prostaglandin E2, plasma and urinary thromboxane B2, and plasma SOD declined.
Conclusion:
The antioxidant status is low in preterm infants at risk for developing hsPDA. SOD may be a key antioxidant regulating functional ductus arteriosus closure. Therefore, low levels may result in persistence of a hsPDA.
