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Gastric Acid (gastric + acid)
Terms modified by Gastric Acid Selected AbstractsClinical trial: intragastric acid control in patients who have Barrett's oesophagus,comparison of once- and twice-daily regimens of esomeprazole and lansoprazoleALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2 2009S. J. SPECHLER Summary Background, Gastric acid control is important for treatment of gastro-oesophageal reflux disease associated with Barrett's oesophagus. Substantial indirect evidence suggests that gastric acid control may have a chemopreventive role in Barrett's oesophagus. Aim, To compare the pharmacodynamic efficacy of esomeprazole and lansoprazole at two dosages for intragastric pH control with Barrett's oesophagus. Methods, Patients with Barrett's oesophagus received open-label consecutive treatment (a 15-day period of once-daily dosing followed by a 10-day period of twice-daily dosing) with esomeprazole (40-mg capsules) and lansoprazole (30-mg capsules) in random order with no washouts. Twenty-four-hour intragastric pH was recorded on the last day of each dosing period. The primary end point was the percentage of time with intragastric pH > 4.0. Results, In the per-protocol once- (n = 46) and twice-daily (n = 41) analyses, the percentage of time with intragastric pH > 4.0 was significantly (P < 0.0001) longer after once- (67.1%) or twice-daily (81.2%) esomeprazole than after once- (50.8%) or twice-daily (64.3%) lansoprazole. The proportion of patients with intragastric pH > 4.0 for >12 h was significantly higher for esomeprazole than lansoprazole with once- (P = 0.004) and twice-daily (P = 0.016) dosing. Conclusion, Esomeprazole 40 mg is significantly more effective than lansoprazole 30 mg in controlling intragastric pH with Barrett's oesophagus. [source] Low-dose intravenous pantoprazole for optimal inhibition of gastric acid in Korean patientsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 9 2007Jung-Hwan Oh Abstract Background and Aim:, Proton-pump inhibitor (PPI) therapy for bleeding ulcers is more efficacious in Asian patients than in non-Asian patients. The aim of this study was to evaluate the efficacy of various doses of pantoprazole on intragastric acidity in Korean patients. Methods:, A prospective randomized study was conducted in 52 patients either with bleeding peptic ulcers after successful endotherapy or who received endoscopic mucosal resection for gastric neoplasms. Patients were randomized into two doses of intravenous pantoprazole: 40 mg q.d. and 40 mg b.i.d. We compared these results with our preliminary study utilizing high-dose pantoprazole (80 mg + 8 mg/h). The potential contribution of CYP2C19 genetic polymorphisms and the presence of Helicobacter pylori were also assessed. Results:, Pantoprazole 40 mg b.i.d. and high-dose pantoprazole demonstrated better inhibition of intragastric acid than pantoprazole q.d. (P < 0.05). The pantoprazole 40 mg q.d. group exhibited significant variations in acid inhibition correlating with CYP2C19 genotype. Median 24 h pH values did not differ significantly between the pantoprazole b.i.d. and high-dose pantoprazole groups, regardless of H. pylori infection status. A median intragastric pH < 6.0 was observed in only three of 28 patients in the 40 mg b.i.d. group; these three patients were extensive metabolizers. Conclusion:, A 40 mg b.i.d. dose of pantoprazole is sufficient to maintain pH > 6.0 in Korean patients, except for patients with extensive metabolizing CYP2C19 genotypes. [source] Clinical trial: gastric acid suppression in Hispanic adults with symptomatic gastro-oesophageal reflux disease , comparator study of esomeprazole, lansoprazole and pantoprazoleALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2 2010D. 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] Omeprazole-Mg 20.6 mg is superior to lansoprazole 15 mg for control of gastric acid: a comparison of over-the-counter doses of proton pump inhibitorsALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2010P. B. MINER JR Aliment Pharmacol Ther,31, 846,851 Summary Background, Over-the-counter (OTC) proton pump inhibitors (PPIs) relieve heartburn by decreasing the production of gastric acid, but may not do so with equal effectiveness. It is important for healthcare professionals to compare the ability of OTC PPIs to control gastric acid when recommending them for patients with frequent heartburn. Aim, To compare the effects of