Gastroesophageal Pressure Gradient Research Articles

Pathophysiological Mechanisms of Gastro-esophageal Reflux After Sleeve Gastrectomy.

To evaluate the mechanisms associated with reflux events after sleeve gastrectomy (SG). Gastro-esophageal reflux (GERD) post-SG is a critical issue due to symptom severity, impact on quality of life, requirement for reoperation, and potential for Barrett esophagus. The pathophysiology is incompletely delineated. Post-SG patients, stratified into asymptomatic and symptomatic, underwent protocolized nuclear scintigraphy (n = 83), 24-hour esophageal pH monitoring, and stationary manometry (n = 143) to characterize reflux patterns. Ten patients underwent fasting and postprandial concurrent manometry and pH for detailed analysis of reflux events. Baseline demographics between cohorts were similar: Age 47.2 ± 11.6 versus 44.1 ± 11.3 years ( P = 0.121); females 73.2% versus 90.8% ( P = 0.005); excess weight loss 53.8 ± 28.1% versus 57.4 ± 25.5% ( P = 0.422), follow-up duration 12.3 versus 7.4 months ( P = 0.503). Nuclear scintigraphy delineated bolus-induced deglutitive reflux events (29.6% vs 62.5%, P = 0.005) and postprandial reflux events [4 (IQR2) versus 4 (IQR 3) events, P = 0.356]. Total acid exposure was significantly elevated in the symptomatic population (7.7% vs 3.6%, P < 0.001), especially fasting acid exposure (6.0% vs 1.3%, P < 0.001). pH/manometry analysis demonstrated acute elevations of the gastro-esophageal pressure gradient (>10 mm Hg) underpinned most reflux events. Swallow-induced intragastric hyper-pressur-ization was associated with individual reflux events in most patients (90% in fasting state and 40% postprandial). We found reflux to be strongly associated with SG and identified 3 unique categories. Bolus-induced deglutitive and postprandial reflux occurred in most patients. Elevated fasting esophageal acid exposure mediated symptoms. Frequent, significant elevation in the gastro-esophageal pressure gradient was the mechanism of reflux and seemed to relate to the noncompliant proximal stomach.

Esophageal High-Resolution Manometry Can Unravel the Mechanisms by Which Different Bariatric Techniques Produce Different Reflux Exposures

IntroductionBariatric surgery is increasingly performed. Since there are numerous surgical techniques, the effects of these on the esophageal function are still poorly understood. We aimed at assessing the effect of different techniques on esophagogastric junction (EGJ), esophageal peristalsis and reflux exposure using high-resolution manometry (HRM), and impedance-pH monitoring (MII-pH). MethodsAll obese patients underwent symptomatic questionnaires, endoscopy, HRM, and MII-pH before and 1 year after surgery. Esophageal function and EGJ were classified according to Chicago Classification V. 3.0. Intragastric pressure (IGP) and gastroesophageal pressure gradient (GEPG) were assessed. Total acid exposure time (AET %), total number of refluxes, and symptom association probability (SAP) were assessed. A group of healthy volunteers (HVs) served as control. ResultsOne hundred and twelve obese subjects and 15 HVs (normal weight) were studied. Thirteen underwent endoscopic balloon placement (BIB), 12 gastric banding (GB), 26 sleeve gastrectomy (SG), 18 Roux-en-Y gastric bypass (RYGB), 15 mini-gastric bypass (MGB), 16 biliointestinal bypass (BIBP), and 12 biliopancreatic diversion (BPD). IGP and GEPG significantly decreased after RYGP, BPD, and BPBP, whereas they significantly increased after GB and SG. Post-operative greater AET (p < 0.05) and increased total number of reflux (p < 0.001) were present after GB and SG. RYGB and MGB showed a significant decrease in AET (p < 0.05) and total number of reflux (p < 0.001). ConclusionsHRM verified that different bariatric techniques produced different modification of IGP and GEPG, leading to different reflux exposure. Only GB and SG can negatively impact on esophageal function and reflux exposure.

