IBD pathogenesis is multifactorial and involves variations in the patient’s genome, environmental factors, and alterations in the intestinal microbiota and the mucosal immune response. The microbiota of people with IBD tends to be less rich and less diverse than in those without IBD. Additionally, in people with IBD, intestinal mucus is thinner and has an altered composition, which leads to a compromised barrier and subsequently increased intestinal permeability. The interplay of these factors, in addition to other environmental triggers, culminates in a dysregulated immune response, involving both innate and adaptive responses, ultimately leading to intestinal inflammation.6,7 Of note, the adaptive immune response produces an immunoglobulin G (IgG) antibody against an epithelial antigen of the colon that is also found in the skin, eyes, joints, and biliary tract and likely plays a role in extraintestinal manifestations of IBD.8 While much of the exact nature of its pathophysiology is unknown, several key risk factors for IBD have been identified:
CD causes full-thickness, transmural inflammation of the intestinal wall. Although CD can affect any portion of the gastrointestinal tract, from the mouth to the anus, approximately 70% percent of patients will have some degree of terminal ileal disease. In approximately 55% of CD patients, inflammation involves both the colon and terminal ileum. Isolated terminal ileal disease and isolated colon disease each account for approximately 15% of those with CD.11
Although the most common CD manifestations are chronic diarrhea, abdominal pain, and weight loss, due to the heterogeneity in disease phenotype, the presentation of a CD flare can vary significantly.8 Active small-bowel inflammation typically presents as an obstruction or ileus, with colicky abdominal pain, distension, nausea, or loose bowel movements.7 Hematochezia is often a sign that the colon is involved and is usually associated with diarrhea and muco-purulent discharge. Patients with perianal disease will present with perianal drainage and pain with sitting and defecating.12 The transmural nature of CD leads to the progression of penetrating disease and the formation of strictures, fistulas, and abscesses,13 complications that have the potential to become surgical emergencies. Additionally, small-bowel disease leads to malabsorption and vitamin deficiencies.
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