Altered plasma proteins released from platelets and endothelial cells are associated with human patent ductus arteriosus

Hou, Hongying; Xi-Zhang,; Wang, Jun; Liu, Lixin; Zhang, Jianfeng; Yang, Qin; He, Guo‐Wei

doi:10.1002/jcp.27433

Cited by 10 publications

(6 citation statements)

References 66 publications

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“…Of note, immunohistochemical studies have demonstrated that fibrinogen, von Willebrand factor, and collagen are expressed in the mice DA lumen [4]. It has been postulated that the coagulation cascade is involved in DA closure in children with persistent ductal patency [26]. Plasma proteomic analysis revealed that concentrations of fibrinogen, platelet factor 4, von Willebrand factor, collagen, and mannose-binding lectin-associated serine protease 1 were significantly lower in children with persistent PDA compared to controls.…”

Section: Discussionmentioning

confidence: 99%

The Thromboelastographic Profile at Birth in Very Preterm Newborns with Patent Ductus Arteriosus

et al. 2020

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Background: The role of hemostasis in the closure of patent ductus arteriosus (PDA) in preterm infants is controversial. Objective: To assess thromboelastography (TEG) at birth in very-low-birth-weight (VLBW) infants affected by PDA. Methods: This was an ancillary study of a prospective observational study aimed at defining the TEG profile in healthy VLBW infants in the first month of life. In this analysis, we included neonates of < 33 weeks' gestational age (GA) with PDA and compared TEG traces based on (1) spontaneous closure versus the need for pharmacological treatment and (2) treatment response. We collected blood samples in the 1st day of life to perform recalcified native-blood TEG (reaction time, maximum amplitude, and lysis at 30 min [Ly30)]), standard coagulation tests, and a full blood count. Results: We enrolled 151 infants with a PDA at the first echocardiogram; 111 experienced spontaneous PDA closure while 40 required treatment. Mean GA was 29.7 ± 1.7 and 27.6 ± 2.1 weeks, and birth weight was 1,158 ± 256 and 933 ± 263 g in the 2 groups, respectively (p < 0.001). The hemostatic profile was similar between groups. Median hematocrit (44.6 and 48.7%; p = 0.01) and platelet count (187 and 216 × 10 3 /μL; p = 0.04) were lower in the treated group, although differences lost significance after controlling for GA and illness severity in the multivariate analysis. Responders to PDA treatment (n = 20) had a significantly lower median Ly30 than nonresponders (0 and 0.7%; p = 0.02). Conclusion: TEG at birth does not predict spontaneous PDA closure in preterm newborns. Fibrinolysis is enhanced in nonresponders to PDA treatment; this observation warrants further investigation.

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Section: Discussionmentioning

confidence: 99%

The Thromboelastographic Profile at Birth in Very Preterm Newborns with Patent Ductus Arteriosus

et al. 2020

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“…Further research on the complex interplay between platelet count and function, other circulating blood cells and the ductal endothelium is warranted in order to understand the developmentally regulated process of ductal closure in preterm infants. 12 , 21 , 26 …”

Section: The Role Of Platelets In Ductus Arteriosus Closurementioning

confidence: 99%

An Update on Patent Ductus Arteriosus and What is Coming Next

Erdeve

Okulu

Singh

et al. 2022

Turk Arch Pediatrics

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Patent ductus arteriosus is the most common cardiovascular condition in preterm infants. There is a significant uncertainty about when and how to close ductus arteriosus in preterm infants due to a high spontaneous closure rate even in very immature preterm infants. Diagnosis and management of patent ductus arteriosus remain a challenge for both neonatologists and pediatric cardiologists. Researchers have tried to define a balance between an expectant approach and active treatment in selected infants. This review aimed to focus on the pathophysiology and management of patent ductus arteriosus and to make suggestions about approaches that might eliminate the association of morbidities with patent ductus arteriosus.

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“…A proteomics-based study on human neonatal plasma identified six differentially expressed proteins (platelet factor 4, fibrinogen, von Willebrand factor, collagen, mannose binding lectin-associated serine protease-2, fibronectin), which were associated with PDA. Interestingly, those proteins are closely related to platelet activation and plasmatic coagulation cascades (39).…”

Section: Platelet Function and Pda Closure In Preterm Infantsmentioning

confidence: 99%

Current Controversy on Platelets and Patent Ductus Arteriosus Closure in Preterm Infants

et al. 2021

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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.

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Altered plasma proteins released from platelets and endothelial cells are associated with human patent ductus arteriosus

Cited by 10 publications

References 66 publications

The Thromboelastographic Profile at Birth in Very Preterm Newborns with Patent Ductus Arteriosus

The Thromboelastographic Profile at Birth in Very Preterm Newborns with Patent Ductus Arteriosus

An Update on Patent Ductus Arteriosus and What is Coming Next

Current Controversy on Platelets and Patent Ductus Arteriosus Closure in Preterm Infants

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