Esophagogastric junction function and gastric pressure profile after minigastric bypass compared with Billroth II

BackgroundMinigastric bypass (MGB) is being performed widely with effective weight loss and improvement in co-morbidities. Because of similarity to Billroth II (BII), there are concerns about bile reflux. ObjectivesTo assess the esophagogastric junction (EGJ) function, esophageal peristalsis, and reflux exposure after MGB and BII. SettingUniversity Hospital, Italy; Public Hospital, Italy. MethodsObese patients underwent symptom questioning, endoscopy, high-resolution impedance manometry, and impedance-pH monitoring, before and 1 year after MGB. Esophageal motor function, EGJ, EGJ–contractile integral, intragastric pressure (IGP), and gastroesophageal pressure gradient were determined. Acid exposure time, number of refluxes, and symptom-association probability were assessed. A group of patients who underwent BII were studied with the same protocol and served as controls. ResultsTwenty-two MGB and 20 BII patients were studied. After surgery, none of the patients reported de novo heartburn or regurgitation. At endoscopic follow-up, esophagitis and bile findings were absent in all. High-resolution impedance manometry features did not vary significantly after MGB, whereas IGP and gastroesophageal pressure gradient statistically diminished (P < .01). BII patients had significantly lower values in IGP, sphincter pressure, and EGJ–contractile integral. In MGB patients, a marked decrease in number of refluxes (from median 41 to 7, P < .01) was observed, whereas BII patients had statistically significant higher acid exposure and number of refluxes (57, P < .001). ConclusionsIn contrast to BII, MGB does not increase any kind of reflux. Also, the differences in IGP and gastroesophageal pressure gradient suggest that bile reflux occurs more readily after BII than after MGB, and that these 2 operations share more differences than similarities.

The Improvement of Gastroesophageal Reflux Disease and Barrett's after Bariatric Surgery.

Obesity and gastroesophageal reflux disease (GERD) are prevalent in Western populations. In obese patients, high-resolution manometry often shows altered gastroesophageal pressure gradients, promoting retrograde gastric content flow into the esophagus and esophagogastric junction disruption, leading to a hiatal hernia. Hernia recurrence is higher in the obese, and recurrence is seen regardless of the operative approach used. Bariatric surgery is the gold-standard treatment for GERD in obese patients, and symptom improvement varies depending on the specific bariatric procedure performed, Roux-en-Y (RYGB), laparoscopic adjustable gastric banding (LAGB), or sleeve gastrectomy (SG). Studies have shown these surgeries significantly improve GERD, but RYGB had the greatest effect. Limited data is available examining the progression or regression of Barrett's following bariatric surgery. We currently recommend RYGB for morbidly obese patients with Barrett's esophagus.

Diaphragmatic breathing for rumination syndrome: efficacy and mechanisms of action.

While high resolution esophageal manometry combined with impedancometry has demonstrated that gastric pressurizations lead to rumination, the contribution of upper esophageal sphincter (UES) and esophagogastric junction (EGJ) function to rumination is unclear. Behavioral therapy with diaphragmatic breathing (DB) can reduce rumination. We aimed to evaluate the pressures in the stomach, EGJ and UES during rumination and the effects of DB augmented with biofeedback therapy. Sixteen patients with rumination were studied with manometry and impedancometry before and after a meal. The postprandial assessment comprised three periods: before, during, and after DB augmented with biofeedback therapy. All patients had postprandial rumination, which was associated (p < 0.001) with increased gastric pressure and reversal of the postprandial gastroesophageal pressure gradient from -4 (-43 to 18) before to 20 (7-79) mmHg during rumination. The EGJ pressure was lower (p < 0.001) during gastric pressurizations that were associated with rumination vs those that were not. The UES also relaxed, almost completely, during rumination. Patients had a median (range) of 5 (2-10) rumination episodes before, 1 (0-2) (p < 0.001) during, and 3 (1-5) after (p < 0.001 vs during) diaphragmatic breathing. During manometry and impedancometry, DB was well-tolerated and learned within 5 min. Diaphragmatic breathing increased EGJ pressure (p < 0.001) and restored a negative gastroesophageal pressure gradient (-20 mmHg [-80 to 7]). Diaphragmatic breathing aided with high resolution esophageal manometry is well-tolerated, effective and averts the gastroesophageal pressure disturbance that leads to rumination.

