gastrins and Esophagitis--Peptic

All vertebrates secrete gastric acid. Acid denatures the proteins in the food and thus makes them more accessible to proteolytic enzymes, and it kills swallowed micro-organisms. Gastric acid plays an important pathogenetic role in peptic ulcer disease and reflux oesophagitis. In these diseases, drugs that inhibit secretion of gastric acid will heal the lesions and suppress the symptoms. However, both reflux oesophagitis and peptic ulcer tend to recur when the acid-inhibitory treatment is stopped. Therefore, these patients often require long-term treatment with acid-inhibitors. In this overview the potential risks of long-term profound inhibition of acid secretion, raising the pH above 4 for a considerable time, resulting in reduced killing of micro-organisms and secondary hypergastrinaemia, are discussed. Gastrin regulates both the function (production and release of histamine) and growth of the enterochromaffin-like (ECL) cell. Hitherto, the role that this cell plays in gastric carcinogenesis appears to have been underestimated.

Topics: Animals; Antacids; Anti-Ulcer Agents; Duodenal Ulcer; Enterochromaffin Cells; Esophagitis, Peptic; Gastric Acid; Gastrins; Histamine; Histamine H2 Antagonists; Humans; Stomach Ulcer

Reflux oesophagitis is a chronic relapsing disorder. When treatment is stopped after successful short-term healing of oesophagitis, high relapse rates (80% within 6 months) indicate that prolonged treatment is necessary in order to maintain remission. The results of three long-term, multicentre, controlled, double-blind clinical trials comparing different regimens of omeprazole with ranitidine are reviewed. Omeprazole, 20 mg daily, was found to be a highly effective maintenance therapy in patients with ulcerative oesophagitis, keeping 67-89% of patients in remission for 1 year, compared with 10-25% of patients treated with ranitidine, 150 mg twice daily. Weekend omeprazole therapy, 20 mg daily every Friday, Saturday and Sunday, was, as with daily ranitidine, relatively ineffective. All treatment regimens were well tolerated and gastric mucosal biopsies showed no qualitative changes in gastric enterochromaffin-like cells.

Topics: Administration, Oral; Australia; Belgium; Biopsy; Double-Blind Method; Endoscopy, Gastrointestinal; Esophagitis, Peptic; France; Gastrins; Humans; Multicenter Studies as Topic; Omeprazole; Randomized Controlled Trials as Topic; Ranitidine; Recurrence; Scandinavian and Nordic Countries

Topics: Esophagitis, Peptic; Follow-Up Studies; Gastrins; Humans; Omeprazole

Gastro-oesophageal reflux (GOR) is common. Nearly all healthy individuals experience occasional or frequent reflux episodes, with or without symptoms, which occur during spontaneous relaxations of the lower oesophageal sphincter, predominantly after meals. It is not known how neural, hormonal and muscular factors contribute to this. A proportion of the patients with reflux disease have normal lower oesophageal sphincter pressures, and their reflux episodes occur during spontaneous sphincter relaxations following the pattern of normals. Nevertheless, most patients with reflux disease have decreased lower oesophageal sphincter pressure, and manoeuvres which increase the intraabdominal pressure provoke "stress" reflux. If the sphincter pressure is very low, "free" reflux occurs; the cause of decreased sphincter pressure is not known. Pharmacological and gastric factors also facilitate GOR. The noxious potency of reflux material on the oesophageal epithelium depends on its components [( H+], pepsin, bile salts, trypsin) and the contact time, which is prolonged during supine and nocturnal reflux episodes, i.e. when clearance function is impaired. In complicated reflux disease it is necessary to consider this multifactorial model of the pathogenesis of reflux disease, and to go on to more sophisticated diagnostic procedures (manometry, scintiscanning, prolonged pH-monitoring) in order to identify an individual patients' predominant pathogenetic factor.

Topics: Cholecystokinin; Esophagitis, Peptic; Esophagogastric Junction; Esophagus; Gastric Emptying; Gastrins; Gastroesophageal Reflux; Hernia, Hiatal; Histamine H2 Antagonists; Humans; Manometry; Middle Aged; Peristalsis; Pressure

Topics: Burimamide; Chemical Phenomena; Chemistry; Cimetidine; Duodenal Ulcer; Esophagitis, Peptic; Gastric Acid; Gastrins; Gastrointestinal Hemorrhage; Histamine; Histamine H1 Antagonists; Histamine H2 Antagonists; Humans; Hypersensitivity; Intrinsic Factor; Kinetics; Malabsorption Syndromes; Metiamide; Pancreas; Pepsin A; Ranitidine; Receptors, Histamine H2; Stomach Ulcer; Stress, Psychological; Zollinger-Ellison Syndrome

The importance of the gastrointestinal hormones to the clinician is considered under three headings: in disease states, diagnostic applications and therapeutic implications. Pearse's APUD (Amine Precursor Uptake and Decarboxylation) theory is referred to, and single and multiple endocrinopathies are discussed with particular referrence to diagnostic criteria and principles of management. The field of gastrointestinal endocrinology is rapidly developing and these peptides will assume an even greater importance to the clinician who must keep abreast with these developments.

Topics: Endoscopy; Esophagitis, Peptic; Gastrins; Gastrointestinal Hormones; Glucagon; Histamine; Humans; Multiple Endocrine Neoplasia; Peptic Ulcer; Secretin; Zollinger-Ellison Syndrome

Topics: Adult; Biomechanical Phenomena; Esophageal Achalasia; Esophageal Diseases; Esophagitis, Peptic; Esophagogastric Junction; Esophagus; Female; Gastrins; Hernia, Hiatal; Humans; Male; Middle Aged; Muscle Tonus; Muscle, Smooth; Parasympatholytics; Pentagastrin

Development of histamine H2-receptor antagonists has enhanced the understanding of histamine physiology and pharmacology. The effect of H2-receptor antagonists on gastrointestinal physiology has been studied extensively. These compounds inhibit gastric acid secretion in response to all known secretagogues and, in contrast to anticholinergic drugs, markedly inhibit food-stimulated acid secretion in duodenal ulcer patients. The relative roles of H2-receptor antagonists, anticholinergic drugs and antacids in the treatment of duodenal ulcer remain to be defined. Cimetidine currently is under investigation for the treatment of duodenal ulcer, gastric ulcer, reflux esophagitis, gastrointestinal bleeding and hypersecretory states. Although the long-term safety of cimetidine has not been established, in short-term clinical trials there have been no significant subjective or objective side-effects. Assuming that toxic effects do not develop, H2-receptor antagonists should improve the treatment of acid-peptic disease.

Topics: Cimetidine; Cyclic AMP; Duodenal Ulcer; Esophagitis, Peptic; Gastric Juice; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Histamine; Histamine H2 Antagonists; Humans; Intrinsic Factor; Metiamide; Pepsin A; Stomach Ulcer

Topics: Digestion; Esophageal Achalasia; Esophagitis, Peptic; Gastric Inhibitory Polypeptide; Gastric Mucosa; Gastrins; Gastritis; Glucagon; Humans; Ileum; Islets of Langerhans; Jejunum; Kidney Failure, Chronic; Liver; Protein Hydrolysates; Pyloric Antrum; Somatostatin; Vagotomy; Vasoactive Intestinal Peptide; Zollinger-Ellison Syndrome

With combined immunofluorescent, cytochemical and electron microscopic investigations the enterochromaffin cell system has been differentiated into 5 distinct endocrine cell types in the human stomach and into 8 cell types in the intestine. These endocrine cells are probably of neuroectodermal origin and belong to the APUD (amine precursor uptake and decarboxylation)-system. Maximal gastrointestinal hormone concentrations as determined by tissue extracts correlate fairly well to the location of each endocrine cell type in various segments of the gastrointestinal tract. In certain gastroenteropathies the pathophysiological disturbances can be explained by pathomorphological alterations of the disseminated endocrine cells. 1. The gastrin-producing G-cell is the predominating endocrine cell in the gastric antrum. Besides immunocytochemistry the G-cell can be demonstrated with argyrophilic reaction (Grimelius, 1968), masked metachromasia and leadhematoxylin. The ultrastructural features are variable, depending on functional activity. The secretory granules are usually only slightly osmiophilic, measuring 200 till 250 nm in diameter. By some working groups a positive immunofluorescence with gastrin-antisera has been demonstrated in A1- or D-cells of the pancreatic islets. However, numerous negative results have been reported, too. Considering physiological conditions, a gastrin-secretion of the human pancreatic islets has not been secured without doubt. 2. The EC-cell produces serotonin and in the intestine motilin, too. Besides the formaldehyde-induced fluorescence, these cells can be demonstrated with diazonium and argentaffin reactions, less specific with argyrophilic methods. Ultrastructurally the EC-granules are easily differeniated from the other endocrine cells by their pronounced osmiophilia and pleomorphism. In experimental conditions the EC-cells demonstrate species- and site-specific alterations. With reserpine no ultrastructural changes were demonstrable in EC-cells of the rat. However, marked ultrastructural alterations with an increase of the hormone-producing organelle system were noticed after administration of parachlorophenylalanine (PCPA) which interferes with serotonine synthesis; 5. The gastric D-cells are characterized by large secretory granules similar to pancreatic D-cells. They secrete the HCl-inhibitory peptide somatostatin. 4. The D1-cell is a cell type with unknown function. The cytoplasm contains small granules with variable elect

Topics: Adenoma, Islet Cell; Anemia, Pernicious; Chromaffin System; Digestive System; Duodenal Ulcer; Endocrine System Diseases; Enterochromaffin Cells; Esophagitis, Peptic; Gastrectomy; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Hormones; Gastrointestinal Neoplasms; Humans; Intestinal Mucosa; Metabolic Diseases; Serotonin; Somatostatin; Stomach Neoplasms; Stomach Ulcer; Syndrome; Zollinger-Ellison Syndrome

Topics: Animals; Electric Stimulation; Esophagitis, Peptic; Esophagogastric Junction; Gastrins; Gastroesophageal Reflux; Hernia, Hiatal; Humans; Mucous Membrane; Pressure; Prostaglandins; Radionuclide Imaging; Stomach

Topics: Antacids; Biopsy; Esophagitis, Peptic; Esophagogastric Junction; Esophagoscopy; Gastrins; Heartburn; Humans; Hydrochloric Acid; Manometry; Methacholine Compounds; Metoclopramide; Muscle, Smooth; Vagus Nerve

Rabeprazole at 10 or 20 mg twice daily (b.i.d.) has been reported to be highly effective in the treatment of proton pump inhibitor (PPI)-resistant reflux esophagitis (RE) that is refractory to the standard once-daily PPI regimen. We evaluated the efficacy and safety of rabeprazole maintenance therapy at 10 mg once daily (q.d.) or b.i.d. for longer than 8 weeks.. Patients with RE refractory to standard PPI regimens for at least 8 weeks were enrolled. They were treated with rabeprazole at 10 or 20 mg b.i.d. for 8 weeks during the open-label treatment period. After endoscopic examination, those with confirmed healing entered the subsequent double-blind maintenance therapy. During this period, the subjects were randomized to receive rabeprazole 10 mg q.d. (control) or 10 mg b.i.d. The primary endpoint was the endoscopic no-recurrence rate at Week 52.. In total, 517 subjects entered the treatment, and 359 subjects continued on maintenance therapy. The full analysis set for central assessment included 343 subjects. The no-recurrence rate at Week 52 was significantly higher in the b.i.d. group (73.9%; p < 0.001, χ. In the maintenance treatment of PPI-resistant RE, rabeprazole at 10 mg b.i.d. exerted a stronger recurrence-preventing effect than 10 mg q.d. over 52 weeks. No particular safety issues were noted during long-term administration. ClinicalTrials.gov number: NCT02135107.

Topics: Aged; Anti-Ulcer Agents; Double-Blind Method; Drug Administration Schedule; Drug Resistance; Endoscopy; Esophagitis, Peptic; Female; Gastrins; Gastroesophageal Reflux; Humans; Japan; Kaplan-Meier Estimate; Male; Middle Aged; Polyps; Proton Pump Inhibitors; Rabeprazole; Recurrence; Secondary Prevention; Treatment Outcome

The study aimed to evaluate the efficacy of on-demand therapy using 20-mg vonoprazan for mild reflux esophagitis (RE).. On-demand therapy by taking one 20-mg tablet of vonoprazan only when reflux symptoms occurred was performed for 24 weeks using 30 patients with mild RE who were receiving maintenance therapy with proton pomp inhibitors (PPIs). The presence or absence of RE, degree of overall satisfaction with the treatment, score of symptoms, and fasting gastrin level before breakfast were examined before and after on-demand therapy. The number of tablets taken during the 24-week period was also noted.. One of the 30 patients dropped out of on-demand therapy 1 week after its initiation. Remission was maintained in 25 (86.2%) of the 29 patients (all 10 [100%] Los Angeles classification grade A patients and 15 (78.9%) of the 19 grade B patients). However, 4 grade B patients exhibited grade B relapse. There were no differences in the degree of overall satisfaction, score of symptoms or the gastrin level between PPI and on-demand therapies. The number of vonoprazan tablets taken during the observation period was 33 tablets (median)/24 weeks.. On-demand therapy using 20-mg vonoprazan tablets is an effective alternative maintenance therapy for mild RE.

