Jay Pravda
New onset ulcerative colitis appearing with or soon after an associated comorbidity represents a unique opportunity to analyze and identify the events that may have triggered the colonic inflammation. The characteristic colonic mucosal inflammatory manifestations observed in ulcerative colitis lends itself to a common pathway analysis within the pathophysiology of associated comorbid triggering conditions. Under these unique circumstances the pathophysiology of one disease becomes the pathogenesis of another, in this case ulcerative colitis. Since the pathophysiology of the triggering comorbidity is usually known, all that remains is to identify a common pathophysiological event in each of the triggering comorbidities that can serve as a common pathway in the pathogenesis of ulcerative colitis (triggered condition). For this common pathway analysis six case reports have been chosen from the literature in which new onset ulcerative colitis is associated with a comorbid condition that is presumed to have triggered the inflammatory bowel disease, with the aim of identifying the common pathway leading to ulcerative colitis. The results suggest a pathogenesis in which an oxidative stress pathway culminates in the production of excess hydrogen peroxide within colonic epithelial cells. Hydrogen peroxide is a toxic by-product of normal metabolism that can initiate mucosal inflammation after diffusing out of colonic epithelial cells.
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