title: Colonic metaplasia in the ileal pouch is associated with inflammation and is not the result of long-term adaptation.
abstract: Ileal pouch-anal anastomosis (IPAA) is the preferred surgical therapy for chronic ulcerative colitis (CUC) and familial adenomatous polyposis (FAP). Previous studies have demonstrated morphologic changes in pouch mucosa such as villous atrophy and crypt hyperplasia. These changes have been labeled "colonic metaplasia." The aims of this study were to determine whether these changes represent "normal" long-term adaptation of the nondiseased pouch or instead are present only in the setting of inflammation. Twenty-four patients were identified, greater than 5 years status post-IPAA for CUC, who underwent pouchoscopy for surveillance and had no history of pouchitis. Thirty-one patients were identified greater than 5 years status post-IPAA for CUC, who had a history of pouchitis and had undergone pouchoscopy at least 5 years status post-IPAA. Eight patients status post-IPAA for FAP were also identified. Biopsy specimens were reevaluated by a single, blinded pathologist for degree of inflammation, the presence of villous atrophy and crypt hyperplasia, and evidence of dysplasia. Among the patients with CUC, the inflammation score was greater in the pouchitis group, 13.2 +/- 1.2, compared to the nonpouchitis group, 4.0 +/- 0.5 (P < 0.0001). Median colonic metaplasia score was greater in the pouchitis group (4 [range 2 to 6]) vs. 2 (9 [range 0 to 6]; P < 0.0001). The colonic metaplasia score correlated with the inflammation score (Spearman coefficient r = 0.83; P < 0.0001). In the eight patients with FAP, the inflammation score was 5.1 +/- 0.9 and the median colonic metaplasia score was 1 (range 0 to 4). There was no evidence of dysplasia in any of the biopsy specimens. Patients without a history of pouchitis or symptoms of pouchitis have only a minimal degree of villous atrophy and crypt hyperplasia. These morphologic changes in the ileal pouch are found primarily in the setting of inflammation, and likely represent a reparative response.
authors.affiliation: Department of Surgery, Boston University School of Medicine, 88 East Newton Street, Boston, MA 02118, USA.
authors.forename: A Brent
authors.initials: AB
authors.lastname: Fruin
authors.forename: Ola
authors.initials: O
authors.lastname: El-Zammer
authors.forename: Arthur F
authors.initials: AF
authors.lastname: Stucchi
authors.forename: Michael
authors.initials: M
authors.lastname: O'Brien
authors.forename: James M
authors.initials: JM
authors.lastname: Becker
mesh_terms: D000222:Adaptation, Physiological; D011125:Adenomatous Polyposis Coli / Q000601:surgery; D001707:Biopsy, Needle; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D003082:Colectomy / Q000379:methods; D003093:Colitis, Ulcerative / Q000601:surgery; D003106:Colon / Q000473:pathology*; D039021:Colonic Pouches / Q000473:pathology*; D003113:Colonoscopy; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007150:Immunohistochemistry; D007413:Intestinal Mucosa / Q000473:pathology; D008297:Male; D008679:Metaplasia / Q000209:etiology; D019449:Pouchitis / Q000150:complications* / Q000473:pathology; D011336:Probability; D016737:Proctocolectomy, Restorative / Q000009:adverse effects* / Q000379:methods; D012189:Retrospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric