Inflammatory bowel diseases (IBD) are chronic inflammatory disorders of unknown etiology involving the GI tract. Peak occurrence is between ages 15 and 30 and between ages 60 and 80, but onset may occur at any age. Epidemiologic features are shown in Table 159-1. Pathogenesis of IBD involves activation of immune cells by unknown inciting agent (? microorganism, dietary component, bacterial or self-antigen) leading to release of cytokines and inflammatory mediators. Genetic component suggested by increased risk in first-degree relatives of pts with IBD and concurrence of type of IBD, location of Crohn's disease (CD), and clinical course. Reported associations include HLA-DR2 in Japanese pts with ulcerative colitis and a CD-related gene called CARD15 on chromosome 16p. CARD15 mutations may account for 10% of CD risk. Other potential pathogenic factors include serum antineutrophil cytoplasmic antibodies (ANCA) in 70% of pts with ulcerative colitis (also in 5–10% of CD pts) and antibodies to Saccharomyces cerevisiae (ASCA) in 60–70% of CD pts (also in 10–15% of ulcerative colitis pts and 5% of normal controls). Granulomatous angiitis (vasculitis) may occur in CD. Acute flares may be precipitated by infections, nonsteroidal anti-inflammatory drugs (NSAIDs), stress. Onset of ulcerative colitis often follows cessation of smoking.
TABLE 159-1EPIDEMIOLOGY OF IBD |Favorite Table|Download (.pdf) TABLE 159-1EPIDEMIOLOGY OF IBD
| ||Ulcerative Colitis ||Crohn's Disease |
|Incidence (North America) per person-years ||2.2–14.3:100,000 ||3.1–14.6:100,000 |
|Age of onset ||15–30 and 60–80 ||15–30 and 60–80 |
|Ethnicity ||Jewish > non-Jewish white > African American > Hispanic > Asian || |
|Male/female ratio ||1:1 ||1.1–1.8:1 |
|Smoking ||May prevent disease ||May cause disease |
|Oral contraceptives ||No increased risk ||Odds ratio 1.4 |
|Appendectomy ||Protective ||Not protective |
|Monozygotic twins ||6% concordance ||58% concordance |
|Dizygotic twins ||0% concordance ||4% concordance |
Colonic mucosal inflammation; rectum almost always involved, with inflammation extending continuously (no skip areas) proximally for a variable extent; histologic features include epithelial damage, inflammation, crypt abscesses, loss of goblet cells.
Bloody diarrhea, mucus, fever, abdominal pain, tenesmus, weight loss; spectrum of severity (majority of cases are mild, limited to rectosigmoid). In severe cases dehydration, anemia, hypokalemia, hypoalbuminemia.
Toxic megacolon, colonic perforation; cancer risk related to extent and duration of colitis; often preceded by or coincident with dysplasia, which may be detected on surveillance colonoscopic biopsies.
Sigmoidoscopy/colonoscopy: mucosal erythema, granularity, friability, exudate, hemorrhage, ulcers, inflammatory polyps (pseudopolyps). Barium enema: loss of haustrations, mucosal irregularity, ulcerations.
Any part of GI tract, usually terminal ileum and/or colon; transmural inflammation, bowel wall thickening, linear ulcerations, and submucosal thickening leading to cobblestone pattern; discontinuous (skip areas); histologic features include transmural inflammation, granulomas (often absent), fissures, fistulas.