Effects of omega-loop bypass on esophagogastric junction function

BackgroundAt present, no objective data are available on the effect of omega-loop gastric bypass (OGB) on gastroesophageal junction and reflux. ObjectivesTo evaluate the possible effects of OGB on esophageal motor function and a possible increase in gastroesophageal reflux. SettingUniversity Hospital, Italy; Public Hospital, Italy. MethodsPatients underwent clinical assessment for reflux symptoms, and endoscopy plus high-resolution impedance manometry (HRiM) and 24-hour pH-impedance monitoring (MII-pH) before and 1 year after OGB. A group of obese patients who underwent sleeve gastrectomy (SG) were included as the control population. ResultsFifteen OGB patients were included in the study. After surgery, none of the patients reported de novo heartburn or regurgitation. At endoscopic follow-up 1 year after surgery, esophagitis was absent in all patients and no biliary gastritis or presence of bile was recorded. Manometric features and patterns did not vary significantly after surgery, whereas intragastric pressures (IGP) and gastroesophageal pressure gradient (GEPG) statistically diminished (from a median of 15 to 9.5, P<.01, and from 10.3 to 6.4, P<.01, respectively) after OGB. In contrast, SG induced a significant elevation in both parameters (from a median of 14.8 to 18.8, P<.01, and from 10.1 to 13.1, P<.01, respectively). A dramatic decrease in the number of reflux events (from a median of 41 to 7; P<.01) was observed after OGB, whereas in patients who underwent SG a significant increase in esophageal acid exposure and number of reflux episodes (from a median of 33 to 53; P<.01) was noted. ConclusionsIn contrast to SG, OGB did not compromise the gastroesophageal junction function and did not increase gastroesophageal reflux, which was explained by the lack of increased IGP and in GEPG as assessed by HRiM.

The puzzling argument of antireflux surgery in obese patients with gastroesophageal reflux disease: can the excellent perioperative safety of antireflux surgery make up for better comprehensive long-term outcomes of bariatric surgery?

The prevalence of obesity has more than doubled in United States over the past 3 decades.1 The increased prevalence of obesity has also corresponded with a parallel increased prevalence of gastroesophageal reflux disease (GERD). In fact, obese patients have a 2.5 times elevated risk of developing GERD symptoms.2 Pandolfino et al 1st proposed a physiopathologic mechanism by which obesity may lead to GERD. Pandolfino et al3 have shown that increased visceral fat in obese patients may increase their intragastric pressure with a resulting increased gastroesophageal pressure gradient and abnormal esophageal acid exposure.

Obesity Is Associated With Increasing Esophageal Acid Exposure in Korean Patients With Gastroesophageal Reflux Disease Symptoms

Background/AimsObesity is regarded as an important contributor to the increasing occurrence of gastroesophageal reflux disease. The aims of this study were to determine whether obesity is associated with gastroesophageal reflux in patients with gastroesophageal reflux disease and to identify the factors affecting increased acid exposure in obese patients.MethodsWe retrospectively analyzed the data of patients who underwent ambulatory 24-hour pH monitoring and esophageal manometry at Seoul St. Mary's Hospital. Obesity was classified according to the Asia-Pacific criteria.ResultsA total of 366 patients were analyzed; 18 were underweight, 152 normal weight, 104 overweight, and 92 obese. Obesity was more frequent in men and younger patients. The percentage time of pH < 4 in the total, upright, and postprandial periods was significantly higher in obese patients than in normal or underweight patients. The DeMeester score was also higher in obese patients. Body mass index correlated positively with reflux parameters. Multivariate analysis showed that being male and obesity were significantly associated with abnormal acid exposure (P < 0.005). The total lower esophageal sphincter length shortened as body mass index increased (P < 0.005). The gastroesophageal pressure gradient increased as body mass index increased (P < 0.05).ConclusionsObesity is associated with increasing esophageal acid exposure. The mechanism responsible for the relationship between gastroesophageal reflux disease and obesity may be associated with shortening of the lower esophageal sphincter length and increasing the gastroesophageal pressure gradient.

