Overview
prospective observational cohort study to explore the relationship between PGE2 metabolite levels and the development of hemodynamically significant PDA in preterm neonates.
Description
Regulation of ductus arteriosus involves (PGE2), produced by the placenta and DA itself, that promotes ductal patency by relaxing smooth muscle.
Prostaglandins are pluripotent lipid mediators derived from membrane glycerophospholipid metabolism. They are synthesized via a multienzyme cascade involving the actions of phospholipases and COX isoforms. Prostanoids, such as prostaglandin E2 and prostaglandin D2 metabolite (PGDM), are produced by various structural and inflammatory cells.
Cyclooxygenase inhibitors restrict the PDA by inhibiting the prostaglandin synthase enzyme, which prevents arachidonic acid from converting to prostaglandin. Acetaminophen is also believed to inhibit the prostaglandin synthesis enzyme's peroxidase portion, resulting in the PDA narrowing.
A significant decrease in serum PGE2 levels was observed following COX inhibitor treatment.
Eligibility
Inclusion Criteria:
- Preterm neonates with gestational age ≤ 32 weeks, admitted to the NICU and diagnosed with patent ductus arteriosus by echocardiography on day 3 of life.
Exclusion Criteria:
- Preterm neonates with evidence of any of the following will be excluded:
Chromosomal anomaly or Congenital malformations Progressive intraventricular hemorrhage Congenital heart defect other than PDA and/or patent foramen ovale Pulmonary hypertension with right to left shunt on PDA Contraindications to the use of Ibuprofen: \[1\] Urine output \<1 mL/kg/hour during preceding 8 hours. Serum creatinine \>1.6 mg/dL. Platelet count \<50 000/mm3. Abnormal coagulation profile. Necrotizing enterocolitis (NEC) or intestinal perforation