Gastroenterology

Gastroenterology

Volume 132, Issue 3, March 2007, Pages 883-889
Gastroenterology

Clinical–alimentary tract
Obesity Is Associated With Increased Transient Lower Esophageal Sphincter Relaxation

https://doi.org/10.1053/j.gastro.2006.12.032Get rights and content

Background & Aims: 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 ≥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 (r2: 0.70, B: 0.28, 95% CI: 0.24–0.33, P < .001) and waist circumference (r2: 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.

Section snippets

Subjects

We prospectively recruited consecutive obese (BMI >30 kg/m2) patients who were referred for globus, noncardiac chest pain, or preoperative assessment of weight reduction procedures because of moderate to severe obesity. During the same study period, nonobese patients with globus and noncardiac chest pain were recruited as controls. All patients with globus and noncardiac chest pain had failure of symptom response to an 8-week therapeutic trial of proton pump inhibitor. The controls were further

Results

From August 2003 to September 2005, 28 obese subjects, 28 overweight subjects, and 28 normal weight controls were studied. Sixteen subjects in each group were male. The demographics and anthropometric data are presented in Table 1. Noncardiac chest pain was the indication for the motility study in 12 (43%) normal weight subjects and 5 (18%) overweight subjects. None of the subjects with globus and noncardiac chest pain had symptom response to proton pump inhibitors. Six (21.4%) patients in the

Discussion

Obesity has been implicated as a major risk factor of GERD and its complication. Many studies have reported an association between obesity, hiatus hernia, and various motility dysfunctions of the upper gastrointestinal tract in GERD patients. However, it is arguable whether obesity predisposes to these conditions or whether they merely coexist in GERD. To solve this controversy, we set out to evaluate the relationship between obesity and functional integrity of GOJ in subjects without GERD. In

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