Imatinib-Induced Psoriasis

Imatinib is a signal transduction regulator that selectively inhibits the tyrosine kinase family, including bcr-abl and c-kit, and the platelet-derived growth factor (PDGF) receptor. It is currently the fi rst-line therapy for newly diagnosed chronic myeloid leukemia (CML) patients [1]. We report the case of a patient who had no previous history of psoriasis but developed psoriasis after starting imatinib. A 21-year-old woman was diagnosed with CML in the chronic phase. Imatinib mesylate was started at a daily dose of 400 mg. The patient achieved a complete hematological response within 3 months. Five months after her CML diagnosis and imatinib usage, she developed an erythematous scaly eruption with plaques of various sizes on her trunk and extremities (Figures 1, 2, and 3). She had no previous history of psoriasis and had not taken any drugs except for imatinib, nor did she have any relatives with a history of psoriasis. The patient underwent a skin biopsy, which revealed a neutrophilic scale crust and loss of the granular cell layer, which are most consistent with psoriasis (Figure 4). The discontinuation of imatinib treatment and subsequent introduction of narrowband ultraviolet B therapy improved the skin condition, and her psoriatic skin lesions had almost disappeared within 3 weeks. Since that time, nilotinib has been started. So far, the patient has not complained of any cutaneous side effects, and she achieved a complete cytogenetic response at 6 months and remains clinically well, currently receiving nilotinib at a dose of 200 mg twice daily. Cutaneous reactions to imatinib are common and may occur in 7% to 88.9% of patients in different series. Maculopapular eruptions, erythematous eruptions, edema, and periorbital edema are the most common adverse events seen [2]. In 2002, Miyagawa et al. reported a patient who had intractable psoriasis but experienced signifi cant improvement while being treated with imatinib for