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

The precise mechanisms that cause gastroesophageal reflux after distal gastrectomy remain unclear. We analyzed the endoscopic findings of the cardia and the position of the remnant stomach, which are related to gastroesophageal reflux. We retrospectively examined the records of 45 patients with Billroth I (B-I) and 39 patients with Roux-en-Y (R-Y) procedure for gastric cancer. Esophagitis was evaluated by the Los Angeles (LA) classification. The endoscopic findings of hiatus hernia were classified according to the criteria of the Keio Cancer Detection Center form (K-form). The valvular appearance of the cardia was classified according to V-grades. The height of the remnant stomach was measured on computed tomography scans. The postoperative findings of esophagitis in the B-I group were significantly worse than the preoperative findings, but no significant change was observed in the R-Y group. The postoperative V-grades and K-forrn findings in the B-I group were worse than their preoperative findings. In the R-Y group, however, there was no significant change in the V-grades or K-form findings. In addition, the height of the remnant stomach was significantly higher in the B-I group than in the R-Y group. This study suggested that an aggravated cardia is associated with the B-I procedure and that the position of the remnant stomach may therefore play an important role in the occurrence of postoperative reflux esophagitis. In contrast, the R-Y operation was shown to preserve the cardia and the position of the remnant stomach better. As a result, R-Y might help prevent not only duodenogastric reflux but also gastroesophageal reflux.
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PMID:Morphologic analysis of gastroesophageal reflux diseases in patients after distal gastrectomy. 1559 45

Gastric cancer has been declining for more than half a century, whereas the incidence of oesophageal cancer is increasing rapidly. The histopathological subtype is also changing with a predominance of oesophageal adenocarcinoma compared with squamous carcinoma. The reasons for these epidemiological changes are not clear, although population-based data have implicated gastro-oesophageal reflux disease as a risk factor. In susceptible individuals reflux of duodeno-gastric contents can lead to the development of a columnar-lined oesophagus, commonly called Barrett's oesophagus. This can then progress to adenocarcinoma via a metaplasia-dysplasia-carcinoma sequence. At the current time, the mortality from oesophageal adenocarcinoma exceeds 80% at 5 years. Therefore, endoscopic surveillance programmes have been generally recommended for patients with Barrett's oesophagus in an attempt to detect early, curable lesions. Unfortunately these programmes are cumbersome and costly and have not yet been proved to reduce population mortality. In order to improve patient outcomes we need to be able to identify patients at high risk and to understand the triggers for disease progression. There is mounting evidence that there is an underlying genetic susceptibility to Barrett's oesophagus and oesophageal adenocarcinoma. However, this is likely to be as a result of multiple low penetrance susceptibility genes which have yet to be identified. Once patients are identified as having Barrett's oesophagus their chance for developing adenocarcinoma is in the order of 0.5%-1% per year. The histological assessment of dysplasia as a predictor of cancer development is highly subjective. Therefore multiple, specific somatic mutations in the tissue have been investigated as potential biomarkers. The most promising markers to date are the presence of aneuploidy, loss of heterozygosity of p53 and cyclin D1 overexpression. However, a study of evolutionary relationships suggest that mutations occur in no obligate order. Combinatorial approaches are therefore being advocated which include genomic profiling or the use of a panel of molecular markers in order to define the common molecular signatures that can then be used to predict malignant progression. An alternative approach would be to use markers for the final common pathway following genetic instability, which is the loss of proliferative control. We have demonstrated an increase in the expression of a novel proliferation marker, Mcm2, which occurs during the malignant progression of Barrett's oesophagus. These Mcm2-expressing cells are detectable on the surface, and hence a cytological approach may be applicable. In view of the role of reflux components in the pathogenesis of Barrett's oesophagus the effect of acid and bile on the cell phenotype have been studied. These studies have demonstrated that pulsatile acid and bile exposure induce cell proliferation. The mechanism for the hyperproliferative response appears to involve p38 mitogen activated protein kinase (MAPK) pathways as well as protein kinase C (PKC) and cyclo-oxygenases. A clinical implication of the laboratory studies is that suppression of acid and bile may need to be profound in order to suppress cell proliferation and, by inference, ultimately prevent the development of dysplasia. There is some support for this concept from short-term clinical studies, and a large randomised chemoprevention trial is being instigated which will evaluate the effect of proton pump inhibitors with or without aspirin. Given the epidemic increase in oesophageal adenocarcinoma and the dismal 5-year mortality rate, a radical approach is necessary to prevent cancer development in individuals with pre-malignant lesions.
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PMID:Genetics and prevention of oesophageal adenocarcinoma. 1564 81

