Gastric ulcer and gastritis

Gear, M. W. L.; Truelove, S. C.; Whitehead, R.

doi:10.1136/gut.12.8.639

Cited by 125 publications

(28 citation statements)

References 9 publications

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“…This could lead to considerable variation between small mucosal samples taken at biopsy. However, if realistic comparison of gastrin cell numbers between patient groups is to be achieved, the importance of antral gastritis deserves more emphasis than it has hitherto received, especially as it is so common in patients with peptic ulceration, as noted by Gear et al (1971) and confirmed by Keuppens et al (1978) and the present study. Asnaes et al (1976) first reported the marked effect of gastritis on immunoreactive gastrin cells and stated that the cells were never found in the presence of intestinal metaplasia.…”

Section: Discussionsupporting

confidence: 68%

“…Chronic gastritis is a common condition found in association with gastric carcinoma and gastric and duodenal ulceration (Morson, 1955;Gear et al, 1971). It is frequently found in patients with no gastrointestinal symptoms (Joske et al, 1955) and is reported to be increasingly prevalent with advancing age in a representative sample of the working population (Siurala et al, 1968 Received for publication 18 September 1978 Material and methods Immediately after removal from the body 38 partial gastrectomy specimens were fixed in formol saline solution or in Bouin's fixative.…”

mentioning

confidence: 99%

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A histological study of the effect of chronic gastritis on gastrin cell distribution in the human stomach.

Sloan¹,

Buchanan²,

McFarland³

et al. 1979

J Clin Pathol

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SUMMARY To determine the effect of varying degrees of gastritis on the distribution of immunoreactive gastrin cells 38 partial gastrectomy specimens have been studied. Routinely stained histological sections of mucosa were compared with serial and adjacent sections stained by specific immunohistochemistry using peroxidase and fluorescent techniques. While chronic superficial gastritis had no obvious effect, mild atrophic gastritis was associated with an uneven distribution of gastrin cells which became more marked with increasing severity of gastritis. In the region of intestinal metaplasia gastrin cells were almost totally absent.Small numbers of gastrin cells were found within areas of pseudopyloric metaplasia in the fundus, a region where those cells are not normally seen. Similarly, gastrin cells were detected within regenerative gastric polypi in both antrum and fundus.Chronic gastritis is a common condition found in association with gastric carcinoma and gastric and duodenal ulceration (Morson, 1955;Gear et al., 1971). It is frequently found in patients with no gastrointestinal symptoms (Joske et al., 1955) and is reported to be increasingly prevalent with advancing age in a representative sample of the working population (Siurala et al., 1968 Received for publication 18 September 1978 Material and methods Immediately after removal from the body 38 partial gastrectomy specimens were fixed in formol saline solution or in Bouin's fixative. After fixation at least five longitudinal strips of mucosa were taken from each specimen. The strips were obtained from non-ulcerated and non-cancerous mucosa on the lesser and greater curvatures and anterior and posterior walls. Both antral and fundal mucosa was included if present. Further samples were also taken from any areas of flat or atrophic mucosa. Mucosal strips were often embedded in the form of a 'Swiss roll' in order to facilitate examination of a large area on a single slide.The tissue was dehydrated and embedded in paraffin wax as for routine histological processing; 5 ,t paraffin sections were dewaxed and stained using haematoxylin and eosin. Adjacent or serial sections were stained for immunoreactive gastrin cells using specific immunohistochemistry. The location and degree of gastritis, if any, in the mucosa was assessed on the H & E section, and the effect of the gastritis on immunoreactive gasti in cells was determined in the adjacent specifically stained section. The morphology of the sections was similar, and it was quite easy to identify localised areas in the specifically stained sections even when immunofluorescence was used by comparing them with the corresponding H & E section. Gastritis was assessed according to the criteria of Whitehead et al. (1972).

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Section: Discussionsupporting

confidence: 68%

mentioning

confidence: 99%

A histological study of the effect of chronic gastritis on gastrin cell distribution in the human stomach.

Sloan¹,

Buchanan²,

McFarland³

et al. 1979

J Clin Pathol

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“…In duodenal ulcer, antral gastritis will persist, while the ulcer improves or remains quiescent [45,46,48]. In gastric ulcer, the same dissociation has been observed [32]. Thus, chronic lesions of gastritis are observed in peptic-ulcer patients; they are limited to the antrum in duodenal ulcer, and spread in the fundus in gastric ulcer.…”

Section: B) Evolution and Significance Of Gastritis In Peptic Ulcermentioning

confidence: 67%

Chronic Gastritis

Lambert¹

1972

Digestion

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“…Over the years several factors, including genetic predisposition, smoking, and acid secretion, have been found to be associated with ulcer development. It has also been known for some years that patients with ulcers have gastritis (32,52,116), a fact that has taken on new significance with reports of bacteria being present.…”

Section: Gastric Diseasesmentioning

confidence: 99%

Campylobacter pylori and gastroduodenal disease

Buck

1990

Clin Microbiol Rev

139

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Campylobacter pylori is a newly described, spiral-shaped, gram-negative bacillus that is oxidase positive, catalase positive, and urease positive and grows slowly in culture. Although observed in human tissue at the beginning of the century, it was not cultured until 1982. Because there are significant morphological and genetic differences between this organism and other species of Campylobacter, it will probably be reclassified in a new genus. Current information indicates that the organism primarily resides in the stomach tissue of humans and nonhuman primates and may occasionally spread to the esophagus or other parts of the alimentary tract under appropriate conditions. Significant evidence has accumulated in the last several years to show that it causes gastritis, and there is mounting evidence that it may participate in the development of duodenal ulcers. It may also be associated with gastric ulcers and nonulcer dyspepsia. It can be detected in patients by culture of biopsy specimens or histological staining of biopsy tissue. Indirect evidence for the presence of the organism can be obtained by detection of urease in a tissue biopsy specimen, by urea breath tests, or by detection of specific antibody. It may not be necessary to implement these procedures for routine use, however, until the role of the organism can be defined better. Ultimately, the discovery of this organism may lead to radical changes in the diagnosis and treatment of gastric disease.

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Gastric ulcer and gastritis

Cited by 125 publications

References 9 publications

A histological study of the effect of chronic gastritis on gastrin cell distribution in the human stomach.

A histological study of the effect of chronic gastritis on gastrin cell distribution in the human stomach.

Chronic Gastritis

Campylobacter pylori and gastroduodenal disease

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