Pomalidomide induced lupus type hypersensitivity reaction.

Abstract Multiple myeloma (MM) is a plasma cell disease characterized by a clonal proliferation of malignant plasma cells. Pomalidomide, a novel immunomodulating imide drug (IMiD), prolongs survival in relapsed or refractory cases. Cutaneous toxicity is one of the most common side effects due to anti-cancer therapy that may even lead to discontinuation of treatment. We report a case of pomalidomide induced cutaneous lupus-like hypersensitivity reaction in a 75-year-old male diagnosed with MM. The patient relapsed on lenalidomide after 7 years. Pomalidomide and Ixazomib were considered the next best treatment option. Treatment was complicated by a generalized rash (grade 3) after 2 cycles (3 weeks on and 1 week off cycle). Multiple pinks, dusky plaques on the lower back and abdomen, some light pink and edematous areas on the chest, abdomen, neck, and hairline, and a few on arms were seen. No pruritis was noted. There was no involvement of the mucosa or palms. No history of a rash with lenalidomide. A punch biopsy showed a moderate number of eosinophils within the inflammatory infiltrate, a finding which favored a lupus-type hypersensitivity reaction rather than true lupus erythematosus or leukemia cutis. Both medications were discontinued and topical betamethasone was administered and the patient's symptoms resolved in 2 weeks. Ixazomib single-agent therapy was subsequently resumed without any adverse effects. It is important to differentiate between disease progression itself drug-induced lupus hypersensitivity reaction vs systemic lupus erythematosus (SLE) vs drug-induced hypersensitivity reaction, therefore all such lesions should always be biopsied. Our case study is unique both because of the incongruent timeline and because it is unusual to expect such a reaction in a patient who had previously tolerated one such treatment. In our case, punch biopsy showed that the patient was having the lupus-like hypersensitivity reaction. Pomalidomide was determined to be the most significant trigger preceding his presentation. Timely identification of the culprit drug is critical. The mainstay of management is to discontinue the drug. In severe cases, systemic steroids can be considered.