Bortezomib‐induced Sweet syndrome

A 59-year-old man was treated with bortezomib (Velcade) for multiple myeloma refractory to VAD (vincristine, adriamycin, dexamethasone), VMBCP (vincristine, BCNU, cyclophosphamide, melphalan, prednisone) and thalidomide. Bortezomib was given at the dose of 1Æ3 mg/m on days 1, 4, 8 and 11, every 21 d. On day 4 of the second cycle, the patient presented with sudden onset of painful round erythematous and oedematous plaques on the head, neck and trunk (as shown), associated with fever up to 38 C and asthenia. There was a slight increase in C-reactive protein (20 mg/l). The white blood cell and neutrophil counts were normal. Skin biopsies confirmed the clinical diagnosis of Sweet syndrome, with neutrophilic infiltration of the dermis, leucocytoclasia and subepidermal oedema in the absence of signs of vasculitis. Cutaneous lesions resolved within 4 d of corticosteroid initiation (methylprednisolone 40 mg/d for 3 d, rapidly tapered over a period of 1 week). Identical but more extensive skin lesions recurred on day 4 of the third cycle. During the fourth cycle, bortezomib was given together with dexamethasone, 20 mg/d given on days 1, 2, 4, 5, 8, 9, 11 and 12. Despite this, skin lesions recurred and were associated with marked constitutional symptoms. Treatment with bortezomib was therefore discontinued. The response after four cycles was excellent, with respect to the patients’ multiple myeloma (IgG level decreased from 62Æ4 to 11Æ1 g/l). The skin lesions did not reappear after the discontinuation of bortezomib. During this period, no other new medications were initiated. The recurring skin symptoms after each cycle of bortezomib strongly suggest a causal link between Sweet syndrome and administration of bortezomib.