Topics: Aged; Esophagitis, Peptic; Fasting; Female; Gastrins; Humans; Japan; Maintenance Chemotherapy; Male; Middle Aged; Patient Satisfaction; Practice Guidelines as Topic; Prospective Studies; Proton Pump Inhibitors; Pyrroles; Recurrence; Severity of Illness Index; Sulfonamides; Treatment Outcome

The aim of this prospective clinical study was to evaluate the efficacy and safety of long-term proton pump inhibitor (PPI) treatment for two years in Japanese patients with reflux esophagitis (RE).. The efficacy and safety of two-year (104-week) treatment with rabeprazole (RPZ) 10 mg were studied in patients confirmed to have been cured of RE by PPI and who required long-term maintenance therapy with PPI. We performed serial endoscopy, checked gastroesophageal reflux disease (GERD) symptoms, adverse events, laboratory values and serum gastrin. We also monitored gastric mucosal histology, atrophy and polyps.. The endoscopic non-relapse rate for RE was 87.3% for the 104-week period. GERD symptoms improved based on the fact that the mean change from baseline in GERD symptom score after treatment was a negative value. Treatment was safe; and atrophy was found to have developed in virtually no cases. A few new benign fundic gland or hyperplastic polyps developed throughout the study, but no ECL carcinoids were found to have developed. Serum gastrin levels tended to increase up to 24 weeks, but there were no subsequent changes thereafter up to 104 weeks.. The results confirmed oral RPZ 10 mg to be effective for maintenance therapy in Japanese patients with RE. Although effects on the gastric mucosa were not ruled out, long-term use of RPZ was confirmed to be safe overall.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Administration, Oral; Aged; Dose-Response Relationship, Drug; Esophagitis, Peptic; Female; Gastric Mucosa; Gastrins; Gastroesophageal Reflux; Humans; Japan; Longitudinal Studies; Male; Middle Aged; Prevalence; Prospective Studies; Proton Pump Inhibitors; Rabeprazole; Treatment Outcome

The acid suppressive effects of omeprazole (OPZ) and lansoprazole (LPZ) are influenced by the CYP2C19 polymorphism. On the other hand, some investigators have reported that acid suppressive effect of rabeprazole (RPZ) was not significantly affected by CYP2C19. The present study was designed to investigate whether the CYP2C19 genotype is related to the healing of reflux esophagitis (RE) in treatment with RPZ 10 mg.. One hundred and three Japanese patients with RE were treated with daily oral administration of 10 mg RPZ. At 4 and 8 weeks after the start of treatment, healing of RE was evaluated endoscopically. The CYP2C19 genotype was investigated before the treatment.. At 4 weeks after the start of treatment, the healing rates for homo-extensive metabolizer, hetero-extensive metabolizer, and poor metabolizer patients were 83.3% (15/18), 77.3% (17/22), and 88.9% (8/9) [corrected] respectively, and at 8 weeks after the start of treatment, the healing rates were 86.1% (31/36), 92.0% (46/50), and 82.4% (14/17), respectively. There were no significant differences in the healing rate of RE among the three genotypes at either 4 or 8 weeks after the start of treatment.. The therapeutic effects of 10 mg/day RPZ administration on RE may be uninfluenced by the CYP2C19 polymorphism.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Aged; Aged, 80 and over; Anti-Ulcer Agents; Aryl Hydrocarbon Hydroxylases; Cytochrome P-450 CYP2C19; Enzyme Inhibitors; Esophagitis, Peptic; Female; Gastrins; Helicobacter Infections; Hernia, Hiatal; Humans; Male; Middle Aged; Mixed Function Oxygenases; Pepsinogens; Polymorphism, Genetic; Prospective Studies; Rabeprazole; Wound Healing

The polymorphic enzyme cytochrome P450 2C19 affects omeprazole metabolism. This influence on metabolism might affect serum gastrin levels, and safety, during long-term treatment of reflux oesophagitis.. To examine the relationship between cytochrome P450 2C19 genotype and the safety profile of long-term omeprazole treatment.. A total of 119 Japanese patients with recurrent reflux oesophagitis underwent cytochrome P450 2C19 genotyping prior to receiving daily omeprazole 10 mg or 20 mg for 6-12 months, during which adverse event frequency, serum gastrin levels and endoscopic findings were monitored.. The incidences of adverse events, serious adverse events and adverse events leading to withdrawal did not differ between homozygous extensive metabolizer (n = 46), heterozygous extensive metabolizer (n = 53) or poor metabolizer (n = 20) groups. In all genotype groups, serum gastrin increased during the first 3 months of dosing but stabilized thereafter. No significant differences were seen either in the rate of reflux oesophagitis healing or symptom improvement among genotype groups.. Long-term treatment with omeprazole was well-tolerated in Japanese patients, irrespective of their cytochrome P450 2C19 metabolic genotype, indicating that dose adjustment depending on metabolic genotype is not required during treatment with omeprazole.

Topics: Adult; Aged; Anti-Ulcer Agents; Aryl Hydrocarbon Hydroxylases; Cytochrome P-450 CYP2C19; Esophagitis, Peptic; Female; Gastrins; Gastroesophageal Reflux; Genotype; Heterozygote; Homozygote; Humans; Male; Middle Aged; Mixed Function Oxygenases; Omeprazole; Polymorphism, Genetic; Recurrence; Treatment Outcome

Erosive gastro-oesophageal reflux disease (GERD) is a chronic condition requiring long-term maintenance treatment. However, few trials of proton pump inhibitors in maintaining healing of erosive or ulcerative GERD are conducted for longer than 1 year.. To compare the efficacy and safety of 10- and 20-mg rabeprazole with placebo in the 5-year maintenance of healing in patients previously diagnosed with erosive/ulcerative GERD healed in an acute efficacy trial.. Patients (N = 497) were randomized to receive once-daily doses of 10- or 20-mg rabeprazole or placebo. The primary efficacy measure was endoscopically documented absence of oesophageal erosions or ulcerations.. After 5 years, relapse rates in both rabeprazole groups were significantly lower than with placebo (rabeprazole 20 mg, 11%; 10 mg, 23%; placebo, 63%; P < 0.001 for rabeprazole vs. placebo; P = 0.005 for rabeprazole 20 mg vs. 10 mg). Both rabeprazole doses were significantly superior to placebo in preventing relapse of heartburn frequency and improving patient quality of life. Analyses of adverse events, biopsy findings and laboratory values showed no evidence of clinically significant effects.. Five-year maintenance therapy with rabeprazole is effective in preventing relapse of erosive or ulcerative GERD and is well tolerated.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adolescent; Adult; Aged; Anti-Ulcer Agents; Benzimidazoles; Dose-Response Relationship, Drug; Double-Blind Method; Esophagitis, Peptic; Female; Gastrins; Gastroesophageal Reflux; Humans; Male; Middle Aged; Omeprazole; Patient Compliance; Proton Pump Inhibitors; Rabeprazole; Secondary Prevention; Treatment Outcome

Proton pump inhibitors can be effective as maintenance therapy in reducing the relapse rate of reflux oesophagitis at a dose lower than that used for acute healing.. Patients (n=396, 18-88 years old) with healed reflux oesophagitis (grade II or III before healing) were included in this multinational, prospective, parallel-group, randomized double-blind study. They took oral pantoprazole 20 mg (n=203) or 40 mg (n=193), once daily for up to 12 months. Scheduled endoscopies were performed at entry, after 6 and 12 months, or when symptoms of at least moderate intensity were perceived on 3 consecutive days; symptoms were assessed every 3 months. The primary efficacy parameter was the time until endoscopically proven relapse of reflux oesophagitis occurred; the secondary parameters included tolerability, safety and time until symptomatic relapse occurred.. Analysis was performed using the 'all-patients-treated' approach. Endoscopic relapse rates in the 20 mg group after 6 and 12 months were 16 and 29%, respectively; in the 40 mg group, they were 7 and 19%, respectively. Symptomatic relapse rates after 6 and 12 months were 14 and 21% in the 20 mg group and 10 and 17% in the 40 mg group, respectively. Pantoprazole 20 mg and 40 mg were well tolerated throughout the study; the type and frequency of adverse events reported were similar for both treatment groups.. The 20 mg dose was proven to be 'at least equivalent' to the 40 mg dose with respect to endoscopic and symptomatic relapse. The 20 mg once daily dose represents an effective and safe maintenance regimen for the majority of patients with healed reflux oesophagitis.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adolescent; Adult; Aged; Aged, 80 and over; Anti-Ulcer Agents; Benzimidazoles; Double-Blind Method; Enzyme Inhibitors; Esophagitis, Peptic; Esophagoscopy; Female; Gastrins; Humans; Male; Middle Aged; Omeprazole; Pantoprazole; Patient Compliance; Prospective Studies; Proton Pump Inhibitors; Secondary Prevention; Sulfoxides

A cross sectional study was designed to elucidate the factors influencing the argyrophil cell population in patients with gastroesophageal reflux disease treated with omeprazole (N = 201) or H2-receptor antagonists (N = 118) and in control patients (N = 215). Fasting gastrinemia and Helicobacter pylori serology were determined. Gastritis, Helicobacter pylori infection, and argyrophil cell density and hyperplasia were evaluated in gastric biopsies. The argyrophil cell density was higher in both treatment groups than in controls (P = 0.002 and P = 0.051), whereas argyrophil cell hyperplasia was similar in the three groups. According to multivariate analysis, positive Helicobacter pylori serology was an independent parameter that decreased both density and grade of hyperplasia of argyrophil cells. Female gender and hypergastrinemia were independent factors increasing argyrophil cell density and hyperplasia, whereas antisecretory therapy, age and active gastritis were not. In addition, atrophic gastritis independently increased argyrophil cell hyperplasia. The prevalence of atrophic gastritis was significantly higher in Helicobacter pylori-positive than in negative patients and lower in the patients treated long-term with omeprazole than in the other groups.

Topics: Adult; Aged; Aged, 80 and over; Anti-Ulcer Agents; Cell Count; Cross-Sectional Studies; Enterochromaffin-like Cells; Esophagitis, Peptic; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Histamine H2 Antagonists; Humans; Hyperplasia; Male; Middle Aged; Multivariate Analysis; Omeprazole; Sex Factors

We conducted a randomized, double-blind, multicenter clinical trial to determine whether lansoprazole was superior to continued therapy with histamine H2-receptor antagonist therapy in healing erosive reflux esophagitis.. Investigators from nine medical centers enrolled 159 patients with endoscopically documented esophageal erosions and/or ulcers that had failed to heal with 12 or more wk of at least standard dosages of histamine H2-receptor antagonist therapy. Patients received ranitidine 150 mg b.i.d. for 8 wk or lansoprazole 30 mg for 4 wk followed by either lansoprazole 30 mg or lansoprazole 60 mg for another 4 wk of treatment. Patients underwent endoscopy at screening and at weeks 2, 4, and 8.. At 2, 4, and 8 wk of therapy, healing rates were significantly higher in the lansoprazole group compared with the ranitidine group (p < 0.001). By 8 wk, 84% of the lansoprazole group were healed as opposed to only 32% of the ranitidine group. Lansoprazole was superior to ranitidine in providing relief of upper abdominal burning and daytime heartburn (p < 0.001) and reducing the need for antacids (p < 0.001). Lansoprazole patients had less interference with sleep and less day time drowsiness than ranitidine patients (p = 0.05). The percentages of patients with adverse events were similar in both groups. Fasting serum gastrin levels at weeks 4 and 8 were significantly higher in the lansoprazole group compared with the ranitidine group.. Eight weeks of lansoprazole therapy is safe, superior to continued ranitidine therapy, and effective in healing more than 80% of patients with erosive reflux esophagitis previously resistant to histamine H2-receptor antagonist therapy.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Aged; Antacids; Anti-Ulcer Agents; Double-Blind Method; Drug Resistance; Esophagitis, Peptic; Esophagoscopy; Fasting; Female; Follow-Up Studies; Gastrins; Heartburn; Histamine H2 Antagonists; Humans; Lansoprazole; Male; Middle Aged; Omeprazole; Ranitidine; Safety; Sleep; Sleep Stages; Ulcer; Wound Healing

This study examined the dose-response effects of the new proton-pump inhibitor rabeprazole on oesophageal and gastric pH in patients with gastro-oesophageal reflux disease.. This study had a single-centre, double-blind, randomized, two-way crossover design. Twenty patients were treated for two 7-day periods separated by a 7-10-day washout period. Patients were randomly assigned to receive either 20 mg of rabeprazole once daily during the first treatment period and 40 mg once daily during the second treatment period, or 40 mg during the first treatment period and 20 mg during the second treatment period. The primary efficacy variable was oesophageal acid exposure determined by 24-hour ambulatory pH monitoring. Acid-reflux time was defined as the percentage of time over 24 h that oesophageal pH was < 4. A dosage was considered effective if reflux time was reduced to < 6%, a number which has been our internal laboratory reference.. Both rabeprazole 20 mg and 40 mg, given once daily, normalized reflux time, with decreases of 79% and 92% in acid exposure by day 7. Both dosages also decreased the mean total number of reflux episodes and the number of episodes lasting > 5 min, with no significant differences between dosages for any reflux parameter. Mean gastric pH increased with 20 mg from 1.86 at baseline to 3.71 on day 1 and 4.17 on day 7. Rabeprazole 40 mg once daily increased gastric pH from 2.01 to 4.37 on day 1, and to 4.65 on day 7. Safety analyses revealed no significant acute side-effects for either dosage.. Pathological oesophageal acid exposure was normalized with both 20 mg and 40 mg dosages of rabeprazole, and the effects of these two doses did not differ. Rabeprazole was well-tolerated in this short-term study.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Anti-Ulcer Agents; Benzimidazoles; Cross-Over Studies; Double-Blind Method; Enzyme Inhibitors; Esophagitis, Peptic; Female; Gastric Acid; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Humans; Hydrogen-Ion Concentration; Male; Omeprazole; Proton Pump Inhibitors; Rabeprazole

Erosive oesophagitis refractory to high dose histamine H2 receptor antagonists (definition: failure to heal fully after > or = 3 months' treatment with cimetidine 3.2 g or ranitidine 0.9 g) responds well to omeprazole 40 mg daily but frequently relapses when the patients are put back on maintenance H2 receptor antagonists at medium or even high dose (e.g. cimetidine 1.6 g and 3.2 g, respectively).. To investigate the efficacy of maintenance omeprazole 20 mg daily in refractory erosive oesophagitis.. In this open, sequential study, patients with H2 receptor antagonist-refractory oesophagitis were healed on omeprazole 40 mg daily and then put on maintenance H2 receptor antagonists (cimetidine 1.6 g or 3.2 g). Relapses were re-treated with omeprazole 40 mg; upon rehealing, patients were put on maintenance omeprazole 20 mg daily for up to 4.5 years.. Healing on omeprazole occurred in 38 out of 39 patients (97%) at 12 weeks. Only six of the 38 patients (16%) relapsed (asymptomatic in half) during subsequent maintenance treatment, whereas all had relapsed earlier on high dose H2 receptor antagonists.. Within the limits of interpretation of an open study, omeprazole 20 mg daily seems effective in maintaining prolonged remission in this group of patients with H2 receptor antagonist-refractory oesophagitis.

