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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence of esophageal tumors, and of adenocarcinoma in particular, has risen markedly in recent years in the developed countries. The use of a variety of histopathological and biological markers is now offering promising prospects for the future. Vertical tumor invasion, intratumoral microvessel density, antimucin monoclonal antibodies, flow cytometry, telomerase activity, and overexpression of cyclin D1 have been correlated with the staging and prognosis of esophageal carcinomas. By combining these markers with Lugol staining, a practical new method of staging esophageal tumors may become available in the coming years. As is well known, Barrett's mucosa is a preneoplastic condition. Discussions in the literature concerning short forms of Barrett's esophagus and their relationship to inflammation of the gastric cardia appear to describe two different scenarios--a gastroesophageal reflux condition for short forms of Barrett's esophagus, and an inflammatory phenomenon (perhaps unrelated to Helicobacter pylori infection) for inflammation of the gastric cardia. Cost-benefit studies of follow-up procedures in Barrett's esophagus have yet to be conducted, and considerable efforts--mainly using biological markers--are being made to identify those patients who are at greatest risk. Although the frequency of gastric tumors has declined in recent years, many as yet unclear aspects of these tumors have been studied. Technological progress has not led to substantial changes in the diagnostic procedures used, although autofluorescence methods and three-dimensional reconstruction have been analyzed. Laparoscopy, preferably combined with the use of ultrasound probes, may be a valuable tool for staging. The suggestion that endoscopy should be avoided in young patients (the "treat but do not scope" approach) has been seriously questioned, as it may lead to early cancer being overlooked. There is thought to be an intermediate stage of gastric cancer (between the early and advanced stages) in which the muscularis propria, but not the serosa, is invaded. Endoscopic ultrasonography is becoming increasingly established as a basic tool for the staging of gastric cancer. Gastric MALT lymphoma can be cured by H. pylori eradication therapy in many cases, but there is still uncertainty regarding the limitations of this approach.
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PMID:Diagnosis of esophagogastric tumors. 1120 80

The incidence of gastroesophageal reflux disease (GERD) and esophageal adenocarcinoma have increased in recent years as the incidence of peptic ulcer disease and distal gastric cancer have declined. Given the simultaneous decline in Helicobacter pylori infection, it is tempting to propose a relationship between H. pylori infection and these opposing time trends. Although H. pylori infection clearly does not cause GERD, it may protect certain susceptible individuals from developing GERD and its complications. The most likely mechanism in which H. pylori infection protects against GERD is by decreasing the potency of the gastric refluxate in patients with corpus predominant gastritis. A variety of implications of H. pylori infection on GERD treatment have also arisen in recent years. These focus on the risk of gastric atrophy while on proton pump inhibitor therapy and the efficacy of proton pump inhibitors before and after eradication of H. pylori. This article puts into perspective our current understanding of the complex, incompletely understood relationship between H. pylori infection and GERD.
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PMID:GERD and H. pylori: is there a link? 1121 51

Since the discovery of Helicobacter pylori(H. pylori), causal linkage between H. pylori infection and some of gastric disease has been generally accepted from the results of many studies. Indeed the usefulness of H. pylori eradication therapy for acute gastritis, peptic ulcer, gastric polyp and MALT lymphoma etc. has been reported. In the low grade MALT lymphoma, the regression rate by this therapy is about 70%. On the other hand, we should pay the caution to several adverse effects, such as drug resistance and GERD, of H. pylori eradication therapy. However, based on the several results of comparative studies between antibiotic therapy and the other one, the antibiotic therapy for peptic ulcer is only covered by national health insurance at present. The reversibility of gastric precancerous conditions such as mucosal atrophy, intestinal metaplasia and dysplasia by antibiotic therapy has been studied, but its significance is not clear yet. In animal experiment, H. pylori infection induced gastric adenocarcinoma in Mongolian Gerbils. However, this phenomenon is limited to this kind of animal only. To proof the causal link between H. pylori infection and genesis of gastric cancer in human being, clinical intervention trials are ongoing in the world. If these trials can clarify it, the H. pylori eradication therapy will be established as preventive measure for gastric carcinogenesis.
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PMID:[Helicobacter pylori & gastric disease]. 1130 2

