Improvement of Bone Marrow Necrosis by Tyrosine Kinase Inhibitor Substitution in a Pediatric Patient With Philadelphia Chromosome-positive Acute Lymphoblastic Leukemia

Abstract

Bone marrow necrosis (BMN) describes necrosis of the myeloid tissues without cortical bone involvement. Imatinib, a tyrosine kinase inhibitor, can trigger BMN during the treatment of malignant disease. In such cases, it is necessary to reduce imatinib dose or discontinue its administration, which could influence treatment outcomes. Here, we report a 6-year-old boy with Philadelphia chromosome-positive acute lymphoblastic leukemia, who developed BMN in response to imatinib. We replaced imatinib with dasatinib, and necrotic lesions gradually disappeared and were never exacerbated. In Philadelphia chromosome-positive acute lymphoblastic leukemia with BMN, tyrosine kinase inhibitor replacement may allow continued chemotherapy without intensity reduction.

Atypical BCR‐ABL1 transcript in mixed phenotype acute leukemia with bone marrow necrosis

“…The pathophysiology of BMN can be due to several processes, for example, fibrin thrombi formation, cytotoxic injury to vessels, tumor embolization, and tumor compression. Ultimately, these factors result in microcirculatory occlusion may be the potential causal mechanisms underlying BMN 9,10 . Patients with BMN usually present with pancytopenia, ostealgia, embolization low immunity, extremely high probability of pulmonary infection 11 .…”

“…Ultimately, these factors result in microcirculatory occlusion may be the potential causal mechanisms underlying BMN. 9,10 Patients with BMN usually present with pancytopenia, ostealgia, embolization low immunity, extremely high probability of pulmonary infection. 11 However, leucoerythroblastic blood picture, high lactate dehydrogenase, and uric acid levels also can be detected.…”