Introduction

Inflammatory bowel diseases (IBDs) are chronic inflammatory disorders of unknown etiology involving the gastrointestinal (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 151-1 Epidemiology of IBD. 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 (UC) 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 UC (also in 5-10% of CD pts) and antibodies to Saccharomyces cerevisiae (ASCA) in 60-70% of CD pts (also in 10-15% of UC 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), and stress. Onset of UC often follows cessation of smoking.