Peptic ulcer disease has been still very actual topic as 10% of western population would fell ill during its life. Substantial changes in understanding of etiopathogenesis were achieved within last hundred years. The first milestone means development of gastric physiology (gastric secretion, histamine, gastrin, cyclo-oxygenase, H2-receptors, proton pump). There is no doubt peptic ulcer is a typically human disease with involvement of the cortico-visceral axis and psychosomatic traits. Others factors play their role in the etiopathogenesis (like genetic, ethnic, environmental and socio-economic factors). However, main etiologic factors are Helicobacter pylori (approximately 90% duodenal and 50% gastric ulcers) and non-steroidal anti-inflammatory drugs (approximately 30% gastric and 10% duodenal ulcers). Diagnostics were determined by technical progress most of all by the construction of flexible digestive endoscopes into clinical practice. Surgery has been step by step replaced by pharmacotherapy (H2-receptor antagonists, proton pump inhibitors, Helicobacter pylori eradication). In near future we can expect further decrease in prevalence of peptic ulcer disease and gastric cancer in developed countries and increase in gastro-oesophageal reflux disease. Let us hope that current controversies in indication of eradication therapy will be overcome by vaccination against Helicobacter pylori.
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PMID:[Gastric and duodenal ulcers--etiopathogenesis, diagnosis and therapy at the milestone of the 20th century]. 1565 Nov 49

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: reasons for eradication]. 1567 64

Over time the relative distribution of cancers of the proximal digestive tract has changed. Squamous cell carcinomas of the esophagus have become less common, while numbers of adenocarcinomas have greatly increased. This shift most likely reflects an increase in the incidence of gastroesophageal reflux. Moreover, there is a decline in the incidence of distal gastric cancer, which in turn may be related to Heliobacter pylori eradication. Simultaneously, there is a time trend toward a more proximal localization of gastric cancer. If the above-mentioned etiopathologic links are correct, this could indicate that the so-called cardia adenocarcinomas are not related to H pylori infection and that they may instead be related to gastroesophageal reflux and eventually may not be considered to be "gastric" cancers. The rapidly growing quantity of literature on this subject is, however, confounding. A major source of discordance would seem to be a Babylonian confusion of tongues concerning the terms cardia and cardiac carcinomas. Unfortunately, this confusion is also apparent in the classification systems available for staging of cancer, thus closing the "vicious" circle.
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PMID:Is adenocarcinoma of the esophagogastric junction or cardia different from Barrett adenocarcinoma? 1567 17

Several epidemiological data indicate that H. pylori infection prevalence in patients with gastroesophageal reflux disease (GERD) is lower than that reported in respective controls, which would suggest that the organism plays a protective role against this disease. On the other hand, most studies demonstrate that the presence of the infection in patients with GERD does not negatively affect the therapeutic efficacy of proton pump inhibitors (PPIs), and, in case of negatively influencing it, the effects are not clinically relevant and are easily controllable with standard antisecretory treatment. Therefore, the decision to administer H. pylori eradication treatment to a patient should not be influenced by the concomitant presence of GERD. In most cases, H. pylori eradication does not seem to induce GERD development, and it does not seem to worsen GERD when it was already present. Nevertheless, when the gastritis pattern is unknown before the antibiotic administration, the effect of H. pylori eradication on gastric acid secretion and the incidence of GERD is unpredictable. In the exceptional cases in which H. pylori eradication could have negative effects on GERD, its clinical relevance will be limited, and reflux symptoms or endoscopic esophagitis will favourably respond to the standard PPI antisecretory treatment. Therefore, again, when H. pylori eradication is indicated in a particular patient, the concomitant diagnosis of GERD should not change our attitude. Finally, is has recently been recommended to eradicate H. pylori infection in those patients with GERD needing long-term treatment with PPI, as some studies have reported that these drugs induce, in presence of the organism, an atrophic gastritis, with the consequent risk of gastric cancer. However, most of these studies have important methodological defects, and several authors have reported contrary results. In any case, the appearance in the gastric mucosa of clinically relevant lesions, such as intestinal metaplasia, dysplasia or adenocarcinoma, in patients treated with PPI for several years, has not yet been demonstrated, although this could simply be a problem of time. This question seems to be too controversial to be answered with the available data, and we should wait until new studies clarify this topic. In the meantime, as it occurs with any controversial indication, the decision of the doctor facing a patient infected by H. pylori and needing maintenance therapy with PPIs should be assessed on a case by case basis.
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PMID:[Indications and consequences of Helicobacter pylori eradication on gastroesophageal reflux disease]. 1589 66

