Year: 2021
Type: review
Abstract: Platelets are critically involved in murine patent ductus arteriosus (PDA) closure. To date, the clinical significance of these findings in human preterm infants with PDA is still controversial. We discuss the available study data on the role of platelets for PDA closure in preterm infants: Several mostly retrospective studies have yielded conflicting results on whether thrombocytopenia contributes to failed spontaneous ductal closure. The same applies to investigations on the role of thrombocytopenia as a risk factor for unsuccessful ductus arteriosus closure by pharmacological treatment with cyclooxygenase inhibitors. Nonetheless, recent meta-analyses have concluded that thrombocytopenia constitutes an independent risk factor for both failed spontaneous and pharmacological PDA closure in preterm infants. However, the available investigations differ in regard to patient characteristics, diagnostic strategies, and treatment protocols. Several studies suggest that impaired platelet function rather than platelet number is critically involved in failure of ductus arteriosus closure in the preterm infant. A recent randomized-controlled trial on platelet transfusions in preterm infants with PDA failed to show any benefit for liberal vs. restrictive transfusion thresholds on PDA closure rates. Importantly, liberal transfusions were associated with an increased rate of intraventricular hemorrhage, and thus should be avoided. In conclusion, the available evidence suggests that thrombocytopenia and platelet dysfunction contribute to failure of spontaneous and pharmacological PDA closure in preterm infants. However, these platelet effects on PDA seem to be of only moderate clinical significance. Furthermore, platelet transfusions in thrombocytopenic preterm infants in order to facilitate PDA closure appear to cause more harm than good.
Source: Frontiers in Pediatrics
Language: English
Subfield: Radiology, Nuclear Medicine and Imaging
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $1,811
Funders: American Heart Association, European Pediatric Pulmonary Vascular Disease Network, Deutsche Forschungsgemeinschaft, Bundesministerium für Bildung und Forschung, National Institutes of Health, National Heart, Lung, and Blood Institute, Eunice Kennedy Shriver National Institute of Child Health and Human Development
Awards: G1033834133, G1250793776, Verbundprojekt: Neue Tryptophan-Hydroxylase Inhibitoren zur inhalativen Behandlung - TPH-Inhibitoren, Teilvorhaben: Testung von TPH Inhibitoren im Lungenhochdruck-Rattenmodell, G1771576154, KATP channels as biomechanical sensors in the regulation of ductus arteriosus tone, G23728244, Mechanisms of Ductus Arteriosus Regulation, G381898139, G4065994052, Pharmacological Validation of Vascular KATP Channels for Modulating Ductus Arteriosus Tone, G5225744738, TPHiPAH - Tryptophanhydroxylase-Inhibitoren als neue Therapeutika für pulmonale arterielle Hypertonie, Studienteil Hannover, G7810301964, G864330851, The role of KATP channels in models of PDA and Cantu Syndrome
OpenAlex ID: W3129925521