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Gastric Acidity (gastric + acidity)

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Medical Sciences	100%

Selected Abstracts

Gastric Acidity in Patients with Follicular Gastritis is Significantly Reduced, but Can be Normalized After Eradication for Helicobacter pylori

HELICOBACTER, Issue 3 2005
Tomohiko Shimatani
ABSTRACT Background., Follicular gastritis is thought to be caused by Helicobacter pylori infection. However, the pathophysiology of it remains unclear. Materials and methods., We assessed gastric acidity in 15 patients with follicular gastritis, aged 20,37 years, using a 24-hour intragastric pH-metry, as well as by histologic and serologic evaluations; and compared it with that in other age-matched groups: 18 cases of H. pylori -positive antrum-predominant gastritis, 12 of pangastritis, and 24 H. pylori -negative normals. In eight cases with follicular gastritis, it was re-assessed 6 months after the eradication therapy for H. pylori. Results., During nighttime, the percentage of time with intragastric pH above 3.0 in follicular gastritis was significantly higher than that in normals (p < .0001), and in antrum-predominant gastritis (p < .001), but was comparable with that in pangastritis. In the daytime period, this parameter in follicular gastritis was significantly higher than that in normal (p < .001), in antrum-predominant gastritis (p < .001), and in pangastritis (p < .05). Marked mononuclear cell and neutrophil infiltration but no apparent glandular atrophy were observed in both the antrum and corpus. Serum pepsinogen I/II ratio was significantly lower in follicular gastritis than that in normals (p < .0001) and in antrum-predominant gastritis (p < .001), whereas serum gastrin was significantly higher than that in normals (p < .0001), in antrum-predominant gastritis (p < .01) and in pangastritis (p < .05). After eradication for H. pylori, all of the parameters in follicular gastritis were altered to the same ranges as those in normals. Conclusions., In follicular gastritis, gastric acidity is significantly reduced, but can be normalized by eradication of H. pylori. It can thus be speculated that inflammatory cytokines or H. pylori -infection,induced prostaglandins might strongly inhibit gastric acid secretion in follicular gastritis. [source]

Cross-Primed CD8+ Cytotoxic T cells Induce Severe Helicobacter -associated Gastritis in the Absence of CD4+ T cells

HELICOBACTER, Issue 5 2007
Toshiro Fukui
Abstract Background:, Although previous studies have reported important roles of CD4+ type1-helper T cells and regulatory T cells in Helicobacter -associated gastritis, the significance of CD8+ cytotoxic T cells remains unknown. To study the roles of CD8+ T cells, we examined the immune response in the gastric mucosa of Helicobacter felis -infected major histocompatibility complex (MHC) class II-deficient (II,/,) mice, which lack CD4+ T cells. Materials and methods:, Stomachs from H. felis -infected wild-type and infected MHC II,/, mice were examined histologically and immunohistochemically. Gastric acidity and serum levels of anti- H. felis antibodies were measured. The expression of pro-inflammatory and anti-inflammatory cytokine, Fas-ligand, perforin, and Foxp3 genes in the gastric mucosa was investigated. Results:,H. felis -infected MHC II,/, mice developed severe gastritis, accompanied by marked infiltration of CD8+ cells. At 1 and 2 months after inoculation, mucosal inflammation and atrophy were more severe in MHC II,/, mice, although gastritis had reached similar advanced stages at 3 months after inoculation. There was little infiltration of CD4+ cells, and no Foxp3 -positive cells were detected in the gastric mucosa of the infected MHC II,/, mice. The expression of the interleukin-1, and Fas-ligand genes was up regulated, but that of Foxp3 was down regulated in the infected MHC II,/, mice. Serum levels of anti- H. felis antibodies were lower in the infected MHC II,/, mice, despite severe gastritis. Conclusions:, The present study suggests that cross-primed CD8+ cytotoxic T cells can induce severe H. -associated gastritis in the absence of CD4+ helper T cells and that Foxp3 -positive cells may have an important role in the control of gastric inflammation. [source]

