Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution and numbers of G cells and of parietal cells were related to the distribution and severity of histopathological alterations (inflammatory cell infiltration, atrophy and intestinal metaplasia) in corresponding mucosal tissue blocks from resected stomachs (12 patients with gastric ulcer, 11 with duodenal ulcer, and 14 with duodenal ulcer and uremia). In all patients the histopathological features were more severe in the pyloric antrum than in the body, and the change in severity corresponded well with the disapperance of G cells at the body-antrum border. The transitional body-antrum zone was histopathologically similar to the remaining antrum. A marked individual heterogeneity of the histopathological alterations was observed. An increasing grade of atrophy was associated with increased severity of inflammation, and the presence of intestinal metaplasia was especially associated with atrophy. No significant correlation was found between the antral G-cell number and the grade of antral inflammatory cell infiltration, whereas there was a reduction in cell number with increasing grade of atrophy in all patient categories. The parietal-cell density in the body mucosa was decreased with increasing grade of inflammation as well as with increasing grade of atrophy. The presence of patchy intestinal metaplasia resulted in a complete absence of G cells and of parietal cells from the corresponding part of the mucosa in the antrum and body respectively.
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PMID:Quantification of gastrin-producing cells (G cells) and parietal cells in relation to histopathological alterations in resected stomachs from patients with peptic ulcer disease. 8 Aug 19

The mucosal distribution of G cells was quantitatively mapped in resected stomachs from 42 patients (12 with gastric ulcer, 11 with duodenal ulcer, 14 with duodenal ulcer and uremia, and 5 with gastric cancer). Along the histological border of the proximal part of the pyloric antrum there was in all patient categories a transitional zone of varying extent, with a low G-cell density before the cells disappeared in the body of the stomach. The proximal end of the duodenum contained considerably fewer G cells than in the antrum, and the number was virtually equal in all groups. Within the antrum there was in the material as a whole a gradual increase in G-cell density from the proximal to the distal part, but this difference was not apparent for the gastric ulcer patients. When corresponding antral segments were compared between the various patient groups, the G-cell density was found to be significantly decreased in the distal antrum of the gastric ulcer patients. In all patient categories, except the duodenal ulcer group with uremia, the circumferential distribution of G cells showed reduced density along the curvatura minor. For the material as a whole there were great individual variations in the overall antral G-cell density, in the antral area corresponding to the distribution of G cells and in the total G-cell mass; these three variables were not significantly related to diagnosis, age or sex.
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PMID:Immunohistochemical investigation of gastrin-producing cells (G cells). Estimation of antral density, mucosal distribution, and total mass of G cells in resected stomachs from patients with peptic ulcer disease. 34 16

The distribution of parietal cells in the body mucosa, and of G cells in the antral mucosa, was quantitatively mapped in resected stomachs from 42 patients (12 with gastric ulcer, 11 with duodenal ucler, 14 with duodenal ulcer and uremia, and 5 with gastric cancer) who preoperatively had had their gastric acid secretion measured. In the material as a whole there was a significant positive correlation between the parietal-cell density and maximal acid output (MAO), and a significant negative correlation between the parietal-cell density and patient age. A significant positive correlation was found between the antral G-cell mass and basal acid output (BAO). When the individual patient categories were analyzed, the correlation between parietal-cell density and MAO were significant in the group with duodenal ulcer and uremia, and in the group with gastric cancer. Correlation between parietal-cell density and age was found only in the group with duodenal ulcer and uremia. There was no correlation between the parietal-cell density and various parameters of the antral G-cell population in the material as a whole or in any of the individual groups.
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PMID:Quantitative studies of gastrin cells (G cells) and parietal cells in relation to gastric acid secretion in patients with peptic ulcer disease. 75 73

Direct immunofluorescence technique with rhodamine-labelled rabbit anti-gastrin IgG conjugate was used for systematic mapping of the G-cell distribution in 16 resected stomachs (8 gastric ulcer patients and 8 duodenal ulcer patients with uraemia). Along the anatomical border of the proximal part of the antrum there was in both groups of patients a tranzitional zone with a low G-cell number per unit mucosa until the cells abruptly disappeared in the body of the stomach. The proximal end of the duodenum contained considerably fewer G cells than the antrum, and the number was equal in both groups. Within the antrum there was in the duodenal ulcer group a gradual increase in G-cell number from the proximal to the distal end, whereas in the gastric ulcer group no significant difference was found in different parts of the antrum. When corresponding antral parts were compared between the two groups, the only significant difference was that the distal part contained more G cells in the duodenal ulcer patients. In both groups the antral G-cell number showed no difference in circumferential distribution.
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PMID:Immunohistochemical investigation of gastrin-producing cells (G cells).The distribution of g cells in resected human stomachs. 79 81

PGE2-like immunoactivity in mucosal specimens from gastric corpus and antrum was measured in individuals with chronic uremia or without renal diseases in absence or presence of gastric ulcerations and in healthy subjects. Regardless the group of patients, compared to normal mucosa, a significant decrease in PGE2-like immunoactivity (50-70%) was found in mucosa from atrophic, but not from superficial gastritis. Whenever patients of the control group or patients with renal diseases suffered from ulcers, PGE2-like immunoactivity, compared to nonulcer subjects, revealed a decrease of about 60-70% in the nonulcerated mucosa. Compared to nonulcerated mucosa, the tissue of the ulcer rim in all patients with gastric ulcer showed a relative increase in PGE2-like immunoactivity, eg, PGE2-like immunoactivity was twice as high in tissue from the ulcer rim. The output of PGE2-like immunoactivity into the gastric juice of subjects without renal diseases was comparable to that found in patients with chronic uremia in both basal and pentagastrin-stimulated conditions. We therefore conclude that gastric mucosal formation is probably not influenced by chronic uremia.
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PMID:Gastric mucosal PGE2 levels in gastric non-ulcer and ulcer patients with chronic renal failure or without renal diseases and in healthy subjects. 225 34