Clinical features, diagnosis, and treatment of colorectal cap polyposis

Abstract

BACKGROUND

Cap polyposis (CP) is a rare benign colorectal disorder characterized by polyps capped with fibrinopurulent exudate and is frequently misdiagnosed as inflammatory bowel disease because of overlapping clinical and histological features. No consensus exists regarding optimal management strategies. The aim of this study was to establish a standardized stepwise management algorithm for CP based on lesion distribution, number, size, and symptom severity, with the hypothesis that such an approach will optimize therapeutic outcomes while minimizing unnecessary interventions.

AIM

To clarify the clinical features, endoscopic findings, treatments and short-term outcomes of colorectal CP and provide clinical information for the diagnosis and treatment of this rare disease.

METHODS

We retrospectively collected data from seven consecutive patients with histologically confirmed CP who were treated at our center between January 2022 and January 2025.

RESULTS

The cohort comprised six males and one female (median age 36 years). Hematochezia was the main symptom (n = 3), and two patients had hypoalbuminemia. Five patients had solitary lesions and two patients had multiple lesions. All the polyps had a characteristic “cap-like” appearance with white fibrinous exudate covering the surface. Histology revealed elongated, dilated crypts and mucosal hyperplasia covered by granulation tissue. One patient with small, asymptomatic lesions was kept under surveillance. Three patients underwent endoscopic mucosal resection, and three underwent transanal excision. Symptoms resolved in all treated patients. During a median follow-up of 18 months (range 10-30 m), no recurrence was detected.

CONCLUSION

In this small series, CP affected mainly males and resulted in rectal bleeding. Both endoscopic and transanal resection relieved symptoms, but larger studies with longer follow-up periods are needed to confirm long-term efficacy.

Key Words: Cap polyposis; Endoscopic resection; Transanal excision; Treatment; Stepwise management

Core Tip: Cap polyposis is a rare inflammatory colorectal disorder characterized by fibrinopurulent-capped polyps. Clinicians frequently misdiagnose it as inflammatory bowel disease. This study retrospectively analyzed seven patients and established a stepwise management algorithm based on lesion distribution, size, and symptoms. Endoscopic or transanal resection achieved sustained symptomatic relief in all treated patients. Protein-losing enteropathy resolved rapidly after definitive surgical intervention.

INTRODUCTION

Cap polyposis (CP) is a rare condition characterized by benign, inflammatory polypoid lesions[1]. The lesions most commonly involve the rectum and sigmoid colon[1]. Polypoid masses are covered by a fibrinopurulent exudate that forms a pathognomonic “cap”[2,3]. Histology shows elongated crypts, mucosal hyperplasia, and inflammatory infiltrates. These features can resemble those of inflammatory bowel disease and make histopathological distinction difficult[4,5]. Patients frequently report hematochezia, mucous discharge, abdominal pain, anemia, or hypoalbuminemia. All of these symptoms impair the quality of life[6-9]. The etiology remains unclear. The proposed mechanisms include mucosal prolapse related to abnormal motility, chronic Helicobacter pylori (H. pylori) infection, and local immune dysregulation with elevated TNF-α expression[10-13]. Management is equally unsettled. Case reports and small series have documented H. pylori eradication, endoscopic resection, transanal excision, segmental colectomy and sporadic use of biological agents. No consensus protocol exists[14,15]. Large systematic studies are lacking. Therefore, we analyzed our institutional cohort to describe the clinical presentation, endoscopic findings, treatment modalities, and short-term outcomes of CP and to outline a practical framework that could guide future standardized care.

MATERIALS AND METHODS

Study sample

We enrolled seven consecutive patients who received a histological diagnosis of colorectal CP at Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, between January 2022 and January 2025. Histopathological diagnosis of CP required consensus by two independent gastrointestinal pathologists. Discrepant cases underwent a third review. Ethics approval was obtained from the Ethics Committee of Sir Run Run Shaw Hospital, Zhejiang University School of Medicine (Approval No. 2024-0669), and all patients provided written informed consent.

