Effect of Helicobacter pylori eradication on antral somatostatin cell density in humans

Tham, T. C. K.; Chen, Li; Dennison, Nathan; Johnston, C.F.; Collins, J. S. A.; Ardill, Joy; Buchanan, K.D.

doi:10.1097/00042737-199804000-00003

Cited by 30 publications

(20 citation statements)

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“…They based this idea on the finding that D cell density increased after eradication, but was unchanged under conditions of persistent infection after three different treatment regimens. 40 Our better controlled study, by comparing the changes in antral and gastric juice SST concentrations between success and failure in eradication with dual therapy in peptic ulcer patients, further confirmed that H. pylori status, but not drugs, affected gastric SST. 41…”

Section: Interventional Human Study Of Somatostatin In H Pylori Infesupporting

confidence: 57%

“…21,37,39 Because many different kinds of drugs have been used to eradicate H. pylori in various studies, one cannot rule out the effect of drugs on SST levels. Tham et al 40 reported that an increase in D cell density accompanied by H. pylori eradication was unlikely to be a nonspecific effect of the eradication therapy itself. They based this idea on the finding that D cell density increased after eradication, but was unchanged under conditions of persistent infection after three different treatment regimens.…”

Section: Interventional Human Study Of Somatostatin In H Pylori Infementioning

confidence: 99%

“…Effects of ammonia solution, administered orally for 2 weeks (white bars) or 4 weeks (black bars), on the number (nb) of somatostatin (D)-, and somatostatin receptor subtype 2 (SSTR-2) peptide[31][32][33][34][35][36][37][38][39][40][41]-labeled cells per unit area (0.29 mm 2 ) in the antral mucosa, and on portal gastrin levels in rats. Each bar represents the mean Ϯ SE value of five rats.…”

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confidence: 99%

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Helicobacter pylori and gut hormones

Kaneko

Konagaya

Kusugami

2002

Journal of Gastroenterology

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Helicobacter pylori infection has been found to decrease the expression of antral somatostatin and to increase the release of the acid-stimulating hormone gastrin. The reversal of these changes in gut hormones by the eradication of H. pylori, and in-vivo and in-vitro studies in animals either infected with H. pylori or exposed to H. pylori-related materials may support the somatostatin-gastrin link theory in the pathophysiology of H. pylori infection. The following mechanisms have been proposed to explain the H. pylori infection-associated changes in gut hormones; (1) ammonia produced by H. pylori and monochloramine, (2) effect on somatostatin receptor subtype-2, (3) action of lipopolysaccharide from H. pylori on somatostatin receptor, (4) inflammatory cells and mediators, and (5) bacterial strain diversity. H. pylori infection can alter gastric acid secretion in both directions. The elevated acid secretion in patients with duodenal ulcer is decreased by H. pylori eradication, and is accompanied by the normalization of gut hormones in patients whose H. pylori-induced gastritis is limited to the antrum with hyperacidity. Corpus gastritis and the subsequent development of mucosal atrophy induced by H. pylori result in decreased acid secretion, although the mechanism underlying H. pylori-induced atrophy in some subjects remains unclear. Hypoacidity enhances corpus atrophy and increases gastrin secretion, mediated via a physiological suppression of somatostatin release, features that are also observed in H. pylori infection. Therefore, the capacity of acid secretion and distribution of gastritis or atrophy should be taken into consideration when we discuss the affect of H. pylori on gut hormones.

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Section: Interventional Human Study Of Somatostatin In H Pylori Infesupporting

confidence: 57%

Section: Interventional Human Study Of Somatostatin In H Pylori Infementioning

confidence: 99%

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confidence: 99%

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Helicobacter pylori and gut hormones

Kaneko

Konagaya

Kusugami

2002

Journal of Gastroenterology

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“…Moreover, it should be noted that 20 out of 21 studies demonstrated the reduced level of serum gastrin by H. pylori eradication therapy, suggesting improvement of inflammation in the corpus (table 2) [18, 19, 21, 22,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49]. The level of somatostatin and the number of D cells have been reported to increase after therapy [38, 45,][50], although this requires biopsy specimens for the estimation.…”

Section: Pepsinogen Gastrin and Gastric Acid Secretionmentioning

confidence: 99%

“…The level of somatostatin and the number of D cells have been reported to increase after therapy [38, 45,][50], although this requires biopsy specimens for the estimation.…”

Section: Pepsinogen Gastrin and Gastric Acid Secretionmentioning

confidence: 99%

Biomarkers in Patients with Gastric Inflammation: A Systematic Review

et al. 2005

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Background: The importance of examining the status of gastric inflammation has been acknowledged; the new classification by the updated Sydney system (USS) allows us to evaluate the quantitative status of gastric inflammation. However, this system is based on the histological classification derived from biopsy specimens. Therefore, more convenient, objective and practical biomarkers are recommended. Aim: We undertook a systematic review to find out potential biomarkers by summarizing the relationship between biomarkers and grades of inflammation. Methods: By a primary search via Medline up to December 2004, we extracted a total of 6,526 papers that described biomarkers for human gastric inflammation. All papers were screened by title and abstract. The authors then retrieved 435 citations for complete review; ultimately 231 were appropriate for inclusion criteria. These papers were subclassified into several categories and summarized by each author. Results: In addition to standard markers such as pepsinogens, we confirmed the close relationship between the levels of several biomarkers including gastrin, interleukin-8, HLA class II molecules, reactive oxygen species, and the histological grades. Conclusions: This review provides valuable information describing the clinical implication of these biomarkers for evaluating the static conditions or dynamic alterations of human gastric inflammation.

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Effect of Helicobacter pylori Infection in Barrett’s Esophagus and the Genesis of Esophageal Adenocarcinoma

Clark

2003

World j. surg.

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The relation between Helicobacter pylori and gastroesophageal reflux disease is unclear. Recent reports have suggested a possible protective role for H. pylori, particularly in preventing the complications of gastroesophageal reflux disease (GERD). The purpose of this article is to present a brief overview of the recent literature regarding the role of H. pylori in the genesis of the complications of GERD, focusing on Barrett's esophagus and esophageal adenocarcinoma. The prevalence of H. pylori infection in the population of the West is around 40% and is not different in cohorts of patients with GERD. When the infection induces pangastritis or corpus-predominant gastritis, there may be concomitant reduced gastric acid secretion. Eradication of the bacteria in this subgroup of patients may enhance gastric acid secretion and provoke reflux symptoms. H. pylori organisms do not colonize the specialized intestinal metaplasia characteristic of Barrett's esophagus. H. pylori infection rates in gastric mucosa of patients with Barrett's esophagus occur at a similar or slightly lower frequency than is found in controls. Gastric infection with cagA-positive strains of H. pylori appears to be uncommon in patients with Barrett's esophagus. Furthermore, epidemiologic studies indicate that cagA-positive strains are protective against esophageal adenocarcinoma. Several investigators have proposed that the decreasing prevalence of H. pylori infection might be an important factor in the rising incidence of this tumor.

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Effect of Helicobacter pylori eradication on antral somatostatin cell density in humans

Cited by 30 publications

References 0 publications

Helicobacter pylori and gut hormones

Helicobacter pylori and gut hormones

Biomarkers in Patients with Gastric Inflammation: A Systematic Review

Effect of Helicobacter pylori Infection in Barrett’s Esophagus and the Genesis of Esophageal Adenocarcinoma

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