title: Obesity is associated with increased transient lower esophageal sphincter relaxation.
abstract: OBJECTIVE
  Obesity has been associated with gastroesophageal reflux disease (GERD) and its complication, but the mechanism is unclear. We evaluated the association between obesity and function of lower esophageal sphincter (LOS) in subjects without GERD.
  
  
  METHODS
  We prospectively recruited consecutive obese (BMI >30) patients referred for weight reduction procedure and age- and sex-matched overweight (BMI 25-30) and normal weight (BMI > or =20 and <25) subjects. Exclusion criteria included esophagitis, reflux symptoms, use of proton pump inhibitor, hiatus hernia >2 cm, and diabetes mellitus with microvascular complication. All participants underwent combined 2-hour postprandial esophageal manometry and pH monitoring after a standard test meal followed by 24-hour ambulatory pH monitoring.
  
  
  RESULTS
  Eighty-four subjects (obese, 28; overweight, 28; normal weight, 28) were studied. All 3 groups had comparable mean LOS pressure, LOS length, and peristaltic function. During the postprandial period, both obese and overweight groups had substantial increase in 2-hour rate of transient lower esophageal sphincter relaxation (TLOSR) (normal weight: 2.1 +/- 1.2 vs overweight: 3.8 +/- 1.6 vs obese: 7.3 +/- 2.0, P < .001), proportion of TLOSR with acid reflux (normal weight: 17.6% +/- 22.0% vs overweight 51.8% +/- 22.5% vs obese: 63.5% +/- 21.7%, P < .001), and gastroesophageal pressure gradient (GOPG) (normal weight: 4.5 +/- 1.2 mm Hg vs overweight: 7.1 +/- 1.4 mm Hg vs obese: 10.0 +/- 1.5 mm Hg, P < .001). Using multiple regression model, BMI (r(2): 0.70, B: 0.28, 95% CI: 0.24-0.33, P < .001) and waist circumference (r(2): 0.65, unstandardized regression coefficient [B]: 0.10, 95% CI: 0.08-0.11, P < .001) were significantly correlated with TLOSR.
  
  
  CONCLUSIONS
  Obesity is associated with increased TLOSR and acid reflux during the postprandial period in subjects without GERD. Abnormal postprandial LOS function may be an early event in the pathogenesis of obesity-related GERD.
authors.affiliation: Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong. justinwu@cuhk.edu.hk
authors.forename: Justin Che-Yuen
authors.initials: JC
authors.lastname: Wu
authors.forename: Lik-Man
authors.initials: LM
authors.lastname: Mui
authors.forename: Carrian Man-Yuen
authors.initials: CM
authors.lastname: Cheung
authors.forename: Yawen
authors.initials: Y
authors.lastname: Chan
authors.forename: Joseph Jao-Yiu
authors.initials: JJ
authors.lastname: Sung
mesh_terms: D000328:Adult; D015992:Body Mass Index; D049628:Body Size; D016022:Case-Control Studies; D049630:Esophageal Sphincter, Lower / Q000503:physiopathology*; D050782:Esophageal pH Monitoring; D005260:Female; D005764:Gastroesophageal Reflux / Q000209:etiology; D006801:Humans; D016014:Linear Models; D008297:Male; D008365:Manometry / Q000379:methods; D008875:Middle Aged; D009126:Muscle Relaxation; D009765:Obesity / Q000150:complications / Q000503:physiopathology*; D010528:Peristalsis; D019518:Postprandial Period; D011446:Prospective Studies; D012307:Risk Factors; D013997:Time Factors