Background: Esophageal hypersensitivity is considered an important pathophysiological mechanism in refractory gastroesophageal reflux disease (GERD) patients. Serotonin (5-HT) plays an important role in the regulation of GI (gastrointestinal) secretion, motility and sensitivity. Previous studies found that altered 5-HT availability has no clear effects on esophageal/GI sensations.
View Article and Find Full Text PDFIntroduction: Gastroesophageal reflux disease (GERD) and functional dyspepsia (FD) are 2 of the most prevalent upper gastrointestinal (GI) disorders in the Western world. Previous Rome definitions excluded patients with predominant heartburn from the definition of FD because they were considered to have GERD. However, more recent studies showed that heartburn and acid regurgitation are also common symptoms in patients with FD.
View Article and Find Full Text PDFBackground: Drugs such as citalopram, "targeting" the serotonin pathway, can alter esophageal mechano-chemical sensitivity and gastrointestinal motility. The aim of this study was to clarify the effect of citalopram on esophageal motility and sphincter function, transient lower esophageal sphincter relaxations (TLESRs), and reflux events.
Methods: Sixteen healthy volunteers (HV) receiving 20 mg citalopram or placebo intravenously, in a randomized cross-over fashion, underwent two high-resolution impedance manometry studies involving liquid swallows and a high-fat, high-caloric meal.
Objectives: Both rumination syndrome and supra-gastric belching (SGB) have limited treatment options. We demonstrated (open-label) that baclofen reduces pressure flow events in these patients. We aimed to study the effect of baclofen in a placebo-controlled, double-blind, cross-over study in patients with clinically suspected rumination and/or SGB.
View Article and Find Full Text PDFAm J Physiol Gastrointest Liver Physiol
May 2017
Esophageal hypersensitivity is important in gastroesophageal reflux disease (GERD) patients who are refractory to acid-suppressive therapy. Stress affects visceral sensitivity and exacerbates heartburn in GERD. Peripheral CRH is a key mediator of the gut stress response.
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