CD infection is a common complication in immunocompromised patients, including those undergoing HSCT, with reported incidences ranging from 4% to 13%. However, there has been no previous detailed report on the clinical impact of positive CD toxin in patients after allogeneic HSCT with current supportive therapies. Therefore, we retrospectively reviewed the medical records of 422 patients who underwent allogeneic HSCT with a variety of preparative regimens at National Cancer Center Hospital from January 2000 to April 2004. CD toxin in stool samples was measured by the Latex particle agglutination method, and selected patients were examined further by endoscopy. Positive results with CD toxin were observed at least once in 51 patients, at a median time of 40 days (range, −1 to 212 days) following allogeneic HSCT. Most patients had severe watery diarrhea, along with other symptoms including fever, nausea, anorexia and abdominal cramping, which mimics pseudomembrane colitis. Twenty-seven of the 51 patients (53%) underwent endoscopic examination, and macroscopic findings were as follows; normal in 4 (15%), extensive edema in 11 (41%), and mucosal sloughing in 12 (44%), while none had pseudomembrane formation. Histological diagnosis revealed that 26 cases (96%) were compatible with GVHD, including 2 complicated with Cytomegalovirus colitis. Thirty-three patients (65%) were treated with oral vancomycin for a median of 14 days (2 to 46 days), while the remaining 18 were followed conservatively without any specific medication. Forty-four patients were evaluable for follow-up, and, regardless of management, all subsequently became negative for CD toxin. These findings suggest that positive CD toxin in the stool detected during the course of allogeneic HSCT may only reflect nonsignificant colonization or proliferation of CD in the gut, and hence may not necessarily imply clinically relevant pseudomembranous colitis which would require intense medical treatment. Additionally, in patients undergoing allogeneic HSCT, signs and symptoms of intestinal involvement may simply reflect concomitant GVHD per se or a pathology closely related to GVHD.

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