Tu1862 Observations of Acid Reflux and Motor Function in Distal Esophagus Using Simultaneous Measurements of Intra-Esophageal pH and Pressure in 8 Directions With Novel Sensor Catheter

G A A b st ra ct s they met criteria for achalasia based on the current Chicago Classification. Of 158 patients (M:F 48:110, age 56.6±15), lower esophageal sphincter pressure (LESP), integrated relaxation pressure (IRP), distal contractile integral (DCI), contractile front velocity (CFV), intrabolus pressure, and distal latency were obtained and reviewed. The data was collected using ManoView ESO 3.0. For statistical analysis, the Spearman correlation was used to investigate the associations between the main outcomes and BMI and abdominal circumference. Results: 54/158 patients were considered obese with a BMI ≥ 30 with a maximum BMI of 67.3 kg m-2. Within the obese group, 21/54 had a hiatal hernia (HH) and 6/21 had .3cm fixed HH. Within the non-obese group, 35/105 had a HH and 14/35 had a fixed HH. Obesity and increased abdominal circumference were significantly associated with increased intragastric pressure in both supine (Spearman correlation coefficient r=0.55, p,0.001; r=0.52, p,0.001 respectively) and upright position (r=0.62, p,0.001; r=0.57, p,0.001 respectively), with upright more prominent. Obesity and increased abdominal circumference were also significantly associated with increased intrabolus pressure during both swallows in both postures (r ranged from 0.31 to 0.47, Figure). The LESP, IRP, DCI, CFV and distal latency were not significantly affected by BMI or abdominal circumference. Conclusion: The results from this study suggest an increased resistance from esophagogastric junction in patients with obesity. The increased resistance is likely a result of increased gastroesophageal pressure gradient, and may have an impact on acid clearance resulting in increased severity and incidence of GERD. This is important in the patients with ineffective peristaltic function, a common condition seen in patients with GERD. Encouraging obese patients to lose weight, specifically abdominal fat, should be a priority in the management of GERD.

Association between metabolic syndrome and prevalence of gastroesophageal reflux disease in a health screening facility in Japan

Abdominal fat accumulation, which induces high intra-abdominal pressure that causes increase in the gastroesophageal pressure gradient and hiatal hernia, as well as obesity, has been shown to increase the prevalence of gastroesophageal reflux disease (GERD). This study was performed to clarify the association between metabolic syndrome and the prevalence of GERD. The study subjects were an adult population who visited a medical center for annual medical check-ups from April 2010 to March 2011. GERD was diagnosed by the presence of endoscopically proven reflux esophagitis, GERD symptoms (QUEST score ≥6), or current medical therapy for GERD. The presence of metabolic or pre-metabolic syndrome was diagnosed based on the Japanese criteria for metabolic syndrome. Six hundred four (16.0%) of 3775 study subjects were positively diagnosed with GERD, with the number of those with metabolic and pre-metabolic syndrome being 477 (12.6%) and 384 (10.2%), respectively. Multiple logistic regression analysis showed that male gender, presence of hiatal hernia, and metabolic or pre-metabolic syndrome, as well as absence of gastric mucosal atrophy, were significant predictive factors for the prevalence of GERD, as were visceral fat accumulation and untreated dyslipidemia. Untreated hypertension and untreated hyperglycemia were also considered to be positive risk factors. Subjects undergoing treatment for hypertension showed an increased risk of GERD, while those undergoing treatment for dyslipidemia and diabetes mellitus showed a decreased risk. Metabolic syndrome is a reliable predictive factor for the prevalence of GERD, and medical therapy for metabolic syndrome may modify the risk of GERD occurrence.

