Gastroesophageal reflux disease and obesity. Pathophysiology and implications for treatment
Gastroesophageal reflux disease and obesity. Pathophysiology and implications for treatment
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DOI：
10.1007/s11605-007-0097-z
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发表时间：
2007-03-01
影响因子：
3.2
通讯作者：
Patti, Marco G.
中科院分区：
文献类型：
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作者：
Herbella, Fernando A. M.;Sweet, Matthew P.;Patti, Marco G.
虽然胃食道反流病(GERD)的病因是多因素的，但病态肥胖患者的疾病病理生理学仍不完全清楚。这项研究的目的是比较病态肥胖(体重指数=35)和非病态患者(体重指数=35)GERD：(A)下食道括约肌(LES)曲线；(B)食管体功能；(C)食管酸暴露。我们回顾了连续599例GERD患者的食道测压和24小时pH监测研究(DeMeester评分14.7)。按BMI分为两组：(1)BMI<35者520例(86.8%)；(2)BMI<35者79例(13.2%)。DeMeester评分在两组间无差异，但病态肥胖患者的LES压力和食道远端蠕动幅度(DEA)较高。在这些患者中，LES和DEA的压力通常是高血压的。线性回归模型显示BMI、LES压力、LES腹长和DEA与DeMeester评分独立相关。这些数据表明：(A)BMI与GERD的严重程度独立相关；以及(B)在大多数患有GERD的病态肥胖患者中，尽管食道运动正常或高血压，仍会发生反流。这些发现表明，病态肥胖患者的GERD的病理生理学可能与非肥胖患者不同，这表明需要不同的治疗方法。
Although the etiology of gastroesophageal reflux disease (GERD) is multifactorial, the pathophysiology of the disease in morbidly obese patients remains incompletely understood. The aims of this study were to compare in morbidly obese (body mass index (BMI) >= 35) and nonmorbidly patients (BMI < 35) with GERD: (a) lower esophageal sphincter (LES) profile; (b) esophageal body function; and (c) esophageal acid exposure. We reviewed esophageal manometry and ambulatory 24-hour pH monitoring studies of 599 consecutive patients with GERD (DeMeester score > 14.7). Patients were divided into two groups according to the BMI: (1) 520 patients (86.8%) with BMI < 35 and (2) 79 patients (13.2%) with BMI >= 35. While the DeMeester score was not different between the two groups, morbidly obese patients bad higher LES pressure and higher amplitude of peristalsis in the distal esophagus (DEA). Among these patients, LES and DEA pressures were often hypertensive. A linear regression model showed that BMI, LES pressure, LES abdominal length, and DEA were independently associated with the DeMeester score. These data showed that: (a) BMI was independently associated to the severity of GERD; and (b) in most morbidly obese patients with GERD, reflux occurred despite normal or hypertensive esophageal motility. These findings show that the pathophysiology of GERD in morbidly obese patients might differ from that of nonobese patients, suggesting the need for a different therapeutic approach.