- Amy Lo, MD
Amy Lo, MD
- Harvard Medical School
- Young-Mee Lee, MD
Young-Mee Lee, MD
- AGA Peer Reviewer
- Adjunct Associate Professor of Medicine
- Tufts University School of Medicine
- Cambridge University Addenbrookes Hospital, Cambridge UK.
Cap polyposis is a rare condition characterized by erythematous, inflammatory colonic polyps covered by a cap of fibrinopurulent mucous. Patients usually present with mucoid diarrhea or rectal bleeding [1,2]. This topic will review the epidemiology, clinical manifestations, diagnosis, and management of cap polyposis. The approach to patient with colorectal polyps and the clinical manifestations, diagnosis, and management of other colorectal polyposis syndromes are discussed separately. (See "Clinical manifestations and diagnosis of familial adenomatous polyposis" and "Familial adenomatous polyposis: Screening and management of patients and families" and "Juvenile polyposis syndrome".)
Cap polyposis is a rare condition. The exact incidence is unknown. Cap polyposis usually occurs during the fifth decade of life; however, cases have been reported in both men and women ranging from 12 to 76 years of age [1,3,4].
ETIOLOGY AND PATHOGENESIS
The pathogenesis of cap polyposis is not well understood. Infection, mucosal ischemia, T cell-mediated inflammation, mechanical stimulation by abnormal bowel motility, and repeated trauma to the colonic mucosa caused by straining, have all been implicated in the pathogenesis.
A possible association with mucosal prolapse syndrome (MPS) has been suggested based upon similar histologic features [5-7]. It is hypothesized that in patients with cap polyposis, abnormal colonic motility may result in mucosal prolapse at redundant transverse folds, resulting in local ischemia, recurrent mucosal trauma, and the development of polyps . Cap polyposis has also been described following pelvic surgery . Persistent mechanical stimulation due to mucosal prolapse may lead to mucosal hyperplasia resulting in hypersecretion of serum proteins into the lumen and a protein-losing enteropathy .
An infectious etiology has been proposed based in part upon symptomatic and endoscopic improvement after treatment of Helicobacter pylori with antibiotics [3,9,11,12]. However, H.pylori has not been isolated within the inflammatory colonic polyps. Postulated mechanisms by which gastric H.pylori causes extra-gastric cap polyposis include molecular mimicry and the release of inflammatory mediators.
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