Restorative proctocolectomy (RPC) with ileal pouch-anal anastomosis is the operation of choice for patients with ulcerative colitis. Pouchitis is the most common cause of pouch dysfunction. Although the pathogenesis of this disease is not well understood, bacteria have been implicated in the disease process. Numerous bacterial studies have been reported over the last 25 years with few unifying findings. In addition, many different treatments for pouchitis have been reported with varying results. Antibiotic treatment remains the most studied and is the mainstay of treatment. In this article we review the aetiology of pouchitis and the evidenced-based treatment options.

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.

While the overall incidence of pouchitis is low, extensive research continues at clinical and experimental levels in attempts to unravel its etiology. The ileal pouch and pouchitis together represent a unique in vivo opportunity to study mucosal adaptation and inflammation in depth. In the recent past, molecular data relating to pouchitis has significantly expanded. These data provide invaluable insight into intracellular and extracellular events that underpin mucosal adaptation and inflammation. Advances in classification, risk factor evaluation, and prevention have meant that a review of this data, as well as its relationship to our current understanding of pouchitis, is both timely and warranted. Therefore, the aim of this review is to summarize recent data in the context of the established literature.

The mode of inactivation of probiotic bacteria may profoundly affect their immune-modulatory properties to the point of reversal of effects in in vitro human intestinal epithelial-like cell cultures (Caco-2). To further investigate the influence of inactivation treatment on cytokine production, three probiotic strains were evaluated-live, heat-inactivated, and formalin-inactivated strains-for their impact on interleukin (IL) 6, IL-8, and IL-10 production in Caco-2-leucocyte cocultures. The tested bacteria induced strain-specific production of IL-6, IL-8, and IL-10. No suppressive effects on cytokine synthesis were observed. Live microorganisms seemed to be slightly more potent inducers of cytokine production than nonviable strains, but differences to inactivated bacteria were not statistically significant. Our results indicate that heat and formalin treatments of probiotic microorganisms are equivalent inactivation methods in terms of induction of IL-6, IL-8, and IL-10 production in Caco-2-peripheral blood mononuclear cell cocultures and do not invert immune-modulatory effects.

This review will highlight the knowledge gained from studies published in the year 2005 on maintenance treatment after surgery for inflammatory bowel diseases.

In Crohn's disease the role of smoking in increasing the risk of relapse and recurrence after surgery is confirmed. Ornidazole seems effective in reducing endoscopic recurrence and clinical relapse after surgery. Probiotics do not appear to be effective in preventing endoscopic recurrence and clinical relapse: a controlled placebo trial showed that Lactobacillus johnsonii is not effective in preventing endoscopic recurrence. A retrospective study suggested that enteral nutrition after surgery may reduce the clinical relapse. Pathophysiological studies underlined the value of probiotics in pouchitis.

In Crohn's disease postoperative maintenance treatment is disappointing. Giving up smoking is still the only effective measure. Mesalamine remains the drug that has been widely studied with large trials and meta-analysis. Encouraging results come from small trials on antibiotics. Azathioprine and 6-mercaptopurine must be evaluated in better designed controlled trials. There is no evidence in favour of probiotics as an effective therapy to prevent recurrence. Enteral nutrition after surgery is a candidate new therapy, but further controlled trials are needed. Pathophysiological studies confirm the beneficial role of probiotics in pouchitis.