ArticleRheumatology (Oxford, England)2026
PPI-refractory GERD in SSc is driven by distinct oesophageal and gastric motility abnormalities.
Article in Rheumatology (Oxford, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectivesGastroesophageal reflux disease (GERD) is highly prevalent in SSc and frequently persists despite proton pump inhibitor (PPI) therapy. We aimed to characterize the contribution of oesophageal and gastric dysmotility to PPI-refractory GERD in SSc.
methodsWe conducted a single‑centre, retrospective study of adults with SSc who underwent ambulatory pH-multichannel intraluminal impedance (pH/MII) monitoring while receiving twice‑daily PPI therapy (2021-25). Oesophageal motility (high‑resolution manometry, HREM) and gastric emptying scintigraphy were integrated to examine associations between gastro-oesophageal dysmotility and reflux phenotypes.
resultsThirty patients were included, of whom 67% had PPI-refractory reflux symptoms and 33% were undergoing pre-lung transplantation evaluation. Refractory GERD was present in 29/30 patients (97%) based on Lyon 2.0 classification, with conclusive evidence in 53% and borderline evidence in 43%. Oesophageal dysmotility was identified in 80%, most commonly absent contractility (67%), and was associated with impaired reflux clearance, reflected by longer acid clearance times [2.20 (1.15-3.75) vs 1.15 (0.43-1.90) min] and more prolonged reflux episode duration [16.60 (4.38-40.63) vs 1.95 (0.53-20.43) min]. Gastric dysmotility was identified in 60.7% and was associated with an increased reflux episode burden [51.00 (30.00-81.50) vs 25.00 (21.00-54.00) episodes/24 h].
conclusionPPI‑refractory GERD is nearly universal in this SSc cohort and reflects heterogeneous, quantifiable abnormalities across the foregut, including impaired oesophageal clearance and increased reflux burden related to gastric retention. These findings support integrated physiologic evaluation to define reflux mechanisms, inform risk stratification (including lung transplantation) and guide targeted, mechanism-based therapies beyond acid suppression.
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