Obesity and Gastroesophageal Reflux Disease (GERD)

| May 1, 2016 | 0 Comments

This column is written by medical students and is dedicated to reviewing the science behind obesity and bariatric surgery.

Column Editor: Daniel B. Jones, MD, MS, FASMBS
Professor of Surgery, Harvard Medical School, Vice Chair, Beth Israel Deaconess Medical Center, Boston, Massachusetts

This month: Obesity and Gastroesophageal Reflux Disease (GERD)

by Ofer Fass, BS, BHS
Medical Student, Harvard Medical School, Boston, Massachusetts

Bariatric Times. 2016;13(5):10–15.

Obesity is a complex medical condition that is associated with a high morbidity and mortality. Gastroesophageal reflux disease (GERD), which affects up to 20 percent of the adult population in the United States, is commonly associated with obesity. Untreated, GERD can result in a symptomatic burden to the patient, poor health-related quality of life, complications, such as esophageal stricture, Barrett’s esophagus, and esophageal adenocarcinoma, and a high direct and indirect cost to the healthcare system. Various pathophysiological mechanisms have been identified to explain the close relationship between obesity and GERD, including a high prevalence of hiatal hernia and increased gastroesophageal pressure gradient. Overall, diagnosis and medical treatment of GERD in patients with obesity are similar to those for patients without obesity. Weight loss in the patient with obesity has also been associated with improved GERD. Bariatric surgery provides a unique opportunity to address both obesity and its associated GERD in this patient population.

Obesity is a highly challenging disorder to our healthcare system that continues to increase in frequency and severity. It has been estimated that greater than one third of American adults (34.9% or 78.6 million people) are classified as having obesity, which is defined as a body mass index (BMI) of 30kg/m2 or more.[1] It is predicted that by the year 2030, the rate of obesity among the general population will surpass 44 percent in all 50 states of the United States.[2] Obesity also poses a substantial financial burden in the United States, with an estimated annual medical cost of $147 billion in 2008 alone.[3]

Similarly, gastroesophageal reflux disease (GERD) is a common gastrointestinal disorder affecting approximately 20 percent of the adult population in the United States, and it has been growing in prevalence.[4,5] GERD is defined as reflux of stomach contents into the esophagus, which can result in bothersome symptoms and complications.[6] It has been proposed that the increase in the prevalence of GERD is partly due to its association with obesity and high BMI. A recent study that was conducted in a cohort of 10,545 women demonstrated a significant association between increasing BMI and patients’ report of GERD symptoms (multivariate P for trend <0.001).[7] As obesity levels continue to rise, it is expected that the prevalence of GERD will follow suit. This is a major cause for concern, given the causal relationship between GERD and Barrett’s esophagus as well as esophageal adenocarcinoma, which is currently the fastest rising cancer in the United States.[8] Thus, through its association with GERD and as an independent risk factor, obesity increases the risk of Barrett’s esophagus and consequently esophageal adenocarcinoma.[9] To better understand the link between obesity and GERD, it is necessary to examine the proposed pathophysiologic mechanisms that lead to the close association of the two disorders.

Several underlying mechanisms have been proposed to be responsible for the close relationship between obesity and GERD (Table 1). One of the important mechanisms is an increased incidence of hiatal hernia in the population with obesity, resulting in GERD symptoms.[10] Hiatal hernia exacerbates GERD symptoms by decreasing the pressure at the lower esophageal sphincter (LES)[11] and by serving as a reservoir for gastric acid above the diaphragm that is difficult for the stomach to clear.[12] Furthermore, a direct correlation between hiatal hernia size and severity of gastroesophageal reflux has been observed.[13] The mechanism by which obesity leads to the development of hiatal hernia is likely secondary to an increase in abdominal pressure forcing the gastric fundus through a weak location in the diaphragm.[14]

