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

Although the standard operation for early cancer of gastric cardia is proximal gastrectomy followed by jejunal interposition, we recently reported a simple and useful technique for proximal gastrectomy with gastric tube reconstruction. The operative procedures included resection of the proximal two-thirds of the stomach, followed by anastomosis between the esophagus and gastric tube, using a circular stapler (Proximate ILS 25; Ethicon, Cincinnati, OH, USA). The gastric tube was about 20 cm long and 4 cm wide. The patient a 76-year-old man had no reflux symptoms such as heartburn, retrosternal pain, and regurgitation. Endoscopy showed no evidence of reflux esophagitis, including mucosal redness, erosion, and ulceration. Ambulatory 24-h pH monitoring indicated that the pH of the lower esophagus was between 6 and 8 when the patient was upright and between 5 and 7 when he was in the supine position. There were nine reflux episodes during the day, and no reflux episode while he was asleep. The duration of each reflux episode was less than 1 min, and the total reflux time was 1 min in the 12-h day (0.1%). These data indicate that reconstruction by gastric tube may prevent esophageal reflux in patients who have undergone proximal gastrectomy for early cancer of the gastric cardia.
Gastric Cancer 1998 Dec
PMID:Long-term survival after perforation of advanced gastric cancer: Case report and review of the literature. 1195 48

Helicobacter pylori (H. p.) causes active chronic antrum gastritis in all infected patients. In a relatively small percentage complications of H. p.-gastritis including duodenal ulcer, gastric ulcer, giant fold gastritis, lymphocytic gastritis, autoimmune gastritis, gastric carcinoma and gastric MALT lymphoma may develop. Strongly recommended indications for eradication therapy include gastroduodenal ulcer disease, giant fold gastritis, lymphocytic gastritis, autoimmune gastritis, gastric MALT lymphoma, atrophic gastritis, corpus-predominant gastritis, post gastric cancer resection and patients who are first degree relatives of gastric cancer patients. Eradication therapy is controversial in patients with gastroesophageal reflux disease, functional dyspepsia and in patients in whom treatment with nonsteroidal antiinflammatory drugs (NSAID) or long-term treatment with proton pump inhibitors (PPI) is planned.
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PMID:[Helicobacter pylori infection--clinical aspects and indications for treatment]. 1199 61

Helicobacter pylori is a gastric pathogen that is a major cause of peptic ulcer disease, has a role in mucosa-associated lymphoid tissue (MALT) lymphoma and is associated with gastric cancer. Yet, in a large proportion of the human population, H. pylori infection has no apparent adverse clinical consequences. Furthermore, recent research suggests that H. pylori may even confer protection against gastroesophageal reflux disease. The conflicting evidence surrounding H. pylori infection was discussed at a sponsored symposium in Helsinki, introduced by Professor P. Malfertheiner, with papers presented by Dr H. J. O'Connor, Professor R. M. Genta, Dr P. Unge and Professor A. T. R. Axon. Emerging epidemiological and retrospective evidence suggests that the presence of H. pylori infection may provide some protection against gastroesophageal reflux disease, but there is other evidence that shows no benefit of H. pylori for the protection of the oesophagus. It was felt that prospective, multicentre studies are needed to explore the H. pylori-gastroesophageal disease relationship further, to avoid confusing potential benefits with known risks. Following the symposium, a discussion on the relative risks and benefits for H. pylori eradication was provided by Professor Axon and Professor Blaser. Eradication of H. pylori has been recommended in a series of management guidelines issued by consensus groups. However, accurate estimates of the relative risks and benefits of H. pylori infection in the general population, as well as in specific patient groups, is essential in order to develop a management strategy.
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PMID:Symposium: Helicobacter pylori and clinical risks--focus on gastro-oesophageal reflux disease. 1200 Mar 12

