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Abstract Lower esophageal sphincter (LES) pathophysiology has been established in gastroesophageal reflux disease (GERD); however, less is understood regarding the role the upper esophageal sphincter (UES) plays in preventing laryngopharynphageal reflux. Sustained UES basal pressure prevents reflux into the pharynx while allowing relaxation during ingestion. We investigate whether GERD influences UES function via HRM and pH Impedance testing. A retrospective analysis of 318 patients who underwent high‐resolution manometry with trans‐nasally placed manometric catheter and 24‐h multichannel intraluminal impedance pH monitoring. One hundred and forty‐seven patients met Lyon consensus criteria for GERD based on acid exposure time >6%. The most common chief concern was heartburn or reflux, present in 59% of these patients. Upper esophageal sphincter basal and residual pressures were not significantly different between patients with GERD when compared to those without GERD, including a subanalysis of patients with extraesophageal symptoms. The LES basal and residual pressures, DCI and MNBI are statistically lower in patients with pathologic GERD. HRM and pH Impedance testing demonstrates no difference in UES basal and residual pressures based on pH diagnosis of GERD. We redemonstrate the association with hypotonic LES, diminished DCI and MNBI with GERD.

Abstract An elevation of serum inflammatory biomarkers in achalasia patients compared with controls recently was demonstrated. It has not been determined whether the elevation of inflammatory cytokines is unique to achalasia or occurs with other diseases involving the esophagus. The primary aim of our study was to compare the differences in plasma immunological profiles (TNF- α receptor, IL-6, IFN-γ, IL-12, IL-17, IL-22, and IL-23) of patients with achalasia, eosinophilic esophagitis (EoE), and gastroesophageal reflux disease (GERD). A secondary aim of this study was to classify these same plasma cytokine profiles in the three achalasia subtypes. Methods Plasma from 53 patients with achalasia, 22 with EoE, and 20 with GERD (symptoms plus esophagitis or + reflux study) were analyzed. Exclusion criteria: malignancy, autoimmune condition, immunodeficiency disorder, and treatment with steroids/immune modulating drugs. Cytokine levels were assayed via multiplex enzyme-linked immunosorbent assay (ELISA). Results Our key finding revealed significant elevations in IL- 6 (p = 0.0158) in achalasia patients compared with EoE patients. Overall, plasma inflammatory biomarker patterns were not different in the three subtypes of achalasia. Conclusion There were no differences between the cytokine levels of any of the measured biomarkers between the achalasia and GERD groups suggesting that luminal stasis does increase biomarker levels for any of the cytokines examined in our study. While these results are an early first step towards clarifying some aspects of the pathogenesis of achalasia, they bring about many more questions that require further investigation and expansion. Further investigation with a larger cohort and a broader panel of biomarkers is needed.