Skip to main content


Log in

Chronic Use of PPI and H2 Antagonists Decreases the Risk of Pouchitis After IPAA for Ulcerative Colitis

  • 2012 SSAT Plenary Presentation
  • Published:
Journal of Gastrointestinal Surgery



Bacteria have been implicated in the development of pouchitis after ileal pouch anal anastomosis. The change in gastric pH with the use of proton pump inhibitors and H2 antagonists may lead to alteration of enteric bacteria. We hypothesized that chronic use of these medications would decrease the incidence of pouchitis.


Patients who had undergone ileal pouch anal anastomosis for ulcerative colitis were classified by history of pouchitis. Patients were further classified by their use of proton pump inhibitors, H2 blockers, antacids, and other known risk factors for pouchitis.


Eighty-five patients were identified. There was a statistically significant increase in the use of daily acid suppression in patients without pouchitis. There was also a statistically significant increase in the use of antacids in patients without pouchitis. Occasional use of acid suppression did not alter the rate of pouchitis.


Our data suggest that the daily use of proton pump inhibitors, H2 antagonists, or antacids is associated with a decreased risk of pouchitis in ulcerative colitis. Occasional use of these agents did not seem to afford the same protection. These data suggest that altering the pH of the gastrointestinal tract may influence the development of pouchitis.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Subscribe and save

Springer+ Basic
EUR 32.99 /Month
  • Get 10 units per month
  • Download Article/Chapter or Ebook
  • 1 Unit = 1 Article or 1 Chapter
  • Cancel anytime
Subscribe now

Buy Now

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others


  1. Meagher AP, Farouk R, Dozois RR, Kelly KA, Pemberton JH. J ileal pouch-anal anastomosis for chronic ulcerative colitis: complications and long-term outcome in 1310 patients. Br J Surg 1998; 85:800–803.

    Article  PubMed  CAS  Google Scholar 

  2. Hurst RD, Molinari M, Chung TP, Rubin M, Michelassi F. Prospective study of the incidence, timing and treatment of pouchitis in 104 consecutive patients after restorative proctocolectomy. Arch Surg 1996; 131:497–500; discussion 501–492

    Article  PubMed  CAS  Google Scholar 

  3. Shen B, Fazio VW, Remzi FH, Delaney CP, Bennett AE, Achkar JP, Brzezinski A, Khandwala F, Liu W, Bambrick ML, Bast J, Lashner B. Comprehensive evaluation of inflammatory and noninflammatory sequelae of ileal pouch-anal anastomoses. Am J Gastroenterol 2005; 100:93–101.

    Article  PubMed  Google Scholar 

  4. Hurst RD, Chung TP, Rubin M, Michelassi F. The implications of acute pouchitis on the long-term functional results after restorative proctocolectomy. Inflamm Bowel Dis 1998; 4:280–284.

    PubMed  CAS  Google Scholar 

  5. Fazio VW, Ziv Y, Church JM, Oakley JR, Lavery IC, Milsom JW, Schroeder TK. Ileal pouch-anal anastomoses complications and function in 1005 patients. Ann Surg 1995; 222:120–127.

    Article  PubMed  CAS  Google Scholar 

  6. Madiba TE, Bartolo DC. Pouchitis following restorative proctocolectomy for ulcerative colitis: incidence and therapeutic outcome. J R Coll Surg Edinb 2001; 46:334–337.

    PubMed  CAS  Google Scholar 

  7. Shen B, Achkar JP, Lashner BA, Ormsby AH, Remzi FH, Brzezinski A, Bevins CL, Bambrick ML, Seidner DL, Fazio VW. A randomized clinical trial of ciprofloxacin and metronidazole to treat acute pouchitis. Inflamm Bowel Dis 2001; 7:301–305.

    Article  PubMed  CAS  Google Scholar 

  8. Lovegrove RE, Tilney HS, Heriot AG, von Roon AC, Athanasiou T, Church J, Fazio VW, Tekkis PP. A comparison of adverse events and functional outcomes after restorative proctocolectomy for familial adenomatous polyposis and ulcerative colitis. Dis Colon Rectum 2006; 49:1293–1306.

    Article  PubMed  Google Scholar 

  9. Penna C, Tiret E, Kartheuser A, Hannoun L, Nordlinger B, Parc R. Function of ileal J pouch-anal anastomosis in patients with familial adenomatous polyposis. Br J Surg 1993; 80:765–767.