Gastric Acidity in Patients with Follicular Gastritis is Significantly Reduced, but Can be Normalized After Eradication for Helicobacter pylori

Pancreatic enzyme replacement therapy: exocrine pancreatic insufficiency after gastrointestinal surgery

HPB, Issue 2009
J. Enrique Domínguez-Muñoz
Abstract Exocrine pancreatic insufficiency (EPI) and resultant maldigestion occurs in up to 80% of patients following gastric, duodenal or pancreatic surgery. Accurate diagnosis is required to determine the appropriate intervention, but the conventional method of faecal fat quantification is time-consuming and not always readily available. The optimized 13C-mixed triglyceride (13C-MTG) breath test is an accurate alternative post-surgery. Pancreatic enzyme replacement therapy (PERT) is indicated post-surgery in patients with clinically evident steatorrhoea, weight loss or maldigestion-related symptoms. Given its favourable safety profile, PERT is also appropriate in asymptomatic patients with high faecal fat excretion as such patients are at high risk for nutritional deficits. However, published data evaluating PERT in this setting are limited. Uncoated powder preparations may be preferred in cases of low gastric acidity and partial or total gastric resection. In clinical studies, enteric-coated microspheres were associated with greater weight gain after surgery vs. uncoated preparations. This was confirmed in a recent study using the 13C-MTG breath test; fat absorption increased from <40% without therapy to almost 60% with enteric-coated minimicrospheres (40 000 lipase units/meal), with >60% of patients achieving normal breath test results (i.e. normal fat digestion) during PERT. A therapeutic algorithm for the treatment of EPI after surgery is also discussed. [source]

Immediate acid-suppressing effects of ranitidine hydrochloride and rabeprazole sodium following initial administration and reintroduction: A randomized, cross-over study using wireless pH monitoring capsules

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 4 2009
Shouko Ono
Abstract Background and Aim:, Histamine 2 receptor antagonists and proton-pump inhibitors, drugs that are widely used for the treatment of acid-related diseases, have different clinical characteristics. The objective of this study was to compare the acid-suppressing effects of ranitidine hydrochloride and those of rabeprazole sodium at the first administration and re-administration after withdrawal. Methods:, The study was designed as an open-label, randomized, two-way cross-over trial. Seven Helicobacter pylori -negative healthy volunteers were enrolled in this study. Ranitidine hydrochloride (300 mg/day) or rabeprazole sodium (20 mg/day) was administered from days 1 to 7 and from days 11 to 13. The percentage of time with gastric pH < 4 and the median gastric pH were evaluated for 15 consecutive days by a Bravo capsule fixed to the stomach. Results:, On day 1, there was no significant difference between the acid-suppressing effects of the two drugs (ranitidine vs rabeprazole: not significant). Although rabeprazole sodium maintained a potent and stable effect from days 2 to 7 (ranitidine vs rabeprazole: P < 0.05), the effect of ranitidine hydrochloride was attenuated after day 4. In addition, the effect of ranitidine hydrochloride at re-administration was attenuated (days 11, 12, and 13 vs pre-administration: not significant). Conclusion:, In view of our observations, we expect symptoms associated with gastric acidity to be more adequately controlled with rabeprazole sodium in the short term when compared to ranitidine hydrochloride. [source]

Clinical trial: gastric acid suppression in Hispanic adults with symptomatic gastro-oesophageal reflux disease , comparator study of esomeprazole, lansoprazole and pantoprazole

