Histomorphological characteristics of gastric mucosa in patients with Zollinger-Ellison syndrome or autoimmune gastric atrophy: Role of gastrin and atrophying gastritis

Lehy, Thérèse; Roucayrol, Anne‐Marie; Mignon, M

doi:10.1002/(sici)1097-0029(20000315)48:6<327::aid-jemt3>3.0.co;2-l

Cited by 30 publications

(18 citation statements)

References 76 publications

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“…Antiulcer medications are known to increase the gastric pH and permit colonization of the stomach by opportunistic pathogens, such as Acinetobacter baumannii, Klebsiella pneumoniae, and Pseudomonas spp., believed to contribute to the development of nosocomial pneumonia (8,36). Patients with pernicious anemia are colonized by organisms other than H. pylori and develop atrophic gastritis and elevated levels of gastrin in serum (9,18). Moreover, 2 weeks of proton pump therapy reduces gastric acid by 75% and is sufficient to permit bacterial colonization of the stomach in healthy volunteers (23).…”

supporting

confidence: 83%

“…In addition, the mouse stomach, which has a gastric acidic range of approximately 3 to 5 eq, provides an environment permissive for colonization by non-H. pylori organisms (42). Consistent with the mouse model presented here, prior studies have reported that increasing gastric pH in the human and mouse stomach results in bacterial overgrowth and subsequently the development of gastritis and metaplasia (9,18,35). In our study, reducing the gastric acidity to 1 to 2 eq was sufficient to observe bacterial overgrowth (42).…”

Section: Discussionmentioning

confidence: 99%

“…However, our study is the first to correlate Acinetobacter colonization with gastric inflammation and metaplasia. It is known that gastritis coincides with an increase in gastric pH and bacterial overgrowth (9,18). Furthermore, gastritis predominating in the corpus is thought to be due to an autoimmune phenomenon or pernicious anemia in which the incidence of H. pylori infection in these patients is low (9,35).…”

Section: Discussionmentioning

confidence: 99%

“…pylori is characterized by its ability to survive in the low-pH milieu of the stomach by generating an alkaline microenvironment. With reduced levels of acid (hypochlorhydria or achlorhydria), the competitive niche established by H. pylori dissipates and the human stomach becomes susceptible to colonization by other organisms (9,18). Gastric colonization by gram-negative bacteria other than H. pylori is common in intensive care unit patients, who often have an alkaline gastric pH due to routine treatment with antacids, proton pump inhibitors, and histamine 2 receptor antagonists.…”

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confidence: 99%

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Gastritis and Hypergastrinemia Due toAcinetobacter lwoffiiin Mice

Zavros

Rieder²,

Ferguson

et al. 2002

Infect Immun

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In mouse models and humans, Helicobacter pylori is associated with an increase in serum gastrin and gastrin-expressing (G) cells with a concomitant decrease in somatostatin-expressing D cells. Inflammation of the gastric mucosa can progress to metaplastic changes in the stomach and to decreased colonization by H. pylori and increased colonization by non-H. pylori organisms. In addition, about 20% of individuals with chronic gastritis are H. pylori negative, suggesting that other organisms may induce gastritis. Consistent with this hypothesis, we report here that Acinetobacter lwoffii causes the same histologic changes as does H. pylori. Gastric epithelial cells were isolated from the entire stomach by an enzymatic method for quantitation by both flow cytometry and morphometric analysis. Two months after mice were inoculated with H. pylori or A. lwoffii, the mucosal T-and B-cell numbers significantly increased. Helicobacter pylori causes chronic atrophic gastritis, and its presence is correlated with the development of peptic ulcer disease and gastric adenocarcinoma (19,25,27). However, there is also an association between colonization of the stomach by non-Helicobacter organisms and chronic atrophic gastritis (7,9,30). Approximately 25% of gastric cancer patients have no evidence of previous or current H. pylori infection based on serology (12). In addition, during long-term acid suppression, the presence of H. pylori and that of non -H. pylori bacteria are independent risk factors for the development of atrophic gastritis (29). Studies of several animal models and humans have clearly shown that bacteria are important in triggering mucosal damage and inflammation in the stomach (15,20,42). In addition, under hypochlorhydric conditions it is known that bacterial overgrowth by non-Helicobacter organisms triggers perturbations in the neuroendocrine and epithelial cell populations (42). The implications are that the pathology observed may not be specific for H. pylori but instead is the general response of the gastric mucosa to colonization by bacteria.H. pylori is characterized by its ability to survive in the low-pH milieu of the stomach by generating an alkaline microenvironment. With reduced levels of acid (hypochlorhydria or achlorhydria), the competitive niche established by H. pylori dissipates and the human stomach becomes susceptible to colonization by other organisms (9, 18). Gastric colonization by gram-negative bacteria other than H. pylori is common in intensive care unit patients, who often have an alkaline gastric pH due to routine treatment with antacids, proton pump inhibitors, and histamine 2 receptor antagonists. Antiulcer medications are known to increase the gastric pH and permit colonization of the stomach by opportunistic pathogens, such as Acinetobacter baumannii, Klebsiella pneumoniae, and Pseudomonas spp., believed to contribute to the development of nosocomial pneumonia (8,36). Patients with pernicious anemia are colonized by organisms other than H. pylori and develop atrophic gastritis an...

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supporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Gastritis and Hypergastrinemia Due toAcinetobacter lwoffiiin Mice

Zavros

Rieder²,

Ferguson

et al. 2002

Infect Immun

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“…In fact, gastrin exerts a trophic effect on ECL-cells, which leads to hyperplasia and, in some cases, to gastric endocrine tumors (Waldum et al 1998, Lehy et al 2000).…”

Section: Introductionmentioning

confidence: 99%

Gastric endocrine tumors type I: treatment with long-acting somatostatin analogs

Campana¹,

Nori²,

Pezzilli³

et al. 2008

Endocrine Related Cancer

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Gastric endocrine tumors associated with autoimmune chronic atrophic gastritis (gastric carcinoid type I) are almost exclusively benign lesions with little risk of deep invasion of the gastric parietal wall. For this reason, the role of octreotide in the treatment of these neoplastic lesions is controversial. Nine patients with more than five type I gastric endocrine tumors each !1 cm in size, without invasion of the muscularis propria and with Ki-67 index lower than 3%, were treated with long-acting somatostatin analogs for 12 months. After 6 months and again after 12 months, all the patients underwent upper gastrointestinal (GI) endoscopy with multiple biopsies. The plasma chromogranin A (CgA) levels and the gastrin levels in the serum were also determined. In all patients, the gastric neoplastic lesions disappeared after 12 months of somatostatin analog therapy. We also observed a significant reduction of CgA and gastrin levels at 6 and at 12 months of therapy as compared with the baseline values. We demonstrate that somatostatin analog treatment provokes the pathological regression of type I gastric carcinoids. This therapeutic approach should be considered as a valid option in selected patients with multiple type I gastric endocrine tumors.

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Introduction to histological studies of gastric secretion

Lamberts

2000

Microsc. Res. Tech.

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Histomorphological characteristics of gastric mucosa in patients with Zollinger-Ellison syndrome or autoimmune gastric atrophy: Role of gastrin and atrophying gastritis

Cited by 30 publications

References 76 publications

Gastritis and Hypergastrinemia Due toAcinetobacter lwoffiiin Mice

Gastritis and Hypergastrinemia Due toAcinetobacter lwoffiiin Mice

Gastric endocrine tumors type I: treatment with long-acting somatostatin analogs

Introduction to histological studies of gastric secretion

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