A new confusing model of GERD: a spectrum of phenotypic progression.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J E Pandolfino.
Explore the source record for details and available documents.
BACKGROUND: Ambulatory pH monitoring is considered the gold standard for measuring oesophageal acid exposure, however, data comparing antimony and glass electrodes are limited. AIM: To compare the accuracy of the Slimline antimony pH monitoring system and a conventional glass electrode catheter pH monitoring system during ambulatory conditions. METHODS: Eighteen subjects (13 males, 23-45 years) underwent simultaneous pH monitoring using the Slimline antimony pH electrode and MIC M3 glass pH electrode pH monitoring systems for 12 h. Acid exposure was analysed and compared by manual extraction of the data onto an excel spreadsheet. RESULTS: There was no statistical difference in the median per cent time the pH was <4 recorded by the two systems (Slimline, 3%, Glass MIC M3, 2%, P = 0.77) and the correlation was excellent (r = 0.84). The difference in recorded reflux events was also not significantly different between the two systems, with the absolute difference being 23 events (s.d., 26). Point-by-point discrepancy was 28% (s.d., 18%), however, the agreement in terms of reflex events was excellent (Kappa value, 0.89, s.d., 0.09). CONCLUSION: Despite substantial point-by-point disagreement, the antimony Slimline pH catheter compares favourably to the Glass MIC M3 pH catheter in terms of measuring standard pH parameters.
The aim of this study was to assess the quantitative differences of acid exposure at 1 cm and 6 cm above the squamocolumnar junction (SCJ) using two radiotelemetry pH capsules affixed to the esophageal mucosa. Ten normal subjects and 10 endoscopy-negative gastroesophageal reflux disease (GERD) patients without hiatus hernia (ages 20-54, 12 male) were studied for a 24-h period using the Bravo pH monitoring system. pH capsules were placed 1 cm and 6 cm above the SCJ. Interpretable data for at least 14 h was obtained in 18 of the 20 subjects (9 normal, 9 GERD). Two failures occurred secondary to early capsule dislodgement. Median esophageal acid exposure was significantly increased at 1 cm above the SCJ compared to 6 cm above the SCJ during the total, upright and postprandial time periods in both normal and GERD subjects. During a 2 h postprandial period the esophageal acid exposure was 8-fold greater in GERD subjects and 5-fold greater in normal subjects 1 cm above the SCJ compared to 6 cm above the SCJ. Confident measurement of esophageal acid exposure at a fixed position 1 cm above the SCJ is feasible with the Bravo system. Acid exposure was significantly higher 1 cm above the SCJ compared to 6 cm above the SCJ in both GERD patients and controls. These findings suggest that measurement of acid exposure 1 cm above the SCJ may improve accuracy of pH monitoring by detecting acid reflux events confined to the distal esophagus.
OBJECTIVE: This study analysed the relative accuracy of the Bravo wireless and the Slimline catheter-Mark III Digitrapper pH systems in the detection of acid reflux events. METHODS: Twenty five asymptomatic subjects were studied. A Bravo capsule was placed 6 cm above the squamocolumnar junction (SCJ), marked by an endoclip, and a Slimline pH catheter was placed 5 cm above the manometrically localised lower oesophageal sphincter. The distance between the SCJ and each pH electrode was measured fluoroscopically. An in vivo pH reference was established using swallows of orange juice (pH 3.88). Concurrent pH data from the two systems were analysed in Excel spreadsheets. RESULTS: Significantly more acid reflux events were reported by the Digitrapper system than the Bravo system (117.0 v 41.8). This was not explained by electrode position as there was no difference in median distance between the SCJ and either pH electrode (7.25 cm v 7.08 cm). The dominant source of discrepancy between systems was inaccuracy in electrode calibration and, after adjustment using the in vivo orange juice pH measurement, the discrepancy improved by 40%. However, discrepancy still existed and was most pronounced with short reflux events (1-15 s for the catheter, 1-17 s for the Bravo) associated with minimal intraoesophageal acidity and poor concordance between systems. CONCLUSION: Substantially more reflux events were reported by the Digitrapper system compared with the Bravo system; 40% of excess events were attributable to a flawed software scheme for electrode thermal calibration while most of the remainder were brief events with poor reproducibility between systems.
Using a simple 'test' to diagnose gastro-oesophageal reflux disease is difficult because accurately measuring gastric refluxate and correlating reflux events with symptom episodes is complex. This paper reviews the safety, tolerability and diagnostic accuracy of Bravo (Medtronic, Shoreview, MN, USA), ambulatory oesophageal pH monitoring technology. Catheter-based pH electrodes inhibit patients' normal activity, and can yield erroneous results because of placement or subsequent migration of the probe or errors in the thermal compensation algorithm that is requisite for antimony pH electrodes. Bravo pH studies reliably discriminated oesophagitis patients from controls, but are less discriminatory in endoscopy-negative gastro-oesophageal reflux disease patients. The Bravo system can be accurately placed using endoscopic landmarks and pH studies demonstrated more accurate in vivo pH recording than with a catheter-based system. The Bravo system detected fewer reflux events of short duration compared with a catheter-based system. Studies examining the correlation between reflux events and symptoms have not yet been conducted using the Bravo system. In conclusion, the Bravo system offers a more user-friendly ambulatory pH monitoring technique that more accurately records pH compared with a catheter-based system. More research is needed to determine whether the detection of reflux events with Bravo will provide a good correlation with symptom episodes.
