prospective observational cohort study to explore the relationship between PGE2 metabolite levels and the development of hemodynamically significant PDA in preterm neonates.
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.
Study Type
OBSERVATIONAL
Enrollment
34
Group1will receive anti-PGE; Ibuprofen (IBU) (brufen)® syrup will be given for 3 days enterally either orally or via a gastric tube with an initial dose of 10mg/kg/day, followed by 5mg/kg/day for the next 2 days. Group 2 will be observed and follow up echocardiography and PGE2 level will be followed up 3 days after treatment or follow up in both groups.
Faculty of Medicine, Ain Shams, University
Cairo, Abbasia, Egypt
RECRUITINGExplore the relationship between PGE2 metabolite levels and the development of hemodynamically significant PDA in preterm neonates.
correlating the initial levels of PGE2 with the significance of PDA
Time frame: initial PGE2 level on the first day of life and follow up the level after 3 days of treatment
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