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2 2010
D. Morgan
Aliment Pharmacol Ther 2010; 32: 200,208 Summary Background, Hispanic-Americans are a rapidly growing population in the United States, yet gastro-oesophageal reflux disease (GERD) is not well studied in this population. Aim, To compare the efficacy of esomeprazole, lansoprazole and pantoprazole in suppressing gastric acid, including the area of the ,acid pocket,' in Hispanics with GERD. Methods, In this open-label, 3-way crossover study, 83 Hispanics with symptomatic GERD were randomized to 1 of 6 possible treatment sequences of three 5,7-day dosing periods with esomeprazole 40 mg, lansoprazole 30 mg and pantoprazole 40 mg daily separated by 10,17-day washout periods. Intragastric pH was measured for 24 h using dual probes with a distal and proximal (area of the ,acid pocket') electrode. Results, Esomeprazole suppressed intragastric acid (pH >4.0) significantly longer over 24 h (primary end point) compared with lansoprazole and pantoprazole (P < 0.0001), and proximal gastric acid (pH >4.0) significantly longer over 24 h compared with lansoprazole (P < 0.05) and pantoprazole (P < 0.0001). Conclusions, Esomeprazole was more effective than lansoprazole and pantoprazole in suppressing gastric acidity at both intragastric distal and proximal (area of the acid pocket) sites in Hispanics with GERD. Future studies are warranted to understand better the role of the acid pocket in GERD (Clinical trial numbers: D9612L00106; ClinicalTrials.gov: NCT00410592). [source]

Factors Influencing Standard Pretravel Health Advice,A Study in Belgium

JOURNAL OF TRAVEL MEDICINE, Issue 5 2007
Kristina Van De Winkel MD
Background Travelers with risk factors, medical conditions such as immunosuppression, medication intake, pregnancy, or elderly age, need adaptation or reinforcement of pretravel health advice. The literature provides little data on the frequency of these risk groups in the travel population. This study intended to investigate whether risk factors influencing standard travel advice are common in the population attending our travel clinic. Methods A prospective survey was carried out over a 2-month period in 2004 at the travel clinic of the Institute for Tropical Medicine in Antwerp, Belgium. A list of risk factors focused on the following three important advice categories: malaria prophylaxis, yellow fever vaccination, and travelers' diarrhea or other enteric infections. We counted how frequently a risk factor was observed for each advice category (potential influence) and, after considering the travel characteristics, how often a real adaptation of advice was necessary (actual influence). Results Of 2,227 travelers, 276 were found to have a possible influencing factor (12.4%). The potential influence was 10.9% (243/2,227) for malaria prophylaxis advice, 6.1% (136/2,227) for yellow fever vaccination, and 1.9% (43/2,227) for travelers' diarrhea advice. The actual influence was lower 8% (184/2,227), 5% (109/2,227), and 1.2% (27/2,227), respectively. The main interfering factors were as follows: for influence on malaria advice, age ,60 years (44%) and neuropsychiatric disorders (15.6%); for yellow fever vaccination, age ,60 years (63.2%) and immunosuppression (10.3%); and for influence on travelers' diarrhea advice, decreased gastric acidity (44.2%) and immunosuppression (32.6%). Conclusion Travelers with risk factors are not infrequently seen at our travel clinic. Some groups are more prominently present and could be the focus of travel group,specific instructions. The study suggests that being informed about risk groups is essential for advising travelers. [source]

Systematic review: impaired drug absorption related to the co-administration of antisecretory therapy

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 12 2009
E. LAHNER
Summary Background, Due to suppression of gastric acidity during antisecretory therapy, an impaired absorption of co-administered drugs may occur. Aim, To review evidence of impaired drug absorption related to the use of co-administered PPIs or H2RAs. Methods, Systematic search of MEDLINE/EMBASE/SCOPUS databases (1980,September 2008) for English articles with keywords: drug malabsorption and absorption, stomach, anti-secretory/acid inhibitory drugs, histamine H2 antagonists, PPIs, gastric acid, pH, hypochlorhydria, gastric hypoacidity. From 2126 retrieved articles, 16 randomized crossover studies were identified investigating impaired absorption of nine different drugs in association with co-administration of PPIs or H2RAs. Information on investigated drug, study type, features of investigated subjects, study design, type of intervention, and study results were extracted. Results, The identified studies investigated the absorption kinetics of nine drugs. Acid suppression reduced absorption of ketoconazole, itraconazole, atazanavir, cefpodoxime, enoxacin and dipyridamole (median Cmax reduction by 66.5%). An increased absorption of nifedipine and digoxin (median AUC increase by 10%) and a 2-fold-increase in alendronate bioavailability were observed. Conclusions, Gastric pH appears relevant for absorption of some cardiovascular or infectious disease agents. Antisecretory treatment may significantly modify the absorption of co-administered drugs. [source]

