Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by a low platelet count due to immune-mediated platelet destruction and impaired thrombopoiesis. It affects both adults and children, with varying incidence and prevalence rates. ITP can be classified as primary or secondary, with primary ITP being more common in adults and often progressing to chronicity. Secondary ITP is associated with other diseases or conditions. The management of ITP involves addressing the underlying immune dysregulation, with treatment options including corticosteroids, intravenous immunoglobulins, thrombopoietin receptor agonists (TPO-RAs), rituximab, and splenectomy. Newer targeted therapies, such as Syk inhibitors, Bruton's tyrosine kinase (BTK) inhibitors, and complement inhibitors, have shown promise in improving platelet counts and quality of life. The pathogenesis of ITP involves multiple mechanisms, including antibody-mediated platelet destruction, T-cell activation, and complement activation. Understanding these mechanisms has led to the development of novel therapies targeting various pathways. Current treatment decisions consider factors such as bleeding risk, platelet count, and patient-specific factors. Despite advances, challenges remain in predicting treatment responses and optimizing individualized care. Ongoing research aims to identify biomarkers and improve therapeutic strategies for ITP.Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by a low platelet count due to immune-mediated platelet destruction and impaired thrombopoiesis. It affects both adults and children, with varying incidence and prevalence rates. ITP can be classified as primary or secondary, with primary ITP being more common in adults and often progressing to chronicity. Secondary ITP is associated with other diseases or conditions. The management of ITP involves addressing the underlying immune dysregulation, with treatment options including corticosteroids, intravenous immunoglobulins, thrombopoietin receptor agonists (TPO-RAs), rituximab, and splenectomy. Newer targeted therapies, such as Syk inhibitors, Bruton's tyrosine kinase (BTK) inhibitors, and complement inhibitors, have shown promise in improving platelet counts and quality of life. The pathogenesis of ITP involves multiple mechanisms, including antibody-mediated platelet destruction, T-cell activation, and complement activation. Understanding these mechanisms has led to the development of novel therapies targeting various pathways. Current treatment decisions consider factors such as bleeding risk, platelet count, and patient-specific factors. Despite advances, challenges remain in predicting treatment responses and optimizing individualized care. Ongoing research aims to identify biomarkers and improve therapeutic strategies for ITP.