Abstract
Crohn’s disease (CD) and ulcerative colitis (UC) are the two major idiopathic inflammatory bowel diseases (IBD). Because there is no pathognomonic, diagnostic feature of either UC or CD, and because of the nonspecific features of intestinal inflammation, these “classic” diagnoses probably represent a spectrum of clinicopathological entities with overlapping features, including a significant proportion of patients with colitis that is “indeterminate,” i.e., colitis with features that defy distinct categorization as UC or CD. Although the pathogenesis of IBD remains obscure, it is believed that, in genetically susceptible hosts, antigens within the intestinal lumen trigger a dysregulated mucosal immune response leading to chronic inflammation (1). Innate immune cells (macrophages, neutrophils), adaptive immune cells (T cells), and nonimmune cells (including epithelial and endothelial cells, cells of the enteric nervous system, and fibroblasts) engage in complex interactions, culminating in the elaboration of pro-inflammatory mediators that overwhelm the homeostatic defenses of the intestine and injure the intestinal epithelium (1). Moreover, the pattern of injury (location along the gastrointestinal tract, severity and penetration of injury) and reparative processes (i.e., intestinal scarring with stricture formation) influence clinical presentation, as well as prognosis and therapeutic approach (2).
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Dassopoulos, T., Hanauer, S. (2003). Presentation and Diagnosis of Inflammatory Bowel Disease. In: Cohen, R.D. (eds) Inflammatory Bowel Disease. Clinical Gastroenterology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-311-8_5
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DOI: https://doi.org/10.1007/978-1-59259-311-8_5
Publisher Name: Humana Press, Totowa, NJ
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Online ISBN: 978-1-59259-311-8
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