Topics: Adult; Aged; Biopsy; Cimetidine; Drug Administration Schedule; Drug Resistance; Enzyme Inhibitors; Esophagitis, Peptic; Esophagus; Female; Follow-Up Studies; Gastric Mucosa; Gastrins; Gastroscopy; Histamine H2 Antagonists; Humans; Hyperplasia; Male; Middle Aged; Omeprazole; Ranitidine; Recurrence; Treatment Outcome; Wound Healing

This study was designed to compare lansoprazole 30 mg, lansoprazole 15 mg, omeprazole 20 mg, and placebo in the treatment of erosive reflux esophagitis.. In a double-blind, multicenter study, 1284 patients with endoscopically diagnosed erosive reflux esophagitis were randomized to received lansoprazole 30 mg (n = 422), lansoprazole 15 mg (n = 218), omeprazole 20 mg (n = 431), or placebo (n = 213) once daily for 8 wk. At 2, 4, 6, and 8 wk, healing was evaluated endoscopically. Patients kept daily diaries of symptoms.. Healing rates at 2, 4, 6, and 8 wk were 65.3%, 83.3%, 89.4%, and 90.0%, respectively, for lansoprazole 30 mg; 56.3%, 74.6%, 80.3%, and 78.8% for lansoprazole 15 mg; 60.9%, 82.0%, 89.7%, and 90.7% for omeprazole 20 mg; and 23.9%, 32.8%, 36.6%, and 40.0% for placebo (all active treatments higher than placebo, p < 0.001). Healing rates with lansoprazole 30 mg were significantly higher than with lansoprazole 15 mg at all time points (p < 0.05). Healing rates with omeprazole 20 mg were significantly higher than with lansoprazole 15 mg at 4, 6, and 8 wk and were similar to those with lansoprazole 30 mg. Based on patient diaries, lansoprazole 30 mg produced better symptomatic relief than lansoprazole 15 mg or omeprazole 20 mg, primarily early in the treatment course.. Both lansoprazole 30 mg and omeprazole 20 mg were more effective than lansoprazole 15 mg in esophageal mucosal healing. Compared with omeprazole 20 mg, lansoprazole 30 mg was as safe, was similarly effective with respect to esophageal healing, and provided superior symptomatic relief, primarily early in treatment. Lansoprazole 30 mg provided greater symptomatic relief than lansoprazole 15 mg.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Dose-Response Relationship, Drug; Double-Blind Method; Enzyme Inhibitors; Esophagitis, Peptic; Female; Gastric Mucosa; Gastrins; Humans; Lansoprazole; Male; Middle Aged; Omeprazole; Proton Pump Inhibitors; Time Factors

This randomized, double-blind study was designed to determine whether the proton pump inhibitor lansoprazole could prevent relapse among patients with healed erosive reflux esophagitis that had been resistant to healing with at least 3 months of H2-receptor antagonist therapy.. By the end of the year, 13% of placebo patients remained healed compared with 67% of lansoprazole 15 mg and 55% of lansoprazole 30 mg patients (p < 0.001 for time to first relapse). All placebo patients were symptomatic by the end of the study whereas only one-third of the lansoprazole patients was symptomatic at the end of the 12-month study period. The two lansoprazole doses were comparably effective in maintaining healing and in symptom control and were well tolerated. Fasting serum gastrin values increased significantly to about 1.5-2 times the baseline values over the first 2 months of lansoprazole treatment; no further increase was noted.. Erosive relapse can be prevented in most patients for up to 1 yr with lansoprazole 15 mg or 30 mg once daily.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Dose-Response Relationship, Drug; Double-Blind Method; Enzyme Inhibitors; Esophagitis, Peptic; Female; Follow-Up Studies; Gastric Mucosa; Gastrins; Histamine H2 Antagonists; Humans; Lansoprazole; Male; Middle Aged; Omeprazole; Proton Pump Inhibitors; Recurrence; Time Factors

Patients with reflux esophagitis have rapid relapses after treatment withdrawal. This study was designed to investigate the relapse rate of symptomatic esophagitis during maintenance treatment with omeprazole or ranitidine.. Patients with endoscopically verified acute erosive or ulcerative esophagitis were initially treated with 20-40 mg omeprazole daily for 8-12 weeks. After healing, the patients were randomized to maintenance treatment with omeprazole (20 or 10 mg each morning) or ranitidine (150 mg twice daily). Control endoscopy was performed at the end of the healing phase and after 12 months of maintenance treatment or symptomatic relapse.. Of 426 initially treated patients, 392 were healed and entered the maintenance study. The months of maintenance treatment with 20 mg omeprazole once daily (n = 131), 10 mg omeprazole once daily (n = 133), and 150 mg ranitidine twice daily (n = 128) were 72%, 62%, and 45%, respectively. Both the 10- and 20-mg doses of omeprazole were significantly better than the dose of ranitidine (P < 0.001 and P < 0.005, respectively). There was no significant difference between the 10- and 20-mg doses of omeprazole (P = 0.06).. Maintenance treatment with omeprazole (20 or 10 mg once daily) is superior to ranitidine (150 mg twice daily) in keeping patients with erosive reflux esophagitis in remission over a 12-month period.

Topics: Adolescent; Adult; Aged; Double-Blind Method; Esophagitis, Peptic; Female; Gastric Mucosa; Gastrins; Humans; Life Tables; Male; Middle Aged; Omeprazole; Parietal Cells, Gastric; Prognosis; Prospective Studies; Ranitidine; Recurrence; Regression Analysis; Remission Induction; Scandinavian and Nordic Countries; Time Factors

Twenty-four-hour integrated intragastric acidity and 24-hr integrated plasma gastrin concentration was measured twice in 23 healthy male volunteers on the seventh day of oral dosing with placebo or ranitidine 150 mg four times a day. The study was a randomized, double-blind, placebo-controlled, two-way crossover investigation. The mean integrated 24-hr intragastric acidity during dosing with ranitidine 150 mg four times a day decreased to 32% of the placebo value (placebo 825 mmol/hr/liter; ranitidine 265 mmol/hr/liter). The mean integrated 24-hr plasma gastrin concentration during dosing with ranitidine 150 mg four times a day was 904 pmol/hr/liter compared with placebo (410 pmol/hr/liter)--an increase of 122%. The median number of hours of pH > 3 during dosing with placebo and with ranitidine 150 mg four times a day were 5 and 11 hr, respectively. Ranitidine 150 mg four times a day caused a significant decrease of mean integrated intragastric acidity for each meal-related interval and also during the night.

Topics: Adult; Dose-Response Relationship, Drug; Double-Blind Method; Drug Administration Schedule; Esophagitis, Peptic; Gastric Acid; Gastric Acidity Determination; Gastrins; Humans; Male; Ranitidine

Thirty two consecutive patients (age range 6 months-13.4 years) with severe reflux oesophagitis were randomised to a therapeutic trial for eight weeks during which they received either standard doses of omeprazole (40 mg/day/1.73 m2 surface area) or high doses of ranitidine (20 mg/kg/day). Twenty five patients completed the trial (12 on omeprazole, 13 on ranitidine). At entry and at the end of the trial patients underwent symptomatic score assessment, endoscopic and histological evaluation of the oesophagus, and simultaneous oesophageal and gastric pH measurement; results are given as median (range). Both therapeutic regimens were effective in decreasing clinical score (omeprazole before 24.0 (15-33), after 9.0 (0-18); ranitidine before 19.5 (12-33), after 9.0 (6-12)), in improving the histological degree of oesophagitis (omeprazole before 8.0 (6-10), after 2.0 (0-60); ranitidine before 8.0 (8-10), after 2.0 (2-6), and in reducing oesophageal acid exposure, measured as minutes of reflux at 24 hour pH monitoring (omeprazole before 129.4 (84-217), after 44.6 (0.16-128); ranitidine before 207.3 (66-306), after 58.4 (32-128)) as well as intragastric acidity, measured as median intragastric pH (omeprazole before 2.1 (1.0-3.0), after 5.1 (2.2-7.4); ranitidine before 1.9 (1.6-4), after 3.4 (2.3-5.3)). Serum gastrin concentration was > 150 ng/l in four patients on omeprazole and in three patients on ranitidine. It is concluded that in children with refractory reflux oesophagitis high doses of ranitidine are comparable with omeprazole for the healing of oesophagitis and relief of symptoms; both drugs resulted in efficacious reduction of intragastric acidity and intra-oesophageal acid exposure.

Topics: Adolescent; Child; Child, Preschool; Esophagitis, Peptic; Esophagus; Female; Gastric Acidity Determination; Gastrins; Humans; Infant; Male; Omeprazole; Ranitidine

Sixty patients who presented with erosive/ulcerative refractory reflux esophagitis were randomized to receive a 4- to 8-week treatment with omeprazole 20 mg daily, or ranitidine 150 mg twice daily. Patients not healed after treatment were given the same drugs at doubled doses for a second period of equal duration. Patients still unhealed after this received open treatment with omeprazole 20 mg twice daily for a third period of 4 to 8 weeks. Endoscopic assessment and clinical and laboratory evaluation were performed every 4 weeks until there was complete esophageal mucosal repair. After 4 weeks, complete healing was observed in 50% of patients on omeprazole 20 mg daily, compared with 20.7% on ranitidine 150 mg twice per day (p < 0.01). After 8 weeks, the figures were 79.3% versus 34.5% (p < 0.5). With doubled doses after 4 weeks, complete healing was achieved in 96.6% of patients on omeprazole 40 mg daily, compared with 64.2% on ranitidine 300 mg twice per day (p < 0.05). The eight still "refractory" patients (one omeprazole, seven ranitidine) healed completely with 8 more weeks of omeprazole 20 mg twice daily. Patients treated with omeprazole experienced faster relief of heartburn, which disappeared in 60% of patients after 4 weeks, as compared to 21% of patients treated with ranitidine (p < 0.006). Apart from the mode of treatment, the only factor that proved to be related to healing at multivariate analysis was the pretreatment severity of gastroesophageal reflux, as measured by esophageal pH monitoring. Our study confirms that omeprazole, even at a low dosage, is the choice for refractory reflux esophagitis.

Topics: Adult; Chronic Disease; Double-Blind Method; Drug Administration Schedule; Drug Resistance; Esophagitis, Peptic; Esophagus; Female; Gastrins; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Omeprazole; Prognosis; Ranitidine; Time Factors; Treatment Outcome

Ninety-eight patients with erosive and/or ulcerative esophagitis unhealed after at least 3 months' treatment with standard doses of cimetidine (greater than or equal to 1200 mg daily) or ranitidine (greater than or equal to 300 mg daily) were primarily included in an acute healing phase study, and 51 were allocated to 40 mg omeprazole once daily and 47 to 300 mg ranitidine twice daily. After 12 weeks of treatment, 46 (90%) patients given omeprazole were healed, compared with 22 (47%) allocated to ranitidine. Healed patients were then given maintenance treatment with either 20 mg omeprazole once daily or 150 mg ranitidine twice daily for 12 months. Plasma gastrin was determined and gastric mucosal biopsy specimens were obtained during the entire study to assess the structure of the exocrine and endocrine cell populations of the oxyntic mucosa. Sixty-seven per cent of the total number of patients randomized to omeprazole were maintained in clinical and endoscopic remission throughout the 12-month study period as compared with only 10% among those given ranitidine (p less than 0.0001). After 4 weeks of omeprazole treatment basal gastrin levels were slightly increased, with a 95% confidence interval for the change of from 8.6 to 16.9 pmol/l. No further increase in basal gastrin levels was observed during the ensuing study months. No significant histopathologic lesion was found in the oxyntic gland mucosa. In conclusion, omeprazole was far superior to ranitidine in preventing recurrence, a goal achieved without adverse events and significant abnormalities in the oxyntic mucosal exocrine or endocrine cells but with a moderate increase in basal gastrin levels.

