2016 Volume 49 Issue 8 Pages 553-558
A 49-year-old male presented with rapidly progressive necrotic ulcers on his fingers. At the age of 44, hemodialysis therapy was commenced to treat end-stage renal failure caused by diabetic nephropathy. At the age of 46, he was diagnosed with chronic myeloid leukemia and was started on imatinib, a first-generation tyrosine kinase inhibitor (TKI, 400 mg daily). Three years later, pain and necrotic ulcers appeared on the fingers of both hands and progressed rapidly within several months. We initially suspected calciphylaxis. The ulcers and necrosis did not respond to medical treatment, and the affected fingers were eventually amputated. A histopathological examination of the amputated finger specimens revealed intimal fibrosis and thickening of the subcutaneous vessels, luminal stenosis, and mildly calcified vessels, which were inconsistent with calciphylaxis. We concluded that imatinib had caused these symptoms because the necrosis stopped progressing when the imatinib treatment was ceased. Recent studies have reported that nilotinib, a second-generation TKI, is associated with progressive peripheral arterial occlusive disease (PAOD). However, imatinib-associated PAOD is rare. We speculate that hemodialysis patients that exhibit hypometabolism are at higher risk of vasculopathy than healthy individuals, and blood vessels exhibiting high-grade arteriosclerosis related to end-stage renal disease might be vulnerable to the effects of TKI.
