gastrins and Esophagitis

Topics: Cimetidine; Duodenal Ulcer; Esophagitis; Gastric Mucosa; Gastrins; Humans; Omeprazole; Ranitidine; Vagotomy, Proximal Gastric

Topics: Adult; Cimetidine; Esophagitis; Female; Gastrins; Humans; Male; Middle Aged; Multiple Endocrine Neoplasia; Parathyroid Glands; Prognosis; Secretin; Zollinger-Ellison Syndrome

Topics: Antacids; Asphyxia; Esophagitis; Esophagoscopy; Gastrins; Gastroesophageal Reflux; Gastrointestinal Hemorrhage; Hernia, Diaphragmatic; Humans; Methods; Parasympatholytics; Radiography; Stomach Ulcer

Topics: Abdomen; Duodenal Diseases; Duodenal Neoplasms; Duodenal Ulcer; Esophageal Achalasia; Esophageal Diseases; Esophageal Neoplasms; Esophagitis; Esophagoplasty; Esophagus; Female; Gastrins; Gastrointestinal Hemorrhage; Hernia, Diaphragmatic; Humans; Male; Peptic Ulcer; Peptic Ulcer Perforation; Postoperative Complications; Rupture, Spontaneous; Stomach Diseases; Stomach Neoplasms; Stomach Ulcer; Stress, Psychological; Vagotomy

To determine the proportion of patients with gastroesophageal reflux disease who are on proton pump inhibitors (PPIs) who could reduce their prior dosage by half, and identify predictors of successful step-down.. Appropriate hypergastrinemia results from gastric acid inhibition. A gender difference in fasting gastrin with higher levels among women than among men on long-term PPI therapy has been demonstrated.. Patients with endoscopically verified erosive esophagitis on long-term PPI therapy were randomized double blindly to step down their dose by half or continue with the same dose for 8 weeks. Fasting gastrin levels were measured before and after treatment. The primary endpoint was successful step-down throughout the study period.. Overall, 100 patients were randomized, 49 (24 females) to continue with the same dose as before and 51 (25 females) to step down. Female patients had higher gastrin levels compared with male patients: 78 pg/mL (IQR, 50 to 99) versus 50 pg/mL (IQR, 36 to 74) (P=0.007). Among those randomized to the step-down intervention only 3/25 (12%) women failed to complete the 2 months of lower-dose therapy versus 9/25 (36%) men (P=0.09). Female gender (P=0.048) was the strongest predictor for successful step-down (odds ratio=1.27; 95% CI, 1.01-1.60). The chance of failing to maintain symptom control was twice as high in the reduction group (24%) as compared with the control group (13%) (P=0.2).. Female patients on long-term PPI therapy were 3 times more likely to tolerate half of their prior dose. Female gender had higher probability for successful step-down. These results indicate that women with gastroesophageal reflux disease might manage with lower doses of PPIs as compared with men.European Clinical Trial Database (https://eudract.ema.europa.eu/), number 2013-002067-26.

Topics: Aged; Dose-Response Relationship, Drug; Double-Blind Method; Esophagitis; Female; Gastrins; Gastroesophageal Reflux; Humans; Male; Middle Aged; Proton Pump Inhibitors; Sex Factors; Time Factors; Treatment Outcome

The potassium-competitive acid blocker vonoprazan (VPZ) has potent acid-inhibitory effects and may offer clinical advantages over conventional therapy for acid-related disorders.. To investigate the efficacy and safety of VPZ in patients with erosive oesophagitis (EO).. In this multicentre, randomised, double-blind, parallel-group, dose-ranging study, patients ≥20 years with endoscopically confirmed EO [Los Angeles (LA) grades A-D] received VPZ 5, 10, 20 or 40 mg, or lansoprazole (LPZ) 30 mg once daily for 8 weeks. The primary endpoint was the proportion of healed EO subjects as shown by endoscopy at week 4.. A total of 732 subjects received VPZ or LPZ. The proportion of healed EO subjects at week 4 was 92.3%, 92.5%, 94.4%, 97.0% and 93.2%, respectively, with VPZ 5, 10, 20 and 40 mg and LPZ 30 mg. All VPZ doses were non-inferior to LPZ when adjusted for baseline LA grades A/B and C/D. Among those with LA grades C/D, the proportions of healed EO subjects were 87.3%, 86.4%, 100%, 96.0% and 87.0%, respectively, with VPZ 5, 10, 20 and 40 mg and LPZ 30 mg. The incidence of adverse events was similar across the groups.. Vonoprazan was effective and non-inferior to LPZ in healing EO. VPZ 20 mg or higher was highly efficacious for severe EO (LA grades C/D). VPZ was associated with no safety concern during this 8-week study, while there was a dose-dependent increase in serum gastrin. Once-daily VPZ 20 mg is the recommended clinical dose for treating EO.

Topics: Adult; Aged; Dose-Response Relationship, Drug; Double-Blind Method; Esophagitis; Female; Gastrins; Humans; Lansoprazole; Los Angeles; Male; Middle Aged; Proton Pump Inhibitors; Pyrroles; Sulfonamides