Mechanisms of Increased Gastroesophageal Reflux in Patients With Cystic Fibrosis

Up to 80% of patients with cystic fibrosis (CF) may have increased gastroesophageal reflux (GER). It has been suggested that increased GER is due to low basal lower esophageal sphincter (LES) pressure and a high number of transient LES relaxations (TLESRs). The aim of our study was to reassess the mechanisms of GER in adult CF patients using state of the art upper-gastrointestinal physiology techniques: high-resolution manometry impedance (HRM-MII). We studied 12 CF patients (age 32 range (19-58), 5 males/7 females) and 11 age-matched healthy volunteers (age 27 range (20-36), 4 males /7 females). HRM-MII was performed in a semi-recumbent position for 30 min during fasting and for 2 h after a standard meal (1,000 kcal). We measured total reflux and proximal extent of reflux with impedance; basal LES pressure, TLESRs, and gastroesophageal pressure gradient (GEPG) with HRM. Basal LES pressure was lower in CF patients compared with healthy controls, both in the pre- and postprandial period (preprandial 13 (7-22) vs. 24 (13-26) mm Hg, P = 0.04; postprandial 10 (8-14) vs. 18 (10-31) mm Hg, P = 0.01) and TLESRs were the main mechanism for reflux both in CF and in controls. We could not find a difference in the number of TLESRs in CF patients compared with healthy (14 (10-20) vs. 13 (10-24), P = not significant). However, reflux during TLESRs was more frequent in CF compared with healthy volunteers (80 (70-95) vs. 42 (20-78) %, P = 0.0058). GEPG during TLESRs was significantly higher in CF than in controls during inspiration (13.5 (9.5-15.8) vs. 7 (4-9.9) mm Hg, P = 0.004). This difference was due to a lower inspiratory intra-thoracic pressure in CF patients (-8.2 (-10.2-(-4.6) vs. -0.08 (-5.7-2.7) mm Hg, P = 0.002). Compared with controls, CF patients had significantly higher number of reflux episodes (13 (6-20) vs. 7 (3-9), P = 0.014) and CF patients also showed a higher proportion of reflux episodes with a high proximal extent compared with healthy volunteers (49 (22-50) vs. 0 (0-17) %, P = 0.0028). CF patients have increased GER with a high proximal extent. Although we could not find a higher number of TLESRs in CF, there is a higher proportion of TLESRs associated with reflux. Unlike non-CF GER disease patients (with increased intra-abdominal pressure), reflux during TLESRs in CF is probably due to an increased GEPG mainly generated by a greater inspiratory negative intra-thoracic pressure.

Gastroesophageal Reflux Disease and Obesity: Not as Simple as We May Think

There is no doubt that, over the last 20 years, westernized countries are seeing a dramatic increase in obesity [1]. This comes at the same time that we are seeing the rates of H. pylori infection in these populations decreasing from 80 % to less than 20 % [2]. Therefore, healthy stomachs with more acid and the refluxogenic contributions of obesity are together leading to an epidemic of GERD and its complications. The epidemiologic data are conclusive that obesity increases the rates of reflux symptoms, frequency and severity of esophagitis, and the frequency of Barrett’s esophagus and adenocarcinoma of the esophagus [3–6]. Recent studies are also suggesting that symptom relief from proton pump inhibitors (PPIs) is more difficult to obtain in the obese patient, with more failing ‘‘on demand’’ therapy and single dose PPIs [7, 8]. Therefore, these patients may more frequently need to be on maintenance once or twice a day PPI regimens, possibly increasing the risk of long-term complications to this class of drugs. What are the physiologic mechanisms by which obesity contributes to GERD? Recent studies suggest that central or abdominal obesity, as measured by the waist-to-hip ratio, may be more important than general obesity as measured by the body mass index (BMI). For example, a large cross-sectional study of 80,111 individuals from the Kaiser Permanente health system found a significant relationship between increased abdominal diameter and reflux symptoms independent of BMI (OR 1.85, 95 % CI 1.55–2.21). Interestingly, this correlation was much more pronounced in the white population and in male subjects [9]. In theory, central obesity should raise intragastric pressure, thereby predisposing to reflux. This was proven in a seminal study by Pandolfino et al. [10] where they studied 285 patients (81 overweight: BMI 25–30 kg/m; and 75 obese: BMI [ 30 kg/m) with high resolution manometry. They found that the pressure morphology within and across the esophagogastric junction is altered in obesity in a fashion that would promote the flow of gastric juices into the esophagus. Particularly, during the inspiratory phase of respiration, increased intragastric pressure and the gastroesophageal pressure gradient (GEPG) were strongly correlated with increased BMI. Both factors correlated even more strongly with waist circumference, suggesting that this is the mediator in the causal pathway of the BMI effect. There was a dose-dependent relationship such that the higher the BMI and waist circumference, the greater the intragastric pressure and GEPG. From an anatomic standpoint, obesity was also associated with increased axial separation between the LES and extrinsic crural diaphragm, an objective measure of the disruption of the esophagogastric junction (EGJ) culminating in the development of hiatal hernia. This confirms older studies where obesity was a significant independent risk factor for hiatal hernia, especially in whites [11]. Not to be forgotten in these mechanistic studies, a prospective study of 84 patients observed that obesity was associated with an increased frequency of transient lower esophageal sphincter relaxation and increased acid exposure [12]. Using both catheter and wireless pH systems, studies have shown that obesity increases acid reflux. In a crosssectional study of 206 patients, El-Serag et al. [13] found that BMI of [30 kg/m (compared to \25 kg/m) was associated with a significant increase in acid reflux J. E. Richter (&) Division of Digestive Diseases and Nutrition, Joy McCann Culverhouse Center for Esophageal and Swallowing Disorders, University of South Florida, Tampa, FL, USA e-mail: jrichte1@health.usf.edu

