We read with great interest the letter by Maunoury and colleagues (Gut 2005;54:313–14). They reported on a case of cap polyposis unresponsive to infliximab, in contrast with the successful report by Bookman and colleagues.1 Maunoury et al stated that the success with infliximab reported by Bookman et al might have been due to spontaneous regression of cap polyposis. Maunoury et al speculated that a role for tumour necrosis factor α (TNF-α) in the pathogenesis of this rare disorder was unacceptable and other mechanism, such as abnormal colonic motility, may be important.
The pathogenesis of cap polyposis has been controversial. In particular, there have been discussions about whether cap polyposis is a specific form of inflammatory disorder or part of a spectrum of “mucosal prolapse syndrome” which is caused by abnormal colonic motility with subsequent local ischaemia and repeated mucosal trauma. We recently experienced a case of cap polyposis, highly suggestive of a role of inflammation in the progression of this disease.2
A 76 year old Japanese woman was diagnosed as having cap polyposis, with typical colonoscopic findings of multiple sessile polyps covered with caps of fibrinopurulent exudates throughout the total colon. Histological findings were also compatible with the disease. She had no history of straining during defecation, and an anorectal motility study was normal. Concomitantly, she had a 5 cm villous adenoma in the sigmoid colon, and underwent laparoscopic sigmoid colectomy for resection of the adenoma. Follow up colonoscopy three months after surgery revealed almost complete spontaneous remission of the cap polyposis throughout the residual colon, except along the anastomotic line where there was confined progression of multiple polyps (fig 1 ). Although the polyps were located in a line on the anastomosis, the adjacent mucosa was normal. She showed no clinical symptoms at that point and so no additional treatment was performed.
Two cases of recurrent cap polyposis after colorectal resection have been reported previously,3,4 of which one was very similar to the present case in that the recurrent polyps were located only along the anastomotic line.4 The process of wound healing on the anastomosis is known to involve a complex network of numerous inflammatory cells and their secretory products, including TNF-α, which accelerates the wound healing process by inducing angiogenesis, fibroblast proliferation, and production of several growth factors.5–7 Therefore, progression of cap polyposis confined along the anastomotic line observed both in the present case and in the report mentioned previously4 may provide evidence that local inflammation plays, at least in part, a role in the progression of cap polyposis. With acceptance on this point, suppression of inflammation could be a clue to treat cap polyposis, as in the case of metronidazole whose anti-inflammatory action plays a central role in the healing of cap polyposis.8