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Mechanisms underlying basal cell hyperplasia in eosinophilic oesophagitis

Eosinophilic oesophagitis is an increasingly recognised cause of dysphagia, characterised by >15 eosinophils/high powered field, basal zone hyperplasia and elongation of vascular papillae. Eosinophils release inflammatory mediators, the most abundant of which is major basic protein (MBP). The extracellular calcium sensing receptor (CaSR) is a G-protein-coupled receptor. The present study using an oesophageal cell line (HET-1A) showed that CaSR responds to MBP-peptide. Furthermore, when HET-1A cells were incubated with MBP-peptide there was a marked increase in fibroblast growth factor 9 (FGF9). Transfecting the cells with short interfering siRNACaSR blocked the production of FGF9 showing this was a CaSR dependent process. The authors also showed that FGF9 stimulates cell proliferation and that paediatric patients with a eosinophilic oesophagitis had a substantial increase in FGF9 in homogenates of oesophageal mucosal biopsies (see fig). Finally, the FGF9 was shown by immunohistochemistry to be increased in eosinophilic oesophagitis. By defining the mechanism whereby eosinophils act this study opens the way to more specific rational therapy of this newly recognised condition. See page 166.

Fibroblast growth factor 9 (FGF9) protein in homogenates of oesophageal mucosal biopsies of patients with normal oesophagus (triangles), gastro-oesophageal reflux disease (GORD, squares) or eosinophilic oesophagitis (EoE, circles), as detected by ELISA (*p<0.05)

The metabolic syndrome increases the risk of progression from non-erosive to erosive reflux disease

The natural course of gastro-oesophageal reflux disease (GORD) is incompletely known. This is also true for risk factors for the progression from a non-erosive to an erosive state. In this issue of Gut, Lee et al report a study of 3669 subjects who underwent repeated upper GI …

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