    Article  PubMed  CAS  Google Scholar 

  10. Tjandra JJ, Fazio VW, Church JM, Oakley JR, Milsom JW, Lavery IC. Similar functional results after restorative proctocolectomy in patients with familial adenomatous polyposis and mucosal ulcerative colitis. Am J Surg 1993; 165:322–325.

    Article  PubMed  CAS  Google Scholar 

  11. Madden MV, McIntyre AS, Nicholls RJ. Double-blind crossover trial of metronidazole versus placebo in chronic unremitting pouchitis. Dig Dis Sci 1994; 39:1193–1196.

    Article  PubMed  CAS  Google Scholar 

  12. Sandborn WJ, McLeod R, Jewell DP. Medical therapy for induction and maintenance of remission in pouchitis: a systematic review. Inflamm Bowel Dis 1999; 5:33–39.

    Article  PubMed  CAS  Google Scholar 

  13. Shen B. Diagnosis and treatment of patients with pouchitis. Drugs 2003; 63:453–461.

    Article  PubMed  Google Scholar 

  14. Gionchetti P, Rizzello F, Helwig U, Venturi A, Lammers KM, Brigidi P, Vitali B, Poggioli G, Miglioli M, Campieri M. Prophylaxis of pouchitis onset with probiotic therapy: a double-blind, placebo-controlled trial. Gastroenterology 2003; 124:1202–1209.

    Article  PubMed  Google Scholar 

  15. Gionchetti P, Rizzello F, Venturi A, Brigidi P, Matteuzzi D, Bazzocchi G, Poggioli G, Miglioli M, Campieri M. Oral bacteriotherapy as maintenance treatment in patients with chronic pouchitis: a double-blind, placebo-controlled trial. Gastroenterology 2000; 119:305–309.

    Article  PubMed  CAS  Google Scholar 

  16. Kuisma J, Mentula S, Jarvinen H, Kahri A, Saxelin M, Farkkila M. Effect of Lactobacillus rhamnosus GG on ileal pouch inflammation and microbial flora. Aliment Pharmacol Ther 2003; 17:509–515.

    Article  PubMed  CAS  Google Scholar 

  17. Pereira SP, Gainsborough N, Dowling RH. Drug-induced hypochlorhydria causes high duodenal bacterial counts in the elderly. Aliment Pharmacol Ther 1998; 12:99–104.

    Article  PubMed  CAS  Google Scholar 

  18. Shindo K, Machida M, Fukumura M, Koide K, Yamazaki R. Omeprazole induces altered bile acid metabolism. Gut 1998; 42:266–271.

    Article  PubMed  CAS  Google Scholar 

  19. Sehgal R, Berg A, Hegarty JP, Kelly AA, Lin Z, Poritz LS, Koltun WA. NOD2/CARD15 mutations correlate with severe pouchitis after ileal pouch-anal anastomosis. Dis Colon Rectum 2010; 53:1487–1494.

    Article  PubMed  Google Scholar 

  20. Fried M, Siegrist H, Frei R, Froehlich F, Duroux P, Thorens J, Blum A, Bille J, Gonvers JJ, Gyr K. Duodenal bacterial overgrowth during treatment in outpatients with omeprazole. Gut 1994; 35:23–26.

    Article  PubMed  CAS  Google Scholar 

  21. Thorens J, Froehlich F, Schwizer W, Saraga E, Bille J, Gyr K, Duroux P, Nicolet M, Pignatelli B, Blum AL, Gonvers JJ, Fried M. Bacterial overgrowth during treatment with omeprazole compared with cimetidine: a prospective randomised double blind study. Gut 1996; 39:54–59.

    Article  PubMed  CAS  Google Scholar 

  22. Sandborn WJ, Tremaine WJ, Batts KP, Pemberton JH, Rossi SS, Hofmann AF, Gores GJ, Phillips SF. Fecal bile acids, short-chain fatty acids, and bacteria after ileal pouch-anal anastomosis do not differ in patients with pouchitis. Dig Dis Sci 1995; 40:1474–1483.

    Article  PubMed  CAS  Google Scholar 

  23. Nasmyth DG, Godwin PG, Dixon MF, Williams NS, Johnston D. Ileal ecology after pouch-anal anastomosis or ileostomy. A study of mucosal morphology, fecal bacteriology, fecal volatile fatty acids, and their interrelationship. Gastroenterology 1989; 96:817–824.

    PubMed  CAS  Google Scholar 

  24. Duffy M, O’Mahony L, Coffey JC, Collins JK, Shanahan F, Redmond HP, Kirwan WO. Sulfate-reducing bacteria colonize pouches formed for ulcerative colitis but not for familial adenomatous polyposis. Dis Colon Rectum 2002; 45:384–388.