Continuous distal oesophageal acidification decreases postprandial gastric acidity in healthy human subjects

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 5 2009
K. BLONDEAU
Summary Background, Previously, we hypothesized that exposing the distal oesophagus to acid signals the stomach to decrease gastric acidity. Aim, To test the hypothesis that exposing the distal oesophagus to acid signals the stomach to decrease gastric acidity. Methods, Twenty-two healthy humans ingested a standard meal containing [14C]octanoic acid and [13C]glycine over 30 min on 2 separate occasions. Gastric pH was measured for 90 min before and 240 min after the meal. 10 mm HCl was infused continuously at 1 mL/min into either the distal oesophagus or stomach in a 2-way crossover fashion for 60 min before and 240 min after the meal. Gastric emptying of solid and liquid were determined with breath tests. Results, Compared to gastric infusion, oesophageal infusion significantly decreased gastric acidity after the meal, but not before the meal and the magnitude of the decrease varied directly with gastric acidity. Gastric emptying of solid or liquid with oesophageal infusion was not significantly different from that with gastric infusion. Conclusions, These findings support the hypothesis of the existence of a physiological oesophago-gastric feedback mechanism that might contribute to regulation of postprandial gastric acidity. Oesophageal acidification might decode gastric information and signal the stomach to decrease gastric acidity. Further studies are needed to assess the characteristics of such feedback mechanism in-patients with gastro-oesophageal reflux disease (GERD). [source]

Comparison of the effects of immediate-release omeprazole oral suspension, delayed-release lansoprazole capsules and delayed-release esomeprazole capsules on nocturnal gastric acidity after bedtime dosing in patients with night-time GERD symptoms

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2 2007
P. O. KATZ
Summary Background Gastro-oesophageal reflux disease (GERD) patients on proton pump inhibitors before breakfast or dinner have acid recovery at night. Bedtime immediate-release omeprazole (IR-OME) demonstrated better control of nocturnal pH than pantoprazole before dinner. Aim To compare repeated once daily bedtime dosing of IR-OME, lansoprazole and esomeprazole on nocturnal gastric acidity. Methods Open-label, randomized, crossover study enrolling 54 patients with nocturnal GERD symptoms comparing IR-OME, lansoprazole and esomeprazole at steady state for nocturnal acid breakthrough (NAB), percentage of time with gastric pH > 4 and median gastric pH. Results Onset of nocturnal acid control with IR-OME was rapid. During the first half of the night, percentage of time with gastric pH > 4 and median gastric pH were significantly higher after IR-OME compared to esomeprazole or lansoprazole (P < 0.001, both comparisons). Over the 8-h night-time period, acid control with IR-OME was significantly better than lansoprazole (P < 0.001), and comparable to esomeprazole. IR-OME reduced NAB compared with esomeprazole and lansoprazole (61% vs. 92% and 92%; P < 0.001, both comparisons). Conclusions Bedtime IR-OME provided more rapid control of night-time gastric pH and decreased NAB compared with esomeprazole and lansoprazole. Nocturnal acid control with IR-OME was superior to lansoprazole and comparable to esomeprazole. Bedtime dosing with IR-OME may be effective for patients with night-time heartburn. [source]

