Korean J Gastroenterol.  2011 Jun;57(6):374-378. 10.4166/kjg.2011.57.6.374.

Left-sided Ulcerative Colitis Reactivated and Aggravated during Clostridium difficile Infection

• Na DK
• Kim JB
• Shin YC
• Shin SL
• Kim HJ
• Baek IH
• Park SH
• Lee MS

• KMID: 1792803
• DOI: http://doi.org/10.4166/kjg.2011.57.6.374

Abstract

Clostridium difficile (C. difficile) infection appears to be closely related to reactivation, diagnostic delay, and disease progression in patients with inflammatory bowel disease. However, whether C. difficile infection triggers the reactivation of inflammatory bowel disease or vice versa is not certain. We report a case of reactivated and progressed left ulcerative colitis following C. difficile infection in a 56-year-old woman. A series of endoscopic findings in this case report strongly supports a causative role of C. difficile infection on the reactivation and progression of ulcerative colitis.

Keyword

Clostridium difficile; Ulcerative colitis; Pseudomembranous colitis

Figure

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  Fig. 1. Initial colonoscopic and pathologic findings. Typical findings suggestive of ulcerative proctitis were noted on the rectal mucosa, while numerous yellowish plaques were scattered proximally starting from the sigmoid colon to cecal base. Well-demarcated active ulceration was noted at upper rectum. In the lower rectum, nonspecific colitis with chronic and acute inflammatory cells in lamina propria was noted. There was no architectural distortion (H&E,×200).

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  Fig. 2. Colonoscopic findings 10 days after oral vancomycin administration. The rectal and proximal mucosal lesions were nearly normalized except for a healing ulcerative lesion at the upper rectum.

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  Fig. 3. Colonoscopic findings 20 days after the cessation of oral vancomycin. Diffuse mucosal erosions, loss of vascularity, and mucosal granularity were noted in a continuous fashion from the lower rectum to distal transverse colon. Abrupt transition to normal mucosa was also noted at the distal transverse colon, suggesting of left-sided ulcerative colitis. Ulcer was still present at the upper rectum. No pseudomembrane was observed. In sigmoid colon, the lamina propria contained a dense infiltrate of pro-minent neutrophils, plasma cells and lymphocytes. The epithelium appear-ed mucin depleted however, histolo-gic feature of active colitis including cryptitis or crypt abscess was not present (H&E, ×200).

Reference

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