Increased intra-abdominal pressure by itself, in the absence of a hiatal hernia, is another proposed mechanism for the development of obesity-related GERD. A study by Mercer et al[15] has demonstrated increased gastroesophageal pressure gradient and delayed esophageal transit time in patients with obesity compared to patients without obesity.[15] Their findings have been substantiated by a more recent study by Pandolfino et al[16] In this study, high-resolution esophageal manometry probe was placed in the stomach, demonstrating a significant correlation between both BMI and waist circumference with increased intra-abdominal pressure. The authors concluded that the increased gastroesophageal pressure favors the movement of gastric contents into the esophagus.[16] The proposed link between obesity, increased intra-abdominal pressure, and GERD symptoms has become widely accepted, however, questions remain as to why weight loss does not necessarily lead to improvement in GERD symptoms.[17]

Another proposed mechanism for the relationship between obesity and GERD relates to diet. Intake of food high in fat content resulst in the secretion of hormones, such as secretin and cholecystokinin, which lead to lower esophageal sphincter (LES) relaxation.[18] A study by Fox et al. demonstrated increased frequency of GERD symptoms with a high-fat diet compared to a low-fat diet irrespective of caloric density.[19] Multiple studies have demonstrated a correlation between chocolate,[20] alcohol,[21] and caffeine[22] intake with GERD symptoms secondary to increased relaxation of the LES.

Ultimately, it is likely that no single mechanism is specifically responsible for the development of GERD in patients with obesity rather than various mechanisms that work in concert to form a pathophysiological process favoring the development of GERD symptoms.

Clinical Presentation
The clinical presentation of GERD in patients with obesity is similar to that in patients without obesity. The most common symptoms associated with GERD include heartburn, regurgitation, sour or bitter taste in the mouth, water brash, and dysphagia.[6] Heartburn, by far the most common presentation of GERD, is often described as a retrosternal burning sensation following the ingestion of food.[6] Regurgitation is commonly described as the feeling of acidic fluid in the back of the throat, although some patients may perceive sub sternal migration of fluid to the upper part of the esophagus.[20] The presence of dysphagia is usually indicative of esophageal inflammation or stricturing as a result of long-standing gastroesophageal reflux.[21]

Extra esophageal manifestations of GERD are due to reflux of gastric contents into the pharynx, larynx, or pulmonary system. These include hoarseness, dysphonia, sore/burning throat, excessive throat clearing, globus sensation, laryngospasm, asthma, and postnasal drip.[22]

Chest pain is a common atypical presentation of GERD, thought to occur in approximately 23.5 percent of patients with gastroesophageal reflux.[23] The chest pain is often described as a substernal squeezing/burning, radiating to the back, neck, jaw, or arms, and lasting from minutes-to-hours.[24] This presentation mimics angina pectoris, causing significant distress. Importantly, 10 to 20 percent of the patients presenting to the emergency department with chest pain are found to have a gastrointestinal etiology to their pain, most commonly GERD.[25]

The diagnosis of GERD is usually made clinically based on the patient’s history and physical examination.[26] A trial of empiric therapy with a proton pump inhibitors (PPI) is highly sensitive, but not specific for the diagnosis of GERD.[27] Most patients will be treated with anti-reflux medications without any diagnostic testing.

In GERD patients, who initially present with chest pain, a cardiac etiology should first be ruled out by a cardiologist. In patients with typical symptoms of GERD, an objective diagnosis may be obtained by ambulatory 24-hour esophageal pH monitoring or upper endoscopy. The American College of Gastroenterology (ACG) recommends ambulatory pH monitoring (catheter based or wireless) in patients refractory to PPI treatment, those with extraesophageal manifestations who do not have typical symptoms of GERD, and in patients with nonerosive reflux disease (NERD) as determined by upper endoscopy.[28] Impedance/pH testing is offered to patients who failed PPI treatment (usually twice per day) and is done on treatment.

