Merit Research Journal of Medicine and Medical Sciences (ISSN: 2354-323X) Vol. 8(10) pp. 600-604, October, 2020 Available online http://www.meritresearchjournals.org/mms/index.htm Copyright © 2020 Author(s) retain the copyright of this article Case Report Imatinib Induced Bullous Pemphigoid as a Late Toxicity: A possible Need for Post Treatment Follow-Up? Walid Shalata 1* , Ala Eddin Neime 2 , Raul Bitran 1 , Abu Saleh Omar 3 , Roxana D. Grinberg 1 , Ismaell Massalha 1 , Alexander Yakobson 1 , Kayed Al-Athamen 4 , Itai Levy 4 Abstract 1 The Legacy Heritage Oncology Center and Dr. Larry Norton Institute, Soroka Medical Center & Ben-Gurion University, Beer-Sheva, Israel 2 Department of Internal Medicine, Soroka University Medical Center, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer Sheva, Israel. 3 Department of Dermatology and Venereology, The Emek Medical Centre, Afula, Israel. 4 Department of Hematology, Soroka University Medical Center, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer Sheva, Israel. *Corresponding Author's Email: walid.shalata@gmail.com Cell: +972 (0)54 2967100. The novel use of Tyrosine Kinase Inhibitors (TKI´s) has shown to be a major breakthrough in the treatment of Chronic Myeloid Leukemia (CML). It has opened the doors for TKIs use in a series of neoplasms with success rates previously unheard of. Nevertheless, its use is not free of adverse effects. Skin, gastro-intestinal and central nervous systems arethe most affected, among which autoimmune response can be observed with a higher incidenceintreated populations. Here we report the case of a patient who presented a rare autoimmune disease, bullous pemphigoid, which wasn’t described before as one of the adverse effects (early or late), most probably as a therapy-related adverse effect two years after stopping Imatinib® treatment. Keywords: Chronic Myeloid Leukemia (CML), Tyrosine Kinase Inhibitors (TKI's), Bullous Pemphigoid (BP), Imatinib INTRODUCTION Chronic Myeloid Leukemia (CML) is a disease that accounts for approximately 15% of the adult leukemias and is characterized by genetic translocation of chromosomes 9 and 22 (derivative (q34; q11) (Philadelphia chromosome; Ph1). The most frequent symptoms and signs include night sweats, anemia and fatigue.As for laboratory parameters, absolute leukocytosis with a left shift and absolute basophilia and eosinophilia (90% of cases) are among the hematological characteristics of this disease. CML patients can be found in one of three phases of disease: chronic phase, accelerated phase and blastic phase. Most patients (85%) will be diagnosed in the chronic phase (Quintás- Cardama and Cortes, 2006; Thompson et al., 2015). The tyrosine kinase inhibitors (TKI's) were first approved by the Food and Drug Administration (FDA) in 2001 when Imatinib® entered the market for CML treatment. Their mechanism of action isbased mainly in the inhibition of specific trans-membrane tyrosine kinase peptide receptors (blockage of domain trans-activation and subsequent target protein phosphorylation).This blockage results in the inhibition of the activity of CML´s fusion product (BCR/ABL), better known as the Philadelphia chromosome. Several studies have shown improvement in results while treating with a TKI, with reported long-term progression of both free disease progrssion and overall survival (Thompson et al., 2015; Chrobák and Voglová, 2019).