Chronic gastritis—a pathogenetic approach

Wyatt, J I; Dixon, M. F.

doi:10.1002/path.1711540203

Cited by 187 publications

(71 citation statements)

References 59 publications

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“…Helicobacter pylon is a microaerophilic, spiral, gramnegative bacterium that has the human gastric mucosa as its exclusive habitat (29). H. pylon has been implicated as a causative agent in chronic active (type B) gastritis (13), gastric and duodenal ulcers (9,10), and gastric adenocarcinoma (22,23).…”

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confidence: 99%

Paracrystalline inclusions of a novel ferritin containing nonheme iron, produced by the human gastric pathogen Helicobacter pylori: evidence for a third class of ferritins

et al. 1993

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An abundant 19.3-kDa Helicobacter pylori protein has been cloned, and the sequence is homologous with a ferritin-like protein produced by Escherichia coli K-12. Homologies are also present with a number of eucaryotic ferritins, as well as with the heme group-containing bacterioferritins. All amino acids involved in chelation of inorganic iron by ferritins from humans and other higher species are conserved in the H. pylori protein. Consistent with the structural data indicating an iron-binding function, E. coli overexpressing the H. pylori ferritin-like protein accumulates almost 10 times more nonheme iron than vector controls, and the iron-binding activity copurifies with the 19.3-kDa protein. Immunoelectron microscopy of H. pylori, as well as of E. coli overexpressing the H. pylori gene, demonstrates that the gene product has a cytoplasmic location where it forms paracrystalline inclusions. On the basis of these structural and functional data, we propose that the H. pylori gene product (termed Pfr) forms the basis for a second class of bacterial ferritins designed to store nonheme iron.

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confidence: 99%

Paracrystalline inclusions of a novel ferritin containing nonheme iron, produced by the human gastric pathogen Helicobacter pylori: evidence for a third class of ferritins

et al. 1993

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“…In the study performed by Stolte et al (47), the frequency of lymphoid follicles in H. pylori-positive patients was found to be 54% and 85% in Zaitonun et al 's (48) study and 27% in the study conducted by Wyatt et al (49). When the results in our country were examined, the frequency of lymphoid follicles in H. pylori-positive patients was found to be 46.3% in Mete et al 's (19) study.…”

Section: Discussionmentioning

confidence: 91%

Retrospective Examination of the Results of Gastroscopy in Bandirma State Hospital in Terms of Helicobacter Pylori and Sydney Classification

Akay¹

2018

Clin Exp Health Sci

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“…The causal relationship between H. pylori and chronic superficial gastritis is well established, but that between H. pylori and peptic ulcer is rather difficult to establish on the basis of the available data [1] . The suggested mechanisms in antral organism cause a duodenal lesion including bacterial colonization of gastric metaplasia in the duodenum [22] , secondary changes in gastric acid or duodenal bicarbonate secretion [23,24] , or the changes caused by the infected organism and/ or the inflammatory response to the host [25,26] . Recently, the changes in gastric acid caused by H. pylori infection have drawn more attention, for inhibition of gastric acid secretion promoted duodenal ulcer healing even in the presence of H. pylori and inflammation of gastric antrum [27] .…”

Section: Discussionmentioning

confidence: 99%

Reduced secretion of epidermal growth factor in duodenal ulcer patients with Helicobacter pylori infection

Chen¹,

Zhang²,

Jiang³

et al. 2011

WJG

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AIM:To investigate the concentration changes of epidermal growth factor (EGF) in duodenal ulcer patients with Helicobacter pylori (H. pylori ) infection. METHODS:Immunoreactive concentration of somatostatin, gastrin and epidermal growth factor of gastric and saliva juice in healthy volunteers, and chronic gastritis and duodenal ulcer patients with H. pylori infection were measured by radioimmunoassay. RESULTS:Gastrin concentration of gastric juice in H. pylori -positive chronic gastritis (P > 0.05) and duodenal ulcer patients (P < 0.01) was higher than that of healthy volunteers (P < 0.05), whereas som atostatin concentration of gastric juice in chronic gastritis (P < 0.05) and duodenal ulcer patients (P < 0.01) was lower than that in healthy volunteers. Furthermore, EGF levels of gastric and saliva juice in duodenal ulcer patients with H. pylori infection (n = 10, 272.0 ng/L ± 96.3 ng/L and 8.3 ng/L ± 2.4 ng/L, respectively) were significantly lower than that in healthy volunteers (n = 12, 405.6 ng/ L ± 35.6 ng/mL and 22.0 ng/L ± 17.0 ng/L, respectively) and in H. pylori -positive chronic gastritis patients (n = 25, 423.0 ng/L ± 104.0 ng/L and 22.0 ng/L ± 11.1 ng/L, respectively (P < 0.05). CONCLUSION:A lower secretion of EGF may be a causative factor in the pathogenesis of H. pylori -positive duodenal ulcer.

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Chronic gastritis—a pathogenetic approach

Cited by 187 publications

References 59 publications

Paracrystalline inclusions of a novel ferritin containing nonheme iron, produced by the human gastric pathogen Helicobacter pylori: evidence for a third class of ferritins

Paracrystalline inclusions of a novel ferritin containing nonheme iron, produced by the human gastric pathogen Helicobacter pylori: evidence for a third class of ferritins

Retrospective Examination of the Results of Gastroscopy in Bandirma State Hospital in Terms of Helicobacter Pylori and Sydney Classification

Reduced secretion of epidermal growth factor in duodenal ulcer patients with Helicobacter pylori infection

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