Correlation between Bispectral Index, Observational Sedation Scale, and Lower Esophageal Sphincter Pressure in volunteers using dexmedetomidine or propofol

SummaryBackgroundMany anesthetics reduce lower esophageal sphincter pressure (LESP) and consequently the gastro-esophageal pressure gradient (GEPG); thus they may promote gastro-esophageal reflux and contribute to aspiration pneumonia. Our goals were to evaluate the association between LESP and 2 measures of sedation: bispectral index (BIS) and the responsiveness component of the Observer’s Assessment of Alertness score (OAA/S).Material/MethodsEleven healthy volunteers were each sedated on 2 separate days. Subjects were given sedative infusions of increasing target plasma concentrations of dexmedetomidine or propofol. LESP and GEPG were recorded after starting each infusion phase. Generalized estimating equation modeling was used to assess the relationship between LESP and, respectively, BIS and OAA/S. The existence of a drug-dependent association was evaluated within these models by testing an interaction term. Wald tests were used to evaluate the relationships within the models.ResultsWe found a significant relationship between LESP and BIS (P=0.0043) after adjusting for the main effect of sedative type – a deepening of sedation as measured by a decrease in BIS of 10% was associated with a decrease [Bonferroni-adjusted 95% CI] in LESP of −1.34 [−2.39, −0.29] mmHg. After adjusting for the main effect of sedative drug, LESP significantly declined with declining OAA/S (P=0.001); a unit decrease of OAA/S was associated with a decrease [Bonferroni-adjusted 95% CI] in LESP of −2.01 [−3.20, −0.81] mmHg.ConclusionsDeeper sedation, as measured by either BIS or OAA/S, significantly reduces LESP.

Effects of Dexmedetomidine and Propofol on Lower Esophageal Sphincter and Gastroesophageal Pressure Gradient in Healthy Volunteers

Survey of Anesthesiology: October 2010 - Volume 54 - Issue 5 - p 256 doi: 10.1097/01.SA.0000387949.25353.bc

Effects of Dexmedetomidine and Propofol on Lower Esophageal Sphincter and Gastroesophageal Pressure Gradient in Healthy Volunteers

Many anesthetics reduce lower esophageal sphincter pressure (LESP). Reduced pressure and consequent reduction in the gastroesophageal pressure gradient (GEPG) thus promotes gastroesophageal reflux and may contribute to aspiration pneumonia and associated morbidity. Therefore, the authors compared LESP and GEPG during dexmedetomidine and propofol sedation. Using a randomized, double-blind, crossover design, 11 healthy volunteers were sedated on 2 separate days. Baseline LESP and GEPG were recorded each day. Subsequently, on each day volunteers received three 40-min-long sedative infusions of increasing doses of 0.6, 1.2, and 2.4 ng/ml dexmedetomidine or 1, 2, and 4 microg/ml propofol. LESP and GEPG were recorded during inhalation and expiration at 20 and 40 min after starting each infusion phase, and these measurements were averaged. Results are presented as mean (95% confidence interval). Two subjects did not return for the dexmedetomidine study day, and the dexmedetomidine results were unusable in another; propofol results in these volunteers were nonetheless retained for analysis. There were no significant differences in LESP and GEPG as a function of drug. However, there was a small but significant 7.4 (-1.6 to -13.2) mmHg (approximately 25%) dose-dependent decrease in LESP over the range of targeted low to high blood levels of each drug. Both dexmedetomidine and propofol have similar effects on LESP and GEPG. Although both of the drugs cause some decrease in LESP at high concentrations, it is unlikely that this effect would promote gastroesophageal reflux during sedation.

