Ulcerative colitis is one of the 2 major types of inflammatory bowel disease (IBD), along with Crohn disease. Unlike Crohn disease, which can affect any part of the gastrointestinal tract, ulcerative colitis characteristically involves the large bowel (see the images below).
Ulcerative colitis as visualized with a colonoscope.
Single-contrast enema study in a patient with total colitis shows mucosal ulcers with a variety of shapes, including collar-button ulcers, in which undermining of the ulcers occurs, and double-tracking ulcers, in which the ulcers are longitudinally orientated.
The exact etiology of ulcerative colitis is unknown, but the disease appears to be multifactorial and polygenic. Proposed causes include environmental factors, immune dysfunction, and a likely genetic predisposition. Some have suggested that children of below-average birth weight who are born to mothers with ulcerative colitis have a greater risk of developing the disease. (See Etiology.)
Histocompatibility human leukocyte antigen (HLA)–B27 is identified in most patients with ulcerative colitis, although this finding is not causally associated with the condition and the finding of HLA-B27 does not imply a substantially increased risk for ulcerative colitis. Ulcerative colitis might also be influenced by diet, although diet is thought to play a secondary role. Food or bacterial antigens might exert an effect on the already damaged mucosal lining, which has increased permeability.
Ulcerative colitis is a lifelong illness that has a profound emotional and social impact on affected patients.
Grossly, the colonic mucosa appears hyperemic, with loss of the normal vascular pattern. The mucosa is granular and friable. Frequently, broad-based ulcerations cause islands of normal mucosa to appear polypoid, leading to the term pseudopolyp (see the image below).
Inflamed colonic mucosa demonstrating pseudopolyps.
The bowel wall is thin or of normal thickness, but edema, the accumulation of fat, and hypertrophy of the muscle layer may give the impression of a thickened bowel wall. The disease is largely confined to the mucosa and, to a lesser extent, the submucosa. Muscle-layer and serosal involvement is very rare; such involvement is seen in patients with severe disease, particularly toxic dilatation, and reflects a secondary effect of the severe disease rather than primary ulcerative colitis pathogenesis. Early disease manifests as hemorrhagic inflammation with loss of the normal vascular pattern; petechial hemorrhages; and bleeding. Edema is present, and large areas become denuded of mucosa. Undermining of the mucosa leads to the formation of crypt abscesses, which are the hallmark of the disease. (See Clinical Presentation.)
The diagnosis of ulcerative colitis is best made with endoscopy and mucosal biopsy for histopathology. Laboratory studies are helpful to exclude other diagnoses and assess the patient's nutritional status, but serologic markers can assist in the diagnosis of inflammatory bowel disease. Radiographic imaging has an important role in the workup of patients with suspected inflammatory bowel disease and in the differentiation of ulcerative colitis from Crohn disease by demonstrating fistulae or the presence of substantial coexisting more proximal small bowel disease in a patient who turns out to actually have Crohn disease. (See Workup.)
The initial treatment for ulcerative colitis includes corticosteroids, anti-inflammatory agents, antidiarrheal agents, and rehydration (see Medication ). Surgery is considered if medical treatment fails or if a surgical emergency develops.
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