The cause of dysphagia in eosinophilic oesophagitis: obstruction to bolus passage not oesophageal dysmotility

Abstract

Background: Eosinophilic Esophagitis (EoE) presents with dysphagia and chest pain; however the cause of symptoms remains uncertain. Endoscopy reveals fibrotic and inflammatory mucosal disease but rarely tight stenosis. Conventional manometry with small volume water swallows is usually normal. However this may not be clinically relevant as most EoE patients report dysphagia on eating bread and meat but not on drinking liquids. This study applied HRM with water and solid bolus swallows to identify abnormal oesophageal function in EoE and to associate abnormal pressure events with reports of oesophageal symptoms. Method(s): Retrospective case review of 14 consecutive patients (10 male; 36 (26-65)) on two sites referred for HRM with a diagnosis of EoE based on biopsy of proximal and distal oesophagus. HRM studies included 10x5ml water swallows and 5-10 solid (dry bread or sandwich) swallows in the seated position. Data from 23 healthy volunteers (11M, age 20- 56) served as control. Association between abnormal pressure events and symptoms was assessed on a per patient and per swallow basis. Result(s): HRM identified oesophageal dysfunction in 3/14 (21%) patients with water swallows and 11/14 (79%) patients with solids (p<0.008). All 11 had increased intra-bolus pressure gradient (IBPG) >=30mmHg with solids (maximum gradient at lower esophageal sphincter (LES) (n=9), mid-oesophagus (n=1) and upper esophageal sphincter (n=1)). Per patient: Typical symptoms were reported with IBPG >30mmHg by 1 (7%) patient with water and 7 (50%) patients with solids (p=0.039). Conversely, 7/11 (64%) patients with IBPG >30mmHg had symptoms (7/7 patients with IBPG >50mmHg). Per swallow: There was temporal association between raised OGPG and patient reports of symptoms (p<0.001). Pan-oesophageal pressurization >30mmHg triggered dysphagia; compartmentalized pressurization >50mmHg in the distal oesophagus between peristalsis and LES triggered either dysphagia or chest pain. No association with symptoms was present for any other pressure event. EoE Patients that had received steroids and/or dilation (n=7) had lower OGPG and reported less symptoms than untreated patients (n=7) (both p<0.001); however, if it occurred, the association between IBPG and symptoms remained. One healthy subject had increased frequency of low-amplitude oesophageal spasm; however none had raised OGPG >30mmHg with solids and none reported symptoms. Conclusion(s): Most EoE patients have normal oesophageal motility and LES function but evidence of structural obstruction to solid bolus passage across the LES, presumably due to reduced compliance due to fibrosis and inflammation. In all but one case this was evident only with solid bolus. Raised OGPG was closely associated with patient reports of symptoms and both improved on treatment.