Regarding the role of upper endoscopy in the evaluation of GERD, the ACG recommends using endoscopy only in the presence of alarm symptoms, such as dysphagia, odynophagia, anorexia, weight loss, and upper GI bleed, and in patients refractory to PPI treatment. The use of upper endoscopy for routine diagnosis of GERD is discouraged.[28] Barium swallow and esophageal manometry are not used routinely in the diagnosis of GERD because of their low sensitivity.[26]

GERD treatment in the patient with obesity is similar to the treatment of other GERD patients. However, studies have repeatedly demonstrated that of all lifestyle modifications, weight loss and elevation of the head of the bed are associated with symptom improvement.[29] Furthermore, in a recent systematic review, it was demonstrated that weight loss can even improve GERD-related objective parameters, such as esophageal acid exposure.[29] Most GERD patients will require some type of medical treatment, which is based on the severity of their disease. Proton pump inhibitors (PPIs) are the most effective treatment that is currently available, primarily because of their profound and consistent acid suppression. Commonly, patients are started on once daily standard dose PPI that is given 30 minutes prior a meal, generally breakfast. Lifestyle modifications, compliance and adherence to the proper time of PPI consumption are encouraged. The dose of PPI is usually doubled if patients demonstrate partial or lack of response to treatment. In this case, one PPI in a standard dose is given half an hour before breakfast and the other half an hour before dinner. There are other medical therapies that are also used to treat GERD either alone or in combination with PPI treatment and they include, antacids, calcium carbonate antacid, histamine 2 receptor antagonists, sucralfate (an anti-ulcer medication), baclofen (a muscle relaxer and an antispastic agent), and prokinetics.

Presently, two endoscopic techniques are available to treat GERD. Neither of them are specific for the patient with obesity.[30] The Stretta system (Mederi Therapeutics, Inc., Norwalk, Connecticut) delivers radiofrequency energy to the esophageal tissue resulting in muscular thickening of the LES and thus fewer transient LES relaxations. The transoral incisionless fundoplication (TIF) technique allows the creation of 2 to 3 cm and 210 to 300-degree fundoplication at the level of the gastroesophageal junction. Anti-reflux surgery has been shown to be less effective in the patient with obesity than in those without obesity. Consequently, it is currently recommended that patients with obesity who are referred for anti-reflux surgery should undergo Roux-en-Y gastric bypass (RYGB) instead.[32]

Role of Bariatric Surgery
As the prevalence of obesity has continued to increase in the United States, bariatric surgery has risen to become an essential strategy for disease management. In 2011 alone, 340,770 bariatric procedures were performed with laparoscopic sleeve gastrectomy (LSG) being the most common.[31] Nearly one-third (101,645) of these procedures were performed in the United States and Canada.[31] Given the rising popularity of bariatric surgery, various studies have attempted to elucidate the relationship between bariatric surgery and GERD symptoms.

In 2013, LSG surpassed Roux-en-Y gastric bypass (RYGB) as the most commonly preformed bariatric surgery in the United States, Canada, Asia, and the Pacific regions.[32] The growing popularity of LSG poses a challenge to clinicians managing patients with obesity suffering from GERD, as the effect of LSG on GERD symptoms remains somewhat controversial. A systematic review by Chiu et al[33] examined the relationship between LSG and GERD. Fifteen key studies were identified, with four studies demonstrating an increase in GERD symptoms and seven demonstrating a decrease postoperatively.[33] Despite these mixed findings, the general consensus remains that LSG increases the incidence of gastroesophageal reflux. A retrospective review by Cecily et al analyzed a cohort of 4,832 patients who underwent LSG. Of those, 2,150 (44.5%) reported preoperative GERD symptoms. Following surgery, the majority of patients continued to have GERD symptoms postoperatively (84.1% of the 2,150 patients with preoperative GERD symptoms) and 8.6 percent of patients with no GERD symptoms preoperatively, reported developing de novo GERD. Furthermore, the presence of preoperative GERD was associated with increased postoperative complications, increased gastrointestinal adverse events, an increased need for revisional surgery, and decreased weight loss.[34]

