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Immune thrombocytopenia : Pathophysiology and impacts of Romiplostim treatment

Semple, John W. LU ; Schifferli, Alexandra ; Cooper, Nichola ; Saad, Hossam ; Mytych, Daniel T. ; Chea, Lynette S. and Newland, Adrian (2024) In Blood Reviews 67.
Abstract

Immune thrombocytopenia (ITP) is an autoimmune bleeding disease caused by immune-mediated platelet destruction and decreased platelet production. ITP is characterized by an isolated thrombocytopenia (<100 × 109/L) and increased risk of bleeding. The disease has a complex pathophysiology wherein immune tolerance breakdown leads to platelet and megakaryocyte destruction. Therapeutics such as corticosteroids, intravenous immunoglobulins (IVIg), rituximab, and thrombopoietin receptor agonists (TPO-RAs) aim to increase platelet counts to prevent hemorrhage and increase quality of life. TPO-RAs act via stimulation of TPO receptors on megakaryocytes to directly stimulate platelet production. Romiplostim is a TPO-RA that has... (More)

Immune thrombocytopenia (ITP) is an autoimmune bleeding disease caused by immune-mediated platelet destruction and decreased platelet production. ITP is characterized by an isolated thrombocytopenia (<100 × 109/L) and increased risk of bleeding. The disease has a complex pathophysiology wherein immune tolerance breakdown leads to platelet and megakaryocyte destruction. Therapeutics such as corticosteroids, intravenous immunoglobulins (IVIg), rituximab, and thrombopoietin receptor agonists (TPO-RAs) aim to increase platelet counts to prevent hemorrhage and increase quality of life. TPO-RAs act via stimulation of TPO receptors on megakaryocytes to directly stimulate platelet production. Romiplostim is a TPO-RA that has become a mainstay in the treatment of ITP. Treatment significantly increases megakaryocyte maturation and growth leading to improved platelet production and it has recently been shown to have additional immunomodulatory effects in treated patients. This review will highlight the complex pathophysiology of ITP and discuss the usage of Romiplostim in ITP and its ability to potentially immunomodulate autoimmunity.

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author
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organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Immune thrombocytopenia (ITP), Immunomodulation, Pathophysiology, Remission, Romiplostim, Therapy free remission
in
Blood Reviews
volume
67
article number
101222
publisher
Churchill Livingstone
external identifiers
  • scopus:85197476231
  • pmid:38942688
ISSN
0268-960X
DOI
10.1016/j.blre.2024.101222
language
English
LU publication?
yes
id
3e13647b-81cd-452f-a11b-3e24b313fc29
date added to LUP
2024-11-28 15:00:18
date last changed
2025-07-11 09:48:49
@article{3e13647b-81cd-452f-a11b-3e24b313fc29,
  abstract     = {{<p>Immune thrombocytopenia (ITP) is an autoimmune bleeding disease caused by immune-mediated platelet destruction and decreased platelet production. ITP is characterized by an isolated thrombocytopenia (&lt;100 × 10<sup>9</sup>/L) and increased risk of bleeding. The disease has a complex pathophysiology wherein immune tolerance breakdown leads to platelet and megakaryocyte destruction. Therapeutics such as corticosteroids, intravenous immunoglobulins (IVIg), rituximab, and thrombopoietin receptor agonists (TPO-RAs) aim to increase platelet counts to prevent hemorrhage and increase quality of life. TPO-RAs act via stimulation of TPO receptors on megakaryocytes to directly stimulate platelet production. Romiplostim is a TPO-RA that has become a mainstay in the treatment of ITP. Treatment significantly increases megakaryocyte maturation and growth leading to improved platelet production and it has recently been shown to have additional immunomodulatory effects in treated patients. This review will highlight the complex pathophysiology of ITP and discuss the usage of Romiplostim in ITP and its ability to potentially immunomodulate autoimmunity.</p>}},
  author       = {{Semple, John W. and Schifferli, Alexandra and Cooper, Nichola and Saad, Hossam and Mytych, Daniel T. and Chea, Lynette S. and Newland, Adrian}},
  issn         = {{0268-960X}},
  keywords     = {{Immune thrombocytopenia (ITP); Immunomodulation; Pathophysiology; Remission; Romiplostim; Therapy free remission}},
  language     = {{eng}},
  publisher    = {{Churchill Livingstone}},
  series       = {{Blood Reviews}},
  title        = {{Immune thrombocytopenia : Pathophysiology and impacts of Romiplostim treatment}},
  url          = {{http://dx.doi.org/10.1016/j.blre.2024.101222}},
  doi          = {{10.1016/j.blre.2024.101222}},
  volume       = {{67}},
  year         = {{2024}},
}