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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acid-related disorders such as gastric and duodenal ulcers and gastro-oesophageal reflux disease have a high prevalence. Traditionally, acid suppression has proved to be the most effective means by which to heal these disorders, but relapse rates are high after cessation of treatment. Recently, Helicobacter pylori infection has been shown to modify several aspects of gastric function. Eradication of H. pylori infection virtually abolishes duodenal ulcer recurrence, implicating this organism in the pathogenesis of peptic ulcers and initiating a whole new strategy in the management of these acid-related disorders. More potent degrees of acid suppression result in faster healing. Moderate acid suppression, as occurs with H2-receptor antagonists, can heal just as many ulcers if treatment is continued for longer. The combination of proton pump inhibitors and antibiotics have successfully eradicated H. pylori in duodenal ulcer patients. Both H2-receptor antagonists and the proton pump inhibitors have satisfactory safety profiles. Due to their superiority in symptom relief, and in the healing of duodenal and gastric ulcers and erosive oesophagitis, and due to their ability to eradicate H. pylori infection in combination with antibiotics, the proton pump inhibitors will probably become accepted as first-line therapy for the treatment of acid-related diseases.
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PMID:The rationale of acid suppression in the treatment of acid-related disease. 791 47

Gastric acid is involved in the pathogenesis of duodenal ulcer, gastric ulcer and gastro-oesophageal reflux disease. Although levels of acid secretion may not be abnormally high in patients with these conditions, pharmacological suppression of acid secretion is associated with healing of mucosal defects and maintenance of healing in the long term. In the case of duodenal ulcer, this was demonstrated before the understanding of the importance of Helicobacter pylori infection. There is a considerable body of published work examining the pharmacological effectiveness of antisecretory drugs in suppressing gastric acid secretion, as well as their therapeutic efficacy in terms of healing ulcers or oesophageal erosions. These two parameters have been significantly correlated in each of the three conditions listed above. The purpose of this article is to review the mathematical relationships established between suppression of gastric acid secretion and healing rates of duodenal ulcer, gastric ulcer and gastro-oesophageal reflux disease.
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PMID:Appropriate acid suppression in the treatment of acid-related conditions. 797 43

In a prospective evaluation of the relationship between Helicobacter pylori infection and gastro-oesophageal reflux disease (GORD), 93 consecutive patients (47 female: 46 male: mean age, 46 years: range 13-93) with symptoms and endoscopic evidence of GORD were studied. A total of 50 patients (54%) were H. pylori-positive on gastric antral biopsies. No significant correlation was detected between H. pylori status and grade of oesophagitis. The prevalence of H. pylori infection showed a gradual increase with age. Of 64 patients with a hiatal hernia, 28 (44%) had histological evidence of H. pylori infection of the hernia mucosa; 27 of these patients (96%) had associated H. pylori in the gastric antrum. Of the 36 patients whose hiatal hernia was H. pylori-negative, only 6 (17%) had antral H. pylori (P < 0.001). Of the 8 patients found to have Barrett's oesophagus, only 1 had H. pylori detected on the Barrett's mucosa. Our results do not support the presence of a significant association between H. pylori infection and GORD.
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PMID:Helicobacter pylori and gastro-oesophageal reflux disease--a prospective study. 800 62

Functional dyspepsia covers various symptoms associated by the physician with the upper gastrointestinal tract without an identifiable organic cause. The existence of dyspepsia subgroups according to different symptom complexes, e.g. so-called "ulcer-like dyspepsia", has not been proved. Gastro-esophageal reflux disease is a distinguishable independent entity. Little is known about the pathogenesis of this common syndrome. Disturbances of gastric motility, especially postprandial antral hypomotility, are found in 50% of these patients but offer no explanation of the dyspeptic symptoms. Neither abnormal gastric acid secretion nor abnormal acid sensitivity has been proved in these patients. Furthermore, no relation between the symptoms and a Helicobacter pylori infection or a functional disturbance of the biliary tract has been established. In some cases fatty foods can provoke dyspeptic symptoms. Unfavorable psychosocial factors can influence the decision to consult a physician for dyspepsia. Recently, a lowered threshold of perception of stomach and small intestine distension in dyspepsia has been demonstrated. This disturbance of perception offers a new basis for further understanding and for possible treatment. Prokinetic agents can be of help in the treatment of functional dyspepsia. H2-receptor antagonists are most effective in patients presenting symptoms of gastro-esophageal reflux disease. Empiric therapeutic trials in this disease entity, which shows a high placebo response rate (between 30% and 60%), are not of proven value.
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PMID:[Functional dyspepsia. Old wine in new bottles?]. 815 99

Thirty-three consecutive patients with idiopathic gastric acid hypersecretion (defined as a basal acid output > 10.0 meq/hr with a normal fasting serum gastrin level and negative secretin stimulation test) who were being treated for duodenal ulcer disease and other acid-peptic disorders were evaluated for the presence of Helicobacter pylori by means of a rapid urease test. Fourteen patients had duodenal ulcer and 19 had other acid-peptic disorders (gastroesophageal reflux in 14, including six with Barrett's esophagus; four with nonulcer dyspepsia; and one with erosive gastritis). Helicobacter pylori was present in 12 of the 14 ulcer patients (86%) compared to only two of the 19 nonulcer patients (11%) (P < 0.0001). The distribution of basal acid output for patients with duodenal ulcer was similar to that for nonulcer patients, and no significant difference in the mean basal acid output was found among Helicobacter pylori-positive compared to Helicobacter pylori-negative patients. Seven of the duodenal ulcer patients with a basal acid output greater than 15.0 meq/hr were Helicobacter pylori-positive, suggesting that the organism can withstand even extreme levels of gastric acidity. In conclusion, this study demonstrates that the prevalence of Helicobacter pylori infection in patients with duodenal ulcer disease associated with idiopathic gastric acid hypersecretion is not different from a majority of ulcer patients with normal acid secretory profiles and offers additional evidence that extreme levels of gastric acid are not bactericidal for the organism.
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PMID:Helicobacter pylori in duodenal ulcer patients with idiopathic gastric acid hypersecretion. 842 Jul 45

This article outlines the clinical management of common gastrointestinal disorders encountered in the primary care setting. The general assessment of a woman presenting with a gastrointestinal concern is reviewed. Diagnosis and management of acute and chronic diarrhea, constipation, irritable bowel syndrome, and anorectal disorders are covered with emphasis on client education. Gastroesophageal reflux disease and peptic ulcer disease is discussed with the latest treatment recommendations for Helicobacter pylori infection outlined. Diagnosis of gallbladder disease and gallstones with alternative treatment options is reviewed. Finally, the diagnosis and management of viral hepatitis is outlined. A case study is given to illustrate the basic principles needed by the nurse-midwife in the assessment, diagnosis, and management of a woman with a gastrointestinal concern.
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PMID:Primary care for women. Management and treatment of gastrointestinal disorders. 869 Dec 76

Acid peptic disorders, including gastric ulcers, duodenal ulcers, and gastroesophageal reflux disease, are commonly occurring conditions with high direct and indirect costs. The pathogenesis of these disorders involves an imbalance between acid secretion and gastric mucosal defenses. Pharmacologic treatment of acid peptic disorders has focused on correcting this imbalance by either improving mucosal defenses with drugs such as sucralfate, bismuth, and prostaglandin analogs, neutralizing acid with antacids, or decreasing acid secretion with histamine2 (H2)-receptor antagonists, or, more recently, proton pump inhibitors. Proton pump inhibitors are more potent inhibitors of acid secretion than H2-receptor antagonists. In clinical comparisons, proton pump inhibitors were shown to be more effective in the treatment of acid peptic disorders than H2-receptor antagonists. Helicobacter pylori infection is a factor in 85% to 100% of duodenal ulcers and 70% to 90% of gastric ulcers; eradicating this organism results in a considerable decrease in the recurrence of ulcers. Current management of peptic ulcer disease includes the use of combination antisecretory and antibiotic therapy for acute treatment of H pylori-associated disease. Patient self-medication with over-the-counter products, including H2-receptor antagonists, may have an impact on the potential for reducing the recurrence of peptic ulcer disease in patients with H pylori infection. Patients with recurrent disease should be informed of the need to seek medical treatment through aggressive education at the point of sale for over-the-counter drugs.
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PMID:Pathogenesis and treatment of acid peptic disorders: comparison of proton pump inhibitors with other antiulcer agents. 885 51

