Platelet function and soluble P-selectin in patients with primary immune thrombocytopenia.


Journal

Thrombosis research
ISSN: 1879-2472
Titre abrégé: Thromb Res
Pays: United States
ID NLM: 0326377

Informations de publication

Date de publication:
03 2023
Historique:
received: 10 11 2022
revised: 22 12 2022
accepted: 12 01 2023
pubmed: 5 2 2023
medline: 4 3 2023
entrez: 4 2 2023
Statut: ppublish

Résumé

The bleeding phenotype in immune thrombocytopenia (ITP) is heterogeneous, but usually mild and only partly dependent on the severity of thrombocytopenia. Platelet reactivity has previously been suggested to underly the mild phenotype. Platelet function was assessed as basal and agonist-induced surface expression of P-selectin and activation of GPIIb/IIIa via flow cytometry, and soluble (s)P-selectin levels were assessed in plasma of 77 patients with primary ITP, 19 hemato-oncologic thrombocytopenic controls (TC) and 20 healthy controls (HC). The association of platelet function with laboratory and clinical parameters such as bleeding manifestations at inclusion and previous thrombosis was analyzed. ITP patients showed tendency towards increased surface P-selectin and elevated levels of activated GPIIb/IIIa. Platelet activation after stimulation with all agonists including TRAP-6, ADP, arachidonic acid and CRP was decreased compared to HC. Compared to TC, only GPIIb/IIIa activation but not surface P-selectin was higher in ITP. Levels of soluble (s)P-selectin were significantly higher in ITP patients compared to TC, but similar to HC. Higher sP-selectin levels were associated with blood group O and current therapy, with highest levels in TPO-RA treated patients. Platelet reactivity was not associated with platelet count or size, platelet antibodies, treatment regime, or blood group. No correlation between platelet activation with the bleeding phenotype or previous thrombotic events could be observed. ITP patients did not have hyper-reactive platelets compared to HC, but partly higher reactivity compared to TC. Further studies are needed to understand the underlying mechanism behind the bleeding and pro-thrombotic phenotype in ITP. 250/250.

Sections du résumé

BACKGROUND
The bleeding phenotype in immune thrombocytopenia (ITP) is heterogeneous, but usually mild and only partly dependent on the severity of thrombocytopenia. Platelet reactivity has previously been suggested to underly the mild phenotype.
METHODS
Platelet function was assessed as basal and agonist-induced surface expression of P-selectin and activation of GPIIb/IIIa via flow cytometry, and soluble (s)P-selectin levels were assessed in plasma of 77 patients with primary ITP, 19 hemato-oncologic thrombocytopenic controls (TC) and 20 healthy controls (HC). The association of platelet function with laboratory and clinical parameters such as bleeding manifestations at inclusion and previous thrombosis was analyzed.
RESULTS
ITP patients showed tendency towards increased surface P-selectin and elevated levels of activated GPIIb/IIIa. Platelet activation after stimulation with all agonists including TRAP-6, ADP, arachidonic acid and CRP was decreased compared to HC. Compared to TC, only GPIIb/IIIa activation but not surface P-selectin was higher in ITP. Levels of soluble (s)P-selectin were significantly higher in ITP patients compared to TC, but similar to HC. Higher sP-selectin levels were associated with blood group O and current therapy, with highest levels in TPO-RA treated patients. Platelet reactivity was not associated with platelet count or size, platelet antibodies, treatment regime, or blood group. No correlation between platelet activation with the bleeding phenotype or previous thrombotic events could be observed.
CONCLUSION
ITP patients did not have hyper-reactive platelets compared to HC, but partly higher reactivity compared to TC. Further studies are needed to understand the underlying mechanism behind the bleeding and pro-thrombotic phenotype in ITP. 250/250.

Identifiants

pubmed: 36738663
pii: S0049-3848(23)00012-9
doi: 10.1016/j.thromres.2023.01.012
pii:
doi:

Substances chimiques

P-Selectin 0
Platelet Glycoprotein GPIIb-IIIa Complex 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

102-110

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest IP has occasionally received honoraria from CSL Behring, Novartis, Amgen and Sobi for lectures and advisory board meetings. JG received honoraria for lectures and advisory board meetings and research funding for the Medical University of Vienna from CSL Behring, Novartis, Amgen and Sobi. CA received honoraria from Bayer, CSL Behring, NovoNordisk, Pfizer, Roche, Sobi and Takeda for lectures and participation in advisory board meetings. DM received honoraria from CSL Behring. The ITP biobank was sponsored by a research collaboration with Novartis, and research grants of Amgen and Sobi.

Auteurs

Dino Mehic (D)

Clinical Division of Hematology and Hemostaseology, Department of Medicine I, Medical University of Vienna, Vienna, Austria; Institute of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.

Jennifer Machacek (J)

Clinical Division of Hematology and Hemostaseology, Department of Medicine I, Medical University of Vienna, Vienna, Austria.

Theresa Schramm (T)

Clinical Division of Hematology and Hemostaseology, Department of Medicine I, Medical University of Vienna, Vienna, Austria.

Lisbeth Buresch (L)

Clinical Division of Hematology and Hemostaseology, Department of Medicine I, Medical University of Vienna, Vienna, Austria.

Alexandra Kaider (A)

Center for Medical Statistics, Informatics and Intelligent Systems, Medical University of Vienna, Vienna, Austria.

Beate Eichelberger (B)

Department of Blood Group Serology and Transfusion Medicine, Austria.

Helmuth Haslacher (H)

Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.

Michael Fillitz (M)

Department of Internal Medicine, Hanusch Hospital, Vienna, Austria.

Barbara Dixer (B)

Department of Internal Medicine, Hanusch Hospital, Vienna, Austria.

Tanja Flasch (T)

Clinical Division of Hematology and Hemostaseology, Department of Medicine I, Medical University of Vienna, Vienna, Austria.

Theresa Anderle (T)

Clinical Division of Hematology and Hemostaseology, Department of Medicine I, Medical University of Vienna, Vienna, Austria.

Anja Rath (A)

Clinical Division of Hematology and Hemostaseology, Department of Medicine I, Medical University of Vienna, Vienna, Austria.

Alice Assinger (A)

Institute of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.

Cihan Ay (C)

Clinical Division of Hematology and Hemostaseology, Department of Medicine I, Medical University of Vienna, Vienna, Austria.

Ingrid Pabinger (I)

Clinical Division of Hematology and Hemostaseology, Department of Medicine I, Medical University of Vienna, Vienna, Austria.

Johanna Gebhart (J)

Clinical Division of Hematology and Hemostaseology, Department of Medicine I, Medical University of Vienna, Vienna, Austria. Electronic address: johanna.gebhart@meduniwien.ac.at.

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Classifications MeSH