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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic Helicobacter pylori infection causes a slight postprandial hypergastinemia, generally referred to as exaggerated or inappropriate gastrin release. This can be ablated by eradication of this infective agent. The expectations that this would further unravel the mysteries of the pathogenesis of peptic ulcer disease have not been fulfilled. It is now well established that of conventional acid secretory patterns such as basal acid secretion, maximum gastrin-stimulated acid secretion, and of sensitivity of the parietal cell to gastrin, only basal acid is modified by chronic H. pylori colonization. This particularly relates to basal secretion in duodenal ulcer patients, as basal secretion of otherwise healthy, chronically H. pylori-infected subjects appears to be affected in only a small proportion of subjects. It is of particular interest, however, that chronic H. pylori infection supplies a solid explanation why acid inhibitory pathways are deficient in duodenal ulcer disease, since this is reversible following H. pylori eradication as demonstrated by elegant studies with gastrin-releasing, peptide-stimulated acid secretion. Furthermore, it has gradually become apparent that exaggerated gastrin response is probably no more than an innocent bystander of chronic H. pylori infection. Paradoxically, in a small subset of patients, hypo-or anacidity accompanying chronic H. pylori infection can be reverted by H. pylori eradication, for currently unknown reasons.
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PMID:Long-term effects of Helicobacter pylori infection on acid and pepsin secretion. 904 96

The study of gastrin continues to serve as an excellent model for gastrointestinal regulatory processes. This review highlights some recent advances in the field by outlining gastrin biosynthesis, summarizing current understanding of gastrin receptors, describing the regulation of gastrin release, and discussing the clinical implications of gastrin in the pathogenesis of peptic ulcer disease. Emphasis is on three emerging areas of gastrin research: the novel finding that one of gastrin's posttranslational processing intermediates has biological activity distinct from that of the mature peptide; elucidation of gastrin's signal transduction mechanisms that mediate the trophic effects of the peptide; and the role of gastrin in peptic ulcer disease pathogenesis secondary to Helicobacter pylori infection.
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PMID:The G cell. 907 65

The pathogenesis of duodenal ulcer appears to be multifactorial, involving an imbalance between "aggressive" (e.g., acid and pepsin) and "defensive" (e.g., prostaglandin production, mucus/mucosal barrier, bicarbonate production, blood flow, cell regeneration) factors. Historically, the management of peptic ulcer disease has focused on controlling gastric acid secretion. Recent evidence suggests that Helicobacter pylori infection underlies many of the acid and gastrin abnormalities observed in duodenal ulcer disease and that it plays a pivotal role in the development of gastritis and ulceration.
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PMID:Ulcerogenesis: integrating the roles of Helicobacter pylori and acid secretion in duodenal ulcer. 912 21

Before the discovery of Helicobacter pylori infection some 12 years ago, three major disturbances in gastric physiology had been identified in patients with duodenal ulcer disease. These abnormalities were: impaired acid inhibition of gastrin release from the antral mucosa, increased basal and stimulated acid secretion by the body of the stomach and increased acid load in the duodenum. Some of these abnormalities in gastric function can now be explained by the effects of H. pylori infection. The increased release of gastrin by the antral mucosa in duodenal ulcer patients, for example, can be entirely explained by the effects of this organism. Other abnormalities, however, appear to have a genetic basis or may be due to environmental factors. Much work has been conducted on the relationship between H. pylori and the development of duodenal ulcer disease and this paper aims to review recent studies in the field and to give an overview of the latest understanding of the pathophysiology of this disease.
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PMID:Pathophysiology of duodenal ulcer disease. 2249 6

To clarify the prevalence of Helicobacter pylori infection in enlarged fold gastritis, serum immunoglobulin (Ig) G antibody to H pylori was determined in 19 patients with severely enlarged gastric body folds (the widest fold greater than 10 mm on the radiograph), 55 patients with moderately enlarged folds (6 to 10 mm) and 44 control subjects (5 mm or less). The prevalence of serum IgG antibody to H pylori in the severe (100%) and moderate groups (100%) was significantly higher than that in controls (34.1%) (P < 0.01). There were significant differences among the three groups in serum gastrin, pepsinogen I and pepsinogen II levels (severe had the highest levels, followed by moderate and then controls, P < 0.001). H pylori colonization in the gastric mucosa was confirmed by culture, urease test or both, and inflammation by hematoxylin and eosin stain in the 25 H pylori seropositive patients who underwent endoscopy and biopsy. Results suggest that H pylori infection is highly prevalent in enlarged fold gastritis. Further studies on enlarged fold gastritis and H pylori infection are needed.
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PMID:High prevalence of serum immunoglobulin G antibody to Helicobacter pylori and raised serum gastrin and pepsinogen levels in enlarged fold gastritis. 928 79

Helicobacter pylori infection is associated with duodenal and gastric ulcer disease, gastric cancer, and gastric mucosa-associated lymphoid tissue lymphoma. Although more than half the world's population harbors H. pylori, only a proportion will develop clinically significant disease. The specific clinical outcome of an individual can be examined as the modulation of host factors by H. pylori infection. Host acid-secretory status and sensitivity to gastrin can be modulated by H. pylori infection. Once H. pylori has established itself in the stomach, virtually everyone develops gastritis, and variations in gastritis patterns have been associated with different gastric acid responses to H. pylori infection. The patterns of gastritis are important because they seem to determine disease outcome. Blood group antigens have been implicated in studies of ulcer disease. Receptors to Lewis antigens in gastric mucosa indicate that host mucosal factors influence H. pylori attachment. Conversely, H. pylori strains express Lewis antigen-like molecules, suggesting an autoimmune component for some H. pylori-associated diseases. HLA genotypes may influence the host response to H. pylori infection, and those of H. pylori-infected individuals have been correlated with histological features. The clinical outcome of H. pylori infection is most likely a result of complex interactions among host, bacterial, and environmental factors. The mechanisms by which these diverse factors influence the pathogenesis of different clinical outcomes remain under investigation.
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PMID:What are the host factors that place an individual at risk for Helicobacter pylori-associated disease? 939 54

