Paradox of gastric cardia: it becomes more acidic following meals while the rest of stomach becomes less acidic.

INTRODUCTION: The proximal cardia region of the stomach has a high incidence of inflammation, metaplasia and neoplasia. It demonstrates less acid buffering following meals than the more distal stomach. Novel high definition pHmetry was employed to investigate acidity at the cardia under fasting conditions and in response to a meal. METHODS: 15 healthy subjects were studied. A custom-made 12-electrode pH catheter was clipped at the squamocolumnar junction with four electrodes recording proximal to and eight distal to the squamocolumnar junction. The most distal pH electrode was located at the catheter tip, and nine electrodes in the region of the squamocolumnar junction were 11 mm apart. RESULTS: The electrode situated in the cardia 5.5 mm distal to the squamocolumnar junction differed from all other intragastric electrodes during fasting in recording minimal acidity (pH <4 = 2.2%) while all other intragastric electrodes recorded high intragastric acidity (pH <4 =or>39%) (p<0.05). The cardia also differed from the rest of the stomach, showing a marked increase in acidity in response to the meal (from 2.2% fasting to 58.4% at 60-70 min after the meal; p<0.05) while the electrodes distal to the cardia all showed a marked decrease in acidity (p<0.05). These changes in acidity at the cardia following the meal caused the gastric acidity to extend 10 mm closer to the squamocolumnar junction. CONCLUSION: Whereas the rest of the stomach shows a marked fall in acidity on ingesting a meal, the cardia paradoxically increases in acidity to become the most acidic region throughout the postprandial period.

Severe reflux disease is associated with an enlarged unbuffered proximal gastric acid pocket.

BACKGROUND: An unbuffered pocket of highly acidic juice is observed at the gastric cardia after a meal in healthy subjects. AIMS: To compare the postprandial acid pocket in healthy subjects and patients with severe reflux disease and define its position relative to anatomical and manometric landmarks. METHODS: 12 healthy subjects and 16 patients with severe reflux disease were studied. While fasted, a station pull-through was performed using a combined dual pH and manometry catheter. Position was confirmed by radiological visualisation of endoscopically placed radio-opaque clips. The pull-through study was repeated 15 min after a standardised fatty meal. Barium meal examination was performed before and following the meal. RESULTS: A region of unbuffered acid (pH

High-resolution esophageal manometry: addressing thermal drift of the manoscan system.

BACKGROUND: The high resolution esophageal manometry system manufactured by Sierra Scientific Instruments is widely used. The technology is liable to 'thermal drift', a change in measured pressure due to change in temperature. This study aims to characterize 'thermal drift' and minimize its impact. METHODS: Response of the system to immediate temperature change (20 °C to 37 °C) was tested. Accuracy of pressure measurement over two hours at 37 °C was examined. Six repetitions were performed and median pressure change calculated for each sensor. Sensors were compared using Kruskal-Wallis test. Current correction processes were tested. KEY RESULTS: There was a biphasic response of the system to body temperature: an immediate change in recorded pressure, 'thermal effect' and an ongoing pressure change with time, 'baseline drift'. Median thermal effect for all 36 sensors was 7 mmHg (IQR 3.8 mmHg). Median baseline drift was 11.1 mmHg (IQR 9.9 mmHg). Baseline drift varied between sensors but for a given sensor was linear. Interpolated thermal compensation, recommended for prolonged studies, corrects data assuming a linear drift of pressures. When pressures were corrected in this way, baseline pressure was almost restored to zero (Median 0.3 mmHg, IQR 0.3). The standard thermal compensation process did not address the error associated with baseline drift. CONCLUSIONS & INFERENCES: Thermal effect is well compensated in the current operation of the system but baseline drift is not well recognized or addressed. Incorporation of a linear correction into current software would improve accuracy without impact on ease of use.

Kinetics of transient hiatus hernia during transient lower esophageal sphincter relaxations and swallows in healthy subjects.

BACKGROUND: Proximal displacement of the gastro-esophageal junction (GEJ) is present in hiatus hernia but also occurs transiently during transient lower esophageal sphincter relaxations (TLESRs) and swallows. Using a novel magnetic-based technique we have performed detailed examination of the GEJ movement during TLESRs and swallows in healthy subjects. METHODS: In 12 subjects, a magnet was endoscopically clipped to the GEJ and combined assembly of Hall-Effect locator probe and 36 channel high-resolution manometer passed nasally. After a test meal the subjects were studied for 90 min. KEY RESULTS: The median amplitude of proximal movement of GEJ during TLESRs was 4.3 cm (1.6-8.8 cm) and this was substantially greater than during swallowing at 1.2 cm (0.4-2.7 cm), P = 0.002. With both TLESRs and swallows proximal GEJ movement coincided with lower esophageal sphincter (LES) relaxation and return to its original position occurred 4 s after return of LES tone. Kinetic modeling of the movement of the GEJ during TLESRs indicated two return phases with the initial return phase having the greater velocity (0.9 cm s(-1) ) and being strongly correlated with amplitude of proximal movement (r = 0.8, P < 0.001). CONCLUSIONS & INFERENCES: The marked proximal GEJ migration during TLESRs represents very severe herniation of the GEJ. The rapid initial return of the GEJ following TLESRs when the crural diaphragm is relaxed and its correlation with amplitude suggest it is due to elastic recoil of the phreno-esophageal ligament. The marked stretching of the phreno-esophageal ligament during TLESRs may contribute to its weakening and development of established hiatus hernia.

