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

Helicobacter pylori plays major causative roles in peptic ulcer disease and gastric cancer. Elevated acid secretion in patients with duodenal ulcers (DUs) contributes to duodenal injury, and diminished acid secretion in patients with gastric cancer allows carcinogen-producing bacteria to colonize the stomach. Eradication of H. pylori normalizes acid secretion both in hyper-secreting DU patients and hypo-secreting relatives of gastric cancer patients. Therefore, we and others have asked how H. pylori causes these disparate changes in acid secretion. H. pylori gastritis more or less restricted to the gastric antrum in DU patients is associated with increased acid secretion. This is probably because gastritis increases release of the antral acid-stimulating hormone gastrin and diminished mucosal expression of the inhibitory peptide somatostatin. Bacterial products and inflammatory cytokines including TNFalpha may cause these changes in endocrine function. Gastritis involving the gastric corpus tends to diminish acid secretion, probably because bacterial products and cytokines including IL-1 inhibit parietal cells. Pharmacological inhibition of acid secretion increases corpus gastritis in H. pylori-infected subjects, so it is envisaged that gastric hypo-secretion of any cause might become self-perpetuating. H. pylori-associated mucosal atrophy will also contribute to acid hypo-secretion and is more likely in when the diet is high in salt or lacking in antioxidant vitamins. Data on gastric acid secretion in patients with esophagitis are limited but suggest that acid secretion is normal or slightly diminished. Nevertheless, H. pylori infection may be relevant to the management of esophagitis because: (i) H. pylori infection increases the pH-elevating effect of acid inhibiting drugs; (ii) proton pump inhibitors may increase the tendency of H. pylori to cause atrophic gastritis; and (iii) successful eradication of H. pylori is reported to increase the likelihood of esophagitis developing in patients who had DU disease. Points (ii) and (iii) remain controversial and more work is clearly required to elucidate the relationship between H. pylori, acid secretion, gastric mucosa atrophy and esophagitis.
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PMID:Helicobacter pylori modulation of gastric acid. 1078 May 81

The cagA gene is a key marker for the Helicobacter pylori cag pathogenicity island (PAI), which may vary in composition in different strains with insertion sequence mediated interruptions and deletions of genes. While presence of cagA has been associated with increased risk for peptic ulcer disease and gastric cancer, the precise link with virulence is controversial. We investigated H. pylori from dyspeptics in one location in England (mid-Essex) with reference to the prevalence and distribution by age cohort of different cag PAI forms to determine if presence of the insertion element IS605 had a modifying effect on the severity of associated disease. H. pylori isolated from gastric biopsies over a 4-year period were screened by specific PCR assays for the presence of cagA, cagD, cagE and virD4 genes in the cag PAI, and for the presence of IS605 in the PAI and elsewhere in the genome. Most (68%) of the 166 isolates of H. pylori contained a PAI based on detection of cagA whereas 29% had no detectable PAI using multiple loci. The cagA+ genotype frequencies were similar in the peptic ulcer and non-ulcer dyspepsia-gastritis groups (79% vs. 74%) whereas frequencies in the NUD-oesophagitis and normal mucosa groups were lower (58%) but not significantly different (P>0.41). Genomic IS605 inserts were present at an overall frequency of 32% and were widely distributed with respect to patient age and disease severity. The combined cagA+/IS- strain genotype was common but not significantly associated with PUD compared to endoscopically normal mucosa (P> or =0.807). We concluded that presence of the IS605 element, whether in cagA+ or cagA- strains of H. pylori, did not systematically modify the severity of associated disease in the study population.
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PMID:Molecular epidemiology of Helicobacter pylori in England: prevalence of cag pathogenicity island markers and IS605 presence in relation to patient age and severity of gastric disease. 1117 93

The aim of surgical treatment of gastric cancer must be complete removal of the tumor including systematic lymphadenectomy. The performance of R0-resection has to take into consideration tumor site as well as the histomorphological type described by Lauren. Therefore, subtotal distal- or total gastrectomy are complementary operative procedures nowadays. From the oncological point of view proximal gastrectomy might be indicated in some situation but increased postoperative morbidity including severe reflux-esophagitis can be obtained. According to the functional outcome subtotal distal gastrectomy should be preferred whenever justified oncologically in comparison to total gastrectomy. Among the different reconstructive methods after total gastrectomy the Roux-en-Y technique is one of the most common procedure performed. Furthermore, some patients can benefit from a reconstruction of a gastric substitute and maintenance of duodenal passage but the superiority of this technique must be evaluated in further prospective studies. The question of the optimal mode of reconstruction of the upper gastrointestinal tract is still open.
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PMID:Functional results of reconstruction after subtotal or total gastrectomy. 1120

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

For over a century duodenogastric reflux (DGR) has been considered the main cause of the primary or secondary alkaline gastritis. In the first case it occurred in patients who had not been operated earlier, in the latter one in those after surgery of stomach, duodenum, gallbladder and bile ducts. Since first time many reports of clinical and experimental studies have demonstrated destructive effect of pancreatic enzymes, bile acids and their by-products on stomach mucose producing in consequence non-specific histologic lesions. It has been also observed that duodenogastric reflux plays the basic role in the patho-genesis of gastritis and other GI tract diseases (gastric ulcer, reflux oesophagitis, progressing metaplasia or oesophageal and gastric cancer). As far as diagnosing of alkaline gastritis requires histologic confirmation, duodenogastric reflux brings many more problems. However, the progress in medicine and technology allow direct measurement of quality and quantity of this reflux.
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PMID:[Pathogenesis and significance of gastroduodenal reflux]. 1145 Jan 55

