Shion Kachi, Mirei Shirakashi, Motoo Nomura, Yoichi Nakayama, Hirokazu Taguchi, Tsuneo Sasai, Ryosuke Hiwa, Hideaki Tsuji, Shuji Akizuki, Akira Onishi, Hajime Yoshifuji, Masao Tanaka, Ran Nakashima, Kosaku Murakami, Akio Morinobu
Immune checkpoint inhibitors (ICIs) can cause de novo inflammatory arthritis and flares of pre-existing rheumatoid arthritis (RA). This study aimed to describe and explore the clinical characteristics and treatment outcomes of these arthritis groups in a single-center, exploratory cohort. We retrospectively analyzed patients who developed inflammatory arthritis after ICI therapy, including pre-existing RA flares and the de novo cases. The de novo cases were operationally classified based on the 2010 ACR/EULAR classification criteria into those who fulfilled the criteria (ICI-RA) and those who did not (ICI-IA). Of 41 de novo cases, 10 and 31 patients were classified into ICI-RA and ICI-IA, respectively. Six patients with RA experienced flares. At baseline, serum IgA was numerically higher in the RA flare group than in the non-flare group (median 482.5 vs. 266 mg/dL). At onset, the ICI-IA group exhibited higher eosinophil counts than the RA flare group (median 140 vs. 7/µL), although prior glucocorticoid exposure may have influenced these values. At 365 days, cumulative treatment discontinuation rates were 34.1% for ICI-IA, 20.0% for ICI-RA, and 0% for RA flares. These operationally defined subgroups exhibited heterogeneous clinical courses. These hypothesis-generating findings support future prospective cohorts with detailed immunophenotyping.