Two primary mechanisms have been proposed to facilitate the increase in GERD symptoms following LSG. First, division of the diaphragmatic crural ligaments and disruption of the angle of His are thought to decreases LES baseline pressure. Second, decreased compliance of the gastric pouch results in increased intragastric pressure. The two mechanisms work in concert to form a pressure gradient favoring the reflux of gastric content into the esophageal lumen.[35]

In an attempt to make LSG accessible to patients suffering from GERD and prevent the development of de novo GERD, a number of investigators have advocated for hiatal hernia exploration and repair concurrently with LSG. In a study by Soricelli et al,[36] zero percent of patients undergoing LSG with hiatal hernia repair developed de novo GERD, compared to 22.9 percent of patients undergoing LSG alone. A prospective cohort study by Daes et al[37] that followed 134 LSG patients showed similar results. Sixty-six patients (49.2%) were diagnosed with preoperative GERD and 34 patients were found to have hiatal hernia intraoperatively. Following LSG and repair of all hiatal hernias, only two patients (1.5%) were found to have GERD symptoms at 6 to 12 months postoperatively.[37] Despite early promising results for combined LSG and hiatal hernia repair, a 2014 study by Santonicola et al[38] found that hiatal hernia repair did not improve GERD symptoms. In this study, 78 patients undergoing LSG with hiatal hernia repair were compared with 102 patients without hiatal hernia who underwent LSG alone. Preoperatively, there was no difference in the prevalence of GERD symptoms between the two groups, however, postoperatively the LSG group demonstrated a significant decrease in GERD symptoms. The LSG plus hiatal hernia repair group was found to have a significantly higher frequency and intensity of GERD symptoms compared to the LSG only group.[38]

Although LSG has overtaken RYGB as the most commonly preformed procedure in the United States and Canada, RYGB remains the most popular bariatric procedure worldwide. Overall, 45 percent of all bariatric procedures preformed in 2013 internationally were RYGB.[32] The effect of RYGB on GERD is considered much more favorable, and has consistently been shown to improve symptoms. A prospective study by Nelson et al[39] examined 239 patients undergoing RYGB with preoperative GERD symptoms. At nine months postoperatively, 94 percent of patients reported improved GERD symptoms, and medication usage decreased from 30 percent preoperatively to five percent postoperatively. The authors ultimately concluded that the observed effect of RYGB on decreased GERD symptoms and medication usage is independent of weight loss, and that RYGB should be the bariatric procedure of choice in GERD patients.[39] Numerous other studies have demonstrated similar findings as Nelson et al, leading experts to recommend RYGB for surgical management of obese patients with GERD.[40]

Multiple mechanisms are believed to cause a decrease in acid reflux following RYGB. First, a small gastric pouch limits acid production secondary to a decrease in the number of parietal cells.[41] Second, a small gastric pouch significantly reduces the reservoir available for regurgitation. Third, the procedure dramatically reduces obesity, decreasing the intra-abdominal pressure and the propensity for gastroesophageal reflux.[40] Finally, RYGB reduces duodenal gastric reflux by eliminating direct communication of the duodenum with the esophagus.[42] However, it should be noted that patients with a short Roux limb are at risk for alkaline reflux, which can perpetuate esophageal ulceration.[40,42]

