Extent Of Atrophic Gastritis Research Articles

Occurrence of gastric cancer in patients with atrophic gastritis during long-term follow-up

Background: Additional data on the incidence of gastric neoplasia in the Chinese atrophic gastritis (AG) population during long-term follow-up are needed and the influence of the endoscopic surveillance interval on gastric neoplasia occurrence remains unknown.Aims: Retrospectively investigated the occurrence of gastric cancer (GC) and precancerous lesions in AG patients during long-term follow-up and assessed risk factors, such as the endoscopic surveillance interval for the development of gastric neoplasia.Methods: This study enrolled 332 AG patients who underwent initial gastroscopy from 2002 to 2005. Following parameters were collected: age, gender, smoking history, H. pylori infection, location of atrophy and intestinal metaplasia (IM), surveillance interval, follow-up duration, and neoplasia occurrence.Results: Gastric neoplasia was diagnosed in 16 patients. The annual incidence rates per person-year of total gastric neoplasia, gastric high-grade intraepithelial neoplasia (HGIN), early GC and advanced GC were 0.53%, 0.07%, 0.20% and 0.33%, respectively. A multivariate Cox analysis not accounting for the extent of AG and/or IM showed that the risk factors for GC development among AG patients included the presence of AG and/or IM involving both antral and corporal (p<.001, HR 2.898) and H. pylori infection (p=.018, HR 3.946). In the extensive AG and/or IM group, a 2- to 3-year surveillance interval might be instructive in early detection of GC (p=.008, HR 0.015).Conclusions: Our data reveal an annual incidence rate of 0.53% per person-year for GC and HGIN in AG patients. A 2- to 3-year surveillance interval may be suitable for patients with extensive AG and/or IM.

New opportunities for the prevention of gastric cancer

The approvals and provisions of the Management of Helicobacter pylori infection-the Maastricht V/ Florence Consensus Report and those of the Kyoto Global Consensus Conference on H. pylori-associated gastritis, concerning with the primary and secondary prevention of gastric cancer (GC), unambiguously suggest that H. pylori infection is the most important risk factor of GC. Accordingly, the basis for the primary and secondary prevention of GC is the optimization of H. pylori eradication therapy. The clear direct relationship of the risk of GC to the severity and extent of atrophic gastritis, intestinal metaplasia and dysplasia and no reversal of intestinal metaplasia and dysplasia in the presence of H. pylori eradication presume that gastroprotective agents should be used for primary and secondary prevention. Experimental and clinical findings can lead to the conclusion that rebamipide is a highly effective and safe agent for the primary and secondary prevention of GC in patients with and without H. pylori infection, by optimizing anti-Helicobacter therapy, its anti-inflammatory effect and ability to restore the cellular structure of the gastric epithelium.

Association of the Extent of Atrophic Gastritis With Specific Dyspeptic Symptoms.

Background/AimsIt remains unclear whether atrophic gastritis can affect dyspeptic symptoms. We aimed to investigate whether the extent of atrophic gastritis is associated with specific dyspeptic symptoms.MethodsConsecutive adults in a routine health-checkup program were enrolled in the study. The extent of atrophic gastritis was classified into 3 groups based on the Kimura-Takemoto criteria; the gastritis with no or little atrophy (group A: C0), the gastritis with atrophy mainly in the antrum (group B: C1 and C2), and the gastritis with atrophy in the large area of the corpus (group C: C3 and O). Upper gastrointestinal symptoms were categorized into “typical reflux symptoms,” “epigastric pain syndrome (EPS)-related symptoms,” and “postprandial distress syndrome (PDS)-related symptoms.”ResultsA total of 1827 patients (1009 males, mean age 45.1 years) were included in the analysis. The subgroups of atrophic gastritis were as follows: group A (n = 1218, 66.7%), group B (n = 392, 21.4%), and group C (n = 217, 11.9%). Typical reflux, EPS-related, and PDS-related symptoms were present in 10.5%, 19.8%, and 16.2% of the subjects, respectively. PDS-related and EPS-related symptoms were significantly more prevalent in the group C of male patients and the group B of female patients, respectively, compared with other groups. PDS-related and EPS-related symptoms were independently associated with the group C in males (OR, 2.123; 95% CI, 1.090–4.136) and the group B in females (OR, 2.571; 95% CI, 1.319–5.025), respectively.ConclusionsThe extent of atrophic gastritis appears to affect the generation of specific dyspeptic symptoms in a gender-dependent manner.

Indicators of apoptosis in the gastric mucosa in patients with atrophic gastritis among the indigenous and nonindigenous dwellers of Evenkia

To study the indicators of apoptosis in the gastric mucosa (GM) in relation to atrophy and the presence of CagA gene- containing Helicobacter pylori strains in the indigenous and nonindigenous dwellers of Evenkia. Clinical and morphological examinations and fibrogastroscopy of GM were performed in 159 Caucasians and 136 Mongoloids (Evenks). The TUNEL assay was used to determine GM apoptosis in 24 Caucasians and 22 Evenks and the H. pylori strains containing the CagA gene were detected in all the 295 patients. The extent of atrophic gastritis in the gastric antrum and body was higher in the Caucasians than in the Evenks. The total indicator of GM apoptosis in the gastric antrum was 5.19 ± 0.26% in the newcomers and 4.04 ± 0.28% in the aboriginals (p = 0.01). Apoptosis in both populations was associated with GM atrophy and the presence of H. pylori strains containing CagA gene. There were ethnic differences in the extent of atrophic gastritis, which may be attributable to differences in the rate of GM apoptosis and the spread of H. pylori strains containing CagA gene in the indigenous and non-indigenous dwellers of Evenkia.

