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Loss of skin pigment caused by imatinib therapy

A 46-year-old Caucasian woman was diagnosed with chronic phase chronic myeloid leukaemia in April 2001. After initial therapy with hydroxycarbamide and interferon, she was commenced on imatinib 400 mg daily. She achieved a complete cytogenetic response within 6 months and with continuation therapy now has a BCR/ABL to ABL ratio of 0Æ001% by quantitative PCR. In May 2004 she reported changes in her skin texture. More recently, she has noted patchy areas of depigmentation and generalized difficulty in maintaining a suntan despite continuing her regular habit of using a sun bed. Her skin shows a generalized loss in background pigmentation though it appears to be preserved within the now prominent lentigines on her chest and arms (bottom). Recent reports describe the loss of skin pigment in patients treated with imatinib, particularly in those with ethnically pigmented skin. Imatinib was developed as a specific BCR– ABL tyrosine kinase inhibitor but is known to be active against at least three other tyrosine kinases, namely platelet derived growth factor receptors a and b and C-kit. The mechanism of skin depigmentation caused by imatinib seems likely to be via its effect on C-kit, which is known, with its ligand stem cell factor, to have a major role in melanogenesis, melanocyte homeostasis and ultra violet B-induced skin pigmentation. Hypopigmentation is reported to be reversible upon imatinib discontinuation or dose reduction. It is likely to be underreported in White patients unless they naturally have a propensity for tanning or live in a sunny climate. It is interesting that our patient usually had a deep tan from foreign travel and the regular use of sunbeds throughout the winter months.