Adjustable gastric bands (AGB) have continued to decline in popularity, falling from 68 percent of weight loss surgeries preformed worldwide in 2008 to 10 percent in 2013.[32] The effect of AGB on acid reflux symptoms, similar to LSG, appears to be somewhat controversial. Studies with shorter follow-up times tend to demonstrate a beneficial affect of AGB on GERD symptoms. A 1999 study by Dixon et al[43] examined the prevalence of postoperative GERD symptoms in a cohort of 48 patients. At 12-month follow up, 76 percent of patients demonstrated complete resolution of symptoms and an additional 14 percent reported improvement of symptoms. Only two patients (4%) reported an increase in symptoms.[43] A more recent publication by Lew et al[44] reported similar results. The authors investigated the relationship between preoperative esophageal manometry, GERD, and outcomes of laparoscopic adjustable silicone gastric banding in a cohort of 77 patients. Follow-up between 6 and 12 months postoperatively demonstrated 1,000-percent resolution of GERD symptoms in patients with abnormal preoperative manometry and 92-percent GERD resolution in patients with normal preoperative manometry.[44] Despite encouraging results, when follow-up times are extended beyond 12 months, the affect of AGB on GERD becomes uncertain. As part of a larger study investigating esophageal motility and reflux symptoms in relation to bariatric surgery, Korenkov et al[45] examined 21 patients who underwent AGB. Patients had an average follow-up time of 22 months. Of the six AGB patients with preoperative reflux symptoms, three experienced resolution of their symptoms, three had no change in their symptoms, and three patients without reflux symptoms preoperatively developed de novo symptoms.[45] A systematic review from 2010 reported similar conflicting results. Analysis of 20 studies with a total of 3,307 patients undergoing AGB demonstrated a decrease in GERD symptoms from 32.9 percent preoperatively to 7.7 percent postoperatively. However, newly developed reflux occurred in 15 percent of patients. The percentage of erosive esophagitis decreased from 33.3 percent preoperatively to 27 percent postoperatively, however, newly developed esophagitis was observed in 22.9 percent of patients postoperatively.[46]

The mechanism by which AGB effects reflux symptoms requires further investigation. A study published by Woodman et al[47] proposed multiple mechanisms leading to decrease in GERD symptoms. These include weight reduction, decrease in intragastric pressure, changes in the frequency of LES relaxation, and reinforcement of the gastroesophageal sphincter.[47]

What is Still Unknown
Studies are still needed to evaluate the effect of obesity on response to medical or endoscopic treatment. It is also unknown if patients with obesity respond better, or the same, to PPI or endoscopic treatment as their normal weight counterparts. It is unclear what diagnostic workup patients with obesity with suspected GERD need to undergo preoperatively. Presently, these patients are evaluated solely by an upper endoscopy prior to bariatric surgery, which may be insufficient to predict the outcome of their GERD post surgery. Moreover, the long-term impact of sleeve gastrectomy and even gastric bypass on gastroesophageal reflux disease and esophageal motility in patients without GERD or mild GERD still needs to be fully elucidated.

Obesity and its associated comorbidities pose a serious challenge to our healthcare system. As the incidence of obesity continues to rise in the United States, GERD is expected to follow suit. As a clinician, it is essential to be familiar with the close relationship between GERD and obesity in order to successfully recognize, diagnose, and treat GERD in this patient population. If GERD remains untreated, it can result in various complications, including peptic stricture, erosive esophagitis, Barrett’s esophagus, and ultimately esophageal adenocarcinoma.[48]

With the advent of weight loss surgery, new therapeutic modalities have become available that have been shown to be more effective in aiding patients lose weight than intensive medical treatment, dieting, and exercise alone.[49] As patients lose weight, many of their obesity-associated comorbidities improve drastically, or even resolve completely.[50] However, the effect of weight loss surgery on GERD has been inconclusive. The literature continues to debate the effect of LSG on GERD symptoms. Although data exist to suggest that LSG when combined with hiatal hernia repair can prevent the occurrence of postoperative GERD symptoms, the current consensus is that LSG should be avoided in patients with severe erosive esophagitis and/or Barrett’s esophagus.[51] It remains difficult to predict who will have their GERD improved and for whom it may get worse after sleeve gastrectomy. Therefore, it may be reasonable for patients who do not want or are not able to undergo a gastric bypass (although best for patients with reflux), to offer a sleeve with the understanding that if GERD worsens they understand that a gastric bypass would be required to potentially treat GERD. The single weight-loss surgery that has been consistently shown to reduce GERD symptoms is RYGB. It remains the surgical treatment of choice for patients with obesity suffering from GERD.

