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The term enteric dysmotility (ED) has been proposed1 to describe patients with recurrent severe gastrointestinal symptoms (nausea, vomiting, abdominal pain, abdominal distension, diarrhoea or constipation) and abnormal small bowel manometry, but without clinical or radiological evidence of previous or current mechanical bowel obstruction, occlusive episodes or bowel dilatation, and without evidence of any medication that could lead to small bowel motor abnormalities. The study in the current issue of Gut by Lindberg et al (see page 1084) represents a potentially significant advance in our understanding of the pathophysiology of motility and functional gastrointestinal disorders (FGIDs), such as ED.2 The authors in this study examined, for the first time, full-thickness small bowel (usually jejunal) biopsies in 65 adult patients with the diagnosis of ED. These patients were found, using tangential sections, to exhibit a histological lesion classified as an inflammatory neuropathy—that is, neuron degeneration associated with an infiltration (mostly low grade) of CD3+ T lymphocytes in and around the ganglia of the myenteric plexus (and in some cases along axons). The prevalence of this inflammatory neuropathy was significantly greater in this group of patients with ED when compared with patients with chronic intestinal pseudo-obstruction who were also evaluated in this report.
The findings in this series extend and strengthen the validity of the findings in a previous report from the same investigators3 that described similar histological findings …
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