Data collection

We recorded demographic information, symptom duration, laboratory results, colonoscopy findings, histopathology, treatment modalities and follow-up data.

RESULTS

Clinical characteristics

Among the 7 patients, 6 were male and 1 was female, with a male-to-female ratio of 6: 1. Patient ages ranged from 16 to 71 years (median: 36 years). Disease duration varied from 2 weeks to 5 years, and 5 patients had symptoms for more than 1 year (Table 1).

Table 1 Clinical features of 7 patients with cap polyposis.

No.	Age (year)	Gender	Symptoms	Lesion site	H. pylori	Hb (g/L)	Alb (g/L)	Treatment	Follow up
1	56	Female	Hematochezia	Rectum	NA	123	46.4	TAMIS	No recurrence
2	36	Male	Constipation	Rectum	Negative	143	41.9	Observation	No increase in size
3	61	Male	Abdominal distension	Transverse colon	Negative	152	46.1	EMR	No recurrence
4	17	Male	Hematochezia; prolapse; mucous discharge	Rectum	NA	146	31	Oral antibiotics, TAMIS	No recurrence
5	71	Male	Hematochezia	Rectum	Negative	142	21	EMR	No recurrence
6	62	Male	Abdominal distension	Sigmoid colon	Negative	157	41.9	EMR	No recurrence
7	20	Male	Prolapse	Rectum	NA	159	49	Transanal excision	No recurrence

H. pylori: Helicobacter pylori; Hb: Hemoglobin; Alb: Albumin; TAMIS: Transanal minimally invasive surgery; EMR: Endoscopic mucosal resection; NA: Not available.

Clinical manifestations

Hematochezia occurred in three patients, anal prolapse in two, abdominal distension in two, constipation in one, and mucous discharge in one. Two patients had hypoalbuminemia (< 35 g/L). H. pylori was not detected in our patients.

Endoscopic findings

The lesion distribution was as follows: Rectum in 5 patients, sigmoid colon in 1 patient, and transverse colon in 1 patient. Five patients had a solitary polyp, and two had multiple polyps (one with dozens). The polyps were broad-based, measured 0.8-3.0 cm, and were covered by white-yellow fibrinous exudate. The mucosa between polyps appeared normal (Figure 1).

Figure 1 Typical endoscopic features of cap polyposis. All polyps had a characteristic “cap-like” appearance with white fibrinous exudate covering the surface.

Pathological features

Microscopic examination revealed polypoid tissue with mucosal proliferation and irregularly dilated and elongated crypts with serpentine changes. The mucosal surface was covered by a “cap” composed of ulcerated and inflamed granulation tissue, fibrin, and inflammatory exudate. The mucosal layer was almost completely replaced by granulation tissue with extensive inflammatory necrosis. Biopsies from adjacent flat mucosa were normal, distinguishing CP from inflammatory bowel disease (Figure 2).

Figure 2 Characteristic histopathological features of cap polyposis. A-C: Hematoxylin and eosin staining. Erosive mucosal surface covered by thick inflammatory granulation tissue (pseudomembrane) with architectural disarray and prominent cystic dilation of crypts (A). Dense mixed inflammatory cell infiltration within the lamina propria (B). Elongated, dilated, and distorted crypts with a preserved glandular architecture and an absence of significant cytological atypia (C); D: Periodic acid-Schiff reaction. Periodic acid-Schiff reaction highlighting the fibrin-rich pseudomembrane overlying the mucosa.

Treatment and outcomes

Among the 7 patients, 1 who had small lesions with minimal symptoms was kept under observation. Three patients underwent endoscopic mucosal resection. Three patients underwent transanal excision [one via transanal minimally invasive surgery (TAMIS) and two via the conventional approach]. Clinical symptoms improved markedly in every patient compared with their pretreatment status, and no recurrence was detected during follow-up.