Helicobacter pylori infection, which is present in 30 - 60% of the population in developed countries and in more than 60% in developing countries, is established to be a major cause of gastritis, peptic ulcer disease and gastric cancer. Eradication therapy has been incorporated into clinical practice over the past 15 years. Treatment regimens include a 2 week bismuth-based triple therapy (a bismuth compound plus metronidazole, tetracycline or amoxycillin), a 1 week proton-pump inhibitor (PPI)-based triple therapy and a 1 week ranitidine bismuth citrate (RBC)-based triple therapy (a PPI or RBC plus any two of the three antibiotics, metronidazole, amoxycillin and clarithromycin). These regimens achieve eradication rates of >> 80%. H. pylori resistance to metronidazole and clarithromycin decreases the clinical efficacy of most regimens, despite the high eradication rates for resistant strains achieved by the RBC-triple therapy in some recent trials. The dose of antibiotics (especially clarithromycin) and the duration of treatment may also influence the eradication rate. Doctors' beliefs impact on clinical practice and, thus, influence the clinical application of eradication therapy. Whereas peptic ulcer disease and primary gastric low-grade B-cell mucosa-associated lymphoid tissue lymphoma (MALToma) have become established as definite indications for eradication therapy, there remain controversies surrounding non-ulcer dyspepsia, gastro-oesophageal reflux disease, atrophic gastritis, intestinal metaplasia, use of non-steroidal anti-inflammatory drugs (NSAIDs) and H. pylori-related extradigestive diseases.
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PMID:Helicobacter pylori infection--current treatment practice. 1133 84

There are now a wide variety of drugs available that are able profoundly to reduce the production of gastric acid. These drugs are currently widely prescribed for the treatment of peptic ulceration and gastro-oesophageal reflux disease. One of the main functions of gastric acid is to kill ingested bacteria. Colonization of the gastric lumen occurs in patients on anti-secretory medication, the degree of bacterial overgrowth depending upon the degree of elevation of the pH. There have been concerns that these bacteria may produce carcinogenic nitrosamines and increase the risk of gastric cancer, but there is at present no definitive evidence in support of this. A profound suppression of gastric acid may also facilitate the colonization of the upper small intestine, leading to deconjugation of the bile salts and malabsorption. There is some evidence that profound gastric acid suppression may decrease the number of ingested pathogens required to produce enteric disease. This chapter discusses these potential bacterial complications of therapeutic acid suppression and the evidence for them.
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PMID:Occurrence and significance of gastric colonization during acid-inhibitory therapy. 1140 43

Over the last several decades, the incidences of gastric cancer and peptic ulcer have declined while the incidences of gastro-oesophageal reflux disease (GORD) and functional dyspepsia have reached virtually epidemic proportions. A similar trend is occurring in oesophageal cancer, with squamous cell carcinoma on the decline and adenocarcinoma on the rise, possibly due to the dramatic increase in GORD. The true clinical spectrum of these disorders, however, is only recently becoming evident: 60% of patients with GORD do not have detectable evidence of oesophagitis; they can be classified as having non-erosive or negative-endoscopy reflux disease (NERD). In this subgroup, a significant proportion will also manifest normal acid exposure on 24-h pH monitoring. Further, patients with NERD appear to be somewhat less responsive to gastric acid suppression with proton pump inhibitors. These differences, combined with the concept of the 'tender' oesophagus and the frequent presence of dyspeptic symptoms in patients with NERD, have important therapeutic implications. Therefore, considering the marked overlap in these disorders, is it realistic or clinically relevant to distinguish the entities of GORD, NERD, and functional dyspepsia? This dilemma has led to general guidelines: should heartburn predominate, treat as GORD; if dyspepsia predominates, treat as functional dyspepsia. In practical terms, each diagnosis requires consideration of the other.
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PMID:Non-erosive reflux disease: part of the spectrum of gastro-oesophageal reflux disease, a component of functional dyspepsia, or both? 1143 May 3

Since the first report of the potential role of Helicobacter pylori as cause of disease of the upper intestinal tract of humans, a major controversial has developed. First, the role of H. pylori as the etiological agent of duodenal and gastric ulcer has been questioned. Second, the possibility of H. pylori as a major risk factor in the development of distal gastric cancer has not been fully accepted. It is interesting that at the time when the etiological role of H. pylori is almost universally accepted, series of publications have suggested that the elimination of H. pylori from asymptomatic individuals might represent a risk for the development of other upper gastrointestinal diseases such as GERD and cancer of the esophagus. The main goal of this revision is to describe the virulence factors associated with H. pylori as well as its interaction with the human host, to establish whether H. pylori should be considered a true pathogen or only a commensal.
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PMID:[Is the association of Helicobacter pylori with humans a classical example of parasitism?]. 1146 23

