Table 1.
Characteristic and clinical outcomes in inflammatory bowel disease patients with concurrent immune-mediated inflammatory diseases
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IMIDs with high prevalence among patients with IBD
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Possible shared immune cells contributing to pathogenesis
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IBD phenotypes
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IBD outcomes
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Possible shared therapies
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| Asthma | Th2 cells | Indefinite | Indefinite | Indefinite |
| Psoriasis | Th1 cells, Th17 cells, and ILC3 | Indefinite | Indefinite | Ustekinumab; TNF inhibitors |
| Rheumatoid arthritis | Th1 cells, Th17 cells, ILC1, and ILC3 | Indefinite | Indefinite | Tofacitinib; TNF inhibitors |
| IMIDs affecting phenotypes or outcomes of IBD | ||||
| PSC | Indefinite (leaky gut theory) | Severe right-sided colitis, rectal sparing, and backwash ileitis | PSC-IBD patients have fewer or no symptoms, and are less likely to require immunosuppressants, hospitalization, and surgery than IBD patients alone | Indefinite |
| Celiac disease | Th17 cells | CD patients with celiac disease are less likely to have ileocolonic involvement than CD patients alone | CD patients with celiac disease are less likely to require TNF inhibitors or azathioprine than CD patients alone. UC patients with celiac disease have an increased risk of colectomy | Indefinite |
| Takayasu arteritis | Th1 cells and Th17 cells | Discontinuous aphthous erosions/ulcers or focal mucosal inflammation | Indefinite | Tofacitinib; Ustekinumab; TNF inhibitors |
IBD: Inflammatory bowel disease; PSC: Primary sclerosing cholangitis; IMIDs: Immune-mediated inflammatory diseases; TNF: Tumor necrosis factor; Th17 cells: Interleukin-17 producing T helper cells; Th1 cells: T helper 1 cells; Th2 cells: T helper 2 cells; CD: Crohn’s disease; UC: Ulcerative colitis; ILC: Innate lymphoid cell.