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Editorials
phoid disease itself and be indicative of worsening bone marrow infiltration by aberrant cells and consequent megakaryocyte hypoplasia and/or dysplasia or be indica- tive of dysregulated immunity leading to ITP, thus not necessarily indicating a worse prognosis, as shown in the study by Jachiet et al.1 Hence, in these circumstances, sep- arating ITP, diagnosed with bona fide criteria, from non- immune thrombocytopenia may be of clinical relevance for both the patient and the treating physician.
In conclusion, the report by Jachiet et al.1 opens new perspectives for a deeper understanding of the pathobio- logical mechanisms linking ITP and some clonal myeloid/lymphoid disorders and of their temporal associ- ation. This will require the collection of large prospective series of patients with either or both disorders and their investigation with extensive next-generation sequencing technology and better immunophenotyping of the cellu- lar components involved. In the meantime, the practicing hematologist should be aware of the difficulties and of the importance of separating ITP from the thrombocy- topenia inherent to the defective megakaryopoiesis of these preleukemic disorders.
Disclosures
No conflicts of interest to disclose
References
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