Imatinib‐induced psoriasiform eruption in a patient with chronic myeloid leukemia
Authors: Connie R. Shi, Vinod E. Nambudiri
Journal: American Journal of Hematology (2017)

A 32-year-old woman with chronic myeloid leukemia (CML) presented for evaluation of a new diffuse cutaneous eruption that developed within one month of initiating therapy with imatinib mesylate at 400 mg daily. The patient endorsed associated pruritus and scaling of the scalp. Notably, the rash improved during a one-week trial off of imatinib and recurred when imatinib was re-initiated. Her only other medication was dexlansoprazole for chronic gastro-esophageal reflux disease. The patient reported no prior personal or family history of skin disease. She achieved a complete hematological response to imatinib for her CML, which she continued to take. Physical examination revealed multiple well-demarcated, thin pink-to-violaceous plaques with hyperkeratotic white scale distributed symmetrically over the dorsal hands (Image 1), bilateral elbows, bilateral lower extremities, and posterior neck, along with scaling and crusting of the scalp and the conchal bowls. Her clinical presentation was consistent with a psoriasiform eruption and the temporal relationship of rash onset with initiation of imatinib was consistent with an imatinib-induced psoriasiform eruption. The patient was treated with topical clobetasol ointment twice daily for two weeks, followed by triamcinolone ointment twice daily for two weeks, while continuing on imatinib for her CML. The lesions demonstrated marked resolution within three weeks of topical therapy. Pink-to-violaceous plaques with hyperkeratotic white scale symmetrically distributed on the (A) dorsal hands and (B) palmar hands and wrists Tyrosine kinase inhibitors such as imatinib mesylate, nilotinib, and dasatinib are associated with a range of cutaneous adverse effects.1 Cutaneous reactions to imatinib occur in up to 69% of patients,2 with the most common being superficial edema and erythematous maculopapular rash.1, 3 Less commonly, hypo- and hyper-pigmentation, lichenoid eruptions, psoriasis and psoriasiform eruptions, pityriasis rosea-like rashes, and Stevens–Johnson syndrome can result, among others.1, 3 It is thought that cutaneous reactions to imatinib are dose-dependent, as these adverse effects are rarely observed at lower doses of the drug (25–140 mg daily) and are much more common at doses of 400–800 mg daily.1, 4 In addition to the classic scaly plaques of psoriasis, scalp involvement and nail dystrophy are characteristic of the condition, with many patients also reporting associated pruritus. Imatinib-induced psoriasis and psoriasiform eruptions are rare and have occurred both de novo and as exacerbations of preexisting disease one to seven months after imatinib initiation.1, 3 Improvement in the psoriasis upon dose reduction or discontinuation of imatinib has been reported,1 as well as recurrence following imatinib re-initiation,5 similar to the case of our patient. Interestingly, there has been one report of improvement in psoriasis following imatinib therapy in a patient with longstanding severe erythrodermic psoriasis.6 Unfortunately, the pathogenesis underlying the association between imatinib and psoriasis or psoriasiform eruptions remains poorly understood. It has been proposed that imatinib's interference with regulatory T cell activity and T-cell receptor signaling pathways results in autoimmune dysregulation, unmasking pathways that ultimately result in the development of autoimmune diseases such as psoriasis.7 However, there remains no experimental evidence elucidating the observed connection between imatinib therapy and psoriasis. Imatinib-induced psoriasiform eruptions are typically successfully managed with standard psoriasis treatments such as topical corticosteroids and vitamin D analogues. Psoriasis is a highly treatable cutaneous condition and development of imatinib- or other tyrosine kinase inhibitor-induced psoriasis or similar eruptions should not automatically preclude continued therapy with these effective medications. The authors report no conflicts of interest. Vinod E. Nambudiri http://orcid.org/0000-0002-4170-7681