In a prospective study of consecutive patients with reflux esophagitis and/or hiatal hernia and Barrett's esophagus, the prevalence of Helicobacter pylori was assessed. Antral biopsy specimens were studied and a serum sample for detection of IgG antibodies against Helicobacter pylori was taken. As a reference group patients presenting with a normal esophagus, stomach, and duodenum were taken. Reflux esophagitis was diagnosed in 118 patients, hiatal hernia without esophageal inflammation in 109, and Barrett's esophagus in 13. Helicobacter pylori was present in 74 (30%) of these patients and in 204 (51%) of the reference group. Prevalence of Helicobacter pylori was significantly lower in all groups compared with the reference group (P < 0.001). There was no difference when patients with esophagitis, Barrett's esophagus, or hiatal hernia were compared. Patients with esophagitis and Helicobacter pylori in their antrum are significantly older than esophagitis patients without concomitant Helicobacter infection, 61.5 (SD, 17) versus 53 (SD, 17) years (P < 0.001). It is concluded that the prevalence of Helicobacter pylori infection in patients with gastroesophageal reflux disease is significantly lower than in the reference group, irrespective of the severity of esophagitis. Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis.
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PMID:Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis. 900 23

A prospective study was performed in 190 control subjects and in 236 patients with different degrees of endoscopic esophagitis in order to determine the prevalence of Helicobacter pylori infection at duodenal gastric and esophageal mucosa and its correlation with histological findings. All patients with pathologic gastroesophageal reflux had 24-h pH monitoring studies confirming the presence of acid reflux into the esophagus. Besides the endoscopic findings, biopsies were taken from the duodenal bulb, gastric antrum, gastric fundus and distal esophagus or at the specialized columnar epithelium in patients with Barrett's esophagus. Patients with pathological gastroesophageal reflux were divided into three groups: 55 with absence of endoscopic esophagitis (gastroesophageal reflux), 81 patients with erosive esophagitis and 100 patients with Barrett's esophagus. There was no H. pylori infection present at duodenal or esophageal mucosa or at the specialized columnar epithelium of the distal esophagus in any case. The prevalence of H. pylori infection at gastric antrum was similar in controls and in any group of patients with reflux disease (20-25% of H. pylori infection). No differences in age and sex distribution were seen. H. pylori infection at gastric fundus was very low (less than 5%). The presence of HP infections was correlated with the finding of chronic active superficial or athrophic gastritis while, in the absence of H. pylori infection, gastric mucosa was normal. In the presence of intestinal metaplasia, no H. pylori infection occurred. Based on these findings, it seems that there is no significant evidence for an important pathogenic role for H. pylori infection in the development of pathologic chronic gastroesophageal reflux, erosive esophagitis or Barrett's esophagus, and the presence of antral gastritis in patients with Barrett's esophagus is closely related to the presence of H. pylori infection, and probably not related to an increased duodenogastric reflux.
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PMID:Prevalence of Helicobacter pylori infection in 190 control subjects and in 236 patients with gastroesophageal reflux, erosive esophagitis or Barrett's esophagus. 907 72

To investigate the prevalence and the significance of Helicobacter pylori duodenal colonization, endoscopic duodenal biopsies were performed in 168 children with chronic abdominal pain, gastroesophageal reflux, gastrointestinal bleeding, and malabsorption syndrome. Helicobacter pylori infection was detected in 68 children (40.4%): in 31 of them H. pylori was present in the gastric antrum, and in 37 in the duodenum also. Duodenitis was observed in 25 children with duodenal H. pylori; gastric metaplasia in 3. Scanning electron microscopy revealed the presence of the micro-organism in 3/13 cases; the bacteria were located in the intercellular spaces and alterations of the epithelial surface were found. In conclusion, H. pylori gastritis in children is often associated with duodenal colonization which can cause duodenitis, and also without gastric metaplasia, which indicates a possible role of the micro-organism in the pathogenesis of the lesions.
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PMID:Helicobacter pylori duodenal colonization in children. 917 19


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