As new bariatric procedures become available to clinicians, further studies will be necessary to investigate their effect on GERD severity and frequency. In 2015, the United States Food and Drug Administration approved the use  two endoscopic intragastric balloon systems—Orbera (Apollo Endosurgery, Austin, Texas) and ReShape Integrated Dual Balloon System (ReShape Medical, San Clemente, California) for obesity treatment. The US FDA also approved vagal nerve blocking therapy (vBloc®, EnteroMedics® Inc., St. Paul, Minnesota), an electrical system targeting vagal innervation of the stomach to limit gastric motility and release of appetite-stimulating hormones. The effect of both of these novel systems on GERD symptoms is an area requiring further investigation.

1.     Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of Childhood and Adult Obesity in the United States, 2011–2012. JAMA. 2014, 311(8):806–814.
2.    Levi J, Segal LM LR, Lang A, Rayburn J: F as in Fat: How obesity threatens America’s future. In: Robert Woods Johnson Foundation & Trust for America’s Health Issue Report. 2012.
3.    Finkelstein EA, Trogdon JG, Cohen JW, Dietz W. Annual Medical Spending Attributable To Obesity: Payer-And Service-Specific Estimates. Health Affairs. 2009;28(5):w822–w831.
4.    El-Serag HB, Sweet S, Winchester CC, Dent J. Update on the epidemiology of gastro-oesophageal reflux disease: a systematic review. Gut. 2014;63(6):871–880.
5.    Farup C, Kleinman L, Sloan S, et al. The impact of nocturnal symptoms associated with gastroesophageal reflux disease on health-related quality of life. Arch Intern Med. 2001;161(1):45–52.
6.    Vakil N, van Zanten SV, Kahrilas P, Dent J, Jones R. The Montreal definition and classification of gastroesophageal reflux disease: a global evidence-based consensus. Am J Gastroenterol. 2006;101(8):1900–1920.
7.    Jacobson BC, Somers SC, Fuchs CS, Kelly CP, Camargo CA Jr. Body-mass index and symptoms of gastroesophageal reflux in women. N Engl J Med. 2006;354(22):2340–2348.
8.    Shaheen N, Ransohoff DF. Gastroesophageal reflux, barrett esophagus, and esophageal cancer: scientific review. JAMA. 2002;287(15):1972–1981.
9.    Thrift AP, Shaheen NJ, Gammon MD, et al. Obesity and risk of esophageal adenocarcinoma and Barrett’s esophagus: a Mendelian randomization study. J Natl Cancer Inst. 2014;106(11). pii: dju252.
10.    Wilson LJ, Ma W, Hirschowitz BI. Association of obesity with hiatal hernia and esophagitis. Am J Gastroenterol. 1999, 94(10):2840–2844.
11.    Kahrilas P, Lin S, Chen J, Manka M. The effect of hiatus hernia on gastro-oesophageal junction pressure. Gut. 1999, 44(4):476–482.
12.    Mittal RK, Lange R, McCallum R. Identification and mechanism of delayed esophageal acid clearance in subjects with hiatus hernia. Gastroenterology. 1987;92(1):130–135.
13.    Fein M, Ritter MP, DeMeester TR, et al. Role of the lower esophageal sphincter and hiatal hernia in the pathogenesis of gastroesophageal reflux disease. J Gastrointest Surg. 1999;3(4):405–410.
14.    Polomsky M, Peters JH, Schwartz SI. Hiatal hernia and disorders of the spine: a historical perspective. Dis Esophagus. 2012;25(5):367–372.
15.    Mercer CD, Rue C, Hanelin L, Hill LD. Effect of obesity on esophageal transit. Am J Surg. 1985;149(1):177–181.
