Joint Disease Activity in Inflammatory Bowel Disease-associated Peripheral Spondyloarthritis Stratifies Therapeutic Response.
Joint Disease Activity in Inflammatory Bowel Disease-associated Peripheral Spondyloarthritis Stratifies Therapeutic Response.
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DOI：
10.1016/j.gastha.2021.12.002
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发表时间：
2022
期刊：
影响因子：
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通讯作者：
Longman, R S
中科院分区：
文献类型：
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作者：
Lai, D;Funez-Depagnier, G;Duenas-Bianchi, L;Lavergne, A;Battat, R;Ahmed, W;Schwartzman, M;Lima, S;Khan, S;Chong, P S;Sonnenberg, G;Artis, D;Lukin, D;Scherl, E;Longman, R S
manifestation associated with active inflammatory bowel disease (IBD). 1, 2 The paucity of cohorts and trials using validated SpA diagnostic criteria and disease activity indices unfortunately limits the available data to define the efficacy of biologic therapy for IBD on joint symptoms. IBD-associated SpA can be classified into axial SpA or peripheral SpA (pSpA)(arthritis, enthesitis, or dactylitis) using diagnostic criteria established by Assessment of SpondyloArthritis International Society (ASAS). 3 Validated clinical SpA disease activity indices are crucial to longitudinally track the response of SpA symptoms in a clinical setting 4, 5. The aim of this study was to apply SpA diagnostic criteria and disease activity indices to assess intestinal and joint response to biologic therapy in IBD subjects with pSpA. We analyzed 1032 IBD subjects (593 Crohn’s disease, 439 ulcerative colitis) with prospective collection of clinical and endoscopic disease activity scores from the JRI Live Cell Biobank at Weill Cornell Medicine. Axial SpA or pSpA was defined by clinical and radiographic criteria established by the ASAS, 3 and joint disease activity was assessed prospectively with the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI). Subjects with pSpA initiating biologic therapy for active intestinal disease were included in the longitudinal cohort. Using ASAS diagnostic criteria, pSpA was the most prevalent extra-intestinal manifestation in IBD subjects and more prevalent in CD compared with UC (23.7% vs 12.4%, P<. 0001, Table and Table A1). Subjects with pSpA were significantly more likely to be on steroids or biologic therapy and have a current or previous exposure to biologic therapy (63% vs 52%, P ¼. 0094, Table). CD subjects with pSpA were less likely to be in clinical remission than those without SpA (43% vs 65%, P<. 0001, Table), but no difference was noted in their Montreal classification (Table A2). Consistent with the overall concordance of pSpA with intestinal symptoms, subjects with active CD had a higher mean BASDAI than those in clinical remission (3.5 vs 2.6, P ¼. 043, N ¼ 106)(Table). No differences were observed in the Simple Endoscopic Score for Crohn’s Disease or Mayo score between IBD and IBD-pSpA cohorts (CD: N ¼ 258, UC: N ¼ 434). Although a higher proportion of subjects with pSpA were treated with ustekinumab(UST) than those without pSpA (15% vs 9%, P ¼. 0013, Table), the impact of UST on pSpA in IBD is not clear. Linear regression analysis of intestinal disease activity (Harvey Bradshaw Index [HBI]) and joint disease activity(BASDAI) revealed a significant correlation for CD pSpA subjects treated with tumor necrosis factor-alpha inhibitors (anti-TNFa, N ¼ 26, R2 ¼ 0.2, P ¼. 04), but not for CD pSpA subjects treated with UST (N ¼ 28)(Figure A). To investigate this discordant response of joint symptoms in CD pSpA treated with UST, 36 sequential patients with IBD-pSpA initiating biologic therapy (21 with UST and 15 with anti-TNFa) for active intestinal disease were longitudinally assessed for intestinal and SpA symptoms before and after induction therapy (Table A3). Similar to previous reports, 6 anti-TNFa therapy significantly reduced the BASDAI (4.3 vs 2.2, P ¼. 006, Figure B) and HBI (12.4 vs 4.2, P ¼. 016, Figure C). In contrast, induction therapy with UST resulted in no change in the BASDAI (4.0 vs 3.5, P ¼. 27, Figure B) despite a significant reduction in the HBI (9.5 vs 6.4, P ¼. 006, Figure C). Assessment of 70% reduction in the BASDAI revealed that a lower proportion of UST-treated patients achieved a joint clinical response in pSpA after induction therapy than anti-TNFa–treated patients (10% vs 40%, 0.03, Figure D …
