Evolving Issues in the Diagnosis, Evaluation, and Management of Irritable Bowel Syndrome

Evolving Issues in the Diagnosis, Evaluation, and Management of Irritable Bowel Syndrome

US Gastroenterology - Volume-4 Issue 1
Published: March 2009
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Irritable bowel syndrome (IBS) is a highly prevalent gastrointestinal motility disorder associated with decreased quality of life1 and significant economic burden to both the individual patient and society.2 For these reasons IBS has remained an area of active clinical research. This article will provide a summary of recent changes in the Rome criteria, discuss how brain imaging broadens our understanding of the brain–gut axis in IBS, and review new data on serotonergic agents, bacterial overgrowth, probiotics, and IBS.

Defining Irritable Bowel Syndrome
The definition of IBS has evolved significantly over the past several decades. The first set of symptom-based criteria was proposed in 1978 by Manning and colleagues, who identified four symptoms that occurred more frequently in IBS.3 These symptoms included looser stools at the onset of pain, increased frequency of bowel movements after the onset of pain, relief of abdominal pain after a bowel movement, and abdominal distension. The Manning criteria had a sensitivity and specificity of 42–90% and 70–100%, respectively, but concerns soon arose about their validity. The 1984 Kruis criteria placed more emphasis on symptom duration; however, these criteria were quite cumbersome to use in clinical practice and rapidly fell out of favor. In 1988 a group of experts met in Rome to discuss functional gastrointestinal disorders (FGIDs). This culminated in the publication of the Rome criteria in 1992. The criteria for IBS were used in research studies but proved unwieldy in clinical practice. In 2000 the Rome criteria were revised to the Rome II criteria, which also proved somewhat cumbersome in clinical practice.

The 2006 Rome III criteria contain several important changes, including a more concise and inclusive symptomatic time-frame for all FGIDs.4 One of the most significant revisions concerns the classification of IBS subtypes. Subtypes are now based on stool consistency rather than stool frequency, and include IBS-C (constipation), IBS-D (diarrhea), IBS-M (mixed), and IBSU (unsubtyped). Validation studies have yet to be published, but the clinical utility of the Rome III criteria is promising.

Brain Imaging
Functional brain imaging evaluates central nervous system activity in patients with IBS. The most common techniques employed in IBS brain imaging are positron emission tomography (PET), functional magnetic resonance imaging (fMRI), and magnetoencephalography (MEG). PET uses radiolabeled isotopes to capture changes in neuronal metabolism or cerebral blood flow, fMRI assesses changes in the concentration of oxygenated hemoglobin, and MEG enables more detailed temporal resolution by mapping the magnetic fields generated by brain activity. As these techniques measure different parameters, they may yield divergent results.

References:
  1. Sandler RS, Everhart JE, Donowitz M, et al., Gastroenterology, 2002;122:1500–11.
  2. Talley NJ, Gabriel SE, Harmsen WS, et al., Gastroenterology, 1995;109:1736–41.
  3. Manning AP, Thompson WG, Heaton KW, Morris AF, BMJ, 1978;2:653–4.
  4. Drossman DA, Program and Abstracts of Digestive Disease Week, May 20–25, 2006;461–9.
  5. Silverman DH, Munakata JA, Ennes H, et al., Gastroenterology, 1997;112:64–72.
  6. Andresen V, Bach DR, Poellinger A, et al., Neurogastroenterol Motil, 2005;17(6):827–37.
  7. Naliboff BD, Berman S, Chang L, et al., Gastroenterology, 2003;124:1738–47.
  8. Wilder-Smith CH, Schindler D, Lovblad K, et al., Gut, 2004;53(11): 1553–5.
  9. Drossman DA, Camilleri M, Mayer EA, Gastroenterology, 2002;123:2108–31.
  10. Kuiken SD, Tygat GN, Boeckxstaens GE, Clin Gastroenterol Hepatol, 2003;1:219–28.
  11. Tabas G, Beaves M,Wang J, et al., Am J Gastroenterol, 2004;99:914–20.
  12. American College of Gastroenterology Functional Gastrointestinal Disorders Task Force, Am J Gastroenterol, 2002;97:S1–S5.
  13. Novick J, Miner P, Krause R, et al., Aliment Pharmacol Ther, 2002;16:1877–88.
  14. Lembo AJ, Olden KW, Ameen VZ, et al., Clin Gasteroenterol Hepatol, 2004;2:675–82.
  15. Singh G, Mithal A, Kahler K, et al., Gut, 2004;53:A66.
  16. Chang L, Chey W, Harris L, et al., Am J Gastroenterol, 2006;101:1069–79.
  17. O’Mahony L, McCarthy J, Kelly P, et al., Gastroenterology, 2005;128:541–51.
  18. Whorwell PJ, Altringer L, Morel J, et al., Am J Gastroenterol, 2006;101:1581–90.
  19. Lin H, JAMA, 2004;292:852–8.
  20. Pimentel M, Park S, Mirocha J, et al., Ann Intern Med, 2006;145:557–63.
  21. Ruff KC, Saito-Loftus YA, Locke GR, et al., Am J Gastroenterol, 2006;102:S488.
  22. Bratten J, Spanier J, Jones MP, Am J Gastroenterol, 2006;102:S479.

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