Severe Peripheral Arterial Disease During Nilotinib Therapy

Abstract

In BCR-ABL-positive chronic myeloid leukemia (CML), the tyrosine kinase inhibitor (TKI) imatinib acts as an antileukemic agent and reconstitutes normal hematopoiesis ( 1 ). Because imatinib-treated patients may develop drug resistance or intolerance, the second generation TKI nilotinib (Tasigna; Novartis Pharmaceuticals, East Hanover, NJ) was designed and has been approved for treatment of CML ( 2 ). In newly diagnosed CML, nilotinib (300 or 400 mg twice daily) was superior to standard therapy with imatinib, with major molecular response rates of 44% (300 mg) and 43% (400 mg) vs 22% for imatinib at 1 year. Adverse events with nilotinib at either dose included reversible constitutional symptoms and elevations in lipase (24%–29% of patients), bilirubin (53%–62%), fasting glucose (36%–41%), and cholesterol (22%) ( 3 , 4 ).