What are the latest advances in Idiopathic Thrombocytopenic Purpura?
Here you can see the latest advances and discoveries made regarding Idiopathic Thrombocytopenic Purpura.
Idiopathic Thrombocytopenic Purpura (ITP) is an autoimmune disorder characterized by low platelet count, leading to increased bleeding and bruising. It is considered idiopathic because the exact cause is unknown. However, recent advances in research and treatment have shed light on this condition, providing new insights and therapeutic options for patients.
1. Pathogenesis: Understanding the underlying mechanisms of ITP has been a major focus of recent research. It is now known that ITP is primarily caused by autoantibodies targeting platelet surface antigens, leading to their destruction by the immune system. The role of T cells and their interaction with B cells in the production of these autoantibodies has also been elucidated. These findings have paved the way for targeted therapies aimed at modulating the immune response.
2. Novel Therapies: Traditional treatment options for ITP include corticosteroids, intravenous immunoglobulin (IVIG), and splenectomy. However, these approaches are not always effective or may have significant side effects. Recent advances have introduced several novel therapies that show promise in managing ITP:
- Romiplostim and Eltrombopag: These drugs belong to a class known as thrombopoietin receptor agonists. They stimulate platelet production by binding to and activating the thrombopoietin receptor on megakaryocytes, the cells responsible for platelet production. Romiplostim and Eltrombopag have demonstrated efficacy in increasing platelet counts and reducing bleeding episodes in patients with chronic ITP.
- Rituximab: This monoclonal antibody targets CD20, a protein found on the surface of B cells. By depleting B cells, Rituximab disrupts the production of autoantibodies, thereby reducing platelet destruction. It has shown promising results in refractory cases of ITP.
- TPO-RAs: Thrombopoietin receptor agonists (TPO-RAs) are a newer class of drugs that directly stimulate platelet production. They work by mimicking the action of thrombopoietin, the hormone responsible for regulating platelet production. TPO-RAs, such as Avatrombopag and Fostamatinib, have shown efficacy in increasing platelet counts and reducing bleeding in patients with chronic ITP.
3. Immune Modulation: Given the autoimmune nature of ITP, therapies aimed at modulating the immune system have gained attention. These approaches focus on restoring immune tolerance and preventing the destruction of platelets:
- Tolerogenic Vaccines: Vaccines designed to induce immune tolerance by targeting specific antigens involved in platelet destruction are being investigated. These vaccines aim to re-educate the immune system and reduce autoantibody production.
- Immune Checkpoint Inhibitors: Immune checkpoint inhibitors, such as anti-PD-1 antibodies, have shown promise in restoring immune tolerance and improving platelet counts in refractory cases of ITP. These inhibitors block the inhibitory signals that prevent immune cells from attacking platelets.
4. Personalized Medicine: Advances in genetic and molecular profiling have opened up possibilities for personalized medicine in ITP. Identifying specific genetic markers or immune profiles associated with treatment response or disease progression can help tailor therapies to individual patients. This approach holds great potential for optimizing treatment outcomes and minimizing side effects.
5. Supportive Care: In addition to novel therapies, advancements in supportive care have improved the management of ITP. This includes the development of guidelines for platelet transfusions, management of bleeding episodes, and psychological support for patients dealing with the chronic nature of the disease.
In conclusion, recent advances in the understanding and treatment of ITP have provided new hope for patients. The identification of key pathogenic mechanisms, development of novel therapies, immune modulation strategies, personalized medicine approaches, and improved supportive care have collectively contributed to better outcomes and quality of life for individuals living with ITP.
Posted Jul 7, 2017 by Theresa 4010
platelet producing drugs
Posted Sep 27, 2017 by jillenid 2570
of patients respond to corticosteroids, and 10%–30% attain durable remission. Splenectomy is avoided in young children because of infection risk and the high prevalence of spontaneous resolution of ITP. Second-line treatments for ITP include immunosuppressive therapy (eg, rituximab). Third-line therapies include TRAs, such as romiplostim and eltrombopag. TRAs are associated with increased platelet counts and reductions in the number of bleeding events. TRAs are considered as a safe and an effective treatment for patients with chronic ITP at risk of bleeding after failure of first- or second-line therapies. Determination of a threshold minimum platelet count or specific age at which a typical patient with ITP should be treated is difficult. The goal of all treatment strategies for ITP is to achieve a platelet count that is associated with adequate hemostasis, rather than a normal platelet count. Therefore, if bleeding symptoms are not found, treatment may not be needed. Patients should be treated with platelet-enhancing agents if the platelet count is ,30 × 109/L and mucosal bleeding has started, although a threshold of 30 × 109/L may not be suitable for children. Treatment may also be appropriate if follow-up cannot be assured, if there are concerns for bleeding due to high levels of activity, or if there is a need for procedures associated with bleeding risk. New therapies and recommendations have emerged in the last decade. However, deciding who should be treated with which treatment option and for how long is not known. The decision to treat should be based on bleeding severity, bleeding risk, activity level, likely side effects of treatment, and patient preference.
Posted Sep 29, 2017 by Marília 3570