New Insights about an Old Foe

New Insights about an Old Foe

Effects of Dexmedetomidine and Propofol on Lower Esophageal Sphincter and Gastroesophageal Pressure Gradient in Healthy Volunteers

Effects of Dexmedetomidine and Propofol on Lower Esophageal Sphincter and Gastroesophageal Pressure Gradient in Healthy Volunteers

The Pathophysiological Mechanisms of GERD in the Obese Patient

Obesity has increased dramatically in the last 30 years, affecting 33% of the adult population in the United States. Increase in body mass index has been shown to be associated with the increase in the prevalence of gastroesophageal reflux disease (GERD) symptoms, esophageal mucosal injury, and GERD complications. The putative mechanisms responsible for the close relationship between GERD and increased body mass index include increased intragastric pressure, increased gastroesophageal pressure gradient, esophageal motor and sensory abnormalities, increase in prevalence of hiatal hernia, increase in serum female hormonal levels, diet, and increase in comorbidities. Whilst the current efforts are to focus on one major underlying mechanism, it is highly likely that multiple factors contribute to the increased prevalence of GERD in the obese patient.

Gastroesophageal Pressure Gradients in Gastroesophageal Reflux Disease: Relations With Hiatal Hernia, Body Mass Index, and Esophageal Acid Exposure

The roles of intragastric pressure (IGP), intraesophageal pressure (IEP), gastroesophageal pressure gradient (GEPG), and body mass index (BMI) in the pathophysiology of gastroesophageal reflux disease (GERD) and hiatal hernia (HH) are only partly understood. In total, 149 GERD patients underwent stationary esophageal manometry, 24-h pH-metry, and endoscopy. One hundred three patients had HH. Linear regression analysis showed that each kilogram per square meter of BMI caused a 0.047-kPa increase in inspiratory IGP (95% confidence interval [CI] 0.026-0.067) and a 0.031-kPa increase in inspiratory GEPG (95% CI 0.007-0.055). Each kilogram per square meter of BMI caused expiratory IGP to increase with 0.043 kPa (95% CI 0.025-0.060) and expiratory IEP with 0.052 kPa (95% CI 0.027-0.077). Each added year of age caused inspiratory IEP to decrease by 0.008 kPa (95% CI -0.015-0.001) and inspiratory GEPG to increase by 0.008 kPa (95% CI 0.000-0.015). In binary logistic regression analysis, HH was predicted by inspiratory and expiratory IGP (odds ratio [OR] 2.93 and 2.62, respectively), inspiratory and expiratory GEPG (OR 3.19 and 2.68, respectively), and BMI (OR 1.72/5 kg/m(2)). In linear regression analysis, HH caused an average 5.09% increase in supine acid exposure (95% CI 0.96-9.22) and an average 3.46% increase in total acid exposure (95% CI 0.82-6.09). Each added year of age caused an average 0.10% increase in upright acid exposure and a 0.09% increase in total acid exposure (95% CI 0.00-0.20 and 0.00-0.18). BMI predicts IGP, inspiratory GEPG, and expiratory IEP. Age predicts inspiratory IEP and GEPG. Presence of HH is predicted by IGP, GEPG, and BMI. GEPG is not associated with acid exposure.

The Relationship Between Obesity and GERD: "Big or Overblown"

The rates of obesity have doubled over the last 22 yr in the United States. Similarly, the prevalence of gastroesophageal reflux disease (GERD) has also been rising in the United States, with studies suggesting it may now be as high as 1 in 5. Given these parallel time trends, it is tempting to speculate that obesity may, in some way, promote the development of GERD. Of the proposed mechanisms, the most attractive ones focus on the mechanical stresses imposed on the antireflux barrier, specifically increased pressure gradients across the esophagogastric junction (EGJ). In this issue of the American Journal of Gastroenterology, de Vries et al. provide a comprehensive retrospective analysis of the relationship among body mass index (BMI), pressure gradients across the EGJ, and objective evidence of GERD. While their results support that increased BMI is associated with increased pressure gradients through the EGJ and the propensity to develop hiatus hernia, they do not illustrate a direct relationship between increased gastroesophageal pressure gradients and abnormal acid exposure in the esophagus. These results highlight the complexity of this relationship and once more support the concept that GERD is a multifactorial disease that cannot be defined by a single anatomical or functional abnormality.