Rebound hypersecretion after omeprazole and its relation to on-treatment acid suppression and Helicobacter pylori status.

BACKGROUND & AIMS: There have been conflicting reports regarding acid secretion after treatment with omeprazole. This study examined acid secretion after treatment with omeprazole and its relation to Helicobacter pylori status and on-treatment gastric function. METHODS: Twelve H. pylori-negative and 9 H. pylori-positive subjects were examined before, on, and at day 15 after an 8-week course of 40 mg/day omeprazole. On each occasion, plasma gastrin, intragastric pH, and acid output were measured basally and in response to increasing doses of gastrin 17. RESULTS: In the H. pylori-negative subjects at day 15 after omeprazole treatment, basal acid output was 82% higher (P < 0.007) and maximal acid output 28% higher (P < 0.003) than before omeprazole. The degree of increase in maximal acid output was related to both on-treatment pH and on-treatment fasting gastrin levels, being 48.0% in subjects with an on-treatment pH of >4 vs. 21. 0% in those with a pH of <4 (P < 0.02) and 49.2% in subjects with an on-treatment gastrin of >25 ng. L-1 vs. 19.8% in those with a fasting gastrin of <25 ng. L-1 (P < 0.006). At day 15 after omeprazole treatment, the H. pylori-positive subjects showed a heterogeneous response with some having increased acid output and others persisting suppression. CONCLUSIONS: Rebound acid hypersecretion occurs in H. pylori-negative subjects after omeprazole treatment. Its severity is related to the degree of elevation of pH on treatment. Persisting suppression of acid secretion masks the phenomenon in H. pylori-positive subjects.

Helicobacter pylori infection potentiates the inhibition of gastric acid secretion by omeprazole.

BACKGROUND: Omeprazole has a greater intragastric pH elevating effect in Helicobacter pylori positive than negative subjects. Ammonia production by H pylori has been suggested as a probable mechanism. AIMS: To assess the effect of H pylori status on gastric acid secretion during omeprazole treatment, and to examine the possible role of ammonia neutralisation of intragastric acid in increased omeprazole efficacy in infected subjects. METHODS: Twenty H pylori positive and 12 H pylori negative healthy volunteers were examined before and six to eight weeks after commencing omeprazole 40 mg/day. On both occasions plasma gastrin and acid output were measured basally and in response to increasing doses of gastrin 17 (G-17). Gastric juice ammonium concentrations were also measured. RESULTS: Prior to omeprazole, measurements were similar in the H pylori positive and negative subjects. During omeprazole, median basal intragastric pH was higher in the H pylori positive (7.95) versus negative (3.75) subjects (p<0.002). During omeprazole basal, submaximal (180 pmol/kg/h G-17), and maximal acid outputs (800 pmol/kg/h G-17) were lower in H pylori positive subjects (0.0, 3.6, 6.0 mmol/h respectively) versus negative subjects (0.3, 14.2, 18.6 mmol/h) (p<0.03 for each). This effect was not explained by neutralisation by ammonia. CONCLUSION: The presence of H pylori infection leads to a more profound suppression of acid secretion during omeprazole treatment. The effect cannot be explained by neutralisation of intragastric acid by bacterial ammonia production and its precise mechanism has to be explained.

The acid response to gastrin distinguishes duodenal ulcer patients from Helicobacter pylori-infected healthy subjects.

BACKGROUND & AIMS: Helicobacter pylori-induced hypergastrinemia is accompanied by increased acid secretion in patients with duodenal ulcer (DU) but not in infected healthy volunteers. The aim of this study was to investigate the mechanism underlying this difference. METHODS: Thirty-four H. pylori-negative and 20 H. pylori-positive healthy volunteers and 15 H. pylori-positive patients with DU were studied. Maximal acid output and sensitivity to gastrin (gastrin concentration required to achieve 50% maximal acid output) were assessed by examining the dose response to gastrin 17. Inhibitory control was tested by comparing the maximal acid response to cholecystokinin octapeptide with that for gastrin 17. RESULTS: Sensitivity to gastrin was similar in patients with DU (median, 69.5 ng.L-1; range, 26.2-142) and H. pylori-negative healthy volunteers (median, 82.2 ng.L-1; range, 17.7-410); H. pylori-positive healthy volunteers were less sensitive than either (164.5 ng.L-1; range, 44.8 to > 3360 ng.L-1). Patients with DU had higher maximal acid output (51.2 mmol.h-1; range, 30.8-73.7 mmol.h-1) than either infected healthy volunteers (37.8 mmol.h-1; range, 0.0-65.0 mmol.h-1; P < 0.04) or uninfected healthy volunteers (35.3 mmol.h-1; range, 21.3-67.3 mmol.h-1; P < 0.002). The maximal acid output in both groups of healthy subjects was similar. The proportion of maximal acid output to gastrin 17 achieved by cholecystokinin was similar in patients with DU (36.6%; range, 21.5%-58.2%) and H. pylori-negative healthy volunteers (28.7%; range, 5.9%-85.8%). CONCLUSIONS: A combination of decreased sensitivity to gastrin in infected healthy volunteers and increased maximal acid secretory capacity in patients with DU underlies their different acid response to H. pylori-induced hypergastrinemia.