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Abstract
The Montreal definition of gastroesophageal reflux disease (GERD) provided a rationale for acid suppression medication without investigation, thus enhancing the management of the substantial symptom burden in these patients. Increased proton-pump inhibitor use has also highlighted their limitations, with one third of “typical” symptoms known to be refractory. Most refractory symptoms are ascribed to reflux hypersensitivity (RH) and functional heartburn (FH). RH may be caused by impaired esophageal mucosal barrier function and sensitization of peripheral esophageal receptors. Central sensitization may also contribute to the perception of non-pathologic reflux in RH, and the perception of physiological stimuli in FH. Importantly, mechanisms underlying GERD, RH, and FH are (in theory) not mutually exclusive, further complicating patient management. Methods used to distinguish GERD from RH and FH are impractical for use in epidemiological studies and pragmatic care and may have limited diagnostic accuracy. This is impeding accurate prevalence estimates and risk factor determination and the identification of new therapies. Direct assessment of mucosal barrier function by measuring impedance is a promising candidate for improved diagnosis. Ultimately though the concept of GERD as a composite, symptom-based entity needs re-evaluation, so that new understandings of upper GI symptoms can direct more precise management.
Highlights
The primary goal of this review was to revisit the concept of gastroesophageal reflux disease (GERD)
Microscopic esophagitis is more prevalent, and esophageal mucosal integrity and chemical clearance more greatly impaired in patients with GERD than in those with reflux hypersensitivity [42, 43]. These findings indicate that patients with reflux hypersensitivity experience heartburn despite comparatively greater mucosal protection of their esophageal receptors from chemical stimuli, invoking mechanisms of enhanced receptor sensitivity
Reflux hypersensitivity and functional heartburn are not technically GERD [7], the complex array of tests required to identify these conditions hinders their exclusion in pragmatic clinical practice [91], where they account for the majority of the substantial symptom burden that exists despite pump inhibitor (PPI) use [35, 92]
Summary
The primary goal of this review was to revisit the concept of gastroesophageal reflux disease (GERD). The majority of studies that quantify the extent to which non-acid (weak acid or weak alkaline) reflux contributes to symptoms in patients with GERD came after the Montreal Consensus These were recently reviewed to show that nearly a third (28%) of reflux-related symptoms are associated with non-acid reflux [11]. Chest pain responsiveness to PPIs increases substantially (50% relief in 56–85% of patients) if those with pathologic esophageal acid exposure are selected, indicating that acid reflux can be a major contributor to this symptom, but that it is one of many possible causes [15]. The proportion of patients who had a positive SAP for acid or non-acid reflux was low for the typical GERD symptoms of unexplained chest pain (18%), heartburn (30%), and regurgitation (52%) [17]. Revisiting Montreal: New insights into Symptoms and their causes, and implications for the... 3
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