Gastroesophageal Reflux Disease and Obesity. Pathophysiology and Implications for Treatment

Abstract

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) > or =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 > or =35. While the DeMeester score was not different between the two groups, morbidly obese patients had 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.

Gastroesophageal reflux disease and severe obesity: Fundoplication or bariatric surgery?

“…While nearly 30% of the 1659 subjects in this study were noted to be obese, specific data regarding severely obese individuals were not described. In contrast, in another large cohort of patients with GERD, mean LESP was in fact significantly greater in subjects with severe obesity (17 ± 9.2 mmHg vs 14 ± 7.6 mmHg), and 62% of severely obese subjects with GERD had a normal (39%) or hypertensive (23%) LES compared to only 46% of individuals with BMI ≤ 35 kg/m 2 ; 10% of whom were noted to have a hypertensive LES [18] . The authors of this study hypothesized that the mechanisms responsible for GERD might be different in the setting of severe obesity, and that the observed increased LESP could represent a compensatory mechanism against the increased pressure gradient between the stomach and esophagus, which ultimately remains inadequate to prevent GERD.…”

Patient factors predictive of 24-h pH normalization following endoluminal gastroplication for GERD

“…Morbidly obese patients with GERD have reflux symptoms and DMS similar to the nonobese, even with normal or hypertensive LES tone and esophageal motility [24,25]. Several theories exist to explain why this occurs in spite of a seemingly normal barrier to reflux.…”

The Intersection of GERD, Aspiration, and Lung Transplantation

“…4 Today, emphasis is also placed on the role of mixed gastroesophageal reflux 5 and on the transdiaphragmatic pressure gradient 6 as both have important therapeutic implications.…”