16.    Pandolfino JE1, El-Serag HB, Zhang Q, et al. Obesity: a challenge to esophagogastric junction integrity. Gastroenterology. 2006;130(3):639–649.
17.    Kjellin A, Ramel S, Rössner S, Thor K. Gastroesophageal reflux in obese patients is not reduced by weight reduction. Scand J Gastroenterol. 1996;31(11):1047–1051.
18.    Nebel OT, Castell DO. Inhibition of the lower oesophageal sphincter by fat—a mechanism for fatty food intolerance. Gut. 1973;14(4):270–274.
19.    Fox M, Barr C, Nolan S, et al. The effects of dietary fat and calorie density on esophageal acid exposure and reflux symptoms. Clin Gastroenterol Hepatol. 2007;5(4):439–444.
20.    Lacy BE, Weiser K, Chertoff J, et al. The diagnosis of gastroesophageal reflux disease. Am J Med. 2010;123(7):583–592.
21.    Vakil NB, Traxler B, Levine D. Dysphagia in patients with erosive esophagitis: Prevalence, severity, and response to proton pump inhibitor treatment. Clin Gastroenterol Hepatol. 2004;2(8):665–668.
22.    Madanick RD. Extraesophageal presentations of GERD: where is the science? Gastroenterol Clin North Am. 2014;43(1):105–120.
23.    Chiocca JC, Olmos JA, Salis GB, et al. Prevalence, clinical spectrum and atypical symptoms of gastro-oesophageal reflux in Argentina: a nationwide population-based study. Aliment Pharmacol Ther. 2005;15;22(4):331–342.
24.    Richter JE. Typical and atypical presentations of gastroesophageal reflux disease. The role of esophageal testing in diagnosis and management. Gastroenterol Clin North Am. 1996;25(1):75–102.
25.    Bösner S, Becker A, Haasenritter J, et al. Chest pain in primary care: epidemiology and pre-work-up probabilities. Eur J Gen Pract. 2009;15(3):141–146.
26.    Kahrilas PJ, Shaheen NJ, Vaezi MF, et al. American Gastroenterological Association Medical Position Statement on the management of gastroesophageal reflux disease. Gastroenterology. 2008;135(4):1383–1391.
27.    Numans ME, Lau J, de Wit NJ, Bonis PA. Short-term treatment with proton-pump inhibitors as a test for gastroesophageal reflux disease: a meta-analysis of diagnostic test characteristics. Ann Intern Med. 2004;140(7):518–527.
28.    Katz PO, Gerson LB, Vela MF. Guidelines for the Diagnosis and Management of Gastroesophageal Reflux Disease. Am J Gastroenterol. 2013;108(3):308–328.
29.    Ness-Jensen E, Hveem K, El-Serag H, Lagergren J. Lifestyle intervention in gastroesophageal reflux disease. Clin Gastroenterol Hepatol. 2016;14(2):175–182.e3.
30.    Lo WK, Mashimo H. Critical assessment of endoscopic techniques for gastroesophageal reflux disease. J Clin Gastroenterol. 2015;49(9):720–724.
31.    Buchwald H, Oien DM. Metabolic/bariatric surgery worldwide 2011. Obes Surg. 2013;23(4):427–436.
32.    Angrisani L, Santonicola A, Iovino P, et al. Bariatric surgery worldwide 2013. Obes Surg. 2015;25(10):1822–1832.
33.    Chiu S, Birch DW, Shi X, Sharma AM, Karmali S. Effect of sleeve gastrectomy on gastroesophageal reflux disease: a systematic review. Surg Obes Relat Dis. 2011;7(4):510–515.
34.    DuPree CE, Blair K, Steele SR, Martin MJ. Laparoscopic sleeve gastrectomy in patients with preexisting gastroesophageal reflux disease: a national analysis. JAMA Surg. 2014;149(4):328–334.