Typical case

We report a clinically instructive case of CP in a 17-year-old male (body mass index = 19.0 kg/m²) who presented on January 29, 2024, with a self-detected perianal protruding mass and intermittent bright red bleeding. Systemic symptoms (abdominal pain, diarrhea, constipation, fever, weight loss) and warning signs (melena, tenesmus) were absent. Digital rectal examination revealed multiple rectal polypoid lesions. The initial workup comprised a contrast-enhanced computed tomography demonstrating a 47-mm intraluminal rectal mass with marked enhancement but intact serosa; magnetic resonance defecography, anorectal manometry, and colonic transit studies confirming no structural or functional anorectal disorder; and colonoscopy identifying scattered polypoid elevations from the anal verge to 6 cm proximal. Initial biopsies revealed chronic active inflammation with granulation tissue and fibrinopurulent exudates—findings frequently misinterpreted as nonspecific proctitis or mucosal prolapse-related changes, a well-documented diagnostic pitfall in CP where superficial sampling fails to capture the characteristic “cap” architecture. The serum albumin concentration was 41.2 g/L, whereas tumor marker levels were normal. A provisional diagnosis of rectal mucosal prolapse was made, and conservative therapy (scheduled defecation training, mesalazine suppositories, probiotics, lactulose) was initiated.

At the 6-month follow-up, symptoms persisted with new-onset mucoid discharge and declining nutritional status (serum albumin concentration: 31 g/L), indicating therapeutic failure. Given the progressive clinical deterioration and inconclusive initial histology, transanal endoscopic microsurgery was performed (Figure 3). Intraoperatively, dozens of polypoid lesions (0.2-1.5 cm) densely carpeted the rectal wall 6 cm from the anal verge. Histopathological examination of en bloc resected specimens confirmed CP: Multiple polyps capped by fibrinopurulent exudate (“cap”), surface erosion, granulation tissue, and chronic inflammatory infiltrate in the lamina propria. Critically, marked crypt dilation with abundant intraluminal mucus retention, prominent goblet cell hyperplasia and extracellular mucus pooling within crypt lumens and superficial lamina propria were identified—distinct from the nonspecific changes seen in initial biopsies (Figure 4). Postoperatively, symptoms resolved completely, and serum albumin levels normalized within 4 weeks. Surveillance colonoscopy at 12 months revealed no residual or recurrent lesions. The patient remains asymptomatic under ongoing endoscopic surveillance.

Figure 3 Endoscopy revealed multiple polyps in the lower rectum of the patient, all of which were covered with fibrinopurulent exudate. Dozens of cap polyps were resected by transanal surgery. No recurrence of cap polyps was observed on follow-up colonoscopy.

Figure 4 Histopathological changes in patient 4 with hypoalbuminemia. A-C: Hematoxylin and eosin staining. Crypts markedly dilated by abundant intraluminal mucus retention (A). Goblet cell hyperplasia with prominent intracellular mucin vacuoles (B). Extracellular mucus pooling within crypt lumens and superficial lamina propria (star; C); D: Periodic acid-Schiff reaction. Periodic acid-Schiff reaction confirming glycoprotein-rich mucus accumulation (intracellular and extracellular).

DISCUSSION

CP is a rare clinicopathological entity, with fewer than 200 cases reported globally. Its true prevalence remains undefined because of frequent misdiagnosis as inflammatory bowel disease, mucosal prolapse, or infectious colitis—particularly in patients who present with rectal bleeding or mucoid discharge. Clinicians should include CP in the differential diagnosis of unexplained protein-losing enteropathy (PLE) and exudative enteropathies, especially when rectosigmoid polyposis coexists with hypoalbuminemia. As exemplified by patient 4’s diagnostic journey, superficial biopsies often reveal only nonspecific inflammation or granulation tissue and miss the pathognomonic surface pseudo membrane; a definitive diagnosis frequently requires full-thickness resection specimens.