A variety of abnormalities contribute to the development of gastroesophageal reflux disease (GERD) including transient lower esophageal sphincter relaxation, low esophageal sphincter pressure, presence of a hiatal hernia, diminished esophageal clearance of refluxed gastric contents, and alterations in esophageal mucosal resistance. Helicobacter pylori infection clearly plays a role in the pathogenesis of peptic ulcer disease and mucosa associated lymphoma of the stomach and is a definite risk factor for distal gastric cancer. The role of H. pylori infection in GERD remains controversial and incompletely understood. Although H. pylori infection does not cause reflux disease, circumstantial evidence suggests that it may protect against the development of GERD and its complications in some patients. The most likely mechanism whereby H. pylori infection protects against GERD is by decreasing the potency of the gastric refluxate in patients with corpus predominant gastritis. A variety of implications of H. pylori infection on GERD treatment have also arisen in recent years. These focus on the risk of gastric atrophy while on proton pump inhibitor therapy and the efficacy of proton pump inhibitors before and after eradication of H. pylori. This article puts into perspective our current understanding of the complex, incompletely understood relationship between H. pylori infection and GERD.
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PMID:The possible role of Helicobacter pylori in GERD. 1147 51

The effect of gastrectomy on the subsequent development of esophageal cancer was investigated, focusing on its multicentric occurrence. We retrospectively evaluated 28 patients who underwent subtotal esophagectomy for intrathoracic esophageal cancer between 1985 and 1999. They were divided into two groups according to whether or not they had previously undergone a gastrectomy: group 1, comprising 7 patients who had undergone gastrectomy and group 2, comprising 21 patients who had not. Clinical profiles of the patients were obtained from the medical records and the whole resected esophagus was histopathologically examined. The interval between gastrectomy and esophagectomy in group 1 was significantly shorter in the patients who had undergone gastrectomy for gastric cancer than in those who had undergone gastrectomy for a peptic ulcer, and also in the patients for whom anastomosis had been performed by Billroth I compared with Billroth II. The patients in group 1 were significantly younger than those in group 2. The multiple occurrence of esophageal cancer was found in 4 of 5 patients (80%) in group 1, and in 2 of 18 patients (11%) in group 2, with significantly higher frequency being seen in group 1. More than two coexisting cancer lesions apart from the primary tumor were detected in all four patients. Histological examination of all the coexisting cancer lesions showed well-differentiated squamous cell carcinoma confined within the superficial mucosal layer. No significant differences were noted in the location of the coexisting lesions between the oral and anal side of the primary tumors. Squamous dysplasia was randomly observed, especially around the cancer lesions. These findings suggest that gastrectomy precipitated subsequent chronic gastroesophageal reflux which in turn induced the development of squamous dysplasia and carcinoma at multiple locations in the esophagus.
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PMID:Multicentric occurrence of esophageal cancer after gastrectomy: a preliminary report. 1151 Jun

In the Western world, there has been an alarming rise in the incidence and prevalence of adenocarcinoma arising at the esophagogastric junction during recent decades. Epidemiological, clinical and pathological data support a sub-classification of adenocarcinomas arising in the vicinity of the esophagogastric junction (AEG) into adenocarcinoma of the distal esophagus (Type I), true carcinoma of the cardia (Type II) and subcardial carcinoma (Type III). While most, if not all, adenocarcinomas of the distal esophagus arise from areas with specialized intestinal metaplasia, which develop as a consequence of chronic gastroesophageal reflux, the etiology and pathogenesis of true carcinoma of the gastric cardia and subcardial gastric cancer is not clear at present. Although a subgroup of true carcinomas of the gastric cardia may also develop within short segments of intestinal metaplasia at the esophagogastric junction, a causal relation between these tumors and gastroesophageal reflux has been difficult to establish. Irrespective of the etiology, a complete removal of the primary tumor and its lymphatic drainage has to be the primary goal of any surgical approach to adenocarcinoma of the esophagogastric junction. Our experience in the management of more than 1000 such patients during the past 18 years suggests that an individualized therapeutic strategy oriented by tumor type and stage results in survival rates superior to those reported with a more indiscriminate approach. This individualized strategy prescribes a transmediastinal esophagectomy with lymphadenectomy in the lower posterior mediastinum and along the celiac axis for Type I tumors, extended total gastrectomy with transhiatal resection of the distal esophagus and D2 lymphadenectomy for Type II and Type III tumors, a limited resection of the esophagogastric junction and distal esophagus with interposition of a pedicled jejunal segment for uT1N0 tumors, and neoadjuvant chemotherapy followed by resection for uT3/T4 tumors. Extensive preoperative staging is essential to allow correct selection of the appropriate therapeutic strategy using this tailored approach.
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PMID:Cancer of the esophagogastric junction. 1152 5


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