Comparison of the effects of immediate-release omeprazole powder for oral suspension and pantoprazole delayed-release tablets on nocturnal acid breakthrough in patients with symptomatic gastro-oesophageal reflux disease

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 12 2005
D. Castell
Summary Background :,Many patients treated with a proton-pump inhibitor for gastro-oesophageal reflux disease or erosive oesophagitis still have substantial night-time gastric acidity. A previous trial of a new immediate-release omeprazole oral suspension suggested that nocturnal gastric acidity could be more effectively controlled with a bedtime dose of immediate-release omeprazole than with a delayed-release proton-pump inhibitor administered before dinner or at bedtime. Aim :,To compare the ability of immediate-release omeprazole with pantoprazole to control nocturnal gastric acidity, when they were dosed once daily and twice daily. Methods :,Thirty-six patients with nocturnal gastro-oesophageal reflux disease symptoms received immediate-release omeprazole and pantoprazole in this open-label, randomized-crossover trial. Median gastric pH, the percentage of time with gastric pH > 4 and the percentage of patients with nocturnal acid breakthrough, were evaluated with 24-h pH monitoring. Results :,Repeated once daily (bedtime) dosing with immediate-release omeprazole suspension produced significantly better nocturnal gastric acid control than repeated once daily (predinner) or twice daily (prebreakfast and bedtime) dosing with pantoprazole delayed-release tablets (median pH: 4.7 vs. 2.0 and 1.7; percentage of time pH > 4: 55 vs. 27 and 34; nocturnal acid breakthrough: 53 vs. 78 and 75). Twice daily dosing (prebreakfast and bedtime) with immediate-release omeprazole 20 and 40 mg achieved the best night-time control of gastric acidity. Repeated once daily bedtime dosing with immediate-release omeprazole 40 mg and twice daily dosing with pantoprazole 40 mg gave similar 24-h pH control. No safety issues were associated with either drug in this trial. Conclusions :,Dosed once daily at bedtime, immediate-release omeprazole reduced nocturnal gastric acidity to a degree not observed with once daily dosing of delayed-release proton-pump inhibitors. [source]

Frequency analyses of gastric pH in control and gastro-oesophageal reflux disease subjects treated with a proton-pump inhibitor

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 11-12 2004
J. D. Gardner
Summary Background :,We are unaware of any solid theoretical or pathophysiological basis for selecting pH 4 or any other pH value to assess gastric acidity. Aim :,To examine the frequency of different gastric pH values in control and GERD subjects. Methods :,Gastric pH was measured for 24 h in 26 control subjects, 26 gastro-oesophageal reflux disease subjects at baseline and the same 26 gastro-oesophageal reflux disease subjects during treatment with a proton-pump inhibitor. Histograms were constructed using the 21 600 values generated from each recording and bins of 0.25 pH units. Results :,The distribution of gastric pH values in gastro-oesophageal reflux disease subjects was significantly different from that in controls and in some instances the distributions detected significant differences that were not detected by integrated acidity. Proton-pump inhibitor treatment significantly altered the distribution of gastric pH values and the nature of this alteration during the postprandial period was different from that during the nocturnal period. Using time pH,4 can significantly underestimate the magnitude of inhibition of gastric acidity caused by a proton-pump inhibitor. Conclusions :,The distribution of gastric pH values provides a rationale for selecting a particular pH value to assess gastric acidity. In some instances, the distribution of gastric pH values detects significant differences between gastro-oesophageal reflux disease and normal subjects that are not detected by integrated acidity. [source]

Effect of low-dose rabeprazole and omeprazole on gastric acidity: results of a double blind, randomized, placebo-controlled, three-way crossover study in healthy subjects