Helicobacter pylori infection increases gastric acid secretion in patients with duodenal ulcers but diminishes acid output in patients with gastric cancer and their relatives. Investigation of the basic mechanisms may show how H. pylori causes different diseases in different persons. Infection of the gastric antrum increases gastrin release. Certain cytokines released in H. pylori gastritis, such as tumor necrosis factor alpha and specific products of H. pylori, such as ammonia, release gastrin from G cells and might be responsible. The infection also diminishes mucosal expression of somatostatin. Exposure of canine D cells to tumor necrosis factor alpha in vitro reproduces this effect. These changes in gastrin and somatostatin increase acid secretion and lead to duodenal ulceration. But the acid response depends on the state of the gastric corpus mucosa. The net effect of corpus gastritis is to decrease acid secretion. Specific products of H. pylori inhibit parietal cells. Also, interleukin 1 beta, which is overexpressed in H. pylori gastritis, inhibits both parietal cells and histamine release from enterochromaffin-like cells. H. pylori also promotes gastric atrophy, leading to loss of parietal cells. Factors such as a high-salt diet and a lack of dietary antioxidants, which also increase corpus gastritis and atrophy, may protect against duodenal ulcers by decreasing acid output. However, the resulting increase of intragastric pH may predispose to gastric cancer by allowing other bacteria to persist and produce carcinogens in the stomach.
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PMID:How does Helicobacter pylori cause mucosal damage? Its effect on acid and gastrin physiology. 939 59

The peptic ulcer of gastric tube using for esophageal reconstruction is rare. We report herein five cases of peptic ulcer of gastric tube used for esophageal reconstruction after esophagectomy for esophageal carcinoma. The reconstructive route, in all cases, was posterior mediastinum. In one case, 10 days after esophagectomy, he had high grade fever and pneumonia of right lower lobe of lung. Endoscopic examination revealed a deep ulcerative lesion on anterior wall of gastric tube and fistula formation on membranous part of trachea. The partial resection of gastric tube was performed for closing to tracheo-gastro fistula. In other four cases, the location of ulcer was middle or lower third of gastric tube. One had multiple peptic ulcer and other had single. Two cases of four underwent post irradiation therapy. One case of then, the Helicobacter infection detected using by rapid urease test and histological examination. We analyzed of Helicobacter pylori infection and serum gastrin level of gastric tube in outpatients who have used gastric tube for esophageal reconstruction after radical esophagectomy. Helicobacter pylori infection was positive at 56% (9/16) of all patients. The serum gastrin level of patients who was positive of Helicobacter pylori infection is not significantly higher than that of patients who was negative. We consider that post operative irradiation therapy and Helicobacter infection might play in development of peptic ulcer of gastric tube.
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PMID:[Five cases of peptic ulcer of gastric tube after radical esophagectomy for esophageal carcinoma and analysis of Helicobacter pylori infection at gastric tube]. 945 13

Helicobacter pylori infection exerts variable effects on gastric acid secretion. It may increase acid secretion, decrease acid secretion or produce no overall change. The effect of the infection on acid secretion depends upon the relative extent to which the Helicobacter pylori gastritis affects the antral and body mucosa of the stomach. When there is antral predominant, body-sparing gastritis, there is increased gastrin release and this is accompanied by increased acid secretion. When there is a significant body gastritis, acid secretion is reduced and subjects may be completely achlorhydric. The majority of subjects have both antral gastritis and body gastritis and this results in no overall change in gastric acid secretion. There is now increasing evidence that the alteration which Helicobacter pylori infection exerts upon gastric acid secretion is a pivotal factor in determining the clinical outcome of the infection. Subjects in whom the infection produces acid hypersecretion develop duodenal ulcer disease due to the increased duodenal acid load. In subjects in whom the infection induces marked hypochlorhydria, there is an increased risk of gastric cancer. The hypochlorhydria probably plays an important role in the carcinogenic process as high intragastric pH markedly raises intragastric nitrite levels, profoundly lowers gastric juice ascorbic acid and allows colonization by nitrosating bacteria. The reason for the different functional responses to Helicobacter pylori infection is unclear but may be related to the host's pre-morbid acid secretory status.
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PMID:Alterations in gastric physiology in Helicobacter pylori infection: causes of different diseases or all epiphenomena? 949 57

Although Helicobacter pylori infection increases gastrin secretion, it is unknown whether this is a direct effect or requires activation of the immune system. We developed an H. pylori-infected human primary antral epithelial cell culture model to address this question. This culture protocol favors growth of H. pylori, and infected cultures could be maintained for up to 48 h. These cultures were enriched for gastrin (10-40%), somatostatin (2-5%), and gastric mucin (60-80%) cells but did not contain immunocytes. Bacterial attachment occurred in a random manner within 2 h of infection, although bacterial density was lower than in sections from infected patients. After 24 or 48 h, the bacterial microcolonies were similar in size to those seen in vivo, and at 24 h ultrastructural studies demonstrated well-developed pedestal formation underlying the bacteria. Coculture with H. pylori increased basal but not stimulated gastrin secretion at all time points >2 h. In conclusion, a newly developed cell culture model has been used to characterize the interactions between H. pylori and normal human antral epithelial cells.
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PMID:Helicobacter pylori-infected human antral primary cell cultures: effect on gastrin cell function. 972 49


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