Topics: Adult; Aged; Biopsy; Chi-Square Distribution; Esophagitis, Peptic; Esophagoscopy; Gastric Mucosa; Gastrins; Humans; Middle Aged; Omeprazole; Ranitidine; Recurrence

Forty-eight patients with erosive reflux esophagitis were allocated to either sucralfate tablets, 4 g/day, or cimetidine, 1.6 g/day, for 8 weeks in a randomized, prospective, single-blind, cross-over therapeutic trial. Pretreatment lower esophageal sphincter (LES) pressure and serum pepsinogen I (PG-I) levels were investigated as possible predictors of healing with either drug. The trial was completed by 41 patients (21 in the sucralfate group and 20 in the cimetidine group); one patient in each group was removed because of side effects. Symptom improvement occurred to a similar extent in both groups. Endoscopic results after 8 weeks of treatment with sucralfate revealed complete healing of esophageal erosions in 48% (cimetidine, 55%) and improvement in an additional 19% (cimetidine, 20%). Neither of these differences was statistically significant. Some patients refractory to one drug had endoscopic healing of esophagitis when treated with the other drug after crossover. LES pressure did not influence outcome in patients treated with sucralfate, whereas significantly (p = 0.024) more patients refractory to cimetidine had an LES pressure less than 7 mm Hg than did those with a good response to the histamine-2 (H2)-receptor blockade. Patients whose esophagitis healed or improved after sucralfate tended to have lower serum PG-I levels than those with treatment failure (104 +/- 35 ng/mL vs 125 +/- 45 ng/mL), whereas the opposite occurred in patients treated with cimetidine (132 +/- 58 ng/mL in responders vs 78 +/- 27 ng/mL in nonresponders, p = 0.048). The results confirm that sucralfate is a valuable alternative to H2-receptor inhibitors for the treatment of reflux esophagitis. They also provide preliminary evidence that LES pressures and serum PG-I levels may have predictive value of the response to one or the other of these two drugs.

Topics: Adult; Cimetidine; Endoscopy, Gastrointestinal; Epoprostenol; Esophagitis, Peptic; Fasting; Female; Gastrins; Gastrointestinal Motility; Humans; Male; Manometry; Middle Aged; Pepsinogens; Pressure; Prospective Studies; Sucralfate; Wound Healing

Ninety-eight patients (26 females), who presented with erosive and/or ulcerative oesophagitis, despite at least a 3-month period of treatment with standard doses of cimetidine (greater than or equal to 1200 mg daily) or ranitidine (greater than or equal to 300 mg daily), were included in a double-blind, randomized trial to compare omeprazole (40 mg o.m.) with a high dose of ranitidine (300 mg b.d.). The treatment was given for 4-12 weeks; endoscopy assessment and laboratory screening were performed on entry to the trial and thereafter every fourth week. Endoscopic healing was defined as complete epithelialization of all macroscopic erosions or ulcers in the squamous epithelium. An 'intention-to-treat' analysis of the clinical data revealed omeprazole to be superior to ranitidine: 63% of those patients who were given omeprazole were healed endoscopically after a 4-week period of treatment, compared with only 17% of those given ranitidine. This difference in healing rate persisted during the 12-week study period (90% vs 47% after 12 weeks; P less than 0.0001). Reflux symptoms were more rapidly and completely relieved with omeprazole: heartburn resolved completely in 86% of patients treated with omeprazole for 4 weeks compared with 32% in the ranitidine group (P less than 0.0001). The mean basal gastrin concentrations increased only in those given omeprazole from 18.9 pmol/L at pre-entry to a mean value of 31.7 pmol/L on the last day of omeprazole administration. In ranitidine-treated patients no significant increase in basal gastrin concentration was observed. Both drugs were well tolerated with few adverse events, which were mainly mild and transient. These results demonstrate the superiority of omeprazole over a high dose of ranitidine in the treatment of resistant reflux oesophagitis.

Topics: Adult; Aged; Double-Blind Method; Endoscopy, Gastrointestinal; Esophagitis, Peptic; Female; Gastrins; Histamine H2 Antagonists; Humans; Male; Middle Aged; Omeprazole; Ranitidine

Twenty-nine nongastrectomized and three partially gastrectomized patients with chronic reflux esophagitis resistant to 12 weeks' treatment with histamine H2-receptor antagonists were treated with a daily oral dose of 20-40 mg of omeprazole for 12-30 months. Basal serum gastrin, serum pepsinogen A, and serum pepsinogen C concentrations were monitored at regular intervals. Serum gastrin levels significantly (P less than 0.01) increased threefold to fourfold during the first 1-2 months of the study when all patients ingested 40 mg of omeprazole daily. Dose reduction to 20 mg did not significantly decrease gastrin levels. Serum gastrin levels showed a trend to further increase after the first 3 months of treatment, reaching statistically significant differences for values from the 3-12-month period (P less than 0.05) and from the 3-24-month period (P less than 0.005). Women and patients with high basal serum gastrin levels before omeprazole treatment were more likely to achieve higher serum gastrin levels during omeprazole treatment. Serum pepsinogen A and C levels were significantly (P less than 0.01) increased at all time intervals during long-term treatment with omeprazole. No significant tendency toward higher serum pepsinogen C levels in time was observed. However, serum pepsinogen A levels and the ratio of pepsinogen A to pepsinogen C further increased significantly (P less than or equal to 0.05) during the initial 3-12-month period. However, this trend was not observed anymore afterward. Antrectomized patients did not show increases in serum gastrin and serum pepsinogen A and C levels, suggesting that hypergastrinemia may be involved in the observed hyperpepsinogenemia.

Topics: Aged; Chronic Disease; Drug Administration Schedule; Esophagitis, Peptic; Female; Gastrectomy; Gastrins; Humans; Male; Middle Aged; Multicenter Studies as Topic; Omeprazole; Pepsinogens; Sex Factors

A total of 143 patients with peptic ulceration of the duodenum, stomach or oesophagus, who did not respond to 3 or more months high-dose treatment with ranitidine (450 mg or more daily), were admitted to oral treatment with omeprazole, 40 mg/day. In 94.4% of the patients, ulcers healed within 2-6 weeks. After healing of their ulcers, 122 patients were admitted to long-term maintenance treatment with omeprazole, 40 mg/day; 91 patients have been on the drug for 1-5.5 years. During maintenance therapy with omeprazole, 40 mg/day, no relapses (verified by endoscopy) have yet occurred and no drug related adverse effects have been observed. There were no significant changes in routine laboratory tests in any patients, including 27 with concomitant liver cirrhosis. Serum gastrin levels were already elevated approximately 2-fold during the initial high-dose ranitidine treatment and rose a further 2-fold at 2-3 months of omeprazole treatment. Thereafter, no further increase of serum gastrin was observed even after 5.5 years of continuous observation. Volume density of G and D cells in the antral mucosa did not change significantly. The volume density of argyrophilic cells in the oxyntic mucosa was 0.73 +/- 0.1% before the start of omeprazole treatment and 0.85 +/- 0.09% after 17-24 months of continuous treatment with omeprazole (ns). In antrectomized patients the volume density was lower (0.23 +/- 0.04%). No clusters of argyrophilic cells were observed in any of the groups. In a control group of patients with gastrinoma the volume density of these cells was higher (1.3 +/- 0.23%, n = 8).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Clinical Trials as Topic; Duodenal Ulcer; Esophagitis, Peptic; Follow-Up Studies; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Long-Term Care; Omeprazole; Ranitidine; Stomach Ulcer

Reflux esophagitis and gastric tube ulcer sometimes cause severe clinical problems in patients undergoing esophagectomy with gastric tube reconstruction. We previously reported that acidity in the gastric tube was decreased for 1 year after esophagectomy, and that lower acidity levels were associated with Helicobacter pylori (H. pylori) infection. However, the long-term changes in gastric acidity remain unknown. We aimed to investigate the long-term changes in gastric acidity after surgery. Eighty-nine patients who underwent esophagectomy with gastric tube reconstruction for esophageal cancer were analyzed. They underwent 24-hour pH monitoring, serum gastrin measurement, and H. pylori infection examination before surgery, at 1 month, 1 year, and 2 years after surgery. The gastric acidity at 1 month and 1 year after surgery was significantly lower than that before surgery (p=0.003, p=0.003). However, there was no difference in gastric acidity before and 2 years after surgery. The gas tric acidity in H. pylori-infected patients was significantly lower in comparison to non-infected patients at each time point (p=0.0003, p<0.0001, p<0.0001, p<0.0001, respectively). In H. pylori-infected patients, gastric acid ity was decreased for 1 year after surgery, and recovered within 2 years after surgery. However, no significant differences were observed in the acidity levels of non-infected patients during the 2-year follow-up period. The serum gastrin level increased after esophagectomy. The acidity levels in the gastric tube recovered within 2 years after surgery. Periodic endoscopy examination is recommended for early detection of acid-related disease, such as reflux esophagitis or gastric tube ulcer, after esophagectomy with gastric tube reconstruction.

Topics: Esophageal Neoplasms; Esophagectomy; Esophagitis, Peptic; Gastrins; Helicobacter Infections; Humans; Ulcer

In clinical practice, most patients with symptoms suggestive of gastroesophageal reflux disease (GERD) undergo esophago-gastro-duodenoscopy (EGD), despite its low sensitivity in detecting reflux stigmata. Gastrin 17 (G-17) has been proposed to be related with GERD, due to the negative feedback between acid secretion and this hormone. We assessed the clinical usefulness of fasting G-17 serum determination for a non-invasive diagnosis of GERD in patients with typical symptoms.. We consecutively enrolled patients complaining of typical GERD symptoms in two different settings: a single referral center and a primary care setting. Control groups consisted of dyspeptic patients. All subjects underwent assessment of serum levels of G-17 and EGD.. At the academic hospital, 100 GERD patients (n=89 with erosive esophagitis and 11 with Barrett's esophagus) had statistically significant low levels of G-17 as compared with 184 dyspeptic patients (1.7±1.2 pg/L vs 8.9±5.7 pg/L p<0.0001). Similarly, in the primary care setting, 163 GERD patients had statistically significant low levels of G-17 as compared with 132 dyspeptic patients (0.5±0.2 pg/L vs. 4.0±2.6 pg/L, p<0.0001). Moreover, in the primary care setting, no statistically significant differences were found for G-17 levels between patients with erosive and non-erosive reflux pattern (0.4±0.2 vs 0.7±0.3; p=0.08). In primary care, the accuracy of G-17 less than 1 pg/L to diagnose non-invasively GERD was 94.3%.. Low levels of G-17 were detected in patients with erosive esophagitis and Barrett's esophagus in a referral center and in patients with typical GERD symptoms in a sample of patients from a primary care setting.

Topics: Adult; Aged; Esophagitis, Peptic; Esophagoscopy; Female; Gastrins; Gastroesophageal Reflux; Humans; Male; Middle Aged

To investigate the efficacy of long-term (52 weeks) maintenance therapy by 10-mg vonoprazan administration for proton pump inhibitor-resistant reflux esophagitis continued from the preceding study.. Sixteen patients with proton pump inhibitor-resistant reflux esophagitis (mean age 70.9 years, eight males) in whom endoscopic healing was achieved by 20-mg vonoprazan administration for 4 weeks and maintenance of remission was maintained by 10-mg vonoprazan administration for 8 weeks were enrolled. Endoscopy was performed at 52 weeks after the initiation of maintenance therapy with 10-mg vonoprazan to evaluate whether there was any recurrence of reflux esophagitis. Changes in the gastric mucosa were investigated at 52 weeks. Symptoms were assessed using the frequency scale for the symptoms of gastroesophageal reflux disease and the fast gastrin level at 8 and 52 weeks following the maintenance therapy.. Endoscopic remission was maintained at 52 weeks in 15 (93.8%) of the 16 patients with proton pump inhibitor-resistant reflux esophagitis. One patient relapsed with grade C of reflux esophagitis. There were no significant differences in the symptom score at 8 and 52 weeks, nor the gastrin level at 8 and 52 weeks. There was no change in the stomach on endoscopy at 52 weeks.. Long-term maintenance therapy by 10-mg vonoprazan administration is very effective for proton pump inhibitor-resistant reflux esophagitis patients in whom endoscopic healing was maintained by 8 weeks maintenance therapy with 10-mg vonoprazan administration.

