Gynecomastia in a Boy with Chronic Myeloid Leukemia during Imatinib Therapy

Chronic myeloid leukemia (CML) is a rare disease in children, accounting for 2%-3% of leukemias in this age group. Current treatment options of CML include tyrosine kinase inhibitors (TKIs) and allogeneic hematopoietic stem cell transplantation (HSCT) for children. Allogeneic HSCT has been recommended following attainment of remission with TKIs. Since long-term outcome and adverse effects of TKIs are uncertain in children, some authors have recommended HSCT within 2 years of treatment with TKIs [1,2,3]. Imatinib mesylate is one of the TKIs; it inhibits all ABL tyrosine kinases and selectively suppresses the ATP-binding site of platelet-derived growth factor receptor (PDGF-R) and c-KIT, which are expressed in various types of neoplasms and also in normal cells. It is well tolerated with mild adverse effects. Common and usually mild side effects of imatinib mesylate include edema, muscle cramps, skin rash, and conjunctival inflammation. An altered bone and mineral metabolism, a reduction of testosterone, and gynecomastia are the other defined side effects of imatinib mesylate, which were attributed to the PDGF-R and c-KIT inhibition in normal cells by imatinib mesylate. Gynecomastia development during the course of imatinib mesylate treatment has rarely been reported in the English literature [4,5,6,7]. Herein, we have described a 14-year-old boy with CML who developed gynecomastia while receiving imatinib mesylate for nearly 1.5 years. A 14-year-old boy was admitted to hospital with complaints of malaise, cough, and pain in the lower extremities. His previous medical history was unremarkable. There was no consanguinity between parents and he had 2 healthy siblings. On his physical examination, he had mild hepatomegaly (2 cm below the costal margin) and massive splenomegaly (18 cm below the costal margin). His laboratory studies revealed that did not show any ongoing infection with these agents. His abdominal ultrasonography revealed hepatosplenomegaly. His echocardiography was normal. Bone marrow aspiration smears revealed hypercellularity and hyperactivity in the myeloid lineage with less than 5% blasts. Cytogenetic study of his bone marrow showed clonal positivity for t(9;22). Thus, the patient was diagnosed with CML in the accelerated phase. After the diagnosis of CML, he received cytosine arabinoside (150 mg/m 2 /day) and mitoxantrone (10 mg/m 2 /day) 2 times at a 1-week interval. Hydration (3000 mL/m 2 /day and 20 mEq/L, NaHCO 3) and allopurinol treatment were continued until his leukocyte count decreased to normal levels. After learning that t(9;22) was positive, imatinib mesylate treatment (260 mg/m 2) was started. Complete hematological response …