Rebound acid hypersecretion after withdrawal of proton pump inhibitor (PPI) may lead to symptom aggravation and difficulties in withdrawing anti-reflux medication. The aim was to investigate pathophysiological and clinical consequences of on-demand treatment with PPI in patients with endoscopy-negative reflux disease.. Twenty-six patients with endoscopy-negative reflux disease were investigated for rebound effects of lansoprazole 15 mg, used on-demand, maximum 4 capsules daily during a 6-month period. P-CgA and s-gastrin were measured before, at termination and 2 weeks after stopping treatment. Symptom score was performed the week before and the second week after treatment, 24-h pH-metry after both periods.. Median daily consumption of lansoprazole was 15.1 mg (95% CI: 10.5; 18.8). S-gastrin before treatment was 31.2 pmol/l, 54.8 at the end (p < 0.01), 31.7 two weeks after withdrawal. P-CgA was 16.7 u/l before treatment, 37.5 at the end (p < 0.01), 17.7 two weeks after withdrawal (p = 0.35). A positive correlation was found between total consumption of lansoprazole and CgA increase during treatment (r = 0.44 p = 0.03). There was a reduction in symptom score during the treatment period from 30 (24-38) before, to 20 (15-36) the second week after treatment, p = 0.06. 32% had increase in symptoms.. Rebound acid hypersecretion is probably an infrequent problem in on-demand treatment with PPI in patients with endoscopy-negative reflux disease. A significant increase in p-CgA and s-gastrin was found after 6 months treatment. Fourteen days after withdrawal, CgA and gastrin returned to pretreatment levels. Overall, no aggravation of symptoms was found, but 1/3 experienced increased symptoms.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Aged; Anti-Ulcer Agents; Chromogranins; Esophagitis; Female; Gastric Acid; Gastrins; Heartburn; Humans; Lansoprazole; Laryngopharyngeal Reflux; Male; Middle Aged; Prospective Studies; Proton Pump Inhibitors; Secretory Rate

To evaluate the effect of Helicobacter pylori (Hp) eradication therapy on blood gastrin levels in long-term PPI users, since proton pump inhibitors (PPIs) and Helicobacter pylori (Hp) are major causes of hypergastrinaemia.. A prospective study.. Twenty seven Hp (+) patients enrolled in the study. Twenty were given eradication treatment (ET group), and the rest were given symptomatic treatment (ST group). Those who remained Hp (+) after eradication therapy were also added into the ST group. Lansoprazol 30 mg/day was given to both groups for three months thereafter.. Fasting and non-fasting blood gastrin levels (FGL and NFGL) were measured initially and one month and four months after treatment. At the end of fourth month, FGL was significantly higher than both initial and first month level (p < 0.01) in the ST group. NFGL in this group did not change significantly (p > 0.05) after eradication therapy. In the ET group, FGL was significantly higher in the fourth month than the first month (p < 0.001) and than the initial level (p < 0.05). NFGL was higher, but not statistically in the fourth month than in the first month (p > 0.05) and significantly lower than the initial level (p < 0.05) in this group.. We suggest that testing for Hp positivity and treating it if detected would be an appropriate approach to avoid hypergastrinaemia, especially in candidate patients for long term PPI treatment.

Topics: Adult; Anti-Ulcer Agents; Esophagitis; Fasting; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Peptic Ulcer; Prospective Studies; Proton Pump Inhibitors; Time

The aim of this study was to determine the effect of 6-12 months of treatment with esomeprazole on the histopathology of the gastric mucosa.. Two identically designed, randomized, placebo-controlled trials of esomeprazole 40, 20, or 10 mg daily for up to 6 months, as well as a noncomparative, multicenter trial of esomeprazole 40 mg daily for up to 12 months, were conducted in 1326 patients with healed erosive esophagitis (1294 negative for Helicobacter pylori [H. pylori]). Gastric biopsy samples were obtained before treatment and on completion of (or discontinuation from) the trials. Samples were evaluated for the presence of H. pylori, characteristics of acute gastritis or atrophic gastritis, and enterochromaffin-like cell pathology.. During treatment with esomeprazole, the number of patients with an improvement in gastric histological scores was typically greater than or equal to the number who worsened. Gastric histological scores worsened for each corporal or antral characteristic of gastritis in <6.2% of patients. Histological scores with esomeprazole and placebo were similar throughout the 6-month trials. Only one among 1326 patients treated with esomeprazole (H. pylori negative) had evidence of treatment-emergent atrophic gastritis. On final biopsy, 5-12% of patients had abnormal enterochromaffin-like cell scores (simple, linear, or micronodular hyperplasia). There were no instances of enterochromaffin-like cell dysplasia, carcinoids, or neoplasia.. Patients with healed erosive esophagitis receiving esomeprazole for up to 12 months had minor fluctuations in gastric histological scores, similar to those experienced in untreated populations. Use of esomeprazole did not raise any safety concerns with respect to the development of atrophic gastritis, or cause clinically significant changes in enterochromaffin-like cells.

Topics: Adult; Anti-Ulcer Agents; Enterochromaffin-like Cells; Esomeprazole; Esophagitis; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Metaplasia

