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

Abstract

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.

Keywords: achalasia; gastroesophageal reflux disease; oesophageal motility disorder; oesophageal ph monitoring; visceral hypersensitivity.

Figure 1

Study protocol. EndoFLIP, Endo Functional Luminal Imaging Probe; HRM, high-resolution manometry; OGJ, oesophagogastric junction; PPI, proton pump inhibitors.

Figure 2

Oesophageal acidification patterns observed during pH-impedance monitoring. (A) Acid reflux with normal clearance: rapid pH drop to below 4, drop rate ≥1 pH unit per second, lasting between 10 s and 5 min. (B) Acid reflux with delayed clearance: rapid pH drop to below 4, drop rate ≥1 pH unit per second, lasting longer than 5 min. (C) Acid fermentation: slow pH drop to below 4, drop rate <1 pH unit per minute, lasting longer than 5 min. (D) Stasis of recently ingested acidic food or drink: pH drop to below 4 during meal/drink, pH below 4 persisting longer than 5 min after meal/drink. The pink-coloured area indicates meal/drink ingestion. (E) Unclassified: pH drop to below 4 not meeting criteria for any of the acid patterns described above.

Figure 3

Results of acid perfusion test in treated achalasia patients with reflux symptoms (RS+), without reflux symptoms (RS–) and healthy subjects (HS). (A) Lag time to initial heartburn perception. (B) Mmaximum symptom intensity expressed by Visual Analogue Scale (VAS). (C) Perfusion sensitivity score ((total perfusion time—lag time to perception) X VAS).