MYELODYPLASIA OR DYSPOIESIS THE MORPHOLOGICAL DIAGNOSIS IN THE CLONAL FORMS TOWARDS THE DYSREACTIVE FORMS: A DIAGNOSTIC TRAP

Just as not all that glitters is gold, not all that is dysplastic is myelodysplastic syndrome (MDS). Hematologists are often called upon to evaluate patients with cytopenias or dysplastic morphology in whom MDS is a possible diagnosis, but many other diagnoses are commonly encountered in routine clinical practice. Dysplasia – referred to as “myelodysplasia” or “dysmyelopoiesis” consists of some combination of peripheral blood (BP) and bone marrow (BM) morphological alterations in the three major myeloid cell series: erythroid lineage dysplasia (dyserythropoiesis), granulocytic lineage dysplasia (dysgranulopoiesis), and megakaryocytic/platelet lineage dysplasia (dysmegakaryopoiesis) (Table 1). These dysplastic changes can be seen in several clinical settings: reactive conditions, due to infections (i.e. Parvovirus B19), injurious effects of a drug or other toxin (smoker); nutritional deficiencies, (B12 or folate); or the clonal, neoplastic disorders that are collectively termed the myelodysplastic syndromes/neoplasms. The diagnostician must be aware that non-MDS disorders can closely mimic MDS in blood and BM, especially megaloblastic anemia but also medication effects, germline disorders, and VEXAS syndrome. In contrast, reactive dysplasia reversible once the inciting factor is corrected. Such reactive abnormalities tend to improve quickly with appropriate therapy.MDS and its mimics show an increased incidence with age, often making it challenging to arrive at the appropriate diagnosis. The assessment of dysplasia on PB and BM smears is the mainstay for the diagnosis of MDS. Counting at least 200 cells in blood smears and 500 cells in bone marrow smears stained on May-Grünwald-Giemsa, including at least 100 erythroblasts and 30 megakaryocytes, is recommended. The recommended requisite percentage of BM dysplastic cells is ≥10% of the nucleated cells in the lineage under consideration. The two most robust types of dysplasia with the highest specificity for MDS are neutrophils that are both hypogranular and hyposegmented, as well as micromegakaryocytes. A comprehensive workup including detailed clinical history, laboratory evaluations, and ancillary molecular and cytogenetic studies is essential to distinguish true clonal MDS from reversible reactive dysplasia.This integrated approach minimizes misdiagnosis and avoids unnecessary interventions, thereby ensuring that patients receive appropriate, targeted management. Table 1. Criteria of myelodysplastic features.