Topics: Aged; Drug Resistance; Endoscopy, Gastrointestinal; Esophagitis, Peptic; Female; Gastric Mucosa; Gastrins; Humans; Maintenance Chemotherapy; Male; Middle Aged; Proton Pump Inhibitors; Pyrroles; Recurrence; Sulfonamides; Symptom Assessment; Time Factors

The long-term administration of proton pump inhibitors (PPIs) is useful for preventing recurrent reflux esophagitis. On the other hand, several adverse reactions, such as an increase in the blood gastrin level, have been reported. The aim of the present study was to examine the increase in the blood gastrin level due to the long-term administration of conventional PPIs compared with vonoprazan.. A prospective cross-sectional study was conducted. We examined the blood gastrin levels of patients taking vonoprazan or conventional PPIs in whom the grade of atrophic gastritis had been endoscopically evaluated in the last year.. The blood gastrin level was significantly higher in the vonoprazan group than that in the PPI group in patients with milder or no atrophic gastritis, irrespective of the administration periods. However, no significant difference was observed between the groups in patients with severe atrophic gastritis.. Vonoprazan more markedly increased the blood gastrin level compared with conventional PPIs in patients with milder or no atrophic gastritis. This indicates that vonoprazan may have stronger acid-suppressing effects in such patients than conventional PPIs. Key Message: We should be aware of the potential development of hypergastrinemia during the long-term administration of vonoprazan, especially in patients with mild or no atrophic gastritis.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Aged; Aged, 80 and over; Cross-Sectional Studies; Esophagitis, Peptic; Female; Gastrins; Gastritis, Atrophic; Humans; Long-Term Care; Male; Middle Aged; Prospective Studies; Proton Pump Inhibitors; Pyrroles; Sulfonamides; Treatment Outcome; Young Adult

Dyspepsia develops in healthy volunteers after withdrawal of proton-pump inhibitors. This phenomenon, attributed to rebound acid hypersecretion, is thought to be mediated by reflex hypergastrinemia.. To measure fasting and postprandial gastrin in patients on long-term proton-pump inhibitor treatment and correlate gastrin levels with the duration of treatment and other potential predictors.. In this cross sectional study patients, with erosive esophagitis, on long-term proton-pump inhibitor treatment and healthy controls underwent gastrin measurements at baseline and four times following a meal and Helicobacter pylori status was determined.. A total of 100 patients and 50 controls were studied. Pre- and postprandial gastrin levels were higher in patients (p<0.001). No significant correlation was found between the area under the gastrin-curve and the treatment duration. Female patients had significantly higher gastrin levels than males pre- and postprandial, whereas such differences was not found in the control group. Female gender was the only independent predictor of s-gastrin levels (OR 2.50 compared to males, 95% CI: 1.08-5.76, p=0.032) in the patient group.. Gastrin values were higher in patients compared to controls. There was no correlation between gastrin levels and treatment duration. Female patients had significantly higher gastrin values than males.

Topics: Aged; Case-Control Studies; Chromogranin A; Cross-Sectional Studies; Dyspepsia; Esophagitis, Peptic; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Postprandial Period; Proton Pump Inhibitors; Sex Factors; Substance Withdrawal Syndrome

The relationship between gastroesophageal reflux disease (GERD) and Helicobacter pylori is controversial. We evaluated endoscopic, 24-h gastric and esophageal acid profile among patients with GERD in relation to H. pylori, as the latter might alter gastric acid secretion.. Patients with GERD (n = 123), who were not on acid-suppressive drugs, and had not received anti-H. pylori therapy, underwent gastroduodenoscopy and tests for H. pylori detection. Esophageal manometry, 24-h pH metry, serum pepsinogen-I (PG-I), PG-II and gastrin-17 ELISA were done in all these patients. Univariate and multivariate analyses were performed to assess independent predictors for erosive esophagitis (EE).. Of 123 patients (mean age 40.5 [13.1] years, 85 [69.1%] men), 59 (47.9%) had H. pylori infection. EE was more common in H. pylori non-infected than infected (49 vs. 32, p < 0.001). Among patients older than 40 years, absence of H. pylori was associated with lower esophageal pH and longer reflux (p = 0.02 and p < 0.001, respectively). PG-I/PG-II ratio was lower in H. pylori infected subjects (p < 0.001). In patients with higher LA grade of esophagitis, elevated PG-I levels and PG-I/PG-II ratio were associated with more acidic stomach (p = 0.04 and p = 0.01, respectively). Multivariate analyses showed low gastrin-17 (p = 0.016), higher age (p = 0.013), hiatus hernia (p = 0.004) and absence of H. pylori (p = 0.03) were independent predictors for risk of EE.. H. pylori infection is associated with less acidic stomach and less severe GERD. Low gastrin-17, higher age, hiatus hernia and absence of H. pylori were the best predictors for EE risk.

Topics: Adult; Age Factors; Endoscopy, Digestive System; Esophagitis, Peptic; Esophagus; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Prospective Studies; Severity of Illness Index; Sex Factors

To investigate the association between the gastric emptying rate and the presence of erosive esophagitis in duodenal ulcer (DU) patients among a population with high prevalence of Helicobacter pylori infection.. Cross-sectional survey was performed in a cohort of 60 male patients with either active or healed DU, with or without the presence of erosive esophagitis. Clinical and social-demographic data, blood level of fasting gastrin, pepsinogen I & I/II ratio, and scintigraphic measurement of half emptying time (t(1/2) ) of the solid phase gastric emptying were evaluated.. Patients with active DU and erosive esophagitis tended to have higher plasma level of fasting gastrin than those without erosive esophagitis (75.11±13.74 vs 45.81±5.06pgmL(-1) , P = 0.059). In the absence of H. pylori infection, patients with healed DU and erosive esophagitis had a trend to have longer half-emptying time (t(1/2) : 96.5±6.4 vs 69.1±11.3min, P=0.0572) than those without erosive esophagitis, and statistically significant longer after excluding those diagnosed with hiatal hernia (t(1/2) : 100.8±7.9min vs 69.1±11.3min, P<0.05) from the former group. Among the healed DU patients, those with negative H. pylori infection, hiatal hernia and overweight (body mass index ≥24) had significantly increased risk of severe esophagitis.. Presence of erosive esophagitis in a subset of Taiwanese patients with healed DU and negative H. pylori status was associated with slower solid phase gastric emptying.

Topics: Adult; Cross-Sectional Studies; Duodenal Ulcer; Esophagitis, Peptic; Gastric Emptying; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Taiwan

Helicobacter pylori (H. pylori) infection is known as a major cause of atrophic gastritis and is associated with serum gastrin, pepsinogen, and gastric acid secretion. There is still a controversial association between gastroesophageal reflux disease and H. pylori infection. This study was designed to investigate the relationship among serum gastrin, pepsinogen, and H. pylori infection in the erosive reflux esophagitis (ERD) patients.. Patients who were diagnosed as ERD by one gastroenterologist at the Kangnam St. Mary's hospital were prospectively enrolled. The persons without ERD in the control group were matched for age and sex. We examined the gastrin, pepsinogen I (PG I), PG II, PG I/II ratio, and H. pylori infection.. Forty five patients were enrolled in ERD group and 66 persons in control group. The H. pylori infection rate in ERD group was lower than that in the control group (11.1% vs. 43.9%, p<0.001). PG I/II ratio in ERD group was higher than that in the control group (7.0+/-3.1 vs. 5.3+/-2.6, p=0.003). The PG II (p=0.016) and gastrin (p=0.029) in ERD group were lower than those in the control group. BMI in ERD group was higher than that in the control group (24.5 vs. 23.1 kg/m2, p=0.013).. The H. pylori infection rate in ERD group was lower and PG I/II ratio was higher than that in the control group. Reflux esophagitis is thought to be reversely associated with the atrophy of gastric mucosa.

Topics: Adult; Aged; Chi-Square Distribution; Esophagitis, Peptic; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogens

The Zollinger-Ellison syndrome is characterized pathophysiologically by a significant hypergastrinemia derived from a gastrin-secreting neuroendocrine tumor with a primary location in the pancreas or duodenum. Chronic hypergastrinemia in turn triggers gastric acid hypersecretion yielding in chronic or recurrent or refractory peptic ulcer disease and/or chronic diarrhea. One half of patients with ZES will have distant metastases in the liver by the time the diagnosis is established and one half of all patients with ZES will experience chronic diarrhea as chief complaint rather than peptic ulcer-related symptoms and signs. Gastrinomas have been reported to either manifest sporadically or to occur in conjunction with the genetic background of the MEN-I syndrome. Diagnosis is based on the patients history which is typically characterized by recurrent episodes of peptic ulcer disease or by severe reflux esophagitis and/or diarrhea or by acid-related symptoms which fail to respond to standard treatment regimens. Upper gastrointestinal tract endoscopy will provide evidence for peptic ulcer disease in anatomical regions located aborally the duodenal bulb within the descending part of the duodenum or even farther distally within the jejunum. Peptic ulcers frequently occur in groups indicating some substantial acid hypersecretion. A gastric pH > 2 is mutually exclusive for ZES. Increased serum gastrin levels confirm the diagnosis biochemically. Gastrin secretion can be determined in the basal state or following stimulation with secretin or calcium. High sensitivity and specificity for the diagnosis of ZES is provided by determining the ratio of basal versus pentagastrin-stimulated gastric acid secretion: The ratio of BAO / MAO > 0.6 is highly specific for gastrinoma. To localize the gastrin-secreting tumor computer-assisted tomography, endoscopic ultrasound, and somatostatin receptor scintigraphy provide useful help but most recently, endoscopic ultrasound with high resolution transducers appear to improve preoperative site localization. If modern imaging techniques fail to elucidate the site of the tumor, intraoperative diaphany may help to detect gastrinomas within the duodenal wall. Definitive treatment will only be achieved by total surgical resection of the gastrin-producing tumor in the pancreas or duodenum including dissection of the regional lymph nodes. Control of symptoms will have to be achieved by administration of highly potent proton pump inhibitors i

Topics: Diagnosis, Differential; Duodenal Neoplasms; Esophagitis, Peptic; Gastric Acidity Determination; Gastrinoma; Gastrins; Humans; Pancreatic Neoplasms; Peptic Ulcer; Proton Pump Inhibitors; Zollinger-Ellison Syndrome

We have previously reported that Helicobacter pylori infection prevents reflux esophagitis (RE) and Barrett's esophagus (BE) by decreasing gastric acid secretion. Gastroesophageal (GE) junction adenocarcinoma, including Barrett's adenocarcinoma, has been thought to be a complication of gastroesophageal reflux disease (GERD). However, the relationship between H. pylori infection, gastric acid secretion, and GE junction adenocarcinoma has not yet been investigated in Japan. The aim of this study was to evaluate this relationship in the Japanese population.. A total of 168 Japanese patients (RE alone: 80, short-segment BE (SSBE): 16, long-segment BE (LSBE): 20, GE junction adenocarcinoma: 12, distal early gastric cancer (EGC): 40; male/female = 106/62; mean age 61.5 yr) and 80 Japanese control subjects who had no localized lesions in the upper gastrointestinal tract (male/female = 43/37, mean age 58.1 yr) were enrolled for this study. The prevalence of H. pylori infection was determined by biopsy, the rapid urease test, and measurement of the serum H. pylori IgG antibody. Gastric acid secretion was assessed by the endoscopic gastrin test (EGT). RE was diagnosed according to the Los Angeles classification.. The prevalence of H. pylori infection in the patients with RE alone (30%) was significantly lower than that in control subjects (71.2%). There was also a tendency for the prevalence of H. pylori infection to be lower in patients with BE (SSBE, 18.7%; LSBE, 0%) when compared to that in patients with RE alone. On the other hand, while the prevalence of H. pylori infection in patients with GE junction adenocarcinoma (58.3%) was significantly lower than that in patients with EGC (87.5%), it tended to be higher than that in patients with RE alone or BE. The mean EGT value in patients with RE alone (3.74 mEq/10 min) was significantly higher than that in control subjects (1.83). The mean EGT value in patients with BE (SSBE, 4.74; LSBE, 4.76) tended to be even higher than that in patients with RE alone. The mean EGT value in patients with GE junction adenocarcinoma (3.94) was significantly higher than that in control subjects and patients with EGC (0.67), but it was comparable to that independent of the H. pylori infection status in patients with RE alone or BE.. Preservation of gastric acid secretion may be important for the development of GE junction adenocarcinoma in Japanese people, irrespective of the H. pylori infection status.

Topics: Adenocarcinoma; Barrett Esophagus; Esophageal Neoplasms; Esophagitis, Peptic; Esophagogastric Junction; Female; Gastric Acid; Gastric Acidity Determination; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Prevalence; Stomach Neoplasms

A comparison was done between the F. Paulino jejunal pouch (FP) and a jejunal pouch (JP) as esophagus-duodenum interpositional graft, for replacing the stomach after total gastrectomy. It was investigated the effect of the two procedures on esophagus histology, nutritional state and serum gastrin in rats.. Male Wistar rats weighing 282 +/- 17g were randomly submitted to sham operation (S), FP and JP after total gastrectomy. After eight weeks the rats were killed with overdose of anesthetic and tissue was taken from the distal esophagus for histology. Serum levels of total proteins, albumin, iron, transferring, folate, cobalamine, calcium, as well as serum gastrin were determined. Survival was considered.. Fourty six rats were operated and thirty survived for eight weeks. Five (33.3%) died after FP and 11 (52.3%) after JP (p < 0.05). Postoperative esophagitis occurred in 6 JP rats. At 8th week, no difference was observed on body weight when compared FP and JP rats (p > 0.05). The JP rats had a significant decrease in serum albumin, glucose, transferrin, iron, folate and calcium, compared to sham (p < 0.05). Serum gastrin, iron and calcium were significantly higher in JP rats than in FP rats (p < 0.05). In FP rats, transferrin and cobalamine showed significant decrease comparing the preoperative with 8th week levels (p < 0.05).. F. Paulino pouch in rats had lower mortality than JP, and esophagitis was not detected in it. JP rats had serum gastrin, iron and calcium unaffected, possibly because of preservation of duodenal passage.

