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The Need to Define The Target of Antibiotic Therapy in IBS Patients: Small Bowel or Colonic Flora?
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Michele Di Stefano, Dr 1st Department of Medicine, University of Pavia, Foundation IRCCS, Gino Roberto Corazza
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m.distefano{at}smatteo.pv.it Michele Di Stefano, et al.
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Dear Sir, we read with interest the recent paper by Pimentel et al (1) on the effect of rifaximin on irritable bowel syndrome (IBS) symptoms and we think it deserves some more comments, in addition to those already depicted by Drossman in his excellent Editorial (2). First of all, it should be underlined that the work hypothesis on which this paper is based is rather confusing. In the “Introduction”, the Authors emphasize the importance of alterations of small bowel bacterial flora in the pathophysiology of IBS. At least three major considerations should be made on this point: first, up to now, no clear demonstration of the causal relationship between small bowel bacterial overgrowth and IBS is available; second, as Drossman righly pointed out, the Authors do not provide any evidence of the presence of bacterial overgrowth in the small intestine; third, in the “Discussion” they refer to bacterial flora commenting on results obtained on fecal samples (3), that reflect the colonic rather than small bowel micro-ecology. If they consider antibiotic treatment useful for IBS patients, they must clearly indicate whether they consider either small bowel or large bowel flora as the target of the therapy. If they consider small bowel flora (i.e. small bowel bacterial overgrowth treatment), they should indicate which mechanism may be suggested for the onset of IBS in SIBO and/or for predisposition to SIBO in IBS. In view of the low discriminating power of the lactulose breath test between ectopic small bowel fermentation and physiological colonic lactulose catabolism (4-6), all their published data (1,7,8) could, actually, also be interpreted on the basis of the modification of fermentation process induced by antibiotics on colonic flora (9,10). In confirmation of this, additional preliminary data report the prevalence of SIBO in IBS at around 10% (11). Once these premises are accepted, the paper only shows the efficacy of rifaximin on bloating severity, and not the correction of SIBO, something which we had already shown around six years ago (9). In addition, our paper showed a significant effect of rifaximin on flatus emission, the only symptom that some Authorities consider as being specific of excessive intestinal gas production (12). We have recently added an important piece of evidence in the puzzle of both the pathophysiology and the treatment of bloating in IBS, since we demonstrated that, in patients with severe bloating and low gas production, a reduction of discomfort threshold is evident when colonic fermentation of orally administered lactulose begins (13). Therefore, the only presence of fermentation seems to be responsible for a sort of colonic hypersensitivity, regardless of the extent of intraluminal gas production. As expected, the administration of rifaximin in this subgroup of patients proved to be unable to modify the severity of bloating, while a significant reduction was obtained in patients with high gas production (9). Hence, a better selection of patients is the key to optimizing therapy of IBS: the identification of homogeneous subgroups, characterized by the same pathophysiological mechanism for symptom onset allows a more precise choice of drug and, consequently, a better treatment outcome. In conclusion, the study of Pimentel et al originates two misleading messages: first, in the treatment of IBS we do not yet have new therapeutic approaches based on improvement of pathophysiological mechanisms; second, rifaximin administration has a minor role in the treatment of IBS. On the contrary, rifaximin administration may be effective when a better selection of patients is performed. Michele Di Stefano, Gino Roberto Corazza 1st Department of Medicine, University of Pavia, Foundation IRCCS “S.Matteo” Hospital, Pavia, Italy References 1. Pimentel M, Park S, Mirocha J, Kane SV, Kong Y. The effect of nonabsorbed oral antibiotic (rifaximin) on the symptoms of the irritable bowel syndrome. Ann Intern Med 2006;145:557-63. 2. Drossman DA. Treatment of bacterial overgrowth in the irritable bowel syndrome. Ann Intern Med 2006;145:626-8. 3. Balsari A, Ceccarelli A, Dubini F, Fesce E, Poli G. The fecal microbial population in the irritable bowel sindrome. Microbiologica 1982;185:185- 94. 4. Corazza GR, Menozzi MG, Strocchi A, Rasciti L, Vaira D, Lecchini L. Gasbarrini G. The diagnosis of small bowel bacterial overgrowth. Reliability of jejunal culture and inadequacy of breath hydrogen testing. Gastroenterology 1990;98:320-9 5. Corazza GR, Sorge M, Strocchi A, Gasbarrini G. Lactose hydrogen breath test in the diagnosis of bacterial overgrowth. Gastroenterology 1990;99:1547. 6. Riordan SM, McIver CJ, Walker BM, Duncombe VM, Bolin TD, Thomas MC. The lactulose breath hydrogen test and small intestinal bacterial overgrowth. Am J Gastroenterol 1996;91:1795-803. 7. Pimentel M, Chow EJ, Lin HC. Eradication of small bowel bacterial overgrowth reduces symptoms of irritable bowel syndrome. Am J Gastroenterol 2000;95:3503-6. 8. Pimentel M, Chow EJ, Lin HC. Normalization of lactulose breath testing correlates with symptom improvement in irritable bowel syndrome: a double- blind, randomised, placebo-controlled study. Am J Gastroenterol 2003;98:412-9 9. Di Stefano M, Strocchi A, Malservisi S, Veneto G, Ferrieri A, Corazza GR. Non-absorbable antibiotics for managing intestinal gas production and gas-related symptoms. Aliment Pharmacol Ther 2000;14:1001-8. 10. Di Stefano M, Miceli E, Tana P, Mazzocchi S, Londoni C, Corazza GR. The reduction of intestinal gas production is not an effective treatment for bloating in patients with irritable bowel syndrome and hypersensitivity to colonic fermentation. Gut 2006;55 (suppl V):A67. 11. Simren M, Ringstrom G, Agerforz P, Bjornsson ES, Abrahamsson H, Stotzer PO. Small Intestinal bacterial overgrowth is not of major importance in the irritable bowel syndrome. Gastroenterology 2003; 124 (suppl 1): A163. 12. Levitt MD, Furne J, Olsson S. The relation of passage of gas and abdominal bloating to colonic gas production. Ann Intern Med 1996; 124: 422-424. 13. Di Stefano M, Miceli E, Missanelli A, Mazzocchi S, Tana P, Corazza GR. Role of colonic fermentation in the perception of colonic distention in irritable bowel syndrome and functional bloating. Clin Gastroenterol Hepatol 2006;4:1242-7. Conflict of Interest:None declared |
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