Imatinib-Induced Hypogammaglobulinemia in Children and Adolescents with Chronic Myeloid Leukemia.
Sidharth TotadriShankar ThipparapuRitu AggarwalMadhulika SharmaShano NaseemRicha JainAmita TrehanPankaj MalhotraNeelam VarmaDeepak BansalPublished in: Pediatric hematology and oncology (2020)
Imatinib-induced tyrosine kinase inhibition extends beyond the BCR-ABL mutation, resulting in adverse effects. We evaluated hypogammaglobulinemia as a potential 'off-target' action of imatinib in children with CML. A cross-sectional, observational study was performed. Patients with CML in chronic phase, age <18-years at diagnosis, receiving imatinib for a duration exceeding 6-months were enrolled. Serum immunoglobulin G, A, and M were measured by end-point nephelometry. Thirty patients were enrolled. The mean age at diagnosis was 10.4 ± 3.1 years (range: 5-18). The mean age at enrollment was 16.4 ± 4.1 years (range: 9-23). The median dose of imatinib was 287.5 mg/m2 (IQR: 267.3, 345.0). The median duration of imatinib-therapy was 6-years (IQR: 3.0, 10.3). The median (IQR) normalized levels of IgG, IgA, and IgM were 33.0% (IQR: -12.8, 58.7), 28.1% (IQR: -17.0, 90.1) and 15.9% (IQR: -9.3, 40.5), respectively. The IgG, IgA, and IgM levels were reduced in 9 (30%), 8 (27%), and 10 (33%) patients, respectively. Five (17%) patients had pan-hypogammaglobulinemia. We suggest checking immunoglobulin levels in patients with CML receiving imatinib with recurrent/unusual infections.
Keyphrases
- chronic myeloid leukemia
- end stage renal disease
- tyrosine kinase
- chronic kidney disease
- ejection fraction
- healthcare
- young adults
- stem cells
- peritoneal dialysis
- patient reported outcomes
- mesenchymal stem cells
- epidermal growth factor receptor
- risk assessment
- endothelial cells
- health insurance
- drug induced
- patient reported