Topics: Analysis of Variance; Anastomosis, Roux-en-Y; Animals; Blood Glucose; Duodenum; Esophagitis, Peptic; Esophagus; Gastrectomy; Gastrins; Jejunum; Male; Nutritional Status; Postgastrectomy Syndromes; Rats; Rats, Wistar; Serum Albumin; Vitamin B 12

Topics: Anti-Ulcer Agents; Drug Administration Schedule; Esophagitis, Peptic; Gastrins; Humans; Long-Term Care; Omeprazole; Proton Pump Inhibitors

Proton pump inhibitors have been proven to have a major role in the management of peptic diseases, especially the long-term control of reflux esophagitis. The potent inhibitory effect of omeprazole on gastric acid secretion is frequently associated with hypergastrinemia, and gastrin and its intermediates have been reported to promote gastrointestinal cellular functions and cell growth. Experimental data suggest that gastrin may affect the proliferation of colon cells and some other cancer cells. However, so far the direct role of gastrin in tumorigenesis is unclear. Although most clinical studies on long-term treatment with omeprazole or other proton pump inhibitors do not report serious adverse effects, the issue of prolonged hypergastrinemia and tissue growth is unsettled, and many clinicians are reluctant to recommend long-term use of omeprazole or of other proton pump inhibitors.. We examined the effect of long-term omeprazole treatment on serum gastrin levels in patients with reflux esophagitis when given either 20 mg daily (group 1) or on alternate days (group 2). During the follow-up period, clinical remission was monitored and maintained in all patients in group 1 and in the majority of patients in group 2.. The mean serum gastrin level was significantly elevated in group 1 (mean +/- SE, 159 +/- 23.6 pg/mL; range, 45-620 pg/mL; n = 31) as compared with the alternate-day treatment group (group 2) (66 +/- 4.8 pg/mL; range, 37-115 pg/mL; n = 21) (p < 0.005). In controls, serum gastrin levels showed similar values to those found in group 2 (54 +/- 4.3 pg/mL; range, 27-94 pg/mL; n = 20). Fourteen patients (45%) in group 1 had serum gastric ranging from 140 to 620 pg/mL, and 8 (25%) had a 6-fold or greater increase in serum gastrin. The follow-up treatment period ranged between 3 and 60 months (mean +/- SE, 16.1 +/- 2.1 months) for group 1 and 3-36 months (9.7 +/- 1.4 months) for group 2. Upon multivariate adjustment for age and duration of treatment, a significantly lower mean serum gastrin level was observed in the alternate-day group as compared with the daily treated group.. Alternate-day, long-term treatment with omeprazole may be adequate to maintain remission in patients with reflux esophagitis. This regimen can assure serum gastrin levels within the normal range, thus reducing the potential risk of prolonged, sustained hypergastrinemia and profound hypochlorhydria.

Topics: Adult; Aged; Aged, 80 and over; Anti-Ulcer Agents; Drug Administration Schedule; Esophagitis, Peptic; Esophagoscopy; Female; Follow-Up Studies; Gastrins; Humans; Long-Term Care; Male; Middle Aged; Omeprazole; Treatment Outcome

Recent studies have clarified a close association between H. pylori infection and gastritis, peptic ulcer disease, and gastric cancer, but there is little information concerning the relationship between H. pylori infection and reflux esophagitis (RE). We investigated the relationship between H. pylori, RE, and corpus gastritis.. Ninety-five patients with RE and 190 sex- and age-matched asymptomatic healthy controls demonstrating no localized lesions in the upper GI tract were studied and evaluated for H. pylori infection, histologic gastritis, serum gastrin, and pepsinogens (PGs).. H. pylori infection was significantly lower in RE patients than in asymptomatic controls (41% vs. 76%, p <.01). Histologic gastritis of both the antrum and corpus was significantly less frequent (antrum; p <.01, corpus; p <. 01), and serum levels of PGI and the PG I/II ratio were significantly higher in RE patients than in controls (PGI; p <.05, PG I/II ratio; p <.01). When the subjects were divided into two age groups (59 years of age and younger and 60 years of age and older), a significant difference was found only among patients over 60 years of age (29% vs. 85%, p <.01). Among subjects in this age group, gastritis in both the antrum and corpus were significantly milder in RE patients than in controls. Although the prevalence of H. pylori infection was similar between the two groups of patients under 59 years of age, corpus gastritis was significantly milder in patients than in controls (p <.05).. A significantly low prevalence of H. pylori infection was found in RE patients over 60 years of age but not in those under 59 in comparison with sex- and age-matched controls. The relative lack of corpus gastritis might play a role in the pathogenesis of RE in our population through preservation of the acid secretion area.

Topics: Age Factors; Aged; Case-Control Studies; Endoscopy, Gastrointestinal; Esophagitis, Peptic; Female; Gastrins; Gastritis; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Humans; Japan; Male; Middle Aged; Pepsinogens; Prevalence; Pyloric Antrum; Stomach

Topics: Anti-Ulcer Agents; Barrett Esophagus; Drug Administration Schedule; Esophageal Neoplasms; Esophagitis, Peptic; Fundoplication; Gastric Mucosa; Gastrins; Gastritis; Gastroesophageal Reflux; Helicobacter Infections; Humans; Omeprazole; Proton Pump Inhibitors; Time

Endoscopic esophagitis is less common in the East than in the West. The reason for this is unknown. This study examines prospectively the relationship between endoscopic esophagitis and lower esophageal sphincter pressure, distal esophageal contractility, esophageal peristaltic performance, esophageal acid exposure, gastric acid output, and Helicobacter pylori (H. pylori) status in a consecutive series of Asian patients.. Esophageal manometry and ambulatory pH monitoring were carried out in 48 patients with endoscopic esophagitis and 208 patients with symptoms suspicious of gastroesophageal reflux disease but without esophagitis. Gastric acid output and H. pylori serology were determined in 22 of the esophagitis group and 36 of the nonesophagitis group.. Compared to the nonesophagitis patients, esophagitis patients had a higher prevalence of hypotensive lower esophageal sphincter (49% vs 24%, p < 0.001), impaired esophageal contractility (45% vs 22%, p < 0.005), poor peristaltic performance (23% vs 12%, p < 0.05), and pathological acid reflux (48% vs 27%, p < 0.005). However, there was no difference in the two groups with respect to gastric acid output and H. pylori positivity.. Lower esophageal sphincter competence, esophageal peristaltic contractility, and esophageal acid exposure were important factors in the pathogenesis of reflux esophagitis--results identical to Western studies. Gastric acid output per se and H. pylori infection might not be responsible for susceptibility to esophagitis.

Topics: Adult; Aged; China; Esophagitis, Peptic; Esophagus; Female; Gastric Acid; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Manometry; Middle Aged; Singapore

Helicobacter pylori gastritis may spread proximally in the stomach during profound acid inhibition.. To examine histological gastric body changes and epithelial cell proliferation before and after treatment with lansoprazole.. Patients diagnosed as having reflux oesophagitis grade 1 or 2 were enrolled and treated for 12 weeks with lansoprazole (30 mg every morning). After 12 weeks, 103 of the 118 patients appeared endoscopically healed and were asymptomatic; they then received maintenance treatment with 15 or 30 mg lansoprazole daily. Biopsy specimens obtained from similar sites before and after treatment, were available from 90 patients after a median of 64 weeks (range 15-73 weeks). Epithelial cell proliferation was determined by the number of Ki-67 antigen positive cells per gland.. Of these 90 patients, 44 (49%) were found to be infected with H pylori. Their median inflammation score had increased from grade 1 before to grade 2 after treatment (p < 0.0001). Initially, the number of Ki-67 antigen positive cells per gland was significantly higher in the H pylori infected than in the uninfected group and increased further after treatment (p < 0.0001). In uninfected patients, no significant change in inflammation or proliferation occurred during treatment.. A marked increase in body gastritis was observed in H pylori infected individuals during long term treatment with the proton pump inhibitor lansoprazole. Epithelial cell proliferation and atrophy also increased in infected but not in uninfected patients.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Aged; Anti-Ulcer Agents; Cell Division; Epithelial Cells; Esophagitis, Peptic; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Lansoprazole; Middle Aged; Omeprazole; Proton Pump Inhibitors; Statistics, Nonparametric; Time Factors

To determine the clinical efficacy of once-daily treatment with omeprazole in refractory acid-related diseases in children.. Endoscopic healing and 24-hour intragastric pH values were assessed in 13 patients with refractory reflux esophagitis (n = 5), refractory and/or giant duodenal ulcer (n = 6), or giant gastric ulcer (n = 2). The mean dose of omeprazole was 0.6 mg/kg per day (range, 0.3 to 0.7 mg/kg per day). Pharmacokinetic studies of omeprazole were performed in seven patients.. The cumulative healing rates at 2, 4, 6, and 8 weeks of treatment were 46%, 85%, 92%, and 92%, respectively. Esophagitis in one patient did not heal despite increases in doses of up to 1.6 mg/kg per day (40 mg/day). The mean intragastric pH of omeprazole-treated patients was 5.2 (range, 3.0 to 6.6) and mean hydrogenion activity was 1.78 mmol/L (range, 0.01 to 10.42 mmol/L). There was wide interindividual variation in the reduction of gastric acid production. Mean intragastric H+ activity in omeprazole-treated patients was significantly lower than that of control subjects (p < 0.005) and that of patients treated with histamine type 2(H2)-receptor antagonists (p < 0.05). Mean intragastric H+ activity was not significantly correlated to the area under the concentration-time curve of omeprazole. No severe adverse effects were reported during treatment or at follow-up.. Omeprazole has a potent antisecretory effect and is a suitable alternative for short-term treatment of refractory acid-related diseases; a relatively low dose (0.6 mg/kg per day) appears to be optimal in most patients. Unhealed esophagitis at 8 weeks of treatment was considered to be refractory to omeprazole.

Topics: Anti-Ulcer Agents; Case-Control Studies; Child; Dose-Response Relationship, Drug; Duodenal Ulcer; Endoscopy, Gastrointestinal; Esophagitis, Peptic; Female; Follow-Up Studies; Gastric Acidity Determination; Gastrins; Histamine H2 Antagonists; Humans; Male; Omeprazole; Stomach Ulcer; Time Factors

Topics: Esophagitis, Peptic; Gastrins; Humans; Omeprazole

Topics: Esophagitis, Peptic; Gastrins; Humans; Omeprazole

To evaluate the long-term efficacy and safety of omeprazole in patients with gastroesophageal reflux disease resistant to treatment with histamine-2 (H2)-receptor antagonists.. Cohort analytic study with a mean follow-up of 48 months (range, 36 to 64 months).. Patients receiving ambulatory care from referral centers.. 91 patients with gastroesophageal reflux disease resistant to treatment with an H2-receptor antagonist but subsequently responsive to 40 mg of omeprazole daily.. Open maintenance therapy consisting of 20 mg of omeprazole daily in 86 patients and 40 mg daily in 5 patients.. Endoscopy to assess healing; side effects, laboratory values, fasting serum gastrin level, and gastric corpus biopsies to assess safety.. Esophagitis recurred in 47% of the patients receiving 20 mg of omeprazole daily, but all rehealed after the dose was doubled. Seven of 40 patients (18%) had a second relapse after a mean follow-up time of 24 months (range, 9 to 36 months) that was successfully treated with a further 20-mg dose increment for a mean period of 36 months (range, 6 to 39 months). Median gastrin levels increased initially from 60 ng/L before study entry to 162 ng/L (P < 0.01) with treatment and reached a plateau during maintenance treatment. Very high gastrin levels (> 500 ng/L) were observed in a subgroup (11%) of patients. The incidence of micronodular hyperplasia increased from 2.5% of the patients at first biopsy to 20% at the last biopsy (P = 0.001), with a corresponding progression of gastritis to subatrophic or atrophic gastritis from less than 1% to 25% (P < 0.001), which was more pronounced in patients with very high serum gastrin levels.. Maintenance therapy with omeprazole was effective for at least 5 years in patients with gastroesophageal reflux disease resistant to treatment with H2-receptor antagonists. Treatment was accompanied by a persistent increase in serum gastrin levels and an increase of micronodular argyrophil cell hyperplasia and subatrophic or atrophic gastritis.

Topics: Barrett Esophagus; Drug Resistance; Esophagitis, Peptic; Female; Gastrins; Gastroscopy; Humans; Life Tables; Male; Omeprazole; Time Factors; Treatment Outcome

Topics: Carcinoid Tumor; Esophagitis, Peptic; Gastrins; Humans; Omeprazole; Stomach Neoplasms

Treatment of omeprazole induces profound inhibition of gastric acid secretion, resulting in hypergastrinaemia. In rats hypergastrinaemia induced by chronic administration of high doses of omeprazole resulted in ECL-cell hyperplasia and subsequent carcinoid formation. This finding may limit long-term therapy in man. The synthetic prostaglandin E2 analogue enprostil not only inhibits gastric acid secretion but also reduces serum gastrin in normal subjects and in peptic ulcer patients. The present study was undertaken to determine whether enprostil reduces serum gastrin in patients on long-term treatment with omeprazole.. Eight patients with reflux oesophagitis treated with 40 mg omeprazole once daily for at least 3 months received 35 micrograms enprostil t.d.s. during a 5-day treatment course. Basal and postprandial serum gastrin concentrations and pepsinogen A and C levels were measured on the day before, the first and the final day, and on the day after cessation of treatment.. Enprostil significantly (P < 0.05) reduced basal serum gastrin from 65 +/- 15 pmol/L to 51 +/- 13 pmol/L on the first treatment day, and to 41 +/- 9 pmol/L on the final day. Enprostil also significantly (P < 0.05) reduced postprandial integrated serum gastrin from 6173 +/- 849 pmol.h/L to 4516 +/- 906 pmol.h/L and to 3532 +/- 706 pmol.h/L on the first and final treatment days, respectively. On the day after cessation of treatment basal (57 +/- 11 pmol/L) and postprandial integrated serum gastrin concentrations (5766 +/- 864 pmol.h/L) were not significantly different when compared to pretreatment values. Enprostil had no significant influence on serum pepsinogens A and C.. Short-term co-administration of enprostil lowers the serum gastrin levels in patients on long-term treatment with omeprazole.

