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[Sustained hematologic response in chronic eosinophilic leukemia with low dose imatinib. Report of one case]
Insights
A rare myeloproliferative variant of hypereosinophilic syndrome was identified. Imatinib therapy effectively reduced eosinophil counts by targeting the FIP1L1/PDGFRA fusion product.
Area of Science:
- Hematology
- Oncology
Background:
- Hypereosinophilic syndrome (HES) can be associated with myeloproliferative neoplasms.
- Identifying specific genetic drivers is crucial for targeted therapy.
Observation:
- A 58-year-old man presented with weight loss, malaise, and headache.
- Laboratory findings revealed significant leukocytosis with marked eosinophilia (absolute eosinophil count 10,465/mL).
- Bone marrow biopsy confirmed eosinophil infiltration.
Findings:
- Conventional treatment with hydroxyurea and prednisone was ineffective.
- Polymerase chain reaction detected the FIP1L1/PDGFRA gene fusion.
- Imatinib therapy led to rapid normalization of eosinophil counts within two weeks.
Implications:
- The FIP1L1/PDGFRA fusion is a key molecular marker in a subset of HES.
- Targeted therapy with imatinib is highly effective for HES associated with this fusion.
- Testing for FIP1L1/PDGFRA should be considered in patients with unexplained eosinophilia.
Abstract:
We report a 58 year-old-man without comorbid conditions, with a history of two months of weight loss, malaise and headache. His initial laboratory analysis showed leukocytosis of 16,100/mL with 65% eosinophils and an absolute eosinophil count of 10,465/mL. Both bone marrow biopsy and aspirate showed infiltration by mature appearing eosinophils. Treatment was started with hydroxyurea, associated with prednisone without satisfactory decrease in the eosinophil count. Polymerase chain reaction showed the presence of the gene fusion product FIP1L1/PDGFRA. Imatinib therapy was initiated, resulting in a rapid and progressive reduction in the absolute eosinophil count, with normalization at the second week of treatment. The incidence of the myeloproliferative variant causing hypereosinophilic syndrome is rare. However, the dramatic response to imatinib emphasizes the need to study the presence of the fusion product FIP1L1/PDGFRA in all patients with eosinophilia of unknown etiology.
