![]() Their patterns of histologic injury can vary, but the presence of increased intraepithelial lymphocytes or increased crypt apoptosis should suggest the possibility of drug-induced injury. Colitis can occur any time during (or even after) treatment. These include CTLA4 inhibitors (ipilimumab) and PD1 inhibitors (nivolumab, pembrolizumab). This diagnosis has become more common with the advent of checkpoint inhibitors, which can prolong the life of patients with metastatic malignancies but have several side effects. Many drugs can cause colitis mimicking inflammatory bowel disease, including nonsteroidal anti-inflammatory drugs and mycophenolate mofetil. However, the polyps in the current case clearly do not have caps of granulation tissue.ĭrug-induced colitis can mimic inflammatory bowel disease clinically and microscopically, requiring careful clinicopathologic correlation. While little is known about this condition, the symptoms are similar to UC, and limited tissue sampling via colonoscopy might suggest UC with pseudopolyposis as a possible diagnosis. The inflammatory polyps all bear a characteristic “cap” of granulation tissue at their surface. Since none of these findings are present in the current case (aside from occasional mild mural inflammation due to disease severity), the findings are more consistent with UC than CD.Ĭap polyposis is a rare form of injury-induced colonic polyposis. Other findings include aphthous ulcers and epithelioid granulomas away from areas of crypt rupture. Microscopically, CD therefore demonstrates transmural chronic inflammation, often forming prominent lymphoid aggregates. The main differences between UC and CD are that the latter can affect the entire gastrointestinal tract and can affect areas discontinuously (“skip lesions”), and the inflammation can involve the entire wall. Surgery is reserved for severe, medically refractory cases.Ĭrohn disease has a similar epidemiology to UC and may also cause inflammatory pseudopolyposis. Immunosuppressant medications are needed for some patients, such as azathioprine and infliximab. Treatment in UC begins with medications aiming to keep the inflammation in check, including anti-inflammatory medications such as sulfasalazine and mesalamine. In patients with severe UC (such as this case), there may be a hint of minor mural inflammation. In most cases, UC only damages the mucosa, with the rest of the colon unaffected. In active disease, acute inflammation is superimposed upon chronic changes it may be mild (cryptitis), moderate (crypt abscesses), or severe (mucosal ulceration). Mucosal changes indicative of chronicity include lamina propria expansion by an increased lymphoplasmacytic infiltrate, crypt distortion, crypt branching, crypt dropout, crypt foreshortening, basal plasmacytosis, and Paneth cell metaplasia in the distal colon. UC can involve most or all of the large intestine, including the rectum, involving the entire mucosa in the affected length (ie, no “skip lesions”). Symptoms lapse and remit they include abdominal pain and bloody, mucoid diarrhea. However, patients may present in the “gap” between the peaks, including with longstanding disease not previously brought to medical attention (as in this patient). ![]() UC has a bimodal distribution, with peak onsets at approximately 15 - 30 years of age and 50 - 70 years of age. ![]() Incidence estimates are as high as 20 cases per 100,000 persons. The disease is more common in Caucasians, with roughly equal prevalence in men and women. Ulcerative colitis (UC) is one of two forms of inflammatory bowel disease, the other being Crohn disease (CD, aka regional enteritis). Overall, the findings are most consistent with ulcerative colitis with extensive pseudopolyposis. Small granulomas, when present, appear to represent a response to ruptured crypts. For the most part, however, the disease is relegated to the mucosa and submucosa. The inflammation extends into the submucosa and very focally into the muscularis propria and beyond. Sections show a segment of colon with numerous polyps that demonstrate marked inflammation and injury, with crypt architectural distortion, crypt abscesses, and expanded lamina propria.
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