Esomeprazole-Induced Subacute Cutaneous Lupus Erythematosus

We report the case of a 74-year-old woman with a history of hypertension, diabetes mellitus, dyslipidemia, spondyloarthritis, and idiopathic thrombocytopenic purpura for which she had undergone splenectomy 5 years previously. She was being followed up by her rheumatologist for joint pain of inflammatory origin with low titers of rheumatoid factor and was taking lorazepam, ranitidine, domperidone, indapamide, AM3, and ursodeoxycholic acid. She attended our clinic with a pruritic disorder that had begun a week earlier and took the form of well-defined discretely desquamative erythematous papules on her back and, to a lesser extent, on her chest, thighs, and proximal upper arms. She had no blisters or mucosal lesions. These signs first appeared during winter, and the patient reported no previous sun exposure. Of interest, she reported starting esomeprazole and a vitamin complex (B1, B6, and B12) 3 weeks before the lesions first appeared. A biopsy specimen of one of the lesions was obtained, and the patient was prescribed mometasone cream twice daily. Esomeprazole and the vitamin supplement were withdrawn. At 3 weeks, the lesions had progressed to confluent annular erythematous-violaceous plaques on the abovementioned sites (fig. 1). The biopsy revealed hyperkeratosis in the epidermis, epidermal atrophy, degeneration of the basal layer, lymphocytic exocytosis, spongiosis, and occasional necrotic keratinocytes. A superficial perivascular lymphohistiocytic inflammatory infiltrate was observed in the dermis (fig. 2). Based on clinical and microscopy findings, the patient was diagnosed with subacute cutaneous lupus erythematosus (SCLE). The results of a complete blood count and routine biochemistry were unremarkable. The immunology workup revealed positive titers for antinuclear antibody (1/160), anti-SSA/Ro antibody, and anti-SSB/La antibody. These results had also been positive in laboratory studies performed 2 years previously in the rheumatology department.