Epidemiological evidence has clearly shown a highly significant relationship between Helicobacter pylori infection and the development of duodenal ulcer and distal gastric adenocarcinoma. Despite H. pylori being a common aetiological factor for both disorders, the two disease phenotypes are virtually mutually exclusive. This indicates that the host response to infection has a pivotal role in determining outcome; these disease phenotypes relate to the effect of infection on gastric acid secretion, duodenal ulcer being closely related to sustained acid secretion whereas gastric cancer follows gastric atrophy and impaired gastric acid secretion. Cancer at the oesophageal junction and that associated with Barrett's oesophagus is now the most rapidly increasing tumour in the gastrointestinal tract. The challenge for the next millennium, therefore, is to try and develop methods for identifying patients at risk of developing oesophagogastric cancer. A common feature in the pathogenesis of both gastric and oesophageal adenocarcinoma is inflammation presenting clinically as gastritis and oesophagitis. The pathway from gastritis to gastric atrophy, dysplasia and carcinoma is thought to be a multi-step process, probably triggered by free radicals within the gastric epithelium and increased exposure to luminal carcinogens. However, it has been unclear as to which aspect of the host response determines whether an individual will move along the neoplasia pathway. Recent work has shown that qualitative aspects of the immune environment in the stomach may account for a substantial part of the phenotypic divergence following H. pylori infection. Interleukin-1 beta polymorphisms relate closely to the propensity for an individual to develop distal gastric cancer and maybe useful for predicting risk in family members. In Barrett's oesophagus, we have recently shown that the immune environment may also be important in determining whether an individual will develop cancer. Although we did not find that Barrett's oesophagus was a profoundly inflammatory condition (unlike esophagitis in the squamous epithelium), where there was evidence of inflammation it was qualitatively different from that of oesophagitis in that a Th-2 response with increased expression of IL-4 predominated in Barrett's, whereas a Th-1 proinflammatory response characterised oesophagitis in squamous epithelium. It seems likely that the specific immune environment within Barrett's metaplasia may be an important driver towards dysplasia and carcinoma. Thus, the immune environment in the stomach and esophagus may be critical in determining whether an individual is at risk of developing neoplastic complications of H. pylori infection and gastroesophageal reflux. Identification of the genetic factors which underpin these responses may ultimately result in development of methods to identify individuals at high risk.
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PMID:Acid, helicobacter and immunity: a new paradigm for oesophagogastric cancer. 1159 70

This is a 12-year follow-up study on screening with a mixture of 2% hydrochloric acid and 18% alcohol for upper digestive tract cancer in a Chinese high-risk population. A public screening for upper digestive tract cancer was conducted from November 1979 to May 1984 by giving a mixture of 2% hydrochloric acid and 18% alcohol to 7280 subjects in high-risk population in Yaocun village, Linxian County, Henan province. The subjects were given 15 ml of this mixture in the morning or at noon before lunch when fasting. Five minutes later, irritative reactions (retrosternal discomfort, warmth, pain or pyrosis) was felt in subjects suffering from oesophageal cancer, oesophagitis, gastritis, mucosal dysplasia or ulcer (positive group). Those with normal oesophageal or gastric mucosa felt nothing (negative group). The overall positive rate was 23.2% (1689/7280). In oesophageal or gastric cancer subjects, the positive rate of these symptoms was 88.7%. In subjects with mucosal dysplasia, it was 71.2%. A total of 26 upper digestive tract cancer patients were found. As a result of 12 years' follow-up, 271 persons with upper digestive tract cancer among the 1689 positive group subjects have been discovered, giving an annual morbidity rate of 1.34%. Among the 5591 negative group subjects, 136 persons have been found to suffer from this cancer, giving an annual morbidity rate of 0.2%. This illustrated that the annual morbidity rate of upper digestive tract cancer in the positive group was 6.65 times of that of the negative group ( <0.0001). In conclusion, screening of upper digestive tract cancer with dilute hydrochloric acid in alcohol is simple, safe, non-traumatic, effective and readily acceptable in a high-risk area in China. It may be feasible in other parts of the world, especially the developing countries.
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PMID:Screening of upper digestive tract cancer with dilute hydrochloric acid and alcohol in a Chinese high-risk population--a follow-up study of 12 years. 1239 50

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

A clutch-like method of esophagojejunal anastomosis on the excluded by the Roux method loop of the small intestine was worked out in experiments on 80 corpses of humans. It was found that the anastomosis should be made at a distance of 3.2 +/- 0.48 cm (two diameters of the patient's esophagus) from the tightly sutured part of the small intestine. In the clinic there were no cases of incompetence of the anastomosis sutures in 86 gastric cancer patients aged from 31 to 71 years (81 gastrectomies and 5 extirpations of the gastric stump). Two patients died (2.3%). The follow-up of the patients during 1-10 years after operation has found that mild reflux-esophagitis developed in 6.1% of the patients, average degree--in 2.04%. No cicatricial strictures of the anastomosis were revealed. The method was used in 6 patients in gastroplasty after Kupriyanov-Zakharov. The dumping syndrome of mild degree developed in 23.6%, average--in 2.7% of the patients. The anastomosis can be used in gastrectomy as a method of choice in extirpation of the gastric stump.
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PMID:[Y Roux anastomosis of small intestine in gastrectomy and esophagectomy]. 1266 Dec 53

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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