Topics: Aged; Aged, 80 and over; Enprostil; Esophagitis, Peptic; Female; Food; Gastrins; Humans; Male; Middle Aged; Omeprazole; Pepsinogens; Radioimmunoassay

The development of gastric enterochromaffin-like (ECL)-cell hyperplasia in humans may be associated with extreme hypergastrinaemia, as occurs in Zollinger-Ellison syndrome (ZES) and pernicious anaemia (type A gastritis). More recently, endocrine cell hyperplasia has been found in all forms of chronic atrophic gastritis and even in cases of focal atrophy. Serum gastrin levels, non-antral gastric endocrine (argyrophil) cell growth, and the severity and type of concomitant gastritis were monitored in 66 unoperated and 8 antrectomized patients with poorly responsive peptic ulcer or reflux oesophagitis during up to 5 years' treatment with high-dose omeprazole, 40 mg daily. A small subgroup of patients (23%) had serum gastrin concentrations of more than four times the normal upper limit. These patients also had hyperplasia of the gastric argyrophil cells. More importantly, the same subgroup of patients had high-grade (atrophic) gastritis. Micronodular hyperplasia of argyrophil cells was significantly more frequent in biopsies showing atrophic gastritis (48%) than in biopsies showing only superficial gastritis (3.6%). It is concluded that, as previously demonstrated in untreated patients with gastric ulcer, the argyrophil cell hyperplasia observed during high-dose omeprazole therapy is related to the progression of chronic atrophic gastritis rather than to serum gastrin levels.

Topics: Biopsy; Esophagitis, Peptic; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Hyperplasia; Longitudinal Studies; Omeprazole; Peptic Ulcer; Severity of Illness Index

Thirty-four patients with H2-blocker-resistant reflux esophagitis subsequently healed by 40 mg omeprazole daily entered a maintenance study with 20 mg omeprazole. In 31 evaluable cases the observation period was at least 12 months (mean 24 months). Esophagitis remained in remission in two thirds of patients despite dose reduction. Relapses of esophagitis occurred in 10 cases within six months, which rapidly healed by increasing the omeprazole dose to 40 mg. No further recurrence with 20 mg omeprazole was found later than six months. Peptic strictures primarily requiring repeated dilatation in six patients during healing with omeprazole did not reappear while on omeprazole maintenance. Major side effects that could be attributed to omeprazole were not observed. Gastrin levels remained within or slightly above the normal range in the vast majority. It is concluded that omeprazole maintenance treatment in severe reflux esophagitis is an effective and safe therapy.

Topics: Adult; Aged; Body Weight; Drug Administration Schedule; Drug Resistance; Esophagitis, Peptic; Esophagoscopy; Female; Follow-Up Studies; Gastrins; Histamine H2 Antagonists; Humans; Lung Diseases; Male; Middle Aged; Omeprazole; Prospective Studies; Recurrence; Remission Induction

The reduction in intragastric acidity and the subsequent increase in plasma gastrin were compared during long-term treatment with either omeprazole or ranitidine in 19 patients with erosive reflux esophagitis. The patients received 40 mg omeprazole in the morning or 300 mg ranitidine twice daily. After healing, half the dose was given as maintenance treatment for 1 year. Intragastric acidity and plasma gastrin were measured 24 h before entry and monthly with the high dose and after 1, 6, and 12 months with the low dose. Omeprazole reduced intragastric acidity more effectively than ranitidine (p less than 0.001). This difference in efficacy was more pronounced during the daytime. Plasma gastrin increased more after omeprazole than after ranitidine (p less than 0.01), and both drugs showed a normal postprandial response and approached fasting levels before the next dose. During long-term treatment with 20 mg omeprazole in the morning no progressive alterations were observed in 24-h intragastric acidity or plasma gastrin.

Topics: Adult; Aged; Aged, 80 and over; Circadian Rhythm; Esophagitis, Peptic; Female; Gastric Acidity Determination; Gastrins; Humans; Male; Middle Aged; Omeprazole; Ranitidine; Time Factors

Topics: Age Factors; Carcinoid Tumor; Esophagitis, Peptic; Female; Gastrins; Humans; Male; Middle Aged; Omeprazole; Peptic Ulcer; Risk Factors; Sex Factors; Stomach Neoplasms

To study the effects of sudden withdrawal of long-term maintenance therapy with omeprazole for up to 4 years, 14 patients with resistant reflux oesophagitis were asked to stop their treatment temporarily. Ten days after withdrawal median basal acid output had increased significantly (p = 0.01) from 0 (range, 0-1.18) on day 1 to 1.95 (range, 0-8.45) mmol/h on day 10. Median serum gastrin levels were raised during treatment with omeprazole but decreased significantly from 166 to 42 ng/l within the 10 days of the study (p = 0.01). The median integrated gastrin response after meal stimulation decreased significantly (p less than 0.001) from 758.6 ng/l on day 1 to 267.9 ng/l on day 10. On day 10 after withdrawal of omeprazole all patients had endoscopic and symptomatic evidence of recurrent oesophagitis. Reflux patients receiving maintenance treatment with omeprazole for up to 4 years showed prompt normalization of serum gastrin levels and return of gastric acid production within 10 days after stopping the treatment. Consequently, there was a fast recurrence of aggravation of reflux symptoms and oesophagitis.

Topics: Adult; Aged; Esophagitis, Peptic; Esophagoscopy; Fasting; Female; Gastric Acid; Gastrins; Histamine H2 Antagonists; Humans; Male; Middle Aged; Omeprazole; Recurrence; Time Factors

Serum gastrin levels were determined in 120 consecutive patients (43 females, 77 males) with peptic disease 24 h post dose after 4 weeks continuous omeprazole (40 mg daily) treatment. Serum gastrin levels were elevated in 33 (28%) but exceeded the twice normal range in only 6 patients (5%). Age and sex did not influence the magnitude of gastrin levels. Gastrin increments induced by omeprazole compared to pretreatment with H2-blockers in 60 cases were similar in both males (42 +/- 10 pg/ml) and females (44 +/- 9 pg/ml). It is concluded that the magnitude of gastrin increases observed during omeprazole therapy are small and independent of age and sex.

Topics: Adolescent; Adult; Age Factors; Aged; Esophagitis, Peptic; Female; Gastrins; Histamine H2 Antagonists; Humans; Male; Middle Aged; Omeprazole; Peptic Ulcer; Sex Factors

A total of 143 patients with peptic ulceration of the duodenum, stomach and oesophagus who did not respond to 3 or more months of high-dose treatment with ranitidine, 450 mg or more daily, were treated with oral omeprazole, 40 mg daily. In 94% of the patients, ulcers healed within 2-8 weeks. After healing, 133 patients underwent long-term maintenance treatment with omeprazole, 40 mg daily, for 1-5 years (continuing). During maintenance therapy with omeprazole, no endoscopically verified relapses occurred, and no drug-related adverse effects were seen. There were no significant changes in routine laboratory tests in any patient, including 27 with concomitant liver cirrhosis. Basal serum gastrin levels, which were already elevated by the previous high-dose ranitidine treatment, rose to 4 times normal levels after 4 months of treatment with omeprazole. Thereafter, no further increases in basal serum gastrin levels were observed, even after 5 years of administration. The volume density of argyrophilic cells in the oxyntic mucosa increased during omeprazole treatment, but no dysplasia of the gastric enterochromaffin-like cells was seen. In conclusion, omeprazole was highly effective in healing ranitidine-resistant peptic ulcers, and subsequent maintenance therapy with omeprazole, 40 mg daily, was found to be effective and safe over the period observed.

Topics: Drug Resistance; Esophagitis, Peptic; Gastrins; Humans; Omeprazole; Peptic Ulcer; Ranitidine; Time Factors

Serum gastrin was determined in 33 patients during treatment with the proton pump inhibitor omeprazole. After 4 weeks of therapy, gastrin levels increased to a median of 55 pg/ml compared to 15 pg/ml prior to omeprazole (P less than 0.001). There was a close correlation (r = 0.939; P less than 0.001) between pre-treatment gastrin and levels at 4 weeks. Comparison of serum gastrin concentrations at 1 month of omeprazole with levels at 6 (n = 21) and 12 months (n = 12) continuous therapy revealed a close correlation (r = 0.961 and r = 0.882, respectively; P less than 0.001) despite dose adjustment. In marked hypochlorhydria documented by continuous pH monitoring, serum gastrin varied from normal up to profound hypergastrinaemia. These results demonstrate that the serum gastrin increase under powerful acid-inhibitory drug therapy depends upon a number of variables. (a) Only in patients with elevated gastrin levels, prior to omeprazole treatment, can moderate to marked hypergastrinaemia during omeprazole be expected. (b) Gastrin increases reached during the initial period of omeprazole treatment remain constant during long-term therapy. (c) Acid inhibition itself is not necessarily associated with an increase in serum gastrin in every patient, which suggests that the individual sensitivity of the gastrin cell to acid inhibition is more important for serum gastrin changes than the degree of acid inhibition itself.

Topics: Esophagitis, Peptic; Gastric Acid; Gastrins; Humans; Omeprazole; Peptic Ulcer; Radioimmunoassay; Vagotomy

As in duodenal and gastric ulcer patients, a highly significant correlation between suppression of 24-h intragastric acidity and healing rates in reflux oesophagitis patients was demonstrated by meta-analysis of data obtained from the literature (r = 0.90; p less than 0.001). Furthermore, we have demonstrated in eight patients with reflux oesophagitis that 2-week treatment courses with 300 mg ranitidine twice daily and 300 mg four times daily progressively decreased 24-h intraoesophageal acidity but only moderately elevated basal and meal-stimulated serum gastrin concentrations, significantly below gastrin values obtained after a 2-week treatment course with 20mg omeprazole once daily. Further studies are awaited to demonstrate long-term effects on both healing rates and serum gastrin responses with high doses of histamine H2-receptor antagonists.

Topics: Adult; Aged; Esophagitis, Peptic; Female; Gastric Acid; Gastric Acidity Determination; Gastrins; Humans; Male; Middle Aged; Omeprazole; Ranitidine

A total of 36 patients with chronic gastric or oesophageal peptic ulceration (including 6 with antrectomy), resistant to high-dose ranitidine treatment for at least 3 months, were successfully treated with omeprazole 20-60 mg/day, for periods up to 3 years. Fasting serum gastrin levels were monitored at regular intervals during therapy and multiple gastric mucosal biopsies were taken during gastroscopy every 3-6 months. Gastrin levels increased significantly during the first 6 months of therapy from a mean of 81.5 to 206 pg/ml; a slight decrease was observed thereafter. There was no significant increase in the volume density of argyrophilic cells in the oxyntic mucosa. No clusters of endocrine cells were found in the oxyntic mucosa and no change of G-cell volume density occurred in the antral mucosa under therapy. Omeprazole therapy did not result in any changes in gastrin levels or oxyntic argyrophilic cells in the antrectomized patients. It is concluded that the moderate hypergastrinaemia observed during long-term omeprazole treatment in man does not induce hyperplasia of argyrophilic cells in the oxyntic mucosa.

Topics: Biopsy; Cell Count; Esophagitis, Peptic; Gastric Acid; Gastric Mucosa; Gastrins; Gastroscopy; Humans; Long-Term Care; Omeprazole; Stomach Ulcer

Twenty patients with gastroesophageal reflux disease (10 with compensated and 10 with decompensated gastroesophageal incompetence) were examined to determine if there was a correlation between the ability of physiological stimuli to tonicize the lower esophageal sphincter (LES) and the response to pentagastrin stimulation (Gastrodiagnost). The pressure of the lower esophageal sphincter as well as blood levels of the hormones/neurotransmitters gastrin, PP and VIP were determined after giving a 300 ml intragastral bolus of either 0.9% NaCl or 20% peptone solution. All patients exhibited per definitionem a positive common-cavity phenomenon on abdominal compression. Intravenous pentagastrin stimulated the LES in patients with compensated gastroesophageal incompetence (GI) but not in those with decompensated GI (p less than or equal to 0.0005). Esophagoscopy revealed a severe esophagitis in 80% of the patients with decompensated GI but in only 10% of the patients with compensated GI. Peptone stimulated the LES in patients with compensated GI (p less than or equal to 0.005) at 5, 10 and 15 minutes, pepton vs. NaCl). Neither NaCl nor peptone increased the tone of the LES in patients with decompensated GI. Peptone but not NaCl caused a significant increase of serum gastrin in all patients: there was no difference between the two groups. Neither NaCl nor peptone influenced VIP levels in peripheral blood. PP levels increased significantly in both groups following peptone. Physiological responsiveness of the LES can be inferred from the manometric data and the results of the pentagastrin test. A negative reaction to pentagastrin is associated with a loss of response to physiological stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Esophagitis, Peptic; Esophagogastric Junction; Esophagoscopy; Female; Gastric Acidity Determination; Gastrins; Gastroesophageal Reflux; Humans; Male; Manometry; Middle Aged; Pancreatic Polypeptide; Peptones; Vasoactive Intestinal Peptide

94 patients with peptic ulcerations of duodenum, stomach, and esophagus, who did not respond to 3 or more months high-dose (450 or 600 mg) treatment with ranitidine, were treated orally with 40 mg omeprazole daily. After healing all patients were offered long-term maintenance therapy with the same dose for 5 years. In 75 patients the peptic ulcerations healed within 4 weeks, in 13 patients within 8 weeks, and in 3 patients only after an increase to 60 mg omeprazole daily. In 3 patients the ulcers did not heal. So far 83 patients have entered long-term maintenance therapy. 59 of these patients are on the drug between 1 and 4 years. During maintenance therapy with 40 mg omeprazole no relapses have occurred up to now as demonstrated by endoscopy and no drug-related adverse effects were observed. Routine laboratory tests remained without significant changes in all patients including 18 patients with concomitant liver cirrhosis. Serum gastrin levels were already elevated during the initial high-dose ranitidine treatment (106 +/- 15.4 pg/ml). 4 weeks after the start of omeprazole treatment serum gastrin levels rose to 4 times normal levels (195 +/- 28 pg/ml). Thereafter, no further increase in serum gastrin was observed even up to 4 years of continuous observation. It is therefore concluded that omeprazole is highly effective in healing ranitidine-resistant peptic ulcerations and that omeprazole maintenance therapy with 40 mg omeprazole is safe during the time observed and highly effective in the prevention of ulcer recurrence.