35.    El-Hadi M, Birch DW, Gill RS, Karmali S. The effect of bariatric surgery on gastroesophageal reflux disease. Can J Surg. 2014;57(2):139–144.
36.    Soricelli E, Iossa A, Casella G, et al. Sleeve gastrectomy and crural repair in obese patients with gastroesophageal reflux disease and/or hiatal hernia. Surg Obes Relat Dis. 2013;9(3):356–361.
37.    Daes J, Jimenez ME, Said N, Daza JC, Dennis R. Laparoscopic sleeve gastrectomy: symptoms of gastroesophageal reflux can be reduced by changes in surgical technique. Obes Surg. 2012;22(12):1874–1879.
38.    Santonicola A, Angrisani L, Cutolo P, Formisano G, Iovino P. The effect of laparoscopic sleeve gastrectomy with or without hiatal hernia repair on gastroesophageal reflux disease in obese patients. Surg Obes Relat Dis. 2014;10(2):250–255.
39.    Nelson LG, Gonzalez R, Haines K, Gallagher SF, Murr MM. Amelioration of gastroesophageal reflux symptoms following Roux-en-Y gastric bypass for clinically significant obesity. Am Surg. 2005;71(11):950–953; discussion 953–954.
40.    Ikramuddin S. Surgical management of gastroesophageal reflux disease in obesity. Dig Dis Sci. 2008;53(9):2318–2329.
41.    Smith CD, Herkes SB, Behrns KE, et al. Gastric acid secretion and vitamin B12 absorption after vertical Roux-en-Y gastric bypass for morbid obesity. Ann Surg. 1993;218(1):91–96.
42.    Johnson WH1, Fernanadez AZ, Farrell TM, et al. Surgical revision of loop gastric bypass procedure: multicenter review of complications and conversions to Roux-en-gastric bypass. Surg Obes Relat Dis. 2007;3(1):37–41.
43.    Dixon JB, O’Brien PE: Gastroesophageal reflux in obesity: the effect of lap-band placement. Obes Surg. 1999;9(6):527–531.
44.    Lew JI, Daud A, DiGorgi MF, et al. Preoperative esophageal manometry and outcome of laparoscopic adjustable silicone gastric banding. Surg Endosc. 2006;20(8):1242–1247.
45.    Korenkov M, Köhler L, Yücel N, et al. Esophageal motility and reflux symptoms before and after bariatric surgery. Obes Surg. 2002;12(1):72–76.
46.    De Jong JR, Besselink MGH, Van Ramshorst B, Gooszen HG, Smout AJ. Effects of adjustable gastric banding on gastroesophageal reflux and esophageal motility: a systematic review. Obes Rev. 2010;11(4):297–305.
47.    Woodman G, Cywes R, Billy H, Montgomery K, et al. Effect of adjustable gastric banding on changes in gastroesophageal reflux disease (GERD) and quality of life. Curr Med Res Opin. 2012;28(4):581–589.
48.    Zagari RM, Fuccio L, Wallander MA, et al. Gastro-oesophageal reflux symptoms, oesophagitis and Barrett’s oesophagus in the general population: the Loiano-Monghidoro study. Gut. 2008;57(10):1354–1359.
49.    Schauer PR, Kashyap SR, Wolski K, et al. Bariatric surgery versus intensive medical therapy in obese patients with diabetes. N Engl J Med. 2012;366(17):1567–1576.
50.    Maggard MA, Shugarman LR, Suttorp M, et al. Meta-analysis: surgical treatment of obesity. Ann Intern Med. 2005;142(7):547–559.
51.    Gagner M. Is sleeve gastrectomy always an absolute contraindication in patients with Barrett’s? Obes Surg. 2016;26(4):715–717.

FUNDING: No funding was provided.

FINANCIAL DISCLOSURES: The author reports no conflicts of interest relevant to the content of this article.

Tags: , , ,

Category: Medical Student Notebook, Past Articles

Leave a Reply