Pathogenesis of and unifying hypothesis for idiopathic pouchitis.
Coffey, J Calvin Rowan, Fiachra Burke, John Dochery, Neil G Kirwan, William O O'Connell, P Ronan
Coffey, J Calvin
Rowan, Fiachra
Burke, John
Dochery, Neil G
Kirwan, William O
O'Connell, P Ronan
Advisors
Editors
Other Contributors
Date
2012-02-01T10:29:47Z
Date Submitted
Keywords
Other Subjects
Subject Mesh
Anal Canal/microbiology/pathology/surgery
Anastomosis, Surgical/methods
Anti-Bacterial Agents/therapeutic use
Bacteria/*growth & development
Colitis, Ulcerative/surgery
Colonic Pouches/microbiology/pathology
Diagnosis, Differential
Humans
Intestinal Mucosa/microbiology/*pathology
Metaplasia/pathology
Postoperative Complications
*Pouchitis/diagnosis/drug therapy/etiology
Anastomosis, Surgical/methods
Anti-Bacterial Agents/therapeutic use
Bacteria/*growth & development
Colitis, Ulcerative/surgery
Colonic Pouches/microbiology/pathology
Diagnosis, Differential
Humans
Intestinal Mucosa/microbiology/*pathology
Metaplasia/pathology
Postoperative Complications
*Pouchitis/diagnosis/drug therapy/etiology
Planned Date
Start Date
Collaborators
Principal Investigators
Alternative Titles
Publisher
Abstract
Ileal pouch-anal anastomosis is the procedure of choice in the surgical management of refractory ulcerative colitis. Pouchitis affects up to 60% of patients following ileal pouch-anal anastomosis for ulcerative colitis. It overlaps significantly with ulcerative colitis such that improvements in our understanding of one will impact considerably on the other. The symptoms are distressing and impinge significantly on patients' quality of life. Despite 30 years of scientific and clinical investigation, the pathogenesis of pouchitis is unknown; however, recent advances in molecular and cell biology make a synergistic hypothesis possible. This hypothesis links interaction between epithelial metaplasia, changes in luminal bacteria (in particular sulfate-reducing bacteria), and altered mucosal immunity. Specifically, colonic metaplasia supports colonization by sulfate-reducing bacteria that produce hydrogen sulfide. This causes mucosal depletion and subsequent inflammation. Although in most cases antibiotics lead to bacterial clearance and symptom resolution, immunogenetic subpopulations can develop a chronic refractory variant of pouchitis. The aims of this paper are to discuss proposed pathogenic mechanisms and to describe a novel mechanism that combines many hypotheses and explains several aspects of pouchitis. The implications for the management of both pouchitis and ulcerative colitis are discussed.
Language
eng
ISSN
1572-0241 (Electronic)
0002-9270 (Linking)
0002-9270 (Linking)
eISSN
ISBN
DOI
10.1038/ajg.2008.127
PMID
19259080