omeprazole-Mg 20.6 mg and lansoprazole 15 mg (OTC doses in the US) on 24-h steady state gastric acid suppression. Methods, This single-centre, randomized, double-blind clinical study compared the steady-state gastric acid control of omeprazole-Mg 20.6 mg vs. lansoprazole 15 mg, dosed before breakfast. Volunteers were enrolled in a 3-period, cross-over design (ABB, BAA) with 24-h gastric pH monitoring on dosing day 5. The primary efficacy variable was the percentage time intragastric pH was >4.0 over 24 h on day 5 of dosing. Results, Forty subjects were enrolled; all completed the study. The mean (SE) percentage time pH was >4.0 was 45.7% (3.45%) for omeprazole-Mg 20.6 mg and 36.8% (3.45%) for lansoprazole 15 mg, an absolute difference of 8.9% (P < 0.0001), and a relative difference of 24.2%. Both drugs were well tolerated. Conclusion, Omeprazole-Mg 20.6 mg provided a statistically significantly (P < 0.0001) greater acid control than lansoprazole 15 mg. [source] Clinical trial: intragastric acid control in patients who have Barrett's oesophagus,comparison of once- and twice-daily regimens of esomeprazole and lansoprazoleALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2 2009S. J. SPECHLER Summary Background, Gastric acid control is important for treatment of gastro-oesophageal reflux disease associated with Barrett's oesophagus. Substantial indirect evidence suggests that gastric acid control may have a chemopreventive role in Barrett's oesophagus. Aim, To compare the pharmacodynamic efficacy of esomeprazole and lansoprazole at two dosages for intragastric pH control with Barrett's oesophagus. Methods, Patients with Barrett's oesophagus received open-label consecutive treatment (a 15-day period of once-daily dosing followed by a 10-day period of twice-daily dosing) with esomeprazole (40-mg capsules) and lansoprazole (30-mg capsules) in random order with no washouts. Twenty-four-hour intragastric pH was recorded on the last day of each dosing period. The primary end point was the percentage of time with intragastric pH > 4.0. Results, In the per-protocol once- (n = 46) and twice-daily (n = 41) analyses, the percentage of time with intragastric pH > 4.0 was significantly (P < 0.0001) longer after once- (67.1%) or twice-daily (81.2%) esomeprazole than after once- (50.8%) or twice-daily (64.3%) lansoprazole. The proportion of patients with intragastric pH > 4.0 for >12 h was significantly higher for esomeprazole than lansoprazole with once- (P = 0.004) and twice-daily (P = 0.016) dosing. Conclusion, Esomeprazole 40 mg is significantly more effective than lansoprazole 30 mg in controlling intragastric pH with Barrett's oesophagus. [source] Systematic review: impaired drug absorption related to the co-administration of antisecretory therapyALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 12 2009E. 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] Systematic review: Heliocobacter pylori infection and impaired drug absorptionALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 4 2009E. LAHNER Summary Background, Impaired acid secretion may affect drug absorption and may be consequent to corporal Heliocobacter pylori- gastritis, which may affect the absorption of orally administered drugs. Aim, To focus on the evidence of impaired drug absorption associated with H. pylori infection. Methods, Data sources were the systematic search of MEDLINE/EMBASE/SCOPUS databases (1980,April 2008) for English articles using the keywords: drug malabsorption/absorption, stomach, Helicobacter pylori, gastritis, gastric acid, gastric pH, hypochlorhydria, gastric hypoacidity. Study selection was made from 2099 retrieved articles, five studies were identified. Data were extracted from selected papers, investigated drugs, study type, main features of subjects, study design, intervention type and results were extracted. Results, In all, five studies investigated impaired absorption of l -dopa, thyroxine and delavirdine in H. pylori infection. Eradication treatment led to 21,54% increase in l -dopa in Parkinon's disease. Thyroxine requirement was higher in hypochlorhydric goitre with H. pylori- gastritis and thyrotropin levels decreased by 94% after treatment. In H. pylori- and HIV-positive hypochlorhydric subjects, delavirdine absorption increased by 57% with orange juice administration and by 150% after eradication. Conclusions, A plausible mechanism of impaired drug absorption is decreased acid secretion in H. pylori -gastritis patients. Helicobacter pylori infection and hypochlorhydria should be considered in prescribing drugs the absorption of which is potentially affected by intragastric pH. [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 diseaseALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 12 2005D. 