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Inflammatory bowel disease (IBD) is the general term used to describe a group of chronic inflammatory disorders of the gastrointestinal tract. The cause for these disorders is unknown, and they have neither pathognomonic features nor strict diagnostic tests. In the strict sense, they remain diagnoses of exclusion, however they have features that are characteristic enough to provide accurate diagnoses in most cases. There are two forms of IBD: chronic nonspecific ulcerative colitis, a mucosal inflammatory condition confined to the colon and rectum; and Crohn's disease, a transmural inflammation which may affect any part of the GI tract.
Although the exact etiology of ulcerative colitis and Crohn's disease is unknown, similar factors are believed to be responsible for each condition. The major theories of the cause for IBD involve infectious or immunologic etiologies.(1) The infectious theory assumes that the body is reacting normally to an as-yet-unrecognized pathogen, whereas the immunologic theory posits that the immune system is responding inappropriately to antigens to which most people are exposed, leading to an autoimmune reaction.(2) Some of the microorganisms suspected of being involved in the pathogenesis of IBD include viruses, protozoans, mycoplasmas, and other bacteria. Even though no definitive infectious cause has been found, the presentation is similar to some invasive pathogens, which produce toxins that cause mucosal damage. Also, bacteria elaborate peptides that have chemotactic properties and cause an influx of inflammatory cells with subsequent release of inflammatory mediators and tissue destruction. Microbes may elaborate super antigens, which are capable of global T-lymphocyte stimulation and subsequent inflammatory response.(3)
Some of the observations in support of the immunologic basis of IBD include the pathology of the lesions (infiltration with lymphocytes, mast cells, plasma cells, macrophages, and neutrophils), systemic manifestations with an immunologic etiology, and IBD is responsive to immunosuppressive drugs. Potential immunologic mechanisms may include both autoimmune and nonautoimmune factors. Ulcerative colitis is confined to the rectum and colon, and affects the mucosa and the submucosa. In some instances, a short segment of terminal ileum may be inflamed; this is referred to as backwash ileitis. Unlike Crohn's disease, the deeper longitudinal muscular layers, serosa, and regional lymph nodes are usually not involved.(4) Since inflammation is usually confined to the mucosa and submucosa, perforations, fistulas, and obstruction are uncommon.
The primary lesion of ulcerative colitis occurs in the crypts of the mucosa (crypts of Lieberkuhn) in the form of a crypt abscess. Here, frank necrosis of the epithelium occurs; it is usually only visible with microscopy but may be seen grossly when coalescence of ulcers occurs.(5) A striking feature of the inflammation is that it is uniform and continuous, with no in-between areas of normal mucosa. The rectum is involved in about 95 percent of cases. There also may be loss of crypt epithelium, with a loss of goblet cells and submucosal edema. Repetitive cycles of inflammation lead to mild submucosal fibrosis.(6) The extent of mucosal damage seen in ulcerative colitis often results in significant diarrhea and bleeding.
Complications of ulcerative colitis may be local, involving the colon or rectum, or may be systemic. In either case, complications may range from mild to life threatening. Some of the complications seen most frequently in ulcerative colitis patients include hemorrhoids, anal fissures, or perirectal abscesses. They are most likely to occur during active colitis episodes. A major complication that may occur in 1 to 3 percent of patients with ulcerative colitis or Crohn's disease is toxic megacolon. In this condition, the pa
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