Association between biologic exposure and relapse incidence in relapsing polychondritis: a retrospective cohort study.
retrospective_cohort · Level III
Where this comes from
- Record sourced from PubMed, PMID 42281284.
- Also identified by DOI 10.1093/rheumatology/keag305.
- No licence information is recorded for this record.
- Because redistribution is not established, this page shows the abstract only. Follow the links below for the full text.
Abstract
Relapsing polychondritis (RP) is characterised by recurrent flares, and comparative evidence for relapse prevention using biologics remains limited. We evaluated the association between biologic exposure and relapse incidence. This single-centre retrospective cohort study (Kyoto University Hospital, 2000-2023) investigated adults with RP. Follow-up was divided into periods without biologics (No Bio), with TNF-α inhibitors (TNFi), or with IL-6 receptor inhibitor (IL-6Ri). Primary outcomes were RP relapse and hospitalised infection. Period-level incidence rate ratios were estimated using negative binomial regression with a log(person-time) offset and adjusted for prespecified covariates, and adjusted absolute event rates and rate differences were estimated by regression standardisation. Over 503.5 person-years, 55 patients were included (never-Bio, n = 28; ever-Bio, n = 27). Within the ever-Bio cohort, crude relapse rates were 46.9, 22.4, and 12.5 per 100 person-years during the No Bio, TNFi, and IL-6Ri periods, respectively. In adjusted models, both TNFi and IL-6Ri were associated with lower relapse rates than the No Bio period (TNFi: IRR 0.4, 95% CI 0.2-0.8; adjusted rate difference, -54.0 events per 100 person-years, 95% CI -141.5 to -5.5; IL-6Ri: IRR 0.2, 95% CI 0.1-0.4; adjusted rate difference, -68.3 events per 100 person-years, 95% CI -149.8 to -21.4). Hospitalised infection estimates were imprecise (TNFi: IRR 0.3, 95% CI 0.1-1.4; IL-6Ri: IRR 0.7, 95% CI 0.2-2.6). Biologic exposure was associated with lower relapse rates than during No Bio periods in RP, whereas estimates for hospitalised infection were imprecise.