{'fraction_non_alphanumeric': 0.03193960511033682, 'fraction_numerical': 0.023519163763066203, 'mean_word_length': 5.001742160278746, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Two cases of skin infection during psoriasis treatment with brodalumab

Dear Editor, The interleukin-17 (IL-17) family of cytokines plays a central role in the pathogenesis of psoriasis. Brodalumab targets IL-17 receptor A. We herein report two cases of skin infection which occurred during brodalumab administration. Case 1, a 40-year-old man with fatty liver and hyperlipidemia, had suffered with psoriasis since the age of 19 years. Brodalumab 210 mg was administrated every 2 weeks. Four weeks into treatment, the patient’s Psoriasis Area and Severity Index (PASI) score improved from 22.2 to 0, and the patient has generally maintained this improvement since then. However, during treatment he suddenly presented multiple, painful, indurated, erythematous nodular skin lesions on his anterior chest, abdomen and upper limbs in winter (Fig. 1a). Furunculosis was diagnosed. Oral cefdinir 300 mg/ day and topical nadifloxacin treatment resolved the eruptions in a few weeks. Brodalumab administration was omitted only once. Case 2, a 57-year-old man with diabetes of approximately 10 years’ duration, hyperlipidemia and fatty liver, had had psoriasis since the age of 30 years. The change in hemoglobin A1c was from 7 to 8. Brodalumab 210 mg every 2 weeks was administrated for 15 months, and his PASI score improved from 20.7 to 0. When the brodalumab dose was reduced to 140 mg every 4 weeks, the psoriatic eruptions worsened. Thereafter, the dose was increased to 210 mg every 2 weeks, but limited improvement in the lesions was observed; the patient achieved a PASI score of only 8.4 and later began experiencing pain in the occipital region. A subcutaneous abscess was diagnosed by magnetic resonance imaging (Fig. 1b). Incision drainage was performed, and cefaclor was administrated but failed to resolve the infection. Methicillin-resistant Staphylococcus aureus was detected in the pus culture. Because of greater susceptibility, cefaclor was switched to minocycline 200 mg/day. Twelve days later, the eruptions resolved and the drainage ceased. Brodalumab administration was omitted only once. Anti-IL-17 agents can produce remarkable improvement in the symptoms of psoriasis. Brodalumab, secukinumab and ixekizumab are commonly used anti-IL-17 agents and, while relatively safe, they may induce characteristic side-effects like candidiasis, exacerbation of Crohn’s disease and neutropenia. Cellulitis and folliculitis are also known adverse effects of brodalumab. Diabetes is an important risk factor for skin infections, but in the present cases brodalumab might have increased this risk. In a murine model, the IL-17 family of cytokines demonstrated a protective effect against skin infections. IL-17A and IL-17F function as either homodimers or heterodimers. Ishigame et al. reported that IL-17A and IL-17F worked complementarily against S. aureus infection. While secukinumab and ixekizumab target only IL-17A, brodalumab targets IL-17 receptor A, thereby inhibiting the anti-infective effects of both IL-17A and IL-17F. Therefore, the risk of infection by extracellular bacteria including S. aureus may increase more during administration of brodalumab than secukinumab or ixekizumab. The differences in the side-effects of these three agents are still unknown, and more data are required for clarification. In summary, we experienced two cases of skin infection while treating psoriasis using brodalumab. IL-17 inhibitors are