To evaluate the safety of lansoprazole in children between 1 and 11 years of age.. In a phase I/II, open-label, multicenter (11 sites) study, children with symptomatic gastroesophageal reflux disease (GERD), erosive esophagitis (> or = grade 2), and/or esophageal pH < 4 for > 4.2% of the 24-hour period were assigned, on the basis of body weight, to lansoprazole 15 mg (< or = 30 kg) or 30 mg (> 30 kg) once daily for 8 to 12 weeks. At the discretion of the investigator, the dosage of lansoprazole was increased up to 60 mg daily in children who continued to be symptomatic after 2 weeks of treatment. Safety for all study participants was monitored by adverse event reports and laboratory evaluations.. Sixty-six children were enrolled in the study and were included in the safety analysis. Throughout the treatment period, no child discontinued therapy because of an adverse event and no clinically significant changes in laboratory values were observed. Three of the 32 children (9%) who received lansoprazole 15 mg once daily (mean exposure 50.3 days) and 6 of the 34 children (18%) who received the 30 mg once-daily dose (mean exposure 49.4 days) experienced one or more treatment-related adverse events before any dose increase. The three children in the lansoprazole 15 mg treatment group were treated with doses of 0.6 mg to 1.2 mg/kg/day; those in the lansoprazole 30 mg treatment group were treated with doses of 0.7 mg to 0.9 mg/kg/day. Only one child experienced a new treatment-related adverse event after an increase in lansoprazole dose to 1.3 mg/kg/day. Treatment-related events experienced by two or more children were: constipation (lansoprazole 15 mg QD, two children; lansoprazole 30 mg QD, one child), and headache (lansoprazole 30 mg QD, two children). Mean fasting serum gastrin levels were significantly increased from 58.0 pg/mL at baseline to 112.4 pg/mL at week 2 and 121.9 pg/mL at the final visit (P < or = 0.001 for each comparison). However, the median fasting serum gastrin levels at the week 2 and the final visit were within the normal range (25-111 pg/mL).. Lansoprazole, when administered on the basis of body weight in children between 1 and 11 years of age, is safe and well-tolerated.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Anti-Ulcer Agents; Child; Child, Preschool; Dose-Response Relationship, Drug; Esophagitis; Female; Gastrins; Gastroesophageal Reflux; Humans; Infant; Lansoprazole; Male; Omeprazole; Proton Pump Inhibitors; Safety

Many children with esophagitis demonstrate histological changes without gross evidence of esophagitis by esophagoscopy. The effect of omeprazole on the histological healing of esophagitis in children is unknown. Therefore, the aim of this study was to determine the effect of omeprazole on refractory histological esophagitis in pediatric patients. Eighteen patients with histological evidence of esophagitis and recurrent symptoms despite therapy with H2-receptor antagonists and prokinetic agents were prospectively treated with omeprazole. Dosing was adjusted by monitoring intragastric pH, and esophagoscopy was repeated after 8-12 weeks of omeprazole treatment. Two patients did not complete the study due to either worsening symptoms or hypergastrinemia. Of the remaining patients, 76% were asymptomatic with omeprazole treatment and 24% reported improvement in their symptoms. Approximately 40% demonstrated complete histological healing of their esophagitis. Three patients (17%) had persistent elevations in serum gastrin levels while on omeprazole treatment, which was associated with both younger patient age and higher omeprazole dosing; however, all elevated gastrin levels returned to normal after discontinuation of the medication. All patients had recurrence of their symptoms after completing a course of omeprazole, even patients with complete histological healing. Omeprazole is efficacious in treating children with esophagitis refractory to H2-receptor antagonist and prokinetic agents. However, none of the patients were able to discontinue acid suppressive therapy even after documented healing of their esophagitis.

Topics: Adolescent; Anti-Ulcer Agents; Child; Child, Preschool; Esophagitis; Esophagoscopy; Female; Gastrins; Humans; Hydrogen-Ion Concentration; Male; Omeprazole; Prospective Studies; Recurrence

A hypothesis suggesting that profound acid inhibition therapy facilitates and hastens the development of gastric glandular atrophy in patients infected with Helicobacter pylori was investigated in this randomized study comparing omeprazole therapy with antireflux surgery (ARS) for chronic gastroesophageal reflux disease (GERD).. Patients with esophagitis and/or chronic GERD were enrolled; 155 patients were randomized to ARS and 155 to long-term omeprazole therapy. Baseline data were obtained and repeated after 3 years in 131 ARS patients and in 139 omeprazole-treated patients. Histopathologic status of the oxyntic mucosa was assessed according to the Sydney system.. Forty omeprazole-treated patients were infected with H. pylori compared with 53 in the ARS group. Basal gastrin levels were significantly higher in H. pylori-infected patients, particularly in the omeprazole group. No further increases in serum gastrin levels were observed during 3 years. Despite 3 years of therapy, only slight changes were found in the prevalence of inflammation in the corpus mucosa of H. pylori-infected subjects. A slow progression of gastric glandular atrophy was observed in these patients irrespective of therapy with no obvious difference between treatment regimens. Intestinal metaplasia (all of type I) was only exceptionally observed with no difference between the treatment arms.. Acid-suppressive therapy in the form of omeprazole maintained for 3 years facilitates neither the development of gastric glandular atrophy of the corpus mucosa nor the occurrence of intestinal metaplasia in H. pylori-infected GERD patients.

Topics: Adolescent; Adult; Aged; Anti-Ulcer Agents; Atrophy; Esophagitis; Female; Gastric Mucosa; Gastrins; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Omeprazole; Prospective Studies

Gastric acid secretion, gastrin release, gastric emptying, and gastroesophageal acid reflux were measured in asymptomatic individuals before and after elimination of Helicobacter pylori gastritis. After basal gastric acid secretion and serum gastrin concentrations were measured, meal-stimulated gastric acid secretion and gastrin release were assessed during in vivo intragastric titration to pH 3. Experiments were repeated 4 wk after treatment with lansoprazole, amoxicillin, and clarithromycin. Esophageal pH was also monitored for 24 h before and after therapy. Basal gastric acidity increased approximately 20 mmol/l in subjects whose infection was eradicated (P < 0.05) but not in those with persistent infection. Basal and meal-stimulated gastric acid secretion did not change after H. pylori eradication, despite a 41% reduction in meal-stimulated gastrin release (P < 0.05). Gastroesophageal acid reflux increased two- to threefold after successful treatment (P < 0. 05) but did not change in subjects with persistent infection. Thus elimination of H. pylori gastritis increases gastric acidity, probably by reducing nonparietal alkaline secretion, and this may facilitate gastroesophageal acid reflux.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Amoxicillin; Anti-Bacterial Agents; Anti-Ulcer Agents; Clarithromycin; Esophagitis; Female; Food; Gastric Acid; Gastric Emptying; Gastric Mucosa; Gastrins; Gastritis; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Lansoprazole; Male; Middle Aged; Monitoring, Physiologic; Omeprazole; Penicillins; Polyethylene Glycols; Postprandial Period; Solvents