Treatment recommendations for H. pylori infection are peptic ulcer disease, MALT lymphoma, atrophic gastritis and following gastric cancer resection as well as first degree relatives of gastric cancer patients. Advisable situations are functional dyspepsia, before introduction of NSAID's or intended long-term proton-pump inhibitor treatment. It is thought that eradication therapy is not associated with gastro-esophageal reflux disease and does not enhance NSAID induced peptic ulcer healing. Therapy should be given as a package which considers first and second line eradication therapies together; in uncomplicated duodenal ulcer patients, eradication therapy does not need to be followed by further antisecretory treatment. First line therapy should be with triple therapy using a proton pump inhibitor (PPI), combined with clarithromycin and amoxycilline or metronidazole. Second-line therapy should use a quadruple therapy with a PPI, bismuth, metronidazole and tetracycline. Where bismuth is not available, second line therapy should be with a PPI triple therapy. If second line quadruple therapy fails in primary care, patients should be referred to the specialist and handled on a case by case basis. Successful eradication should always be confirmed by urea breath test (UBT), or endoscopy-based tests if endoscopy is clinically indicated. Stool antigen test is the alternative if UBT is not available. A 'test and treat' approach based on non-invasive testing can be offered to adult patients presenting in primary care with persistent dyspepsia under the age of 45 years (the age cut-off may vary locally), having excluded those with predominantly gastroesophageal reflux disease (GERD) symptoms, NSAID users, and patients with alarm symptoms.
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PMID:[Helicobacter pylori--2002]. 1207 Oct 78

Gastric carcinoma is thought to develop via the actions of inducers and promoters of carcinogenesis. Tryptophan in charred fish or animal meat, ultraviolet rays, and irradiation, which damage genes of normal cells, have long been regarded as inducers of carcinoma, and agents such as alcohol, tobacco, aflatoxin, and nitrosoamine as promoters, with tobacco having both activities. The interaction between these environmental factors, principally diet, and Helicobacter pylori (Hp) is important in the genesis of gastric carcinoma. In this report, the histopathological feature of the Hp gastritis-carcinoma sequence is outlined, and the pathological characteristics of gastroesophageal reflux disease (GERD) and endoscopically negative reflux disease (ENRD) and the risk factors for lower esophageal carcinoma after Hp eradicated status in particular are discussed regarding aspects of cell cycle-associated factors. We conclude that (1) Infection with Hp increases the risk of gastric cancer in two histological phenotypes (i.e., diffuse undifferentiated type and intestinal differentiated type). Excessive cell replication and interrupting the mucus secretion mechanism may result in a large proportion of cells with genetic abnormalities. (2) Genetic alterations in gastric carcinogenesis may differ from those in colonic carcinogenesis. (3) The degree of GERD in Japanese patients is milder than that in patients from Western countries, although the incidence of GERD increases the status after successful eradication of Hp. It is also possible that accumulation of genetic abnormalities increases the number of cardiac and lower esophageal cancers. Investigation of cell cycle factors in GERD including ENRD can be expected to reveal the risk of carcinogenesis.
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PMID:Pathological issues of gastric and lower esophageal cancer: helicobacter pylori infection and its eradication. 1210 62

Since 1990, laparoscopic surgery for gastrointestinal disease has been accepted worldwide because it is minimally invasive, associated with less pain, and results in early recovery. For the surgical management of gastroesophageal reflux and perforated peptic ulcer, laparoscopic procedures are recognized as the standard. Laparoscopic gastrectomies for cancer have developed since 1991. Laparoscopic wedge resection and intragastric mucosal resection are performed for the treatment of early gastric cancer without the risk of lymph node metastasis. For early gastric cancer with the risk of perigastric lymph node metastasis, laparoscopy-assisted Billroth-I gastrectomy with D1 lymph node dissection has been successfully performed. Thus, laparoscopic approaches play an important role in the management of gastroduodenal disease.
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PMID:[Laparoscopic surgery for gastroduodenal disease]. 1241 41