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2004
S. Bruley des Varannes
Summary Background :,The treatment of acid-related symptoms requires rapid and consistent acid suppression, especially with on-demand regimens. Aim :,To compare the antisecretory activity of low-dose rabeprazole and omeprazole in healthy, Helicobacter pylori -negative subjects. Methods :,In this randomized, double-blind, placebo-controlled, three-way crossover study, 27 volunteers were given rabeprazole 10 mg, omeprazole 10 mg, or placebo once daily for 7 days with a 10,14-day washout between treatments. Intragastric pH was monitored for 24-h on days 1 and 7 of each treatment. Results :,Median gastric pH was significantly higher with rabeprazole than with omeprazole or placebo: day 1: 2.3, 1.4 and 1.3, respectively (P = 0.0056, rabeprazole vs. omeprazole; P < 0.0001, rabeprazole vs. placebo); day 7: 3.7, 2.2 and 1.3, respectively (P = 0.0016 rabeprazole vs. omeprazole; P < 0.0001, rabeprazole vs. placebo). Time with gastric pH above 4 was significantly higher with rabeprazole than with omeprazole: day 1, 5.8 h vs. 3.7 h, respectively (P < 0.02); day 7, 10.5 h vs. 4.6 h, respectively (P = 0.0008). Conclusions :,Rabeprazole 10 mg provides more rapid acid inhibition compared with omeprazole 10 mg. After 7 days, the time with pH above 4 is more than doubled with rabeprazole 10 mg vs. omeprazole 10 mg. [source]

Cisapride inhibits meal-stimulated gastric acid secretion and post-prandial gastric acidity in subjects with gastro-oesophageal reflux disease

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 10 2002
J. D. Gardner
Summary Background and aims : KCNQ1 potassium channels in human gastric parietal cells are thought to be involved in gastric acid secretion. As cisapride can inhibit similar channels in other tissues and is an effective treatment for nocturnal heartburn, we examined the effects of cisapride on gastric and oesophageal acidity, gastric emptying and heartburn severity in subjects with gastro-oesophageal reflux disease. Methods : Subjects (n=11) had suffered from heartburn four times or more per week for at least 6 months. Gastric pH and oesophageal pH were measured before, during and after a standard meal ingested over 15 min. Each subject received placebo or 10 mg cisapride orally, 30 min before the beginning of the meal. Meal-stimulated gastric acid secretion was calculated from the amount of HCl required to titrate the homogenized standard meal to pH 2 in vitro and the time required for the pH of the ingested meal to decrease to pH 2 in vivo. Heartburn severity was assessed at 15-min intervals beginning at the end of the meal. Gastric emptying of solids was measured using a [13C]-octanoic acid breath test. Results : Cisapride significantly decreased meal-stimulated gastric acid secretion by 20%, decreased integrated gastric and oesophageal acidity by 50,60% and transiently increased the expiration of 13CO2. Cisapride did not significantly alter heartburn severity. Conclusions : The cisapride-induced decreases in meal-stimulated gastric acid secretion, gastric acidity and oesophageal acidity in subjects with gastro-oesophageal reflux disease can account for its beneficial clinical effects. These results also raise the possibility that gastric KCNQ1 potassium channels are important in meal-stimulated gastric acid secretion and possibly in the pathophysiology of gastro-oesophageal reflux disease. [source]

Control of intragastric pH with omeprazole 20 mg, omeprazole 40 mg and lansoprazole 30 mg

