Increased risk of developing Crohn’s disease or ulcerative colitis in 17 018 patients while under treatment with anti‐TNFα agents, particularly etanercept, for autoimmune diseases other than inflammatory bowel disease
Summary Background Anti‐TNFα agents have revolutionised management of chronic inflammatory diseases. Paradoxically, these agents might provoke development of de novo autoimmune diseases. Aim To examine whether there is an increased risk of developing Crohn's disease (CD) and ulcerative colitis (UC) while under treatment with anti‐TNFα agents for diseases other than inflammatory bowel disease (IBD) Methods A nationwide cohort study, based on Danish health registries, of all patients who utilised anti‐TNFα agents for non‐IBD indications. Included were patients, who had diseases for which anti‐TNFα agent is indicated (rheumatoid arthritis, psoriasis/psoriatic arthritis, ankylosing spondylitis, others). The observation period for development of de novo IBD started from 2004. Exposed patients had received at least one dose of anti‐TNFα. Results In total 17 018 individuals with autoimmune diseases were exposed to anti‐TNFα (the vast majority had infliximab, etanercept and adalimumab), and 63 308 individuals were not. Patients treated with etanercept had an increased risk of being diagnosed with CD and UC while under treatment, adjusted hazard ratio 2.0 [95% CI: 1.4‐2.8] and 2.0 [95% CI: 1.5‐2.8], respectively. The corresponding hazards ratios for infliximab were 1.3 [95% CI: 0.8‐2.2] and 1.0 [95% CI:0.6‐1.6], and for adalimumab 1.2 [95% CI: 0.8‐1.8] and 0.6 [95% CI: 0.3‐1.0]. Conclusions Patients treated for autoimmune diseases with anti‐TNFα had an increased risk of being diagnosed with CD or UC while under treatment with etanercept. The nature of this association is uncertain. This finding has relevance to clinical care and insights into common mechanisms of the pathophysiology of these diseases..
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2019 |
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| Erschienen: |
2019 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:50 |
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| Enthalten in: |
Alimentary Pharmacology & Therapeutics - 50(2019), 3, Seite 289-294 |
| Beteiligte Personen: |
Korzenik, Joshua [VerfasserIn] |
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| BKL: |
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| Anmerkungen: |
Copyright © 2019 John Wiley & Sons Ltd |
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| Umfang: |
6 |
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| doi: |
10.1111/apt.15370 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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WLY002330865 |
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| 520 | |a Summary Background Anti‐TNFα agents have revolutionised management of chronic inflammatory diseases. Paradoxically, these agents might provoke development of de novo autoimmune diseases. Aim To examine whether there is an increased risk of developing Crohn's disease (CD) and ulcerative colitis (UC) while under treatment with anti‐TNFα agents for diseases other than inflammatory bowel disease (IBD) Methods A nationwide cohort study, based on Danish health registries, of all patients who utilised anti‐TNFα agents for non‐IBD indications. Included were patients, who had diseases for which anti‐TNFα agent is indicated (rheumatoid arthritis, psoriasis/psoriatic arthritis, ankylosing spondylitis, others). The observation period for development of de novo IBD started from 2004. Exposed patients had received at least one dose of anti‐TNFα. Results In total 17 018 individuals with autoimmune diseases were exposed to anti‐TNFα (the vast majority had infliximab, etanercept and adalimumab), and 63 308 individuals were not. Patients treated with etanercept had an increased risk of being diagnosed with CD and UC while under treatment, adjusted hazard ratio 2.0 [95% CI: 1.4‐2.8] and 2.0 [95% CI: 1.5‐2.8], respectively. The corresponding hazards ratios for infliximab were 1.3 [95% CI: 0.8‐2.2] and 1.0 [95% CI:0.6‐1.6], and for adalimumab 1.2 [95% CI: 0.8‐1.8] and 0.6 [95% CI: 0.3‐1.0]. Conclusions Patients treated for autoimmune diseases with anti‐TNFα had an increased risk of being diagnosed with CD or UC while under treatment with etanercept. The nature of this association is uncertain. This finding has relevance to clinical care and insights into common mechanisms of the pathophysiology of these diseases. | ||
| 700 | 1 | |a Larsen, Michael Due |4 aut | |
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