LAUSR

Dear Editor, A 65-year-old female was referred by the hematologists to the supportive dermato-oncology clinic for dermatologic evaluation of a skin rash. The patient was diagnosed with advanced stage multiple myeloma (MM) IgAκ type, with high-risk cytogenetic features 2 months ago, and was treated with bortezomib 1.5 mg/m sc, cyclophosphamide 500 mg p.o., and dexamethasone 20 mg p.o, οn days 1, 8, 15, and 22. The skin rash appeared after the fourth infusion of bortezomib and according to the patient and as documented by the hematologist, it displayed periodic exacerbation connected to bortezomib administration. Analytically, the eruption was flaring up immediately after bortezomib infusion and was gradually improving, without disappearing, until the next dose. Furthermore, withholding of one bortezomib dose resulted in almost complete resolution, however, after drug rechallenge the patient experienced a relapse. Clinical examination revealed generalized, asymptomatic purpuric macules, and patches, involving the trunk and extremities (Figure 1A,B). Laboratory tests, including complete blood count, coagulation tests, and biochemistry profile were unremarkable; in addition, IgE levels and eosinophil rate were within normal limits. The patient under the diagnosis of drug eruption was initially managed with 20 mg of systemic prednisone for 5 days. Cessation of prednisone resulted in recurrence immediately after bortezomib infusion. A skin biopsy was performed, and histologic examination confirmed the diagnosis of cutaneous leucocytoclastic vasculitis (LV) (Figure 1C). In collaboration with the dermatologists, the patient received a daily dose of 20 mg of prednisone concomitantly to VCD (bortezomib, cyclophosphamide, and dexamethasone) treatment, until complete remission of MM that was documented after six cycles. Systemic prednisone adequately controlled cutaneous LV, and allowed the unhindered treatment of MM, without the need of bortezomib discontinuation, or dose modification. MM is a plasma cell dyscrasia, resulting in impaired immunoglobulin secretion, with IgG being the most prevalent monoclonal protein. Cutaneous LV in the context of MM may represent a manifestation of paraneoplastic syndrome or it may be linked to other common causes of LV like cryoglobulinemia and infections. It is not unusual neoplasiaassociated LV to develop as the initial manifestation of the disease, guiding the diagnosis of MM. LV due to drug hypersensitivity, as in