|Classification and external resources|
|This article needs additional citations for verification. (June 2012)|
Pouchitis is inflammation of the ileal pouch (an artificial rectum surgically created out of ileal gut tissue in patients who have undergone a colectomy), which is created in the management of patients with ulcerative colitis, indeterminate colitis, FAP, or, rarely, other colitides.
A variety of pathophysiological mechanisms have been proposed for pouchitis, but the precise pathogenesis (biological cause) remains unknown. A pilot study on the effect of reducing dietary FODMAP intake on bowel function in patients without a colon ran by Croagh C, Shepherd SJ, Berryman M, Muir JG, Gibson PR indicates there might be a relation between Pouchitis and FODMAP content of diets.
Patients with pouchitis typically present with bloody diarrhea, urgency in passing stools, or discomfort while passing stools. The loss of blood and/or dehydration resulting from the frequent stools will frequently result in nausea. Extreme cramping and pain can occur with pouchitis.
Endoscopy in patients with pouchitis usually reveals erythematous pouch mucosa, loss of pseudocolonic vaculature or other architecture, and friability of the mucosa. Biopsies show evidence of inflammatory cells or red blood cells in the lamina propria.
Once a diagnosis of pouchitis is made, the condition is further classified. The activity of pouchitis is stratified as:
- remission (no active pouchitis).
- mild to moderately active (increased stool frequency, urgency, infrequent incontinence).
- severely active (hospitalised for dehydration, frequent incontinence).
The duration of pouchitis is defined as acute (less than or equal to four weeks) or chronic (four weeks or more) and the pattern classified as infrequent (1-2 acute episodes), relapsing (three or fewer episodes) or continuous. Finally, the response to medical treatment as labelled as treatment responsive or treatment refractory, with the medication for either case being specified.
There is no clinically approved treatment for pouchitis. First line treatment is usually with antibiotics, specifically with ciprofloxacin and metronidazole. Ampicillin or Piperacillin can also be considered as alternatives to empiric Ciprofloxacin and metronidazole). Administration of metronidazole at a high daily dose of 20 mg/kg can cause symptomatic peripheral neuropathology in up to 85% of patients. This can be a limiting factor in the use of maintenance metronidazole to suppress chronic pouchitis.
Other therapies which have been shown to be effective in randomised clinical trials include probiotic therapy, the application of which usually begins as soon as any antibiotic course is completed so as to re-populate the pouch with beneficial bacteria. Biologics, such as anti-TNF antibodies, may also be useful but the evidence for their use is largely anecdotal. In addition, discussion by patients using related internet forums appears to give evidence of benefits (again, after cessation of antibiotics) from certain diets, such as the Specific Carbohydrate Diet, Paleolithic Diet, and Low FODMAP Diet. In particular, attention has been drawn to the exclusion of complex carbohydrates, as well as other foods with high starch content (such as grains, rice, and potatoes) and certain dairy products including milk and soft cheese.
Antisense inhibitors which target the inflammatory process have been used to treat Pouchitis in clinical trials. Antisense inhibitors function by binding to messenger RNA (mRNA) produced by a gene and deactivating it, effectively turning that gene "off". Specifically applied to pouchitis, antisense inhibitors would be used to switch off the inflammatory process.
- "Pouchitis". Mayo Clinic.
- Mahadevan, Uma; Sandborn, William J. (2003). "Diagnosis and management of pouchitis". Gastroenterology 124 (6): 1636–50. doi:10.1016/S0016-5085(03)00325-1. PMID 12761722.
- Croagh, Catherine; Shepherd, Susan J.; Berryman, Melissa; Muir, Jane G.; Gibson, Peter R. (2007). "Pilot study on the effect of reducing dietary FODMAP intake on bowel function in patients without a colon". Inflammatory Bowel Diseases 13 (12): 1522–8. doi:10.1002/ibd.20249. PMID 17828776.
- Penna, C; Dozois, R; Tremaine, W; Sandborn, W; Larusso, N; Schleck, C; Ilstrup, D (1996). "Pouchitis after ileal pouch-anal anastomosis for ulcerative colitis occurs with increased frequency in patients with associated primary sclerosing cholangitis". Gut 38 (2): 234–9. doi:10.1136/gut.38.2.234. PMC 1383029. PMID 8801203.
- The FSE Group
- Gosselink, MP; Schouten, WR; van Lieshout, LM; Hop, WC; Laman, JD; Ruseler-van Embden, JG (September 2004). "Eradication of pathogenic bacteria and restoration of normal pouch flora: comparison of metronidazole and ciprofloxacin in the treatment of pouchitis.". Diseases of the colon and rectum 47 (9): 1519–25. doi:10.1007/s10350-004-0623-y. PMID 15486751. Cite uses deprecated parameter
- Tremaine, W. J.; Sandborn, W. J.; Wolff, B. G.; Carpenter, H. A.; Zinsmeister, A. R.; Metzger, P. P. (1997). "Bismuth carbomer foam enemas for active chronic pouchitis: A randomized, double-blind, placebo-controlled trial". Alimentary Pharmacology and Therapeutics 11 (6): 1041–6. doi:10.1046/j.1365-2036.1997.00253.x. PMID 9663827.
- "Pouchitis Treatment". Mayo Clinic.
- Miner, P.; Wedel, M.; Bane, B.; Bradley, J. (2004). "An enema formulation of alicaforsen, an antisense inhibitor of intercellular adhesion molecule-1, in the treatment of chronic, unremitting pouchitis". Alimentary Pharmacology and Therapeutics 19 (3): 281–6. doi:10.1111/j.1365-2036.2004.01863.x. PMID 14984374.
- Morcos, PA. (2007). "Achieving targeted and quantifiable alteration of mRNA splicing with Morpholino oligos". Biochem Biophys Res Commun 358 (2): 521–7. doi:10.1016/j.bbrc.2007.04.172. PMID 17493584.