Wu Justin Che-Yuen, Mui Lik-Man, Cheung Carrian Man-Yuen, Chan Yawen, Sung Joseph Jao-Yiu
Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong.
Gastroenterology. 2007 Mar;132(3):883-9. doi: 10.1053/j.gastro.2006.12.032. Epub 2006 Dec 19.
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.
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.
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.
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.
肥胖与胃食管反流病（GERD）及其并发症相关，但机制尚不清楚。我们评估了无GERD受试者中肥胖与食管下括约肌（LOS）功能之间的关联。
我们前瞻性地招募了连续的肥胖（BMI>30）患者，这些患者因减重手术前来就诊，并纳入了年龄和性别匹配的超重（BMI 25 - 30）和正常体重（BMI≥20且<25）的受试者。排除标准包括食管炎、反流症状、使用质子泵抑制剂、裂孔疝>2 cm以及伴有微血管并发症的糖尿病。所有参与者在标准试验餐后接受了2小时餐后食管测压和pH监测，随后进行24小时动态pH监测。
共研究了84名受试者（肥胖组28名、超重组28名、正常体重组28名）。所有3组的平均LOS压力、LOS长度和蠕动功能相当。在餐后期间，肥胖组和超重组的2小时短暂食管下括约肌松弛（TLOSR）发生率均显著增加（正常体重组：2.1±1.2 vs超重组：
