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Pain is common and strongly associated with poor quality of life and disability, constituting a major burden for affected individuals and for society as a whole. As gastroenterologists, we can appreciate this fact in our clinical practice: pain and discomfort are by far the most important causes for consultative visits. In the majority of cases, our diagnostic efforts do not identify an underlying cause, resulting in the diagnosis of a functional disease. Whether it is irritable bowel syndrome (IBS), functional dyspepsia or gastroparesis, a subgroup of patients will recall an acute event, typically infectious, preceding the onset of their chronic illness. Understanding how a transient process triggers lasting symptoms may thus provide important insight into mechanisms of visceral pain, which in turn could translate into better treatments. We cannot prospectively dissect the relationship between a sensitising event and the development of pain in humans. However, we can use animal models of human disease to obtain very detailed information about the effects of inflammation on the properties of afferent neurons. So, what can such animal models teach us about the physiology and pathophysiology of visceral sensation? In this issue of Gut, Hughes et al1 (see page 1333) report an elegant series of experiments that convincingly demonstrate lasting increases in the excitability of afferent nerve fibres following transient colitis. Thus, we have hypersensitivity (more afferent input), which may well translate into hyperalgesia (more pain).
A case for nociceptors
The results fit into a growing body of literature implicating hypersensitivity as a cause for chronic visceral …
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