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] Review article: potential gastrointestinal effects of long-term acid suppression with proton pump inhibitorsALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2000Laine This review examines the evidence for the development of adverse effects due to prolonged gastric acid suppression with proton pump inhibitors. Potential areas of concern regarding long-term proton pump inhibitor use have included: carcinoid formation; development of gastric adenocarcinoma (especially in patients with Helicobacter pylori infection); bacterial overgrowth; enteric infections; and malabsorption of fat, minerals, and vitamins. Prolonged proton pump inhibitor use may lead to enterochromaffin-like cell hyperplasia, but has not been demonstrated to increase the risk of carcinoid formation. Long-term proton pump inhibitor treatment has not been documented to hasten the development or the progression of atrophic gastritis to intestinal metaplasia and gastric cancer, although long-term studies are required to allow definitive conclusions. At present, we do not recommend that patients be tested routinely for H. pylori infection when using proton pump inhibitors for prolonged periods. Gastric bacterial overgrowth does increase with acid suppression, but important clinical sequelae, such a higher rate of gastric adenocarcinoma, have not been seen. The risk of enteric infection may increase with acid suppression, although this does not seem to be a common clinical problem with prolonged proton pump inhibitor use. The absorption of fats and minerals does not appear to be significantly impaired with chronic acid suppression. However, vitamin B12 concentration may be decreased when gastric acid is markedly suppressed for prolonged periods (e.g. Zolllinger,Ellison syndrome), and vitamin B12 levels should probably be assessed in patients taking high-dose proton pump inhibitors for many years. Thus, current evidence suggests that prolonged gastric acid suppression with proton pump inhibitors rarely, if ever, produces adverse events. Nevertheless, continued follow-up of patients taking proton pump inhibitors for extended periods will provide greater experience regarding the potential gastrointestinal adverse effects of long-term acid suppression. [source] Sensory neurone responses to mucosal noxae in the upper gut: relevance to mucosal integrity and gastrointestinal painNEUROGASTROENTEROLOGY & MOTILITY, Issue 5 2002P. Holzer Abstract ,The digestive tract is supplied by extrinsic and intrinsic sensory neurones that, together with endocrine and immune cells, form a surveillance network that is essential to gut function. This article focuses on the responses of extrinsic afferent neurones to chemical insults of the gastrointestinal mucosa and their pathophysiological relevance to mucosal integrity and abdominal pain. Within the gastroduodenal region, spinal afferents subserve an emergency function because, in case of alarm by influxing acid, they stimulate mechanisms of mucosal protection via an efferent-like release of transmitters. Other sensory neurones signal chemical noxae to the brain, a task that is not confined to spinal afferents because vagal afferents communicate gastric acid and peripheral immune challenges to the brainstem and in this way elicit autonomic, endocrine, affective and behavioural reactions. Emerging evidence indicates that hypersensitivity of extrinsic afferent pathways to mechanical and chemical stimuli makes an important contribution to the abdominal hyperalgesia seen in functional dyspepsia and irritable bowel syndrome. Sensitization may be brought about by inflammatory processes that lead to up-regulation and functional alterations of receptors and ion channels on sensory neurones. Such sensory neurone-specific molecules, which include vanilloid (capsaicin) receptors, may represent important targets for novel drugs to treat abdominal pain. [source] Nonsteroidal anti-inflammatory drug-induced experimental gastropathy: Is gastric acid the major trigger?CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 7 2010Thomas Brzozowski No abstract is available for this article. [source] | ||||||||||