title: Distension during gastroesophageal reflux: effects of acid inhibition and correlation with symptoms.
abstract: We studied spontaneous gastroesophageal reflux (GER)-induced esophageal distension using ultrasound imaging and its role in the genesis of esophageal symptoms before and during esomeprazole therapy. Ten controls and 10 GER disease (GERD) patients were studied by combined impedance, esophageal pH, manometry, and ultrasonography before and during esomeprazole therapy. Physiological data and symptoms were recorded for 2 h following a standardized meal. From ultrasound images, the esophageal cross-sectional area (CSA) at the peak of GER-induced distension was determined and compared between controls vs. patients, symptomatic vs. asymptomatic GER episodes, and before vs. during esomeprazole in GERD patients. The mean lumen CSA is greater in the patients than controls (271 +/- 71 mm(2) vs. 163 +/- 56 mm(2), P = 0.001) but not different among asymptomatic reflux episodes, and those associated with regurgitation (290 +/- 110 mm(2)) or heartburn (271 +/- 67 mm(2)). Eight chest pain episodes associated with reflux revealed a tendency toward larger mean esophageal distension (459 +/- 40 mm(2)) compared with asymptomatic reflux (268 +/- 70 mm(2), P = 0.058). Following esomeprazole treatment, most GER episodes were nonacidic and asymptomatic except in two patients in whom cyclical reflux was associated with large esophageal distensions. Esomeprazole did not alter the lumen CSA during GER. Esophageal distension is greater in the GERD subjects compared with controls; however, it is unlikely that the GER-induced distension of the esophagus plays a significant role in the genesis of heartburn sensation. Esomeprazole therapy does not alter the GER-induced distension of the esophagus.
authors.affiliation: Division of Gastroenterology, San Diego Veterans Affairs Health Care System and University of California, San Diego, California 92161, USA.
authors.forename: Neelesh A
authors.initials: NA
authors.lastname: Tipnis
authors.forename: Poong-Lyul
authors.initials: PL
authors.lastname: Rhee
authors.forename: Ravinder K
authors.initials: RK
authors.lastname: Mittal
mesh_terms: D000328:Adult; D000897:Anti-Ulcer Agents / Q000494:pharmacology / Q000627:therapeutic use*; D016022:Case-Control Studies; D004108:Dilatation, Pathologic; D017097:Electric Impedance; D019160:Endosonography; D004791:Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D064098:Esomeprazole / Q000494:pharmacology / Q000627:therapeutic use*; D050782:Esophageal pH Monitoring; D004947:Esophagus / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D005260:Female; D005764:Gastroesophageal Reflux / Q000150:complications / Q000188:drug therapy* / Q000201:enzymology / Q000473:pathology; D017506:H(+)-K(+)-Exchanging ATPase / Q000378:metabolism; D006356:Heartburn / Q000188:drug therapy / Q000201:enzymology / Q000209:etiology* / Q000473:pathology; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D008365:Manometry; D008875:Middle Aged; D011312:Pressure; D054328:Proton Pump Inhibitors; D016896:Treatment Outcome
chemical_list: D000897:Anti-Ulcer Agents; D004791:Enzyme Inhibitors; D054328:Proton Pump Inhibitors; D017506:H(+)-K(+)-Exchanging ATPase; D064098:Esomeprazole