Both proton pump inhibitor drug treatment and Helicobacter pylori infection cause hypergastrinaemia in man.. To determine whether eradicating H pylori is a means of reducing hypergastrinaemia during subsequent proton pump inhibitor treatment.. Patients with H pylori were randomised to treatment with either anti-H pylori or symptomatic treatment. One month later, all received four weeks treatment with omeprazole 40 mg/day for one month followed by 20 mg/day for six months. Serum gastrin concentrations were measured before and following each treatment.. In the patients randomised to anti-H pylori treatment, eradication of the infection lowered median fasting gastrin by 48% and meal stimulated gastrin by 46%. When gastrin concentrations one month following anti-H pylori/symptomatic treatment were used as baseline, omeprazole treatment produced a similar percentage increase in serum gastrin in the H pylori infected and H pylori eradicated patients. Consequently, in the patients in which H pylori was not eradicated, median fasting gastrin concentration was 38 ng/l (range 26-86) at initial presentation and increased to 64 ng/l (range 29-271) after seven months omeprazole, representing a median increase of 68% (p < 0.005). In contrast, in the patients randomised to H pylori eradication, median fasting gastrin at initial presentation was 54 ng/l (range 17-226) and was unchanged after seven months omeprazole at 38 ng/l (range 17-95).. Eradicating H pylori is a means of reducing the rise in gastrin during subsequent long term omeprazole treatment. In view of the potential deleterious effects of hypergastrinaemia it may be appropriate to render patients H pylori negative prior to commencing long-term proton pump inhibitor treatment.

Topics: Adult; Alginates; Aluminum Hydroxide; Amoxicillin; Antacids; Anti-Ulcer Agents; Drug Combinations; Drug Therapy, Combination; Esophagitis; Female; Gastrins; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metronidazole; Middle Aged; Omeprazole; Organometallic Compounds; Peptic Ulcer; Silicic Acid; Sodium Bicarbonate

To investigate the efficacy of daily maintenance treatment with omeprazole 10 mg in reducing the relapse rate of healed erosive oesophagitis.. Three hundred patients with erosive oesophagitis (grade 2 or greater) received omeprazole 20 mg daily for 12 weeks, followed by 40 mg daily for a further 12 weeks if required. After healing, patients were randomised to double blind treatment with omeprazole 10 mg daily or placebo for up to 18 months. On relapse the treatment cycle was repeated.. The cumulative healing rate at 12 weeks in the initial healing period was 95%, and 96% and 98% on rehealing courses after relapse in the first and second maintenance periods respectively. After 12 weeks of treatment, 98% of patients were free from heartburn and 97% were free of all reflux related symptoms. Relapse in the subgroup of patients who relapsed in both maintenance periods was infrequent on omeprazole 20 mg daily: only 9% at two years. Gastrin concentrations rose above normal in one third of patients. One patient had linear hyperplasia of endocrine cells and another had micronodular hyperplasia. There were no side effects definitely attributable to omeprazole.. Maintenance treatment with omeprazole 10 mg daily keeps about 60% of patients with erosive oesophagitis in prolonged remission. Patients relapsing once are likely to do so again; they can subsequently be treated effectively with omeprazole 20 mg daily.

Topics: Anti-Ulcer Agents; Double-Blind Method; Drug Administration Schedule; Endoscopy, Gastrointestinal; Esophagitis; Female; Gastrins; Humans; Male; Middle Aged; Omeprazole; Recurrence; Treatment Outcome

Treatment with H2 receptor antagonists (H2RAs) and proton pump inhibitors (PPIs) induces hypergastrinemia and causes rebound hypersecretion of gastric acid after treatment, and during treatment with H2RAs tolerance develops. In the present study we investigated whether a treatment period with a PPI induced tolerance to an H2RA.. Thirteen patients with esophagitis were given omeprazole for 90 days. Twenty-four-hour pH monitorings without and with ranitidine were performed before and after treatment with omeprazole. Blood samples and biopsy specimens from the oxyntic mucosa were analyzed for gastrin, histamine, and chromogranin A.. An increase in mucosal histamine and a reduction in the effect of ranitidine on gastric pH was found 14 days after discontinuing omeprazole compared with before treatment in Helicobacter pylori-negative but not in H. pylori-positive patients.. Treatment with omeprazole reduces the effect of ranitidine in H. pylori-negative patients. This is caused by an increase in histamine released by the enterochromaffin-like cell secondarily to hypergastrinemia, corresponding to the tolerance towards H2RAs seen in patients with Zollinger-Ellison syndrome.

Topics: Adult; Aged; Chromogranin A; Chromogranins; Drug Tolerance; Esophagitis; Female; Gastric Acid; Gastrins; Gastroesophageal Reflux; Gastrointestinal Agents; Helicobacter Infections; Helicobacter pylori; Histamine H2 Antagonists; Histamine Release; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Omeprazole; Proton Pump Inhibitors; Ranitidine

Esophagitis is common in children with cerebral palsy. Because histamine2-receptor antagonists such as ranitidine have not been uniformly effective, we treated disabled children with esophagitis with greater than usual doses. Endoscopy and pH monitoring were used to monitor dose and response to treatment. A dose of 9.3 +/- 0.9 mg/kg/day did not improve visual or microscopic esophagitis after 3 months. A dose of 14.8 +/- 3.9 mg/kg/day resulted in only slight microscopic improvement, but symptoms were improved. There was no correlation between esophageal reflux index at enrollment and either severity of esophagitis or response to treatment. Elevation of gastric pH by ranitidine was infrequent. These results affirm that pH monitoring does not reliably identify disabled children with reflux esophagitis nor does ranitidine reliably heal this disorder.

