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New insights into visceral hypersensitivity—clinical implications in IBS

Nature Reviews Gastroenterology & Hepatology volume 8, pages 349–355 (2011)Cite this article

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Abstract

A subset of patients with IBS have visceral hypersensitivity and/or somatic hypersensitivity. Visceral hypersensitivity might have use as a clinical marker of IBS and could account for symptoms of urgency for bowel movements, bloating and abdominal pain. The mechanisms that lead to chronic visceral hypersensitivity in patients who have IBS are unclear. However, several working models may be considered, including: nociceptive input from the colon that leads to hypersensitivity; increased intestinal permeability that induces a visceral nociceptive drive; and alterations in the expression of microRNAs in gastrointestinal tissue that might be delivered via blood microvesicles to other target organs, such as the peripheral and/or central nervous system. As such, the chronic visceral hypersensitivity that is present in a subset of patients with IBS might be maintained by both peripheral and central phenomena. The theories underlying the development of chronic visceral hypersensitivity in patients with IBS are supported by findings from new animal models in which hypersensitivity follows transient inflammation of the colon. The presence of somatic hypersensitivity and an alteration in the neuroendocrine system in some patients who have IBS suggests that multisystemic factors are involved in the overall disorder. Thus, IBS is similar to other chronic pain disorders, such as fibromyalgia, chronic regional pain disorder and temporomandibular joint disorder, as chronic nociceptive mechanisms are activated in all of these disorders.

Key Points

  • Visceral and somatic hypersensitivity are present in some patients with functional gastrointestinal disorders

  • Injury to visceral afferents is the most common underlying cause of visceral hypersensitivity that is maintained by either peripheral and/or central nervous system mechanisms

  • Animal models of hypersensitivity have been used to examine the neural mechanisms of hypersensitivity following inflammatory injury, such as alterations in the N-methyl, D-aspartate receptor, dorsal horn neurons or c-Fos

  • Increased intestinal permeability might lead to hypersensitivity and abdominal pain in patients with functional gastrointestinal disorders

  • Functional gastrointestinal disorders are similar to other chronic pain disorders in which persistent nociceptive mechanisms are activated

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Figure 1: Hypersenstivity in IBS.

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Acknowledgements

The authors would like to acknowledge the support of NIH grants (NS053090, AT005291) and a VA Merit Review Award from the Medical Research Service of the Department of Veterans Affairs.

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Authors and Affiliations

  1. Department of Medicine, Research Service, Cincinnati VA Medical Center, 3200 Vine Street, Cincinnati, 45220, OH, USA

    QiQi Zhou

  2. Department of Medicine, The Ohio State University, 1799 W 5th Avenue, Columbus, 43212, OH, USA

    G. Nicholas Verne

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Both authors contributed equally to all aspects of this review.

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Correspondence to G. Nicholas Verne.

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Zhou, Q., Verne, G. New insights into visceral hypersensitivity—clinical implications in IBS. Nat Rev Gastroenterol Hepatol 8, 349–355 (2011). https://doi.org/10.1038/nrgastro.2011.83

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