Topics: Adult; Aged; Duodenal Ulcer; Esophagitis, Peptic; Female; Gastrins; Humans; Male; Middle Aged; Omeprazole; Ranitidine; Stomach Ulcer; Time Factors

Ambulatory oesophageal pH, oesophageal manometry and fasting serum gastrin concentrations were carried out on 28 patients with reflux oesophagitis, before and during treatment with ranitidine 300 mg bd. Fourteen patients healed endoscopically at six weeks (group A) and 14 had residual oesophagitis (group B). Group A were characterised by a lower serum gastrin concentration before treatment (4.52 pmol/l; 2.4-10: mean and range) than group B (11.1 pmol/l; 3.5-21: p less than 0.05) and showed a marked reduction in acid reflux on treatment to near normal values. Mean per cent time below pH4 fell from 14.9 to 4.2 in group A (p less than 0.05) but was not affected in group B (14.2-15.6, not significant). Abnormal oesophageal motility was found in 13 patients from each group. This did not inhibit the response to ranitidine, and was not improved by healing of oesophagitis.

Topics: Adolescent; Adult; Aged; Deglutition; Esophagitis, Peptic; Esophagus; Female; Gastrins; Gastrointestinal Motility; Humans; Hydrogen-Ion Concentration; Male; Manometry; Middle Aged; Peristalsis; Ranitidine

Under basal conditions serum gastrin concentration was compared with lower oesophageal sphincter pressure (pull-through perfusion manometry) and gastrooesophageal reflux (continuous pH measurements) in 72 patients. Between patients with low, middle and high basal gastrin level no differences were obtained for mean sphincter pressure. Mean reflux frequency and total reflux duration were increased significantly in patients with high gastrin level compared with patients with low gastrin level. Mean basal gastrin level was found to be higher in patients with symptoms of reflux than in patients without symptoms.

Topics: Esophagitis, Peptic; Female; Gastric Acidity Determination; Gastrins; Gastroesophageal Reflux; Humans; Male; Manometry; Pentagastrin

The effects on the oesophagus of an aromatic oil, guaiacol, has been examined in a group of 20 patients with reflux oesophagitis and also normal volunteers. This agent produced a rapid and sustained rise in resting lower oesophageal sphincter pressures and the peristaltic pressures induced in response to swallowing liquids. This compound may prove useful in the treatment of patients with reflux oesophagitis and other disorders of oesophageal motility.

Topics: Esophagitis, Peptic; Esophagus; Gastrins; Guaiacol; Humans; Peristalsis; Pressure

In a pancreatic adenoma approximately 78.7% of the endocrine cells reacted specifically with antisera to neurotensin, 17.5% to gastrin, 2.8% to pancreatic polypeptide, and 1% to glucagon. The electron microscope revealed that the majority of the endocrine cells were N-cells--morphologically similar to the ileal N-cells which are known to represent the neurotensin-producing cells. Neurotensin was extracted from the tumor and identified by Sephadex, ion-exchange, and high-pressure liquid chromatography. Gastrin, pancreatic polypeptide, and glucagon cells were also identified by the electron microscope; the peptides were extracted and demonstrated by chromatography. The serum concentrations of these hormones were elevated. After total gastrectomy which was necessary because of Zollinger-Ellison syndrome, a jejunoesophageal alkaline reflux, reaching the upper esophagus appeared. As intravenous infusion of synthetic neurotensin in rats caused an increase of luminal enteric pressure, it is suggested that severe jejunoesophageal reflux after gastrectomy may be a clinical feature of a neurotensinoma.

Topics: Adenoma; Adult; Esophagitis, Peptic; Gastrins; Glucagon; Histocytochemistry; Humans; Jejunal Diseases; Male; Neurotensin; Pancreatic Neoplasms; Pancreatic Polypeptide

Topics: Adult; Diagnosis, Differential; Esophageal Stenosis; Esophagitis, Peptic; Esophagoscopy; Gastrins; Humans; Male; Zollinger-Ellison Syndrome

Topics: Adolescent; Adult; Esophagitis, Peptic; Female; Gastrins; Humans; Male; Middle Aged

A 61-year-old man with a 20-year history of recurrent gastric peptic ulcerations had an adenocarcinoma of the esophagus resected. The carcinoma was associated with columnar cell-lined (Barrett's) esophagus with carcinoma in situ. The patient had hypergastrinemia (gastrin level, 1,000 pg/dl), and at autopsy two months after the operation, a 3-mm pancreatic adenoma was discovered. In addition to the rarity of this clinical constellation, the case is of interest in suggesting that hypergastrinemia does not protect against peptic esophagitis and its sequelae.

Topics: Adenocarcinoma; Esophageal Diseases; Esophageal Neoplasms; Esophagitis, Peptic; Gastrins; Humans; Male; Middle Aged; Zollinger-Ellison Syndrome

Topics: Adult; Duodenal Ulcer; Esophagitis, Peptic; Gastrins; Gastritis; Humans; Middle Aged

Topics: Duodenitis; Esophagitis, Peptic; Female; Gastrins; Gastritis; Humans; Male; Peptic Ulcer; Postgastrectomy Syndromes; Stomach Diseases; Stomach Neoplasms

New manometric techniques in for examining the lower oesophageal sphincter (LOS) were applied an investigation of the oesophago-gastric junction after partial gastric resection. Pressure and blood gastrin data are reported for eight cases examined before and after surgery, under basal conditions and after stimulation with a protein meal. It was found that gastric resection leads to a decrease in LOS performance (43.6% fall in maximum pressure) and length (-33.3%). There is also a 93.5% decrease in the pressure response to a protein meal, and hence a predisposition to gastroesophageal reflux.

Topics: Adult; Aged; Esophagitis, Peptic; Esophagogastric Junction; Gastrectomy; Gastrins; Gastroesophageal Reflux; Humans; Male; Manometry; Middle Aged; Pressure

Lower esophageal sphincter pressure, basal gastric pH, fasting plasma gastrin, and plasma concentrations of estrone, estradiol, and progesterone were measured in pregnant volunteers at 12, 24, and 36 weeks of gestation, and again at 1 to 4 weeks postpartum. In addition, basal and pentagastrin-stimulated acid secretory responses at each time were measured. No differences in basal gastric pH, basal, and peak acid outputs were observed during pregnancy when compared to the postpartum values. In contrast, lower esophageal sphincter pressure was reduced at all times during pregnancy, reaching a nadir at 36 weeks. Postpartum lower esophageal pressures were normal. As expected, plasma concentrations of progesterone and both estrogens increased progressively during pregnancy. These data are consistent with earlier studies in women ingesting oral contraceptives. Moreover, they provide support for the thesis that the progressive increase in plasma progesterone alone or in combination with estrogens that occurs during pregnancy is responsible for the reduction of lower esophageal sphincter pressure which allows esophageal reflux to occur with the resultant development of symptomatic heartburn.

Topics: Adolescent; Adult; Esophagitis, Peptic; Esophagogastric Junction; Estradiol; Estrone; Female; Gastrins; Heartburn; Humans; Hydrogen-Ion Concentration; Pregnancy; Pregnancy Complications; Pressure; Progesterone

Tissue gastrin was determined in 36 biopsies obtained from the esophagus and 35 biopsies from the stomach in 12 patients with Barrett's esophagus. Histology of the mucosa from the area adjacent to the biopsy sites was also examined. Esophageal biopsies were obtained from three different sites in each patient. The gastric biopsies were obtained from the antrum, fundus, and the area just distal to the lower border of the lower esophageal sphincter. The columnar mucosa lining the esophagus was of three distinct types, namely, fundic, transitional (cardiac), or specialized. None of these epithelia nor the squamous epithelium showed any detectable gastrin. In contrast, antral mucosa had very high gastrin content; smaller amounts of gastrin were detected in duodenal epithelium, whereas fundic mucosa sometimes contained small amounts of gastrin.

Topics: Adult; Aged; Biopsy; Esophageal Stenosis; Esophagitis, Peptic; Esophagus; Female; Gastric Mucosa; Gastrins; Hernia, Diaphragmatic; Humans; Male; Middle Aged; Mucous Membrane; Pyloric Antrum; Syndrome

Topics: Esophagitis, Peptic; Esophagogastric Junction; Esophagoscopy; Esophagus; Gastric Juice; Gastrins; Gastroesophageal Reflux; Humans; Hydrogen-Ion Concentration; Manometry; Muscle, Smooth; Muscles; Reflex

Four cases of Barrett's esophagus are presented. Three cases presented with significant esophageal bleeding and one case presented with high esophageal stricture. Gastrointestinal panendoscopy was done in each case and multiple biopsies were taken. The biopsies were utilized for histomorphology, pepsinogen agar gel electrophoresis, and tissue gastrin assays. Tissue gastrin levels in esophageal mucosa were elevated in 2 cases when compared to controls with and without hiatus hernia. Pepsin and acid secretory studies were done by isolating the esophagus. Barrett's esophagus was shown to produce pepsin by both chemical studies (2 cases) and agar gel electrophoresis at pH 5.7 (3 cases), and was also shown to produce acid. The mucosa contained either cathepsin or cathepsin and pepsinogens in all cases. Nissen's fundoplication was performed in all of the patients. Of 3 patients who were bleeding, 2 who consented for this operation stopped bleeding after the operation. It is to be noted that the usual clinical treatment of antacids, bedrest, and raising the head end of the bed failed in all of the patients. The follow-up of 9 months to 3 years postoperatively has shown persistence of Barrett's mucosa with no evidence for any reversion to normal esophageal type.

Topics: Electrophoresis, Agar Gel; Esophageal Stenosis; Esophagitis, Peptic; Esophagus; Female; Gastrins; Hernia, Diaphragmatic; Histocytochemistry; Humans; Male; Middle Aged; Mucous Membrane; Pepsin A; Pepsinogens

Findings in this study correlated a low circulating gastrin level with an incompetent lower esophageal sphincter mechanism and abnormal reflux. Such reflux, in amounts causing esophagitis distally, was treated surgically by a mechanically simple method of fundoplication. The success of this reefing method of fundoplication was explained by using physiologically active sling fibers of the gastric fundus to augment the lower esophageal sphincter. Available gastrin was used more effectively in this manner. The high incidence of associated foregut diseases suggested an embryologic factor in the development of gastroesophageal reflux. The dilated hiatus and its attendant hernia had no apparent relationship to the development of reflux esophagitis. The term symptomatic sliding hiatal hernia, therefore, seemed to be a diagnostic and therapeutic misnomer.

Topics: Adolescent; Adult; Aged; Duodenal Ulcer; Esophagitis, Peptic; Esophagogastric Junction; Female; Gastrins; Gastroesophageal Reflux; Hernia, Diaphragmatic; Hernia, Hiatal; Humans; Male; Manometry; Middle Aged; Muscle Tonus; Postoperative Complications; Suture Techniques; Vagotomy

The purpose of this study is to determine whether lower esophageal sphincter (LES) incompetency is a common occurrence in patients with liver cirrhosis and contributes to the development of variceal bleeding. Resting LES pressure (17.8 +/- 1.1 mm Hg) in 35 patients with cirrhosis was similar to that of our control population (17.3 +/- 2.0 mm Hg). No differences were found among patients with ascites, variceal hemorrhage, or with different degrees of hepatic decompensation. In both patients and control subjects the LES responded with a significant pressure increase to gastric alkalinization. Symptoms and radiological evidence of gastroesophageal reflux were extremely uncommon in patients with liver cirrhosis. Based on these data it is unlikely that acid-pepsin regurgitation is a significant factor in the development of variceal hemorrhage.

Topics: Adult; Aged; Ascites; Esophageal and Gastric Varices; Esophagitis, Peptic; Esophagogastric Junction; Gastric Acidity Determination; Gastrins; Gastroesophageal Reflux; Gastrointestinal Hemorrhage; Humans; Liver Cirrhosis; Liver Function Tests; Manometry; Middle Aged; Muscle Contraction

Topics: Anemia, Pernicious; Bicarbonates; Duodenal Ulcer; Endocrine System Diseases; Esophagitis, Peptic; Esophagus; Gastric Juice; Gastrins; Humans; Hyperplasia; Intestines; Kidney Failure, Chronic; Pancreas; Pheochromocytoma; Pyloric Antrum; Stomach; Stomach Neoplasms; Stomach Ulcer; Vagotomy; Zollinger-Ellison Syndrome

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