As an update to previously published recommendations for the management of Helicobacter pylori infection, an evidence-based appraisal of 14 topics was undertaken in a consensus conference sponsored by the Canadian Helicobacter Study Group. The goal was to update guidelines based on the best available evidence using an established and uniform methodology to address and formulate recommendations for each topic. The degree of consensus for each recommendation is also presented. The clinical issues addressed and recommendations made were: population-based screening for H. pylori in asymptomatic children to prevent gastric cancer is not warranted; testing for H. pylori in children should be considered if there is a family history of gastric cancer; the goal of diagnostic interventions should be to determine the cause of presenting gastrointestinal symptoms and not the presence of H. pylori infection; recurrent abdominal pain of childhood is not an indication to test for H. pylori infection; H. pylori testing is not required in patients with newly diagnosed gastroesophageal reflux disease; H. pylori testing may be considered before the use of long-term proton pump inhibitor therapy; testing for H. pylori infection should be considered in children with refractory iron deficiency anemia when no other cause has been found; when investigation of pediatric patients with persistent or severe upper abdominal symptoms is indicated, upper endoscopy with biopsy is the investigation of choice; the 13C-urea breath test is currently the best noninvasive diagnostic test for H. pylori infection in children; there is currently insufficient evidence to recommend stool antigen tests as acceptable diagnostic tools for H. pylori infection; serological antibody tests are not recommended as diagnostic tools for H. pylori infection in children; first-line therapy for H. pylori infection in children is a twice-daily, triple-drug regimen comprised of a proton pump inhibitor plus two antibiotics (clarithromycin plus amoxicillin or metronidazole); the optimal treatment period for H. pylori infection in children is 14 days; and H. pylori culture and antibiotic sensitivity testing should be made available to monitor population antibiotic resistance and manage treatment failures.
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PMID:Canadian Helicobacter Study Group Consensus Conference: Update on the approach to Helicobacter pylori infection in children and adolescents--an evidence-based evaluation. 1601 Mar

Epidemiological studies demonstrate a negative association between Helicobacter pylori infection and gastro-oesophageal reflux disease and its complications. This might represent a protective effect because of the tendency for H. pylori infection to lower gastric acid secretion with advancing age. However, studies of the effect of H. pylori eradication on gastro-oesophageal reflux disease have failed to show any worsening of gastro-oesophageal reflux disease symptoms. Several interactions between H. pylori and proton-pump inhibitor therapy used to treat gastro-oesophageal reflux disease need to be considered. Helicobacter pylori infection improves the control of gastric acidity by proton-pump inhibitors and this produces a small advantage in clinical control of reflux disease. The infection prevents rebound acid hypersecretion occurring when proton-pump inhibitor therapy is discontinued. However, concerns have been expressed that the body gastritis induced by proton-pump inhibitor therapy in H. pylori-infected subjects might increase the risk of gastric cancer. At present, it is unclear whether H. pylori should be eradicated in gastro-oesophageal reflux disease patients.
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PMID:Review article: Helicobacter pylori and gastro-oesophageal reflux disease. 1604 57

Helicobacter pylori is a common gastric infection that causes serious complications in a minority of individuals. A great deal is known about the disease, but many unanswered questions remain. Among these, perhaps the most enigmatic is that we do not know how the organism is transmitted. We are uncertain why the prevalence of the disease is falling within the developed population. There is still debate as to its relationship with gastroesophageal reflux disease. It is unclear why there are differences in the international incidence of gastric cancer. Similar uncertainties relate to the reasons why the complications of H. pylori infection have changed over time. In this article, I have hypothesized that a number of these unanswered questions may be related to a putative increase in gastric acid secretion that may have taken place during the past 200 years. To date, there is little confirmatory evidence for this, and it remains a fascinating area that merits more scientific research.
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PMID:Helicobacter pylori: what do we still need to know? 1634 Jun 27

Carbonated soft drinks (CSDs) have been associated with gastroesophageal reflux, an established risk factor for esophageal adenocarcinoma. As both CSD consumption and esophageal adenocarcinoma incidence have sharply increased in recent decades, we examined CSD as a risk factor for esophageal and gastric cancers in a U.S. multicenter, population-based case-control study. Associations between CSD intake and risk were estimated by adjusted odds ratios (ORs), comparing the highest versus lowest quartiles of intake. All statistical tests were two-sided. Contrary to the proposed hypothesis, CSD consumption was inversely associated with esophageal adenocarcinoma risk (highest versus lowest quartiles, OR = 0.47, 95% confidence interval = 0.29 to 0.76; Ptrend = .005), due primarily to intake of diet CSD. High CSD consumption did not increase risk of any esophageal or gastric cancer subtype in men or women or when analyses were restricted to nonproxy interviews. These findings indicate that CSD consumption (especially diet CSD) is inversely associated with risk of esophageal adenocarcinoma, and thus it is not likely to have contributed to the rising incidence rates.
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PMID:Carbonated soft drink consumption and risk of esophageal adenocarcinoma. 1667 Mar 93


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