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Cap polyposis

Cap polyposis
Literature review current through: Jan 2024.
This topic last updated: Jun 05, 2023.

INTRODUCTION — 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".)

EPIDEMIOLOGY — 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 males and females ranging from 11 months to 76 years of age [1,3-6].

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 [7-9]. 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 [10]. Cap polyposis has also been described following pelvic surgery [11]. 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 [12,13].

An infectious etiology has been proposed based in part upon symptomatic and endoscopic improvement after treatment of Helicobacter pylori with antibiotics [3,11,14,15]. 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. The role of altered intestinal microbiome (dysbiosis) has also been suggested in pathogenesis of cap polyposis. In one case study, antibiotic treatment lead to regression of cap polyposis through significant alterations in fecal microbiota composition [16].

CLINICAL FEATURES

Clinical manifestations — Patients with cap polyposis may be asymptomatic [17]. Symptomatic patients usually present with rectal bleeding (82 percent) and mucoid diarrhea (46 percent). Symptoms may be present for weeks to months prior to the diagnosis [18]. Other clinical manifestations include abdominal pain, tenesmus, weight loss, and constipation [10]. In rare cases, patients have mild peripheral edema due to protein-losing enteropathy. (See 'Etiology and pathogenesis' above and "Protein-losing gastroenteropathy", section on 'Clinical features'.)

Laboratory findings — Laboratory studies including markers of inflammation (eg, C-reactive protein) are typically normal [3]. However, in rare cases patients may have hypoproteinemia due to protein-losing enteropathy and iron deficiency anemia due to rectal bleeding. (See "Protein-losing gastroenteropathy", section on 'Laboratory studies'.)

DIAGNOSIS — The diagnosis of cap polyposis is often made incidentally during endoscopic evaluation of the colon for symptoms of hematochezia or diarrhea. The diagnosis should be suspected in patients with erythematous colonic polyps with an adherent mucoid cap and is established by biopsy.

Endoscopy — Polyps in patients with cap polyposis are typically located in the rectosigmoid colon, but can occur elsewhere in the colon [17,19]. They range in size from a few millimeters to two centimeters and in numbers from one to over a hundred. Polyps may be sessile or pedunculated and are usually located at the apices of enlarged transverse mucosal folds [1]. Cap polyps typically have an erythematous surface and an adherent white mucoid cap (picture 1 and picture 2A-C) [3,20]. There may be associated central pitting. Magnification colonoscopy shows a mixture of round crypts in the depressed center with long branching crypts in the surrounding elevated areas [21]. The intervening mucosa is normal.

A mild form of cap polyposis, characterized by multiple patches of erythematous, edematous mucosa separated by normal mucosa, has been described [3]. Whether these patients progress to the more classic form of cap polyposis is unclear.

Histology — On histologic evaluation, cap polyps are non-neoplastic lesions composed of elongated, hyperplastic-appearing glands with a mixed inflammatory infiltrate in the lamina propria and fibromuscular obliteration of the lamina propria (picture 3). There are varying degrees of surface ulceration and a characteristic overlying cap formed by an inflammatory exudate composed of mucus, fibrin, and leukocytes. In contrast with normal mucosa, the overlying mucus has a predominance of non-sulfated mucins. However, the abnormal mucins do not appear to have a direct pathologic effect and are not specific to cap polyposis but rather appear to reflect abnormally differentiated epithelium [22-27].

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of cap polyposis on endoscopy includes inflammatory pseudopolyps due to inflammatory bowel disease (eg, ulcerative colitis, Crohn disease), inflammatory polyps associated with diverticular disease, solitary rectal ulcer syndrome, colorectal adenomatous polyposis syndromes (eg, familial adenomatous polyposis, MUTYH polyposis), and juvenile polyposis syndromes (eg, familial juvenile polyposis) [28,29]. However, despite similarities in the endoscopic appearance, cap polyposis can be differentiated from these conditions by histology. (See 'Histology' above.)

MANAGEMENT — There are limited data from case reports and small retrospective series to guide the management of cap polyposis. The goal of management is to improve clinical symptoms of the disease. (See "Management of chronic constipation in adults".)

Overall approach — Asymptomatic patients do not require treatment unless symptoms develop. In symptomatic patients, we perform endoscopic polypectomy. Patients with a history of constipation should be treated with laxatives given the potential role of straining in the pathogenesis of cap polyposis. (See 'Etiology and pathogenesis' above and "Management of chronic constipation in adults", section on 'Initial management'.)

In patients with recurrent polyps after polypectomy, we test for H. pylori and treat patients with evidence of an infection with eradication therapy. We reserve surgery for patients with intractable symptoms due to polyps that are too numerous to clear endoscopically. (See "Indications and diagnostic tests for Helicobacter pylori infection in adults" and "Treatment regimens for Helicobacter pylori in adults".)

