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Cap polyposis is a rare condition that predominantly affects the rectosigmoid with distinctive clinicopathological features. The common symptoms are mucoid and bloody diarrhoea with abdominal pain and tenesmus. At endoscopy, polyps are red, sessile, and located at the apices of enlarged transverse mucosal folds with a normal intervening mucosa. Microscopic features include elongated hyperplastic looking glands with a mixed inflammatory infiltrate in the lamina propria. A cap of fibrinopurulent exudate covers the polyps. Treatment of this condition remains empiric. Metronidazole and steroids have been effective in some cases. Symptoms are often relieved by polypectomy but rectosigmoid resection may be required to control diarrhoea.
Some years ago, we reported in Gut on a 52 year old woman who needed sigmoid resection for cap polyposis.1 Following surgery, she did well until 1998 when she again complained of abundant mucoid diarrhoea with severe postprandial abdominal pain requiring daily antispasmodic therapy. Endoscopy with histology displayed the characteristic features of recurrent cap polyposis in the rectum (fig 1). This was again refractory to multiple therapies, including several courses of mesalamine, antibiotics, steroids, and laser photocoagulation of polyps. At that time, we were aware of a case of cap polyposis that was successfully treated with infliximab.2 This was a 36 year old woman who had a one year history of cap polyposis and who experienced complete clinical, endoscopic, and histological remission following four infliximab infusions at eight week intervals. This encouraging observation led us to treat our patient with infliximab. Two infusions of infliximab 5 mg/kg were administered at four week intervals. In order to gain some insight regarding the potential involvement of tumour necrosis factor α (TNF-α) in this condition, TNF-α mRNA was measured in the rectal mucosa using real time polymerase chain reaction before and after treatment, and compared with control values. Unfortunately, no clinical or endoscopic improvement occurred following infliximab infusions. TNF-α levels in the mucosa were not different compared with controls before and after treatment.
The reason for the discrepancy between this failure and the spectacular improvement observed by Bookman and colleagues2 is unclear. Our patient suffered from this condition for more than 10 years and may have had a more refractory form of the disease. One should also remember that in the case described by Bookman and colleagues, no control was available and spontaneous regression of cap polyposis has already been observed.3,4 The pathogenesis of cap polyposis remains unclear. Our data do not support the hypothesis that TNF-α plays a role in the pathogenesis of cap polyposis. An infectious or ischaemic aetiology has been suspected. Histological features similar to cap polyposis have been described in other disorders where mucosal prolapse is the underlying mechanism such as solitary rectal ulcer syndrome or prolapsed colostomies.5 It has therefore been suggested that abnormal colonic motility may be an important aetiological factor.
Conflict of interest: None declared.
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