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 5 2001
P. O. Katz
Background: Single daily doses of proton pump inhibitors, omeprazole and lansoprazole provide effective acid suppression and equal healing and symptom relief in patients with GERD. Despite this, controversy exists as to the efficacy of available proton pump inhibitors in the control of gastric acidity. Aim: To assess the efficacy of omeprazole 20 mg vs. lansoprazole 30 mg and omeprazole 40 mg vs. lansoprazole 30 mg in intragastric pH control. Methods: Study I: 12 Helicobacter pylori -negative volunteers (mean age 33 years) were treated with omeprazole 20 mg and lansoprazole 30 mg in random order before breakfast for 7 days. Study II: 24 subjects (mean age 36 years) were similarly treated with omeprazole 40 mg and lansoprazole 30 mg for 7 days after a baseline pH study. One week washout was allowed between studies. Subjects had the same meal on each study day. On day seven, a 24-h intragastric pH study was performed. The percentage time for which gastric pH > 4 was analysed (Gastrosoft, Synectics Medical Inc.) and expressed as mean ± s.d. Results: (1) Omeprazole 20 mg and lansoprazole 30 mg showed no significant difference in the percentage time for which gastric pH > 4 in the daytime and night-time periods. (2) The percentage time for which pH > 4 with omeprazole 40 mg was significantly greater than lansoprazole 30 mg in both daytime (61 ± 19% vs. 48 ± 14%, P < 0.001), and night-time periods (34 ± 21% vs. 26 ± 14%, P < 0.05). (3) A large inter-subject variation existed in both studies. (4) In 10 subjects who participated in both studies, omeprazole 40 mg showed a significantly higher percentage time for which pH > 4 in the daytime (69 ± 18% vs. 51 ± 15%, P=0.015) than omeprazole 20 mg. Conclusion: These pH data support the therapeutic equivalency of FDA approved doses of omeprazole and lansoprazole. [source]

The effects of capsaicin on reflux, gastric emptying and dyspepsia

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2000
Rodriguez-Stanley
Aims: To evaluate capsaicin's effects on heartburn, dyspepsia, gastric acidity and emptying, and gastro-oesophageal reflux, and to test the hypothesis that capsaicin induces heartburn and exacerbates symptoms by sensitizing the oesophagus. Methods: Eleven heartburn sufferers underwent two separate pH monitoring sessions and assessments of gastric emptying (13C-octanoic acid breath test), heartburn and dyspepsia (100 mm VAS) after a non-irritant meal. The meal consisted of a sausage biscuit with egg, cheese and 30 g raw onion, 8 oz chocolate milk and a peppermint patty. Thirty minutes prior to meal consumption, subjects were administered a placebo capsule. On visit 1, subjects consumed the meal containing 100 ,l 13C-octanoic acid cooked in the egg, over 15 min. On visit 2, subjects consumed the meal plus 5 mg capsaicin in gelatin capsules. Results: Oesophageal and gastric pH profiles and gastric emptying were not different between meals. Capsaicin did not alter mean heartburn and dyspepsia scores (P > 0.05), but significantly decreased time to peak heartburn (120 min vs. 247 min; P < 0.003). Time to peak dyspepsia was not altered by capsaicin (P > 0.05). Conclusion: Capsaicin enhances noxious postprandial heartburn, presumably by direct effects on sensory neurons. [source]

Oxyntic lesions may be provoked in the rat both by the process of acid secretion and also by gastric acidity

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2000
Waldum
Background: Gastric ischaemia appears to be a common pathogenetic factor for stress ulcers. These ulcers occur predominantly in the oxyntic mucosa, suggesting that the acid secretory process or its stimulation is involved in the pathogenesis. Methods: We examined separately the role of the acid secretory process and gastric luminal acidity in the pathogenesis of gastric lesions using the isolated vascularly perfused acid-secreting rat stomach. Results: Pentagastrin-stimulated acid secretion induced submucosal bleeding in the oxyntic mucosa whether accompanied by perfusion of the gastric lumen with saline or a phosphate buffer at pH 7.0. On the other hand, acidity, whether endogenous or introduced by luminal perfusion, induced erosions in both the oxyntic and antral mucosa. Conclusion: It is concluded that the acid secretory process itself contributes to the particular vulnerability of the oxyntic mucosa to ischaemia. Histamine released upon stimulation of gastric acid secretion or shortage of energy due to the requirements for acid secretion may both contribute to this vulnerability. Furthermore, these findings suggest that inhibition of gastric acid secretion should be superior to antacids in preventing stress ulcers. [source]