Polypoid mucosal prolapse complicating low rectal adenomas: Beware the inflammatory cloacogenic polyp!
Department of Histopathology, Gloucestershire Royal Hospital, Great Western Road, Gloucester, UK. Histopathology
(Impact Factor: 3.45).
08/2008; 53(1):91-6. DOI: 10.1111/j.1365-2559.2008.03035.x
Polypoid mucosal prolapse near the anorectal junction mimics adenomas endoscopically and histopathologically. The aim was to describe the phenomenon of polypoid mucosal prolapse arising secondary to adenomas at the anorectal junction.
Four cases of low rectal adenoma with polypoid mucosal prolapse were assessed histopathologically, as well as with p53 and Ki67 antibodies. Two were male and two female; the mean age was 45 years. Available follow-up has revealed no recurrence in any patient. All cases showed mucosal expansion with ulceration or erosion, crypt architectural irregularity, fibromuscular proliferation between crypts and variable epithelial serration and inflammation. Each case also showed unequivocal dysplasia, often co-mingled with features of prolapse, highlighted by p53 and Ki67 immunohistochemistry, which demonstrated positivity within dysplastic areas.
Histopathologists must recognize the potential for adenomatous/dysplastic foci in anorectal lesions to superficially resemble inflammatory cloacogenic polyps. We recommend use of immunomarkers p53 and Ki67 to aid the interpretation of challenging cases. We believe that polypoid mucosal prolapse changes can be a secondary phenomenon, due to adenomas close to or at the anorectal junction.
Available from: Alexandros G Georgakilas
- "Mucosal prolapse accompanies 50% of reported ICP cases (Levey et al. 1994) and therefore it has been proposed that ICPs is due to mucosal prolapse (Levey et al. 1994; Saul 1987; Du Boulay et al. 1983). ICPs may mimic adenomas and even adenocarcinomas, both endoscopically and histologically (Parfitt & Shepherd 2008). There are reports of squamous cell carcinoma in situ arising in ICPs (Saul 1987; Hanson & Armstrong 1999; Jaworski et al. 1969) and in some of these cases HPV type 16 was demonstrated in the areas of squamous carcinoma in situ in the polyps by polymerase chain reaction (PCR) (Jaworski et al. 1969). "
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ABSTRACT: Background: We report two rare cases of inflammatorycloacogenic polyps of the anorectum. The first case involves a 50year old white female who presented with chronic diarrhea,prolapse, and rectal bleeding. The second case presents a 67 year oldwhite male who presented with hemorrhoids and rectal bleeding. Itis hypothesized that correction of prolapse will resolve thepathologic changes. In these two patients, at one year follow-up,there has been gradual resolution of pathologic changes followingresection of lesions and correction of prolapse with stapledtechnique.Investigation: Physical examination, colonoscopy, andhemorrhoidectomy with correction of prolapseDiagnosis: The pathologic findings of these lesions are presented.A review of the literature in relation to this colonic lesion ispresented.Management: Inflammatory cloacogenic polyps (ICPs) are benignlesions arising from the transitional zone of the anorectal junctionand may macroscopically resemble anorectal malignancies. ICPsare being recognized lately with increasing frequency and treatmentoptions are similar as to those for other submucosal lesions of thecolon and may include conservative therapy, and endoscopicresection for small lesions. Surgical resection for larger lesions canbe used as treatment if there is a threat of obstruction, a question ofunderlying malignancy, or if they are prolapsed induced. Surgery isthe most common path for treatment. Surveillance is necessary withpatients that show severely dysplasic ICPs since they have beenassociated with anal neoplasias as well as squamous cellcarcinomas. It is hypothesized that correction of the prolapse willresolve the pathologic changes.
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ABSTRACT: The differential diagnosis of rectal serrated polyps is challenging due to its unique anatomic location, the evolving concept of serrated polyps over the past several years, and to histologic changes seen in rectal mucosal prolapse. We reclassified 95 rectal polyps diagnosed originally as "sessile serrated adenoma" (SSA), "serrated polyp," or "hyperplastic polyp (HP) with features of SSA" in a 5-year period based on World Health Organization classification criteria for colorectal serrated polyps. BRAF (V600E) mutation assay was performed to explore its value in the differential diagnosis for serrated polyps. Twenty-six originally diagnosed SSAs were reclassified as SSA (15/26, 57.7%), HP with mucosal prolapse (HP-P; 7/26, 26.9%), and HP (4/26, 15.4%). Fifty-two polyps originally diagnosed "HP with features of SSA" were reclassified as HP-P (24/52, 46.2%), HP (10/52, 19.2%), inflammatory-type polyp (5/52, 9.6%), and serrated polyp unclassifiable (13/52, 25.0%). Thirty-one of the 78 originally diagnosed SSA or HP with features of SSA were reclassified as HP-P, which accounted for 32.6% of the rectal polyps in this study. Mucosal prolapse along with chronic inflammation and tissue embedding artifact were the most common features that led to misdiagnosis in rectal serrated polyps. BRAF mutation was identified in 8 of 11 HP, 4 of 4 SSA, and 8 of 11 unclassifiable serrated polyp of the rectum, and was absent in control tissue. Thus, histopathologic changes suggesting prolapsed rectal mucosa should take precedence over BRAF results.
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