    Article  PubMed  CAS  Google Scholar 

  25. McLaughlin SD, Walker AW, Churcher C, Clark SK, Tekkis PP, Johnson MW, Parkhill J, Ciclitira PJ, Dougan G, Nicholls RJ, Petrovska L. The bacteriology of pouchitis: a molecular phylogenetic analysis using 16S rRNA gene cloning and sequencing. Ann Surg 2010; 252:90–98.

    Article  PubMed  Google Scholar 

  26. Tannock GW, Lawley B, Munro K, Lay C, Taylor C, Daynes C, Baladjay L, McLeod R, Thompson-Fawcett M. Comprehensive analysis of the bacterial content of stool from patients with chronic pouchitis, normal pouches, or familial adenomatous polyposis pouches. Inflamm Bowel Dis 2012; 18:925–934.

    Article  PubMed  Google Scholar 

  27. Elmer GW. Probiotics: “living drugs”. Am J Health Syst Pharm 2001; 58:1101–1109.

    PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations


Corresponding author

Correspondence to Lisa S. Poritz.

Additional information


Dr. Scott D. Goldstein (Philadelphia, PA): This paper is a small retrospective, but intriguing study. If the study’s findings are found to be accurate after future randomized controlled trials, it could lead to a significant new approach to the management and prevention of pouchitis in ulcerative colitis patients.

The frequency of pouchitis is seen in approximately 23–40 % of patients undergoing J-pouch reconstruction by 10 years, with 70 % experiencing their first attack within 1 year. The mechanism of pouchitis is thought to be the result of a dysbiosis in the pouch lumen. Viable sulfate-reducing bacteria are seen in the pouches of ulcerative colitis patients, but not in FAP patients. Normal pouches harbor large numbers of anaerobes. During pouchitis episodes, a reduction in anaerobes and an increased number of aerobic bacteria and Clostridium perfringens are seen.

The natural history of pouchitis appears to be an acute process of bacterial origin, which may develop into a chronic disease of persistent inflammation. Antibiotics have a beneficial effect by altering the bacterial flora of the pouch to a more normal state and are usually effective in the management of pouchitis. Other approaches, such as probiotics, may also be beneficial.

This paper proposes that a change in the gastric pH may lead to a beneficial alteration in enteric bacteria, resulting in a decrease in the incidence of pouchitis.

I have three questions for the authors:

(a) What sparked your interest in this study? Was there a simple clinical observation, or was it based upon theoretical grounds?

(b) Were any qualitative or quantitative bacteriologic studies performed on the pouchitis and normal pouch patients?

(c) If pH-altering therapy proves to be effective, which groups of patients would you suggest using this form of therapy for, i.e.,

(1) Antibiotic responsive

(2) Antibiotic dependent

(3) Antibiotic refractory

(4) All ulcerative colitis patients

Closing Discussant

Dr. Lisa S. Poritz: Dr. Goldstein, thank you very much for your comments.

1. I got the idea for the study while listening to a grand rounds lecture on the consequences of chronic acid reduction on the stomach. The speaker discussed the effects of chronic acid suppression on bacterial overgrowth in the upper gastrointestinal tract and I became curious about the potential effects on the bacterial flora in an ileal pouch.

2. At the time that we presented this study we had not as of yet done any qualitative on quantitative studies of the bacterial flora. These studies are now currently ongoing.

3. We would anticipate that altering the pH would be most beneficial in patients with antibiotic dependent pouchitis. This group of patients essentially requires chronic antibiotic therapy. If acid suppression could reduce the need for long term antibiotics in this group that would be a benefit to the patient. Those patients with antibiotic responsive pouchitis have relatively infrequent episodes and respond well to a course of antibiotics. There is probably not enough benefit to those patients to warrant chronic acid suppression. On the other hand, patients with antibiotic refractory pouchitis probably have disease that is too severe to be significantly improved with acid suppression. As far as the use in all ulcerative colitis pouch patients, there might be potential in starting post-operative patients on acid suppression in an attempt to prevent pouchitis in the first place.

This was a plenary podium presentation at the SSAT Annual Meeting in San Diego, CA, May 2012.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Poritz, L.S., Sehgal, R., Berg, A.S. et al. Chronic Use of PPI and H2 Antagonists Decreases the Risk of Pouchitis After IPAA for Ulcerative Colitis. J Gastrointest Surg 17, 1027–1031 (2013).

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: