Editorial: Immune thrombocytopenia (ITP) - diagnosis and treatment, volume II

Immune Thrombocytopenia (ITP) is characterized by an abnormally reduced platelet count in peripheral blood, arising from a dysregulated immune response that compromises both platelet production and survival. Recent evidence indicates that, beyond classical antibody-mediated platelet destruction, this disease encompasses defects in cytotoxic lymphocyte-mediated injury, perturbations in mesenchymal stem-cell immunoregulatory functions, activation of apoptotic pathways in platelets (caspase 3, 8, and 9 activation and phosphatidylserine exposure) and expansion of T follicular helper (Tfh) cells. However, despite numerous diagnostic advances, ITP is principally identified through the systematic exclusion of other potential etiologies.The main goal of ITP treatment is to prevent and control bleeding by maintaining platelet counts within safe hemostatic limits. Advances in the understanding of ITP pathophysiology have facilitated the development of several novel ITP therapies.Nevertheless, considerable obstacles remain in both the accurate diagnosis and effective management of ITP, underscoring the need for a more comprehensive understanding of the disease. This overview highlights key challenges in the diagnosis and management of ITP.Diagnostic considerations include here the emerging links of ITP with gut microbiome alterations, the dynamic relationship between platelet counts and psychological state after COVID-19 infection as well as disease characteristics of ITP in adolescents and young adults. This ITP volume also discusses therapeutic considerations that may affect the outcomes of corticosteroids and thrombopoietin receptor agonists (TPO-RAs), particularly in patients with comorbidities. Khiabani A. et al. (DOI: 10.3389/fmed.2025.1511612) conducted a systematic review to evaluate evidence on gut microbiome alterations in ITP. After screening 480 records, 12 studies comparing ITP patients with controls were included, revealing notable but inconsistent changes across major bacterial phyla. Several taxa and microbial metabolites were linked to immune mechanisms involved in platelet destruction and impaired production. Overall, the review suggests a potential association between gut dysbiosis and ITP, though heterogeneity among studies limits firm conclusions and highlights the need for standardized, well-designed research. The contributions collected in this volume explore multiple, and in many cases insufficiently characterized, dimensions of the disease. Advancing research based on these observations will be essential to deepen diagnostic insight and improve therapeutic strategies in ITP.