Current evidence indicates that CP is a benign reactive condition. No cases of dysplasia or malignant transformation have been documented. The etiology of CP remains unclear. The proposed mechanisms include mucosal prolapse, chronic infection, and local immune dysregulation. We performed histology and H. pylori stool antigen testing in four patients; all the results were negative. This contrasts with the findings of select Asian case series reporting a higher H. pylori association[9], suggesting geographical or methodological variability and implying that H. pylori was not a universal trigger for CP in our cohort.

Critically, CP can manifest as clinically significant PLE. Patient 4 (a 17-year-old male) developed hypoalbuminemia for more than six months despite receiving conservative therapy, including scheduled defecation training, mesalazine suppositories, probiotics and lactulose, with concurrent mucoid discharge. Histopathological examination of the en bloc TAMIS-resected specimen revealed marked crypt dilation with abundant intraluminal mucus retention, prominent goblet cell hyperplasia and extracellular mucus pooling. Rapid albumin normalization postresection provides compelling evidence of a causal relationship. This observation parallels that of Kreisel et al[14], who reported similar refractory mucoid symptoms, hypoalbuminemia, histologically confirmed cap-like lesions, and rapid metabolic recovery following resection. This consistent response highlights CP as a treatable cause of PLE and supports the use of persistent hypoalbuminemia as an objective indicator for definitive intervention.

With respect to medical therapy, isolated reports describe trials examining 5-aminosalicylates, corticosteroids, or immunosuppressants[15,16]; however, the evidence remains anecdotal. In our cohort, conservative management failed to resolve symptoms or correct hypoalbuminemia in patient 4, which is consistent with the literature suggesting the limited efficacy of medical therapy for patients with established CP. Therefore, we emphasize timely endoscopic or surgical intervention for symptomatic or protein-losing patients.

No consensus treatment algorithm exists. A systematic review of 57 patients revealed symptom resolution in 82% of patients after endoscopic or transanal resection at a 14-month median follow-up[13]. Our cohort achieved similar results (0/6 recurrences; median follow-up, 18 months), although a longer follow-up period is needed to confirm the long-term effectiveness.

On the basis of our data and the published literature, we propose a pragmatic stepwise strategy. We suggest that patients with rectal CP who have three or fewer polyps and a maximum polyp diameter of ≤ 2 cm should undergo endoscopic mucosal resection or endoscopic submucosal dissection. For those with larger or more numerous rectal polyps, we advise transanal local excision. When the colon is involved, we recommend endoscopic removal of the polyps in patients with three or fewer colonic polyps, each ≤ 2 cm in size. If the colon harbors multiple cap polyps and the patient experiences related symptoms such as diarrhea or hypoalbuminemia, we suggest that clinicians evaluate surgical risk and consider segmental colectomy. In contrast, for patients with multiple colonic cap polyps but no symptoms, clinical follow-up can be considered, and we advise annual colonoscopy. For all patients with confirmed CP, we recommend a colonoscopy one year after treatment; if no new or residual lesions are found, the next examination may be scheduled after two to three years[17-19]. The suggested management flow is shown in Figure 5.

Figure 5 Suggested management flow for cap polyposis patients. EMR: Endoscopic mucosal resection; ESD: Endoscopic submucosal dissection.

Our study has several limitations. The median follow-up was 18 months, which was shorter than the 3-5 years required to assess late recurrence. The single-center, retrospective design and small sample size may have introduced selection bias, potentially over-estimating the frequency of symptomatic disease requiring invasive therapy. Multicenter prospective registries with longer surveillance are necessary to define true recurrence rates and to validate the proposed management algorithm.

CONCLUSION

Colorectal CP predominantly affects young males and presents with rectal bleeding. Endoscopic or transanal resection provides sustained symptomatic relief in most cases. Annual follow-up is recommended for all patients until evidence-based surveillance protocols are established.