Pathogenesis of and unifying hypothesis for idiopathic pouchitis.

Hdl Handle:
http://hdl.handle.net/10147/207507
Title:
Pathogenesis of and unifying hypothesis for idiopathic pouchitis.
Authors:
Coffey, J Calvin; Rowan, Fiachra; Burke, John; Dochery, Neil G; Kirwan, William O; O'Connell, P Ronan
Affiliation:
School of Medicine and Medical Sciences University College Dublin, St Vincent's, University Hospital, Dublin, Ireland. calvincoffey@hotmail.com
Citation:
Am J Gastroenterol. 2009 Apr;104(4):1013-23. Epub 2009 Mar 3.
Journal:
The American journal of gastroenterology
Issue Date:
1-Feb-2012
URI:
http://hdl.handle.net/10147/207507
DOI:
10.1038/ajg.2008.127
PubMed ID:
19259080
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
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
ISSN:
1572-0241 (Electronic); 0002-9270 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorCoffey, J Calvinen_GB
dc.contributor.authorRowan, Fiachraen_GB
dc.contributor.authorBurke, Johnen_GB
dc.contributor.authorDochery, Neil Gen_GB
dc.contributor.authorKirwan, William Oen_GB
dc.contributor.authorO'Connell, P Ronanen_GB
dc.date.accessioned2012-02-01T10:29:47Z-
dc.date.available2012-02-01T10:29:47Z-
dc.date.issued2012-02-01T10:29:47Z-
dc.identifier.citationAm J Gastroenterol. 2009 Apr;104(4):1013-23. Epub 2009 Mar 3.en_GB
dc.identifier.issn1572-0241 (Electronic)en_GB
dc.identifier.issn0002-9270 (Linking)en_GB
dc.identifier.pmid19259080en_GB
dc.identifier.doi10.1038/ajg.2008.127en_GB
dc.identifier.urihttp://hdl.handle.net/10147/207507-
dc.description.abstractIleal 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.en_GB
dc.language.isoengen_GB
dc.subject.meshAnal Canal/microbiology/pathology/surgeryen_GB
dc.subject.meshAnastomosis, Surgical/methodsen_GB
dc.subject.meshAnti-Bacterial Agents/therapeutic useen_GB
dc.subject.meshBacteria/*growth & developmenten_GB
dc.subject.meshColitis, Ulcerative/surgeryen_GB
dc.subject.meshColonic Pouches/microbiology/pathologyen_GB
dc.subject.meshDiagnosis, Differentialen_GB
dc.subject.meshHumansen_GB
dc.subject.meshIntestinal Mucosa/microbiology/*pathologyen_GB
dc.subject.meshMetaplasia/pathologyen_GB
dc.subject.meshPostoperative Complicationsen_GB
dc.subject.mesh*Pouchitis/diagnosis/drug therapy/etiologyen_GB
dc.titlePathogenesis of and unifying hypothesis for idiopathic pouchitis.en_GB
dc.contributor.departmentSchool of Medicine and Medical Sciences University College Dublin, St Vincent's, University Hospital, Dublin, Ireland. calvincoffey@hotmail.comen_GB
dc.identifier.journalThe American journal of gastroenterologyen_GB
dc.description.provinceLeinster-

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