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

Objective: After 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.

Design: Forty 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.

Results: Total 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.

Conclusion: Reflux 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.