Case Report Fatal Outcome of Imatinib in a Patient with Idiopathic Hypereosinophilic Syndrome Ashraf Abugroun , Ahmed Chaudhary , and Gabriel Rodriguez Advocate Illinois Masonic Medical Center, Chicago, IL, USA Correspondence should be addressed to Ashraf Abugroun; ashraf.abugroun@advocatehealth.com Received 25 October 2017; Revised 5 February 2018; Accepted 25 February 2018; Published 26 March 2018 Academic Editor: Peter F. Lenehan Copyright © 2018 Ashraf Abugroun et al. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Cytokine storm is a poorly explained clinical entity caused by an undesired and aggrandized immune system response leading to unregulated activation of the proinflammatory cascade, often contributing to multisystem organ failure and even death. Its potentially diverse etiologies and sepsis-like presentation have made it even more challenging to diagnose, and so far, no well- establishedtreatmentprotocolhasbeenproposed.Itsassociationwithcertainmedications,especiallywithmonoclonalantibodies, has well been reported in literature. To the best of our knowledge, so far, no previous case of cytokine storm associated with imatinibhasbeenreported.Wehereinpresentacasereportofa77-year-oldmalewithapastmedicalhistoryofhypereosinophilic syndrome who developed acute fatal cytokine storm following treatment with imatinib. is study highlights a life-threatening complication of the medication that may be underrecognized. 1. Introduction Imatinib is a tyrosine kinase inhibitor that is used in various hematologic malignancies, including idiopathic hyper- eosinophilic syndrome (IHES) which is a myeloproliferative disorder characterized by sustained, nonreactive, un- explained persistent hypereosinophilia that commonly re- sults in multiorgan dysfunction. is case highlights the development of a cytokine storm with severe uncontrolled systemic inflammatory response with a fatal outcome fol- lowing the initiation of imatinib in a patient with IHES. 2. Case Presentation A 77-year-old male with a history of IHES, COPD, CKD stage III, and active Mycobacterium avium complex (MAC) infection on treatment with rifampin, azithromycin, and levofloxacin was sent to the ER from oncology clinic for evaluation of progressive weakness, lethargy, and hyperkalemia. e patient had outpatient workup for unexplained hypereosinophilia. He underwent lymph node biopsy which showed no evidence of lymphoma (Figure 1). Peripheral blood flow cytometry showed myeloid and lymphoid cells with unremarkable immunophenotypic expression. Bone marrow biopsy showed eosinophilia that varied from ap- proximately 25% in the aspirate smears to 60% in the core biopsy (Figure 2). e infiltrate of eosinophils consisted of eosinophilic myelocytes and mature eosinophils. ere were no increase in blasts and no morphologic evidence of lymphoma. e patient had negative fluorescence in situ hybridization (FISH) results using a panel for hyper- eosinophilia containing probes for 4q12 (SCFD2, LNX, and PDGFRA) rearrangement, 5q32 (PDGFRB) rearrangement, 8p11.2 (FGFR1) rearrangement, and 9q34 and 22q11.2 (BCR/ABL1) rearrangement on a bone marrow specimen. He had normal cytogenetic studies and male-type karyotype. A final diagnosis of idiopathic hypereosinophilic syndrome was made. His disease was resistant to steroids and brief course of chemotherapy with methotrexate. Onhiscurrentadmission,hewaslethargicandcachectic. Vital signs were normal. Skin examination showed wide- spread erythroderma, scaling, and excoriations. Initial lab- oratory workup revealed potassium 6.9 mmol/L, creatinine Hindawi Case Reports in Oncological Medicine Volume 2018, Article ID 6291614, 5 pages https://doi.org/10.1155/2018/6291614