Reflux symptoms and oesophageal acidification in treated achalasia patients are often not reflux related

Abstract

ObjectiveAfter treatment, achalasia patients often develop reflux symptoms. Aim of this case–control study was to investigate mechanisms underlying reflux symptoms in treated achalasia patients by analysing oesophageal function, acidification patterns and symptom perception.DesignForty treated achalasia patients (mean age 52.9 years; 27 (68%) men) were included, 20 patients with reflux symptoms (RS+; Gastro-Oesophageal Reflux Disease Questionnaire (GORDQ) ≥8) and 20 without reflux symptoms (RS−: GORDQ <8). Patients underwent measurements of oesophagogastric junction distensibility, high-resolution manometry, timed barium oesophagogram, 24 hours pH-impedance monitoring off acid-suppression and oesophageal perception for acid perfusion and distension. Presence of oesophagitis was assessed endoscopically.ResultsTotal acid exposure time during 24 hours pH-impedance was not significantly different between patients with (RS+) and without (RS−) reflux symptoms. In RS+ patients, acid fermentation was higher than in RS− patients (RS+: mean 6.6% (95% CI 2.96% to 10.2%) vs RS−: 1.8% (95% CI −0.45% to 4.1%, p=0.03) as well as acid reflux with delayed clearance (RS+: 6% (95% CI 0.94% to 11%) vs RS−: 3.4% (95% CI −0.34% to 7.18%), p=0.051). Reflux symptoms were not related to acid in both groups, reflected by a low Symptom Index. RS+ patients were highly hypersensitive to acid, with a much shorter time to heartburn perception (RS+: 4 (2–6) vs RS−:30 (14-30) min, p<0.001) and a much higher symptom intensity (RS+: 7 (4.8–9) vs RS−: 0.5 (0–4.5) Visual Analogue Scale, p<0.001) during acid perfusion. They also had a lower threshold for mechanical stimulation.ConclusionReflux symptoms in treated achalasia are rarely caused by gastro-oesophageal reflux and most instances of oesophageal acidification are not reflux related. Instead, achalasia patients with post-treatment reflux symptoms demonstrate oesophageal hypersensitivity to chemical and mechanical stimuli, which may determine symptom generation.