The aim of this study was to adapt impedance methodology to study esophagogastric junction (EGJ) sphincter opening and compare opening patterns of the EGJ during deglutitive LES relaxation (dLESR) and transient LES relaxation (tLESR). We studied eight healthy subjects with a novel 12-lumen combined impedance/manometry catheter, the main element of which was a 6 cm sleeve sensor with six side hole sensors and six impedance rings spaced at 1 cm increments along its length. Subjects underwent an air infusion protocol after standard assessment and data tracings and isocontour plots were analysed to assess opening characteristics of the EGJ during dLESRs and tLESRs. Our results revealed that during dLESR the opening pattern was top to bottom, occurred in 0-2.7 s and in 29 of 35 (83%) cases the leading edge of the bolus was liquid. Opening during tLESR began between -7.8 and +8.6 s relative to the onset of nadir LES relaxation. The opening pattern during tLESR was bottom to top, occurred in 0-7.7 s, and in 22 of 29 (76%) the leading edge was liquid. These results support that impedance monitoring can be adapted to identify sphincter opening, to distinguish sphincter opening from sphincter relaxation, and to determine luminal contents during the opening period.
This study aimed to determine the effect of glucagon-induced gastric relaxation on the frequency of transient lower oesophageal sphincter relaxations (TLOSRs). Eight normal subjects (four male, age 18-52 y) were studied after a 6-h fast using a combined manometric barostat assembly. The recording was divided into two 1-h sessions: (1) a baseline period with the barostat set at minimal distending pressure (MDP) + 2 mmHg and (2) a period with continuous glucagon or placebo infusion with barostat set at MDP + 2 mmHg. Patients were studied on two different days and randomly received glucagon (4.8 microg kg(-1) bolus followed by 9.6 microg kg(-1) h(-1) infusion) on 1 day and placebo (saline) on another. Lower oesophageal sphincter (LOS) pressure, frequency of TLOSRs, and barostat bag volumes were determined for both placebo and glucagon infusion. Glucagon induced significant fundal relaxation compared with placebo (P < 0.05) and significantly decreased baseline LEOS pressure (P < 0.05). The frequency of TLOSRs was not altered by glucagon infusion compared with placebo. Despite causing substantial proximal stomach relaxation, glucagon did not increase TLOSR frequency. This suggests that the relevant gastric mechanoreceptors responsible for triggering TLOSRs do not respond to passive elongation.
It is neither practical nor necessary to embark on a diagnostic evaluation of every patient with classic symptoms of gastroesophageal reflux disease (GERD). In most cases a well-taken history is usually sufficient to confirm the diagnosis of GERD and begin therapy. However, some patients may present with atypical symptoms; and many with classic symptoms are refractory to standard medical therapy. In these cases one must rely on diagnostic studies to confirm that abnormal acid reflux is present and potentially responsible for the symptoms in question. Modern technology has given us many different modalities to quantify esophageal acid exposure and determine whether symptoms are correlated to reflux events. Unfortunately, these studies are not perfect and the work-up of refractory patients typically requires more than one test. The goal of the following review will be to summarize the currently available techniques for diagnosis of GERD and also discuss the possible impact of new techniques, such as intraluminal impedance monitoring and wireless ambulatory pH monitoring.
This study characterized oesophageal shortening during secondary peristalsis and transient lower oesophageal sphincter relaxation (TLOSR) in an attempt to determine its contribution to the opening mechanism. Eight healthy subjects (four males, 26 +/- 1 years) had metal clips affixed at 0, +3, and +8 cm relative to the squamocolumnar junction (SCJ), defining two distal oesophageal segments. Axial clip movement was assessed with concurrent videofluoroscopy and manometry during primary peristalsis, secondary peristalsis and TLOSR. Clip-defined oesophageal segment length change was measured at 0.5-s intervals. The magnitude of the most distal segment shortening was least with TLOSR, greatest with primary peristalsis and intermediate with secondary peristalsis. Conversely, maximal overall oesophageal shortening during TLOSR, evidenced by SCJ movement, was similar to that during primary peristalsis. In 3/12 TLOSRs, the moment of LOS opening and gas reflux was optimally imaged; SCJ excursion was 0.3 +/- 0.1 cm prior to LOS opening and 1.4 +/- 0.7 cm immediately after gas reflux. The segmental pattern of oesophageal shortening was distinct during primary peristalsis, secondary peristalsis and TLOSR. During TLOSR, significant elevation of the SCJ occurred only after LOS opening, suggesting that this was a consequence of oesophageal distension induced by gas reflux rather than a component of the opening mechanism.
Explore the source record for details and available documents.
The role of smoking in the pathogenesis of gastrooesophageal reflux disease has been controversial since the early 1970s when Stanciu reported the two to be 92% epidemiologically associated (a study subsequently challenged by inconsistencies in the observational data). Mechanistically, reflux disease is caused by excessive oesophageal acid exposure, which is potentially attributable to excessive reflux events and/or prolonged acid clearance. Currently, the best available pH monitoring data confirm that smoking increases oesophageal acid exposure. Smoking reduces lower oesophageal sphincter (LOS) pressure and predisposes to strain-induced reflux. Consistent with this, smoking has been shown to cause an increased number of reflux events that are not attributable to increased transient LOS relaxations, but rather are associated with deep inspiration and coughing. Once reflux occurs, acid is cleared from the oesophagus by a two-step process consisting of oesophageal peristalsis followed by neutralization of the residual acid by swallowed saliva. Smoking prolongs acid clearance by decreasing salivation. The effects of smoking on LOS tone and acid clearance are most likely mainly due to nicotine but are incompletely understood. Transdermal nicotine has similar effects to smoking on LOS pressure and salivation. Thus, although perhaps not a dominant risk factor, smoking and nicotine impact on pathophysiological variables of gastro-oesophageal reflux disease. In itself, smoking cessation is unlikely to cure severe gastrooesophageal reflux disease, but, along with appropriate pharmacological therapy, it may be beneficial.