Topics: Adolescent; Child; Child, Preschool; Developmental Disabilities; Dose-Response Relationship, Drug; Esophagitis; Female; Gastrins; Humans; Hydrogen-Ion Concentration; Male; Ranitidine

Patients (106) with peptic ulceration of the oesophagus, stomach and duodenum, unresponsive to 3 or more months of high-dose treatment with ranitidine, were initially given pantoprazole (40-80 mg, p.o.) daily. In 96.7% of the patients ulcers healed within 2 to 8 weeks, and in 2.3% of patients the ulcers healed within 12 weeks. In just one patient with severe oesophagitis, the lesion took more than 6 months to heal. After ulcer healing, patients (98 to date) were treated with pantoprazole (40 mg/day) as long-term maintenance therapy. Eighty-eight of the 98 patients have been taking pantoprazole for 6 months to 3 years. During maintenance therapy, peptic disease was kept in remission in most patients with 40 mg pantoprazole. Twelve patients with oesophagitis and two patients with gastric ulcers needed higher doses (80-120 mg) to control the disease. One female patient developed peripheral oedema which disappeared quickly after stopping treatment. No further drug-related adverse effects were observed. Seven patients withdrew from the study and two patients died, all for non-drug-related reasons. Routine laboratory tests remained without significant changes in all patients. Mean (+/- S.E.M.) serum gastrin levels were already elevated during the initial high-dose ranitidine treatment (128 +/- 23 pg/ml). Within one year of the start of the pantoprazole treatment, serum gastrin levels rose to 3 times normal values (189 +/- 32 pg/ml). Thereafter, no further increases in serum gastrin were observed for up to 2.5 years. Enterochromaffin-like (ECL) cell density increased very slightly from 0.19% to 0.24% within one year.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Benzimidazoles; Duodenal Ulcer; Enterochromaffin Cells; Esophagitis; Female; Gastrins; Humans; Longitudinal Studies; Male; Omeprazole; Pantoprazole; Peptic Ulcer; Proton Pump Inhibitors; Ranitidine; Stomach Ulcer; Sulfoxides

Forty-two patients with peptic ulceration of the duodenum, stomach or oesophagus, who had not responded to 3 or more months of high-dose treatment with ranitidine (450 or 600 mg/day), were treated with oral lansoprazole at 30-60 mg daily. In 40 patients (95.2%) the ulcers healed within 2-12 weeks. In the remaining 2 patients healing took several months but eventually all ulcers healed. After healing, 40 patients underwent long-term maintenance treatment with 30-60 mg lansoprazole daily for 1-3 years (continuing). During maintenance therapy with lansoprazole, no endoscopically verified relapses occurred when the drug was taken regularly. In 1 patient treatment had to be discontinued because of a drug-related colitis that disappeared soon after treatment had been stopped. There were no significant changes in routine laboratory tests in any patient. Basal serum gastrin concentrations, which were already elevated by the previous high-dose ranitidine treatment (125 +/- 25 pg/ml), rose to four times the normal values after 4 weeks of treatment with lansoprazole (255 +/- 65 pg/ml). Thereafter no further increases in basal serum gastrin concentrations were observed, even after 3 years of administration. The volume density of argyrophilic cells in the oxyntic mucosa increased slightly during lansoprazole treatment; until now no dysplasia of the enterochromaffin-like cells has been observed. In conclusion, 30-60 mg lansoprazole daily healed ranitidine-resistant peptic ulcers, and subsequent maintenance therapy with 30-60 mg lansoprazole daily was found to be highly effective and safe over the time observed.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Anti-Ulcer Agents; Dose-Response Relationship, Drug; Drug Administration Schedule; Drug Resistance; Duodenal Ulcer; Enterochromaffin Cells; Esophagitis; Female; Follicle Stimulating Hormone; Gastric Mucosa; Gastrins; Humans; Lansoprazole; Luteinizing Hormone; Male; Omeprazole; Peptic Ulcer; Pyloric Antrum; Ranitidine; Stomach Ulcer; Testosterone

Twenty-four-hour intragastric pH and serum gastrin profiles were monitored in six male asymptomatic patients who previously were found to have esophagitis on endoscopy and biopsy. They received cimetidine 300 mg qid (C), ranitidine 150 mg bid (R), or placebo (P) for one week each, utilizing the Latin-square design. The mean BAO was 0.4 +/- 0.2 mmol/hr, and the pentagastrin-stimulated MAO was 21.2 +/- 3.2 mmol/hr. In the P-treated patients, the pH fluctuated between 1.8 and 3.5 and over 90% of the readings were less than pH 4. As compared to P, both C and R significantly suppressed H+ after breakfast, overnight, and over the 24-hr period. The mean pH after lunch was significantly higher in R than in P, but not in C. Over the 24-hr period, a higher percentage of the readings were above pH 4.0 in R as compared to C. During the night, 50% of the pH readings were above pH 4.0 in C and R, whereas in P 50% of the pH readings were less than pH 2.0. The integrated gastrin responses after each meal were similar in C and R and were greater than in P. The biphasic response of the ratio of H+ and gastrin (H+/G) following each meal was suppressed by both H2-receptor antagonists, with numerically lower values obtained in R than in C. This study suggests that ranitidine 150 mg bid is superior to cimetidine 300 mg qid in suppressing the 24-hr intragastric acidity.

