Addressing thrombosis concerns in immune thrombocytopenia: the role of fostamatinib in immune thrombocytopenia management

ABSTRACT

Introduction

Immune thrombocytopenia (ITP), a disease that commonly presents with an increased risk of bleeding, can also paradoxically produce an increased risk of thromboembolic events. The risk of thromboembolism can be associated with patient-related factors (e.g. co-morbidities, age and history of thrombosis), disease-related factors (e.g. a greater proportion of younger, more reactive platelets, and the presence of microparticles and pro-inflammatory cytokines) and treatment-related factors (e.g. splenectomy, thrombopoietin receptor agonists, and IVIg).

Areas covered

Aspects of the pathophysiology of ITP and the effects of treatment are discussed with emphasis on individualizing treatment based on the patient’s thromboembolic risk, treatment options and preferences.

Expert opinion

An increased understanding of the pathophysiology of ITP has led to the development of new agents such as fostamatinib, a spleen tyrosine kinase inhibitor. Further research into the factors contributing to the risks for bleeding and thromboembolic events can contribute to the development of more specific therapies for ITP and allow greater individualization of therapy based on each patient’s medical history and clinical status.

KEYWORDS:

• Bleeding
• fostamatinib
• immune thrombocytopenia
• platelets
• thromboembolism

Article highlights

• Immune thrombocytopenia (ITP), usually considered a bleeding disorder can also carry increased risk of thromboembolism

• The relative risk of thromboembolism in ITP depends on patient-related and disease-related factors and can be influenced by the choice of ITP treatment.

• Greater understanding of the pathophysiology of ITP has led to the development of new agents, e.g. fostamatinib and can lead to greater personalization of treatment for each patient.

• Agents such as fostamatinib can be a therapeutic alternative for patients in which thromboembolic risk must be minimized.

Declaration of interest

D Provan acknowledges the following competing interests: research support from Amgen, and Novartis; honoraria from Amgen, Novartis, SOBI, UCB, and argenx; consultancies with UCB, MedImmune, Ono, SOBI, argenx, and Takeda. J Thachil has received honoraria from Amgen, Grifols and Novartis. MT Alvarez-Roma has served as a speaker or an advisory board member with Novartis, Bayer, Takeda, Roche, Pfizer, Octapharma, Amgen, Novartis, CSL Behring and Sobi. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or material discussed in the manuscript apart from those disclosed.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Previous presentations

This material was previously presented in a symposium at The International Society on Thrombosis and Haemostasis 2022 Congress, London, 9 July 2022 (Sponsored by Grifols).

Acknowledgments

Michael K. James, PhD, CMPP (Grifols) is acknowledged for medical writing assistance and Roser Mir, PhD and Jordi Bozzo, PhD, CMPP for editorial assistance.

Additional information

Funding

The preparation and submission of this manuscript were funded by Grifols.