Gastric Juice Prostaglandins and Peptide Growth Factors as Potential Markers of Chronic Atrophic Gastritis, Intestinal Metaplasia and Gastric Cancer: Their Potential Clinical Implications Based on this Pilot Study

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Abstract

Background

Gastric secretion can provide valuable information especially when Helicobacter pylori ( Hp) infection results in chronic atrophic gastritis (CAG) and intestinal metaplasia (IM) preceding adenocarcinoma (AdCa).

Aims

Looking for a potential biomarker of malignant transformation in the setting of chronic inflammation we studied the levels of prostaglandin E2 (PGE ₂), as well as peptide growth factors [epidermal growth factor (EGF) and transforming growth factor α (TGFα)], harbingers of injury and repair, in gastric juice aspirated at endoscopy from patients with CAG, CAG/IM, AdCa, and controls.

Methods

The PGE ₂, EGF and TGFα concentrations in the gastric juice were measured using radioimmunoassays (RIAs).

Results

In patients with AdCa gastric juice PGE ₂ increased fivefold versus controls ( P < 0.01) and almost threefold versus patients with CAG ( P < 0.05). The EGF levels in patients with AdCa were fourfold higher versus controls ( P < 0.001) and almost threefold higher versus CAG ( P < 0.05). In patients with CAG/IM the EGF levels were also almost 3 times higher versus controls. The TGFα levels in patients with AdCa were half the value of controls and CAG ( P < 0.05). In patients with CAG/IM the levels were as low as 1/5 of controls or CAG ( P < 0.05).

Conclusions

Testing the gastric juice for PGE ₂, EGF, and TGFα in patients with endoscopy and biopsy proven CAG, may be helpful in follow up of patients who may potentially progress to IM and ultimately AdCa. This could be considered as an adjunct to histologic assessment especially that even the best surveillance biopsy specimen regimens are inherited with sampling errors.

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Most cited references 40

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Nonsteroidal anti-inflammatory drugs (NSAIDs) represent one of the most highly utilized classes of pharmaceutical agents in medicine. All NSAIDs act through inhibiting prostaglandin synthesis, a catalytic activity possessed by two distinct cyclooxygenase (COX) isozymes encoded by separate genes. The discovery of COX-2 launched a new era in NSAID pharmacology, resulting in the synthesis, marketing, and widespread use of COX-2 selective drugs. These pharmaceutical agents have quickly become established as important therapeutic medications with potentially fewer side effects than traditional NSAIDs. Additionally, characterization of the two COX isozymes is allowing the discrimination of the roles each play in physiological processes such as homeostatic maintenance of the gastrointestinal tract, renal function, blood clotting, embryonic implantation, parturition, pain, and fever. Of particular importance has been the investigation of COX-1 and -2 isozymic functions in cancer, dysregulation of inflammation, and Alzheimer's disease. More recently, additional heterogeneity in COX-related proteins has been described, with the finding of variants of COX-1 and COX-2 enzymes. These variants may function in tissue-specific physiological and pathophysiological processes and may represent important new targets for drug therapy.

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Prostanoids are the cyclooxygenase metabolites of arachidonic acid and include prostaglandin (PG) D(2), PGE(2), PGF(2alpha), PGI(2), and thromboxne A(2). They are synthesized and released upon cell stimulation and act on cells in the vicinity of their synthesis to exert their actions. Receptors mediating the actions of prostanoids were recently identified and cloned. They are G protein-coupled receptors with seven transmembrane domains. There are eight types and subtypes of prostanoid receptors that are encoded by different genes but as a whole constitute a subfamily in the superfamily of the rhodopsin-type receptors. Each of the receptors was expressed in cultured cells, and its ligand-binding properties and signal transduction pathways were characterized. Moreover, domains and amino acid residues conferring the specificities of ligand binding and signal transduction are being clarified. Information also is accumulating as to the distribution of these receptors in the body. It is also becoming clear for some types of receptors how expression of their genes is regulated. Furthermore, the gene for each of the eight types of prostanoid receptor has been disrupted, and mice deficient in each type of receptor are being examined to identify and assess the roles played by each receptor under various physiological and pathophysiological conditions. In this article, we summarize these findings and attempt to give an overview of the current status of research on the prostanoid receptors.

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Recent epidemiologic evidence indicates that Helicobacter pylori infection increases the risk for gastric carcinoma. Infection with H. pylori leads to chronic gastritis, which usually persists for life unless treated with antimicrobial drugs. Because the great majority of gastritis patients never develop neoplasias, research concerning those who do may provide clues about carcinogenesis. In affluent populations, H. pylori infection leads to nonatrophic gastritis, predominantly involving diffusely the antrum (diffuse antral gastritis), the basic lesion seen in patients with duodenal ulcer, which has not been associated with increased risk for gastric carcinomas. In populations with high gastric cancer risk, H. pylori infection is associated with multifocal atrophic gastritis, which frequently advances to intestinal metaplasia, occasionally to dysplasia, and rarely to carcinoma. H. pylori infection increases the rate of proliferation of the gastric epithelial cells and decreases the gastric secretion of ascorbic acid, processes that may modulate the process of carcinogenesis. Infection with H. pylori is characterized by infiltration of lymphocytes, polymorphonuclear leukocytes, and macrophages in the gastric mucosa. There is considerable interest in investigating oxygen radicals originating in white blood cells and the possibility that they induce mutations with carcinogenic potential in the gastric epithelium.

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Author and article information

Contributors

: +1-915-5456626 , +1-915-5456634 , jerzy.sarosiek@ttuhsc.edu

Journal

Journal ID (nlm-ta): Dig Dis Sci

Title: Digestive Diseases and Sciences

Publisher: Springer US (Boston )

ISSN (Print): 0163-2116

ISSN (Electronic): 1573-2568

Publication date (Electronic): 22 June 2011

Publication date PMC-release: 22 June 2011

Publication date (Print): November 2011

Volume: 56

Issue: 11

Pages: 3220-3225

Affiliations

[1 ]Department of Internal Medicine, TTUHSC Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, 4800 Alberta Avenue, El Paso, TX 79905-2709 USA

[2 ]Medical University of Lublin, Lublin, Poland

[3 ]Collegium Medicum, UMK, Bydgoszcz, Poland

Article

Publisher ID: 1758

DOI: 10.1007/s10620-011-1758-z

PMC ID: 3208809

PubMed ID: 21695403

SO-VID: 8330bf73-1bd4-45d2-aa38-476df8531874

History

Date received : 25 August 2010

Date accepted : 14 May 2011

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ScienceOpen disciplines: Gastroenterology & Hepatology

Keywords: gastritis,intestinal metaplasia,peptide growth factors,adenocarcinoma,prostaglandins,helicobacter pylori

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ScienceOpen disciplines: Gastroenterology & Hepatology

Keywords: gastritis, intestinal metaplasia, peptide growth factors, adenocarcinoma, prostaglandins, helicobacter pylori

Gastric Juice Prostaglandins and Peptide Growth Factors as Potential Markers of Chronic Atrophic Gastritis, Intestinal Metaplasia and Gastric Cancer: Their Potential Clinical Implications Based on this Pilot Study

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Abstract

Background

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Conclusions

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Karger: Gastroenterology

Most cited references 40

Cyclooxygenase isozymes: the biology of prostaglandin synthesis and inhibition.

Prostanoid receptors: structures, properties, and functions.

Helicobacter pylori and gastric carcinogenesis.

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