Topics: Adult; Aged; Cimetidine; Double-Blind Method; Eating; Esophagitis; Gastric Acid; Gastric Acidity Determination; Gastrins; Gastroesophageal Reflux; Humans; Male; Middle Aged; Radioimmunoassay; Ranitidine; Time Factors

A new pH capsule telemetry technique was used to measure the pH fluxes in the upper part of the gastrointestinal tract in normal volunteers, symptomatic patients and in those with hiatal herniorrhaphy during the preoperative and postoperative period. The Darvon-sized pH capsule is swallowed with ease and with minimal discomfort by a fasting patient. The pH of the surrounding media activates an FM radio transmitter within the capsule to emit a continuous radio signal which is converted by a receiver to a linear graph on a strip chart recorder. This pH capsule telemetry test is easy to perform on an ambulatory basis and allows an accurate and reproducible determination of the presence or absence of esophageal reflux in patients with and without a hiatal hernia. Its correlation with symptomatic reflux is higher than that found with a conventional gastrointestinal series examination. The technique allows a much clearer distinction to be made between those patients with real symptomatic esophagitis secondary to actual reflux and those with other esophageal, cardiac or pulmonary symptoms existing withour reflux. This study also reveals a consistently lower fasting gastric pH in patients with signs and symptoms of reflux than in normal individuals without reflux. The technique enabled a more accurate assessment of the efficacy of hiatal hernia repair and revealed a reduced degree of esophageal reflux in those patients who had undergone successful repair with fundic plication.

Topics: Clinical Trials as Topic; Esophagitis; Gastric Acidity Determination; Gastric Juice; Gastrins; Gastroesophageal Reflux; Hernia, Hiatal; Humans; Hydrogen-Ion Concentration; Radiography; Telemetry

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Esophagitis; Female; Gastrins; Humans; Male; Proton Pump Inhibitors

Withdrawal of proton pump inhibitors (PPIs) may induce symptoms in healthy volunteers, suggesting that discontinuing PPI therapy induces acid-peptic disease. Similar assessments in patients with documented acid-related disorders are lacking.. We performed a retrospective analysis of data from 287 Helicobacter pylori-negative erosive esophagitis (EE) patients healed after 4 or 8 weeks of therapy with dexlansoprazole modified release (MR) or lansoprazole, and then randomized to placebo in 6-month maintenance trials. We compared serum gastrin levels and 24-h heartburn severity before enrollment in the healing trials (baseline) and after receiving placebo in the 6-month maintenance trials.. Mean gastrin values at maintenance months 1 and 3 were essentially unchanged (median changes, 1.0 and -1.0 pg/ml), showing that gastrin normalized within 1 month of discontinuing PPIs and remained flat. Mean heartburn severity at maintenance month 1 was <1 on a 5-point scale (1=mild) and significantly lower than at baseline (median decrease, 0.41 points; P≤0.001). Heartburn severity in patients healed at week 4 or 8 with either PPI was generally similar, suggesting that neither longer exposure nor more potent therapy was associated with rebound. In those with month 2 data, mean heartburn severity at months 1 and 2 was significantly lower than baseline (median decrease, 0.54 and 0.58 points; both P<0.001), indicating an ongoing symptom response for 2 months after PPI withdrawal.. In H. pylori-negative EE patients, there was no indication of recurring heartburn symptom worsening beyond baseline levels within 2 months of discontinuing 4-8 weeks of PPI therapy.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Aged; Dexlansoprazole; Esophagitis; Female; Gastric Acid; Gastrins; Heartburn; Humans; Lansoprazole; Male; Middle Aged; Proton Pump Inhibitors; Randomized Controlled Trials as Topic; Retrospective Studies; Severity of Illness Index; Withholding Treatment

The objective of this work was to assess the efficacy of continuous proton pump inhibitor (PPI) therapy in children and to evaluate changes in biochemical, endoscopic, and histologic parameters during such treatment. A retrospective review of children receiving PPI therapy continuously for 1 year or more with baseline and follow-up esophageal and gastric biopsies on treatment was conducted to assess type, frequency, and duration of PPI dosing, symptom relief, gastrin levels, histologic findings, and adverse events. A total of 113 children (59 male, median age 4.5 years) were identified. Of these, 31% (35/113) were neurologically impaired. The median treatment duration was 35.2 months. Elevated serum gastrin levels occurred in 73% of children with no statistically significant differences in gastrin level by PPI type, dose, and dosing frequency or treatment duration. Adverse events were reported by 12% of children: diarrhea (5%) and constipation (4%) were the most frequent. Long-term PPI therapy appears to be effective, safe and well tolerated in children despite some biochemical, endoscopic, and histologic changes.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Child; Child, Preschool; Esophagitis; Female; Gastrins; Humans; Lansoprazole; Liver Function Tests; Male; Omeprazole; Pantoprazole; Proton Pump Inhibitors; Rabeprazole; Retrospective Studies; Vitamin B 12

We aim to investigate the effects of different electroacupuncture (EA) frequencies at ST-36 on esophageal motility, and to compare the effect of EA on serum gastrin (GAS), motilin (MTL), and vasoactive intestinal peptide (VIP). Thirty-two cats were divided into four equal groups. All animals underwent a Heller myotomy. After esophagitis developed two frequencies (2/15 Hz or 2/100 Hz) of EA were delivered into ST-36 (LEA group [low EA], HEA group [high EA]). Animals submitted to EA on a non-point region (EANP) were used as controls (LEANP group, HEANP group), respectively. Esophageal motility was continuously monitored. The lower esophageal sphincter pressure (LESP) decreased significantly after myotomy. The LESP decreased in both LEA and LEANP cats, and in LEA cats the pressure decrease was greater. The LESP increased in the HEA group, which was higher than that in the HEANP group (P < 0.05). High-frequency EA significantly increased the peak amplitude in esophageal peristalsis. There was a decrease in serum GAS and MTL in LEA cats compared with LEANP cats (both P < 0.01). GAS and MTL were higher in the HEA group than in the HEANP group (both P < 0.01). Serum VIP decreased in the HEA group (P < 0.05), while it increased in the LEA group (P < 0.05), compared with EANP groups, respectively. EA with a high frequency at ST-36 enhances LESP as well as esophageal motility, while EA with a low frequency decreases LESP. The effect of EA is acupoint-specific, and this effect appears to be mediated through GAS, MTL and VIP.

