Reproductive Hormone Profiles during Imatinib Therapy in Men with Chronic Myeloid Leukemia

Imatinib mesylate is a potent inhibitor of the oncogenic tyrosine kinase BCR-ABL1, and a targeted therapeutic agent in the treatment of chronic myeloid leukemia (CML). The small molecule also inhibits tyrosine kinases associated with cKIT and platelet derived growth factor (PDGF) receptors [1]. Though the drug is generally well tolerated [2], impaired testosterone production after imatinib therapy has been reported [3,4]. Reduced testosterone levels can, amongst other symptoms, result in gynecomastia, which has been reported as a side effect of tyrosine kinase inhibitor therapy [3,5-8]. Additionally, case reports of imatinib-related severe oligozoospermia have appeared [9,10]. Pathophysiologically, inhibition of cKIT and PDGF receptors is thought to be involved in these unintended testicular effects, in that both play crucial roles in Leydig and Sertoli cell development and function and in germ cell differentiation [11-13].