Bile reflux and intestinal metaplasia in gastric mucosa.

Sobala, G. M.; O'Connor, H.J.; Dewar, E. P.; King, R. F. G. J.; Axon, Anthony; Dixon, M. F.

doi:10.1136/jcp.46.3.235

Cited by 223 publications

(140 citation statements)

References 13 publications

Supporting

Mentioning

130

Contrasting

Unclassified

Order By: Relevance

“…Such areas may also become malignant after long-term influence of refluxed bile (6,13). Obtained results do not show such intensity of changes as suggested by a number of sources (14,15,16). It may be due to a relatively short observation time, which is a consequence of the short lifespan of examined animals.…”

Section: Discussionmentioning

confidence: 65%

See 1 more Smart Citation

Morphological Changes in the Stomach Mucosa of Rats Caused by Endogenous Bile Acids

Rudnicki¹,

Мазур

Slusarczyk

et al. 2007

Polish Journal of Surgery

View full text Add to dashboard Cite

"Bile reflux" is a common term to denote a process of placing duodenal contents in the stomach and/or lower oesophagus. It is most often associated with functional or organic failure of the pylorus and is a not uncommon postoperative condition after pyloric section, resection or by-passing. Gastrotoxicity of the replaced small intestinal mixture leading to lesions in gastric mucosal barrier, is caused by an increased ability to reabsorb hydrogen ions along with migration of blood proteins and electrolytes towards lumen of the stomach. Consequently, histamine secretion becomes increased, leading to inflammatory and haemorrhagic changes or ulcer niches. The aim of the study was to demonstrate histological and microscopic changes in the gastric mucosa following reflux and to determine if long-term exposure to refluxed duodenal contents will produce tumorous changes in the organs tested. Material and methods. The study consisted of 25 mature female Wistar rats weighing 180-200 g. Bile reflux to the stomach was produced experimentally by surgical drainage. Final evaluation was performed after 55 weeks. Results. Findings were as follows: gastric changes were noted in basal and parietal cells, no tumorous foci were found in histological samples. Slight morphological changes can be caused by short periods of gastric mucosa exposure to the gastrotoxic small intestinal mixture. Conclusions. Endogenous bile acids cause morphological changes in the stomach mucosa of rats. In particular, these changes affect the ultrastructure of basal and parietal cells. No neoplastic foci were found in the examined organs.

show abstract

Section: Discussionmentioning

confidence: 65%

“…In patients who did not undergo any procedures, "bile reflux" can be asymptomatic and is by some sources treated as a physiological phenomenon (8,9,10).…”

Section: Discussionmentioning

confidence: 99%

Morphological Changes in the Stomach Mucosa of Rats Caused by Endogenous Bile Acids

Rudnicki¹,

Мазур

Slusarczyk

et al. 2007

Polish Journal of Surgery

View full text Add to dashboard Cite

show abstract

“…Increased bile concentrations in the stomach are positively associated with intestinal metaplasia and particularly so in those individuals infected with H. pylori. 5 The incidence of cancer in patients who have previously been operated on for duodenal ulcer is higher than the normal population, in spite of the fact that two-thirds of the stomach may have been removed at the original operation. This Ôsurgical experimentÕ is important because unoperated patients with duodenal ulcer are at lower risk of gastric cancer than the general population.…”

Section: Introductionmentioning

confidence: 99%

Gastric cancer and Helicobacter pylori

Axon

2002

Aliment Pharmacol Ther

View full text Add to dashboard Cite

SUMMARYGastric cancer is the second commonest cause of death from malignancy in the world. Its pathogenesis is comparatively well understood and its aetiology multifactorial. Non-cardia gastric cancer usually arises in a stomach that has been inflamed over a long period and where atrophy and intestinal metaplasia have supervened. The commonest cause of gastric inflammation is infection with Helicobacter pylori. Colonization with this organism increases the relative risk of developing this cancer by about six [Helicobacter and Cancer Collaborative Group. Gut 2001; 49: 347-53]. Its likelihood increases with the severity and extent of the gastritis. Severity is influenced by the virulence of the infecting organism, the genetics of the host, bile reflux, dietary factors and the presence of hypochlorhydria which influences the extent, as well as the severity, of the inflammation. The only predisposing factor which can easily be manipulated is H. pylori infection, which can be successfully treated in 80-90% of cases using a 1-week therapeutic regimen. INTRODUCTIONGastric cancer is the second commonest malignancy in the world and after lung cancer kills more people than any other malignant tumour.1 Although the incidence of the disease is falling in developed countries, changes in demography suggest that numbers dying from this condition will increase in the foreseeable future. The prognosis for gastric cancer once a diagnosis has been made is poor. In most developed countries only around 10% survive for 5 years. The only exception to these dismal statistics is Japan where, for a variety of reasons, the condition is often identified at an early stage and in younger and fitter patients. Preventative measures for gastric cancer are likely to be the most effective method of reducing the mortality from this disease and this in turn depends upon a knowledge of its aetiology. In recent years it has become apparent that the most important single factor responsible for the development of non-cardia gastric cancer (by far the commonest type) is infection with the organism Helicobacter pylori. This article addresses the relevance of this organism in the pathogenesis of gastric cancer and its interrelationship with other factors that predispose to the disease.Factors associated with gastric cancer Table 1 sets out the conditions known to be associated with gastric cancer. Considerable epidemiological research devoted to this disease shows that its incidence varies widely throughout the world and can differ markedly within individual countries. Although gastric cancer incidence has consistently fallen in developed countries, mortality rates remain high in the developing world. The disease is more common in the Far East than in the West and higher in Eastern and Central Europe than in Western Europe. It seems to be less common in Africa, but there are hotspots in South America. In general, the risk of cancer seems to be higher in those communities that are socio-economically disadvantaged, an exception to this rule being Japan. Wit...

show abstract

“…The clinical application of Bilitec 2000 technology for the 24 h bile reflux monitoring revealed that bile reflux into the stomach or even the esophagus was a frequent phenomenon (1-3). Dixon et al believed that bile reflux might be related to the intestinal metaplasia of gastric antral mucosa (4)(5)(6). Recent studies have shown that bile reflux is not only related to reflux esophagitis but also is a significant cause of Barrett's esophagus (7)(8)(9)(10)(11) and esophageal adenocarcinoma (12)(13)(14)(15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%