Topics: Animals; Cats; Electroacupuncture; Esophagitis; Gastrins; Gastrointestinal Motility; Motilin; Vasoactive Intestinal Peptide

Whereas severe duodenal ulcer is the hallmark of acid hypersecretion in Zollinger-Ellison syndrome (ZE) and similar states, the esophagus also is at high risk. We quantified the incidence of esophagitis and various risk factors that might contribute to it.. Sixty-eight acid hypersecretors (basal acid output >15 mmol/h), 50 patients with ZE, and 18 patients without ZE with normal gastrin levels were studied by gastric analysis, serum gastrin levels, and endoscopy. In 44 of 68 patients, esophageal manometry was performed after the esophagus had healed.. Erosive esophagitis, grade 2 or worse, was found in 65%; an additional 15% had heartburn only, for a total reflux disease incidence of 80%. ZE accounted for 95% of severe esophagitis. Patients with and without esophagitis had the same high overnight fasting gastric residual volume and acidity, as well as basal and peak acid and pepsin outputs. However, patients with esophagitis had a lower median lower esophageal sphincter pressure (LESP) of 15.5 vs. 23 mm Hg in those without symptoms; the critical discriminator threshold was 16 mm Hg. Multivariate analysis further identified frequent vomiting and obesity as positive predictors of esophagitis, whereas Helicobacter pylori was a strong negative predictor (odds ratio, 0.16), possibly related to an elevated LESP in patients infected with H. pylori.. Erosive esophagitis is very common in acid hypersecretors. Identified risk factors that could promote abnormal esophageal exposure to the high acid and pepsin levels in our population of hypersecretors were vomiting, LESP < 16 mm Hg, and obesity, whereas H. pylori appeared to protect the esophagus not by reduced acid, but through an elevated LESP.

Topics: Adult; Age Distribution; Analysis of Variance; Body Weight; Case-Control Studies; Esophagitis; Esophagoscopy; Female; Gastric Acid; Gastric Acidity Determination; Gastrins; Helicobacter pylori; Humans; Incidence; Male; Manometry; Middle Aged; Multivariate Analysis; Probability; Prognosis; Risk Factors; Sampling Studies; Severity of Illness Index; Sex Distribution; Zollinger-Ellison Syndrome

The association between gastroesophageal reflux disease and end-stage renal disease remains unclear. We aimed to assess the prevalence of gastroesophageal reflux disease and also to identify possible pathogenetic factors in the development of reflux in symptomatic end-stage renal disease patients.. The study involved 42 end-stage renal disease patients with upper GI symptoms (group I) and 46 age- and sex-matched controls who did not have renal disease but had the same symptoms (group II). Endoscopy, endoscopic biopsies, and 24-h esophageal pH studies were used to diagnose gastroesophageal reflux disease. Subjects were also investigated for Helicobacter pylori gastritis and GI amyloidosis.. The prevalences of gastroesophageal reflux disease in the two groups were similar (81% vs 84.8%, p = 0.423). The prevalence of H. pylori infection was significantly lower in group I than in group II (38.1% vs 67.4%, p = 0.01). There were II cases of GI amyloidosis in group I. Multivariate logistic regression analysis in group I showed that GI amyloidosis (OR = 7.28, 95% CI = 1.13-46.93), chronic ambulatory peritoneal dialysis treatment (OR = 5.54, 95% CI = 1.01-30.43), and absence of H. pylori infection (OR = 3.75, 95% CI = 1.01-13.9) were significantly associated with reflux esophagitis.. Upper GI symptoms are important in predicting gastroesophageal reflux disease in end-stage renal disease patients. Chronic ambulatory peritoneal dialysis, GI amyloidosis, and absence of H. pylori infection seem to be risk factors for the development of gastroesophageal reflux disease in end-stage renal disease patients.

Topics: Adult; Amyloidosis; Esophagitis; Esophagus; Female; Gastrins; Gastritis; Gastroesophageal Reflux; Gastrointestinal Diseases; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Male; Middle Aged; Monitoring, Physiologic; Multivariate Analysis; Prevalence; Risk Factors

The efficacy and safety of long-term acid suppression remains a subject for debate. We report data from patients with refractory reflux esophagitis who were undergoing maintenance therapy with >/=20 mg omeprazole daily for a mean period of 6.5 years (range, 1.4-11.2 years).. Patients with severe reflux esophagitis resistant to long-term therapy with H(2)-receptor antagonists and who were not eligible for surgery were evaluated at least annually for endoscopic relapse and histological changes in the gastric corpus.. In 230 patients (mean age, 63 years at entry; 36% were >/=70 years), there were 158 relapses of esophagitis during 1490 treatment years (1 per 9.4 years), with no significant difference in relapse rates between Helicobacter pylori-positive and -negative patients. All patients rehealed during continued therapy with omeprazole at the same or higher dose. The annual incidence of gastric corpus mucosal atrophy was 4.7% and 0.7% in H. pylori-positive and -negative patients, respectively, which was mainly observed in elderly patients who had moderate/severe gastritis at entry. In patients with baseline moderate/severe gastritis, the incidences were similar: 7.9% and 8.4%, respectively. Corpus intestinal metaplasia was rare, and no dysplasia or neoplasms were observed. The adverse event profile was as might be expected from this elderly group of patients.. Long-term omeprazole therapy (up to 11 years) is highly effective and safe for control of reflux esophagitis.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Anti-Ulcer Agents; Barrett Esophagus; Child; Drug Resistance; Esophagitis; Female; Gastric Mucosa; Gastrins; Gastritis; Gastroesophageal Reflux; Helicobacter Infections; Humans; Hyperplasia; Male; Middle Aged; Omeprazole; Time Factors; Treatment Outcome

