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Eosinophilic oesophagitis (EO) is essentially a new disease not generally recognised in the UK or many other western European countries until early this decade. It is characterised by dysphagia, usually intermittent with a wide range of symptom severity and disruption to quality of life. The mechanism underlying the symptom of dysphagia is often not clear in EO because the changes seen at endoscopy are very variable. In this issue of Gut (see page 1056), Mittal’s group from San Diego address the pathophysiology of dysphagia using endoscopic ultrasound, and their results are intriguing.1
Korsapati et al propose that the mechanism of dysphagia is through a discoordination of longitudinal muscle of the oesophagus.1 Standard manometry fails to show an abnormality of peristalsis in most patients with EO,2 and this is confirmed by Korsapati et al. They then use endoscopic ultrasound to measure the thickness (as a marker of muscle contraction) of the circular and longitudinal muscle of the oesophagus and observe its reaction to an edrophonium stress test. The combined thickness of the muscle and submucosal layers is significantly greater at rest in patients with EO compared with controls. During contractions, however, the thickness of the muscle in patients has a lower peak than in controls, indicating dysfunctional contraction. In patients with symptomatic EO suffering dysphagia, they observed that the longitudinal muscle fails to react normally, with both a weaker contraction and a time delay (asynchrony) during the edrophonium stress, whereas the circular muscle seems to be unaffected …
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