Genetic factors may also critically influence this particular immune reaction. They found an isoform of tropomysin, which is expressed in all the organs that can be affected by EIM of IBD as well as in the gut and postulated an autoimmune reaction towards this molecule as a cause of EIM in IBD patients.
The immune system is incapable of distinguishing the two epitopes and therefore attacks both, as shown by Bhagat et al. The inflamed intestinal mucosa may trigger an extraintestinal immune response due to specific epitopes that are detectable in, e.g. This allows the assumption, that there is at least some genetic influence. Most patients with EIM present with a severe colitis and some of them also reveal a positive family history for IBD. In the SIBDCS this constellation occurred in 15% of Crohn’s disease (CD) and 8% of ulcerative colitis (UC) patients. Previous studies showed that almost one quarter of patients with EIM present with a combination of several EIMs suggesting that the appearance of one EIM favours the onset of at least one other EIM. We have recently shown that in 25.8% of patients of the Swiss IBD Cohort Study (SIBDCS) EIM occur even before IBD is diagnosed. Other EIM, such as primary sclerosing cholangitis (PSC), pyoderma gangrenosum, uveitis and spondylarthropathy, are considered independent from intestinal activity. Peripheral arthritis, erythema nodosum and aphtous ulcers are associated with the activity of the intestinal disease. Inflammatory bowel disease (IBD) patients are commonly affected by extraintestinal manifestations (EIM) affecting the joints, skin, eyes, and biliary ducts, the overall appearance ranges from 6% to 47% and up to 10% at the time of IBD diagnosis.
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