The main form of gastrin in antral mucosa, the amidated heptadecapeptide G17, is generated from an inactive precursor, progastrin, by steps involving endopeptidase cleavage and amidation. Gastrin cells are normally inhibited by gastric acid and in this study we have examined how suppression of acid by treatment with omeprazole for 6-8 weeks influences gastrin production in patients with oesophagitis. Plasma concentrations of total amidated gastrins in the fasting state increased from 18 to 43 pmol l-1; assays specific for G17-immunoreactivity indicated that the plasma concentrations of this form increased from 6 to 12 pmol l-1. In endoscopic biopsies of antral mucosa there was no change with omeprazole treatment in the concentrations of total amidated gastrins, or their immediate precursors, the Gly-extended gastrins. However, assays using an antibody that reacts with progastrin, together with size exclusion chromatography, indicated that tissue progastrin concentration increased 6-fold. The data suggest a modest net increase in gastrin production with omeprazole-treatment; because the ratio of tissue concentrations of total amidated gastrins to Gly-extended gastrins did not change, it would seem that the amidating capacity of the gastrin cell was maintained. However, the increase in progastrin concentrations suggests a relative failure of the initial steps of post-translational processing, and consequently that in certain circumstances endopeptidase cleavage of progastrin may be rate limiting.

Topics: Amino Acid Sequence; Esophagitis; Female; Gastric Mucosa; Gastrins; Humans; Male; Middle Aged; Molecular Sequence Data; Omeprazole; Peptide Fragments; Protein Precursors; Protein Processing, Post-Translational; Pyloric Antrum; Tissue Distribution

Topics: Adolescent; Child; Esophagitis; Female; Gastrins; Humans; Male; Stomach

To determine whether the use of pedicled full-thickness gastric patches would be feasible and safe in esophageal reconstruction, studies were undertaken in eleven dogs. The results demonstrate that patches containing parietal cell mucosa are likely to produce localized adjacent esophagitis. Patches containing antral mucosa do not produce esophagitis and are not associated with a subsequent increase in circulating serum gastrin levels.

Topics: Animals; Dogs; Esophagitis; Esophagoplasty; Gastric Mucosa; Gastrins; Stomach; Transplantation, Autologous

Topics: Adult; Aged; Esophagitis; Female; Gastrins; Gastrointestinal Diseases; Glutamine; Humans; Male; Middle Aged; Proglumide

Antral gastrin concentration (AGC) was measured in prepyloric mucosa specimens obtained by forceps biopsy during endoscopic examination of 174 clinic and hospital patients. AGC in 32 patients who had normal endoscopic findings, the control group, varied widely from 2 to 38.6 ng gastrin/mg tissue. The mean AGC of the control patients was 14.2 +/- 1.4 (mean +/- 1 SE) ng gastrin/mg tissue. AGC was similar to control values in 18 patients with duodenal ulcer, 14.7 +/- 2.1; 12 patients with a pyloric channel or antral ulcer, 16.4 +/- 3.5; and 48 patients with miscellaneous diagnoses, 14.3 +/- 1.5. AGC was significantly less than control values in 13 patients with a ulcer in the body or fundus of the stomach, 5.9 +/- 1.5, and 4 patients with the Zollinger-Ellison syndrome, 4.9 +/- 2.4. AGC was significantly greater than in control values in 16 patients with gastritis, 25.8 +/- 4.3;22 patients with esophagitis, 23.2 +/- 3.0; and 9 patients with gastric atrophy and fasting serum hypergastrinemia 44.6 +/- 12.3. In group of 77 of these patients with heterogeneous diagnoses, meal-stimulated 3-hr integrated gastrin output was directly related to AGC (r = 0.47, P less than 0.001). In a group of 106 patients AGC was inversely related to histalogstimulated maximum acid output. The correlation was very weak (r = -0.20) but significant (P less than 0.05).

Topics: Atrophy; Biopsy; Duodenal Ulcer; Esophagitis; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Humans; Pyloric Antrum; Stomach; Stomach Ulcer; Zollinger-Ellison Syndrome

Topics: Esophageal Achalasia; Esophagitis; Esophagogastric Junction; Gastrins; Gastroesophageal Reflux; Gastrointestinal Hormones; Humans

Topics: Adult; Celiac Disease; Diarrhea; Esophagitis; Female; Gastrins; Humans; Hyperparathyroidism; Male; Middle Aged; Neoplasm Metastasis; Radiography; Zollinger-Ellison Syndrome

Topics: Antacids; Esophagitis; Esophagoscopy; Esophagus; Gastrins; Gastroesophageal Reflux; Heartburn; Hernia, Diaphragmatic; Humans; Hydrogen-Ion Concentration; Parasympatholytics; Perfusion; Pressure; Radiography

Topics: Antacids; Diet Therapy; Dietary Proteins; Esophagitis; Esophagitis, Peptic; Gastrins; Gastroesophageal Reflux; Humans; Parasympatholytics