Helicobacter pylori infection has been recognized as the most important pathogenetic principal of peptic ulcer disease, atrophic gastritis, gastric adenocarcinoma and MALT lymphoma. At the moment efforts are made to clarify it's role in functional dyspepsia, and gastro-esophageal reflux disease. The complex interactions between H. pylori infection and NSAIDs is another field of ongoing research. Diagnosis and eradication therapy are standardized. Established indications are peptic ulcer disease, low-grade gastric MALT lymphoma, early gastric cancer treated by mucosal resection and partial gastrectomy for gastric cancer. Atrophic gastritis, known to be a precancerous lesion, as well as first degree relatives of patients with gastric cancer is another widely accepted indication for eradication therapy. The recommended eradication regimens combine a proton pump inhibitor with clarithromycin and either amoxicillin or metronidazole--for a week.
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PMID:[Helicobacter pylori. Update 2002]. 1250 73

The falling prevalence of Helicobacter pylori infection and related diseases (peptic ulcer disease, gastric cancer) in developed countries has been paralleled by an increased recognition of gastro-oesophageal reflux and its complications. These epidemiological data do not support a role for H. pylori in the pathogenesis of reflux disease, but suggest a negative association with the increasing incidence of oesophageal diseases. This has led some investigators to propose a 'protective' role of H. pylori infection against the development of oesophageal diseases. In these patients, pre-existing lower oesophageal sphincter dysfunction, susceptibility to reflux, unmasking of latent reflux and the patterns and severity of gastritis are probably important factors contributing to the development of oesophageal diseases. The most likely mechanism by which H. pylori infection may protect against reflux is by decreasing the potency of the gastric refluxate in patients with corpus-predominant gastritis. The prevalence of H. pylori infection in patients with reflux disease is probably no greater than that in those without reflux, and there are conflicting data indicating that reflux symptoms or erosive oesophagitis develop after H. pylori eradication. It is also unclear whether H. pylori augments the antisecretory effects of proton pump inhibitors or accelerates the development of atrophic gastritis.
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PMID:Review article: Helicobacter pylori and reflux disease. 1256 42

Helicobacter Pylori infection has been identified as a pathogenic factor in a number of gastroduodenal diseases, most importantly in gastric and duodenal ulcer disease. This association and the development of H. PYLORI eradication therapies has had a tremendous influence on the surgical therapy for these disorders. Decades ago, surgery was the therapy of choice for gastric and duodenal ulcers. Now, however, the first line of therapy includes treatment of H. PYLORI infection, suppression of gastric acid secretion, and protection of gastric mucosal barriers combined with a range of endoscopic procedures. These developments have had a major impact on the indications for surgery in benign gastroduodenal diseases. In addition, advances in our understanding of the pathogenetic mechanisms of H. PYLORI infection have also changed our views of gastric mucosa-associated lymphoid tissue lymphoma, gastric cancer, and gastroesophageal reflux disease.
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PMID:How Helicobacter Pylori changed the life of surgeons. 1268 75

The relationships between Helicobacter pylori (H. pylori)and gastroesophageal reflux disease (GERD) remain controversial. Epidemiological studies do not support an important role of H. pylori in the pathogenesis of GERD although some studies showing a low prevalence of the infection in GERD patients suggest that it could protect against the development of either symptoms or esophagitis. This hypothesis has been reinforced by the increased prevalence of esophagitis following H. pylori eradication in duodenal ulcer patients, although conflicting results have been reported. An increased gastric acid secretion following H. pylori eradication in patients who previously had corpus gastritis may explain this phenomenon. H. pylori eradication does not exacerbate GERD symptoms and may, in some cases, improve them. H. pylori-associated gastritis enhances the efficacy of antisecretory drugs as evidenced by the lower gastric pH values after eradication; however, as far as healing rates and symptom relief are concerned, the differences are probably not clinically relevant. Long term treatment with proton pump inhibitors could accelerate the development of atrophic gastritis, and therefore increase the risk of gastric cancer. However, conflicting results have been reported, so that further studies are needed before considering eradication of H. pylori systematically before long-term medical treatment for GERD.
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PMID:[Does H. pylori infection or its eradication play a role in gastroeosphageal reflux disease?]. 1270 Apr 99


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