Endoscopic polypectomy — Snare polypectomy with argon plasma coagulation or endoscopic mucosal resection have been associated with complete resolution of symptoms [18,30-33]. However, polyps can recur following polypectomy, especially in patients with multiple polyps [7,18]. Repeat colonoscopy has been recommended to monitor for persistent disease and possible progression. However, there is no documented malignant potential of these polyps. The need and timing of colonoscopy should be individualized based on the adequacy of resection, number of polyps, and the presence of symptoms. (See 'Disease course' below and "Endoscopic removal of large colon polyps", section on 'Polyp removal techniques'.)

Test for and eradicate H. pylori — Small case series have reported symptomatic improvement within three months of eradication of H. pylori infection and endoscopic resolution in six to eight months [3,5,15,34]. The diagnosis and management of H. pylori are discussed in detail separately. (See "Indications and diagnostic tests for Helicobacter pylori infection in adults", section on 'Noninvasive testing' and "Treatment regimens for Helicobacter pylori in adults", section on 'Clarithromycin-based therapy'.)

Surgery — Colectomy is necessary in symptomatic patients if the multiplicity of polyps precludes endoscopic resection. Full colonoscopic evaluation should be performed just prior to surgery to determine the extent of disease. The preferred operation depends on the severity and distribution of colorectal polyps. In general, patients with a large number of cap polyps in the rectum require proctocolectomy with ileal pouch anal anastomosis. Patients with few rectal polyps can undergo less extensive surgery with a total colectomy with ileorectal anastomosis.

There are few studies that have evaluated long-term outcomes of patients undergoing surgery for cap polyposis. In one series of 11 patients, four patients undergoing anterior resection were symptom-free at a median of 48 months [18]. However, symptomatic polyposis can recur and lesions may evolve along the anastomotic line after surgery [7,8,19,35].

Other — Several other approaches have been described in case reports and small series including the use of aminosalicylates, anti-inflammatory agents (eg, topical and systemic steroids), antibiotics (eg, metronidazole), and immunomodulators (eg, infliximab) [3,10,14,35-39]. However, the evidence to support their use has been conflicting.

DISEASE COURSE — Data on the natural history of cap polyposis are limited to small case series with limited follow-up [18]. Cap polyposis may begin as a solitary pedunculated lesion. Other lesions may extend distally or proximally [40]. The lesions may also evolve along the anastomotic line after surgery [8,19]. There have been no reports of malignant transformation. Most patients have chronic recurrent symptoms requiring multiple treatment modalities, although spontaneous resolution has been reported [41]. In one series of seven patients, spontaneous remission occurred in three patients 18, 54, and 72 months after their initial diagnosis [37]. Spontaneous remission has been reported up to nine years after the initial diagnosis [42].

SUMMARY AND RECOMMENDATIONS

Cap polyposis is a rare condition characterized erythematous, inflammatory colonic polyps covered by a cap of fibrinopurulent mucous. Cap polyposis usually occurs during the fifth decade of life. (See 'Introduction' above.)

The most common presenting symptoms of cap polyposis include rectal bleeding (82 percent) and mucoid diarrhea (46 percent), which may be present for weeks to months prior to the diagnosis. Other clinical manifestations include constipation, abdominal pain, tenesmus, and weight loss. In rare cases, patients have mild peripheral edema due to protein-losing enteropathy. (See 'Clinical manifestations' above.)

Laboratory studies are usually normal. However, in rare cases patients may have hypoproteinemia due to protein-losing enteropathy or iron deficiency anemia due to rectal bleeding. (See 'Laboratory findings' above.)

The pathogenesis of cap polyposis is not well understood. Infection with Helicobacter pylori, dysbiosis of gut microbiota, 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. (See 'Etiology and pathogenesis' above.)

The diagnosis of cap polyposis is often made incidentally during colonoscopy for evaluation of symptoms of bleeding or diarrhea. The diagnosis is suspected in patients with erythematous polyps with an adherent mucoid cap on colonoscopy and is established by biopsy. (See 'Diagnosis' above.)

On histologic evaluation, cap polyps are non-neoplastic lesions composed of elongated, hyperplastic-appearing glands with a mixed inflammatory infiltrate in the lamina propria and fibromuscular obliteration of the lamina propria (picture 3). There are varying degrees of surface ulceration and a characteristic overlying cap formed by an inflammatory exudate composed of mucus, fibrin, and leukocytes. (See 'Histology' above.)

The differential diagnosis of cap polyposis includes inflammatory pseudopolyps due to inflammatory bowel disease, diverticular disease, solitary rectal ulcer syndrome, colorectal adenomatous and juvenile polyposis syndromes. Cap polyposis can be differentiated from these conditions by histology. (See 'Differential diagnosis' above.)

Optimal treatment has not been established, and thus recommendations are based mainly on clinical experience. Our approach to the management of cap polyposis is as follows:

Asymptomatic patients do not require treatment unless symptoms develop.

In symptomatic patients, we perform endoscopic polypectomy and treat patients with a history of constipation with laxatives.

In symptomatic patients with recurrent polyps after polypectomy, we test for H. pylori and treat patients with evidence of an infection with eradication therapy.

We reserve surgery for patients with intractable symptoms due to polyps that are too numerous to clear endoscopically.

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