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Guselkumab for treating immune checkpoint inhibitor-induced psoriatic arthritis

Rheumatic immunerelated adverse events (irAEs) occur in approximately 10% of patients receiving immune checkpoint inhibitors (ICIs). Here, we report a case of psoriatic arthritis (PsA) that occurred during ICI treatment for lung cancer and was successfully treated with guselkumab. A 64yearold man with stage IIIC lung cancer was treated with definitive concurrent chemoradiotherapy followed by six cycles of weekly carboplatin and paclitaxel. He was then started on biweekly durvalumab (antiprogrammed deathligand 1 antibody) monotherapy. After the sixth cycle of durvalumab administration, he developed shoulder pain, a skin rash, and nail changes. Due to the high possibility of irAEs, durvalumab was discontinued and prednisolone 20 mg/day was started. However, his symptoms continued to worsen; therefore, he was referred to our department of oncorheumatology. Before starting durvalumab, he had never experienced such skin rashes or nail changes and had no family history of any autoimmune disease. On physical examination, tender entheses on the shoulders, distal interphalangeal joint arthritis of the fingers, and dactylitis of the left fourth toe were observed without any signs of axial involvement. Welldemarcated, scaly, erythematous papules and plaques were present on the trunk, hands and feet. Onycholysis, oildrop discolouration and nail bed hyperkeratosis were also present (figure 1A–C), leading to the diagnosis of plaque psoriasis and nail psoriasis. His C reactive protein level was normal (4.53 mg/dL), while the rheumatoid factor level was elevated (115 U/mL, normal range 0–10), and the anticitrullinated peptide antibody assay revealed negative results. The patient was diagnosed with PsA (Composite Psoriatic Disease Activity Index (CPDAI) score 9), for which celecoxib 200 mg/day in combination with calcipotriol/betamethasone dipropionate ointment was started; prednisolone 20 mg/day was continued. However, the symptoms worsened over the next 4 weeks; hence, we introduced guselkumab. His active PsA symptoms improved from week 3 of guselkumab treatment. Therefore, we discontinued celecoxib and tapered prednisolone dosage. Two months after guselkumab initiation, all symptoms except nail psoriasis disappeared, but he developed pulmonary tuberculosis despite a negative interferongamma release assay result before starting guselkumab. We terminated guselkumab after two doses (weeks 0 and 4) and administered antituberculosis drugs. After 8 months of guselkumab treatment, prednisolone dosage was reduced to 2 mg/day, and the symptoms of PsA remained absent except some residual toenail psoriasis (CPDAI score 0) (figure 1D–F). Treatment of pulmonary tuberculosis was successful, and there was no recurrence or metastasis of lung cancer. Durvalumab was not rechallenged. Psoriasis and PsA develop in some patients after ICI initiation. In our patient, PsA developed 4 months after ICI initiation and worsened rapidly thereafter, suggesting its development as an irAE. When using biologic agents for PsA treatment, it is necessary to exercise caution for patients with underlying ICItreated malignancies. Tumour necrosis factor alpha (TNF-α) inhibitors can increase risk of infection, and interleukin (IL)17 inhibitors may reduce the antitumour effect of ICIs. Guselkumab is a specific IL23 inhibitor used to treat PsA, with a joint efficacy comparable to that of subcutaneous TNF-α and IL17 inhibitors. It is particularly robust against skin manifestations and is relatively safe without side effects such as serious infections or any malignancy. Although a similar drug, IL12/23 inhibitor ustekinumab, was used for refractory irAE colitis, this is the first case of using an IL23 inhibitor for treating an irAE. While pulmonary tuberculosis developed after guselkumab initiation, the patient had also been receiving prednisolone 15–20 mg/day for 3–4 months, Letter