An 87-year-old man presented with a 3-month history of weight loss, fatigue, and weakness. A complete blood count showed leukocytosis (14.6 × 109/L) and anemia (9.1 g/dL). The manual differential count revealed 24% segmented neutrophils, 6% band neutrophils, 3% metamyelocytes, 10% myelocytes, 20% promyelocytes, 1% myeloblasts, 21% eosinophils, 13% lymphocytes, 2% monocytes, and 0% basophils. The eosinophil count was elevated to 3.0 × 109/L. A trephine core bone marrow biopsy (panel A; hematoxylin-and-eosin stain, original magnification ×630) and bone marrow aspirate smear demonstrated marked hypercellularity, with 60% mature, sometimes aberrant, eosinophils (panel B, black arrows; May-Grünwald-Giemsa [MGG] stain, original magnification ×400). Granulopoiesis showed dysplastic changes (panel C, red arrow; MGG stain, original magnification ×400) and multiple inclusions of long pointed structures, identified as Charcot-Leyden crystals (CLCs) (panels A-C, green arrows; panel C inset: MGG stain, original magnification ×1000). Cytogenetic analysis revealed trisomy 1q in 10% of the cells. A diagnosis of chronic eosinophilic leukemia (CEL) not otherwise specified was established. Unfortunately, the patient died shortly after treatment with imatinib was started.

CLCs are colorless crystals and may be seen in reactive hypereosinophilia as well as in hematologic malignancies with eosinophilia. Eosinophils contain a large amount of CLC protein (galactin-10). Eosinophil cytolysis is the result of eosinophil extracellular trap cell death (EETosis), which mediates CLC formation. Although CLCs were first described in 1853 and are frequently seen in CEL, their role and their diagnostic and prognostic value are still unknown.

An 87-year-old man presented with a 3-month history of weight loss, fatigue, and weakness. A complete blood count showed leukocytosis (14.6 × 109/L) and anemia (9.1 g/dL). The manual differential count revealed 24% segmented neutrophils, 6% band neutrophils, 3% metamyelocytes, 10% myelocytes, 20% promyelocytes, 1% myeloblasts, 21% eosinophils, 13% lymphocytes, 2% monocytes, and 0% basophils. The eosinophil count was elevated to 3.0 × 109/L. A trephine core bone marrow biopsy (panel A; hematoxylin-and-eosin stain, original magnification ×630) and bone marrow aspirate smear demonstrated marked hypercellularity, with 60% mature, sometimes aberrant, eosinophils (panel B, black arrows; May-Grünwald-Giemsa [MGG] stain, original magnification ×400). Granulopoiesis showed dysplastic changes (panel C, red arrow; MGG stain, original magnification ×400) and multiple inclusions of long pointed structures, identified as Charcot-Leyden crystals (CLCs) (panels A-C, green arrows; panel C inset: MGG stain, original magnification ×1000). Cytogenetic analysis revealed trisomy 1q in 10% of the cells. A diagnosis of chronic eosinophilic leukemia (CEL) not otherwise specified was established. Unfortunately, the patient died shortly after treatment with imatinib was started.

CLCs are colorless crystals and may be seen in reactive hypereosinophilia as well as in hematologic malignancies with eosinophilia. Eosinophils contain a large amount of CLC protein (galactin-10). Eosinophil cytolysis is the result of eosinophil extracellular trap cell death (EETosis), which mediates CLC formation. Although CLCs were first described in 1853 and are frequently seen in CEL, their role and their diagnostic and prognostic value are still unknown.

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