A case of subacute cutaneous lupus erythematosus as a result of ranibizumab (Lucentis) treatment
An 82-year-old female was referred to a dermatologist with a generalized, scaly, symmetric, non-palpable but very erythematous, almost hemorrhagic rash which was painful and associated with a mild itch. It was initially on the face, neck and forearms in light-exposed areas [Figs. and ]. The presence of the rash on her legs [] at that stage is uncertain as they were bandaged following surgery and subsequent ulceration. It had developed over two weeks following an injection of Lucentis as part of her treatment for neovascular AMD.\nShe had been diagnosed with “wet” AMD in 2002. Over the following two years, she was treated with seven doses of Verteporfin (Visudyne) and a single dose of Bevacizumab (Avastin). Her general health was good and, in addition to AMD, her medical history consisted of well-controlled hypothyroidism, hypertension and recently stripped varicose veins. Her medications included aspirin, thyroxine, amlodipine, and calcium and cholecalciferol supplements, all of which she had been using for a prolonged period.\nIn August 2008, she received a single 2.3-mg intravitreal injection of ranibizumab. Five days later, she developed a few “flat, brown spots” which over the next 10 days, evolved into the rash described above. Her dermatologist prescribed topical methylprednisolone ointment for the face and betamethasone ointment for the rest. None of the other medications had been changed or added in the months preceding this episode. Arthralgia and myalgia were not present.\nA biopsy [] showed a prominent lichenoid inflammatory process with some necrotic keratinocytes in keeping with a drug reaction and, considering the clinical history, consistent with the diagnosis of drug-induced, subacute cutaneous lupus erythematosus (SCLE).\nImmunofluorescence was negative but she had already been using steroids. She was commenced on oral steroids which were initially ceased by her vascular surgeon due to slow healing of her leg wounds. They were restarted and she improved markedly at 25 mg/day.\nThe dose was being weaned until it was again ceased, this time by an immunologist. The rash flared quite markedly and steroids were recommenced. In February 2009, hydroxychloroquine (Plaquenil) was introduced as a steroid-sparing agent and surprisingly, her rash flared again. A second biopsy in April was also suggestive of SCLE.\nHer standard bloods were unremarkable except for a mild anemia (111 g/L). Erythrocyte sedimentation rate (ESR) was initially elevated at 30 mm/h (normal < 20 mm/h) which decreased to 4 mm/h over several months. Antinuclear antibodies (ANA)/anti-SSA in particular SSA (Ro60) and SSB (La) were present. Anti-DNA, complement, ANCA, cardiolipin, and mitochondrial and ribosomal antibodies were all within normal limits.\nBy July 2009, she was on 15 mg of prednisolone and, excluding her upper back, the rash was much improved. Her chest, face and arms were virtually clear.