Helicobacter pylori-Induced Signaling Pathways Contribute to Intestinal Metaplasia and Gastric Carcinogenesis.

Helicobacter pylori (H. pylori) induces chronic gastric inflammation, atrophic gastritis, intestinal metaplasia, and cancer. Although the risk of gastric cancer increases exponentially with the extent of atrophic gastritis, the precise mechanisms of gastric carcinogenesis have not been fully elucidated. H. pylori induces genetic and epigenetic changes in gastric epithelial cells through activating intracellular signaling pathways in a cagPAI-dependent manner. H. pylori eventually induces gastric cancer with chromosomal instability (CIN) or microsatellite instability (MSI), which are classified as two major subtypes of gastric cancer. Elucidation of the precise mechanisms of gastric carcinogenesis will also be important for cancer therapy.

M1908 Extent of Atrophic Gastritis Graded by Autofluorescence Imaging is Predictive for Metachronous Gastric Cancer After Helicobacter pylori Eradication in Patients With History of Endoscopic Resection for Early Gastric Cancer

M1908 Extent of Atrophic Gastritis Graded by Autofluorescence Imaging is Predictive for Metachronous Gastric Cancer After Helicobacter pylori Eradication in Patients With History of Endoscopic Resection for Early Gastric Cancer

Circulating acylated ghrelin level decreases in accordance with the extent of atrophic gastritis

We attempted to clarify the significance of atrophic change of gastric mucosa for reduction of plasma ghrelin concentration irrespective of Helicobacter pylori (Hp) infection. Plasma acylated (acyl-)ghrelin concentration in 220 subjects, both with and without atrophic gastritis, was measured with an enzyme immunoassay kit. The extent of atrophic change of gastric mucosa was assessed and graded endoscopically. Hp infection was determined by assay of the anti-Hp antibody with an ELISA assay kit. Plasma acyl-ghrelin concentration was significantly lower in the Hp positive than the Hp negative group, and Hp eradication significantly increased plasma acyl-ghrelin concentrations in Hp positive subjects. Plasma acyl-ghrelin was significantly lower in subjects with severely atrophic gastritis than in those with mild or moderate atrophic gastritis, irrespective of Hp infection or age group (<60 years old or > or = 60 years old). In male subjects with a normal body mass index, plasma acyl-ghrelin concentrations in subjects with severely atrophic gastritis were significantly lower than those in subjects with mildly or moderately atrophic gastritis, suggesting that the results of the study are independent of emaciation or obesity. Logistic regression analysis showed that gastric atrophy is the key factor that modulates plasma acyl-ghrelin levels. The results suggest that plasma acyl-ghrelin concentration decreases in accordance with the extent of atrophic change in gastric mucosa irrespective of Hp infection, indicating that the low plasma acyl-ghrelin level of subjects with Hp infection is mainly caused by the progress of atrophic changes in gastric mucosa.

Relation of Helicobacter pylori infection to plasma vitamin B12, folic acid, and homocysteine levels in patients who underwent diagnostic coronary arteriography

The aim of this study was to test the hypothesis that chronic atrophic gastritis induced by Helicobacter pylori (H. pylori) causes malabsorption of vitamin B12 and folate in food, leading ultimately to an increase in circulating homocysteine levels. We performed endoscopy with stomach biopsy and measured fasting plasma homocysteine, vitamin B12, and folate levels in 93 patients who underwent diagnostic coronary arteriography. The patients were divided into two groups according to the presence (n = 57) or absence (n = 36) of H. pylori infection. Positive H. pylori infection was defined as positive H. pylori histology of biopsy specimens from the stomach. The extent of atrophic gastritis was endoscopically graded from 0 to 6. There were no differences in age, sex, or traditional coronary risk factors between the two groups. Atrophy scores of the stomach were greater in patients with H. pylori infection than in patients without (3.9 +/- 1.4 vs 2.2 +/- 1.8, p < 0.0001). Patients with H. pylori infection had lower levels of vitamin B12 (630 +/- 222 vs 747 +/- 259 pg/ml, p = 0.02) and folate (6.2 +/- 2.1 vs 7.4 +/- 2.8, p = 0.046), as well as higher levels of homocysteine (11 +/- 4.9 vs 8.3 +/- 2.1 nmol/ml, p = 0.01), than did patients without H. pylori infection. Plasma homocysteine levels correlated inversely with plasma vitamin B12 and folate levels and positively with atrophic scores. This study suggests that H. pylori-induced chronic atrophic gastritis decreases plasma vitamin B12 and folic acid levels, thereby increasing homocysteine levels. However, this effect does not seem to be strong.

Relation of Helicobacter pylori infection to plasma vitamin B 12, folic acid, and homocysteine levels in patients who underwent diagnostic coronary arteriography

OBJECTIVE: The aim of this study was to test the hypothesis that chronic atrophic gastritis induced by Helicobacter pylori ( H. pylori) causes malabsorption of vitamin B 12 and folate in food, leading ultimately to an increase in circulating homocysteine levels. METHODS: We performed endoscopy with stomach biopsy and measured fasting plasma homocysteine, vitamin B 12, and folate levels in 93 patients who underwent diagnostic coronary arteriography. The patients were divided into two groups according to the presence (n = 57) or absence (n = 36) of H. pylori infection. Positive H. pylori infection was defined as positive H. pylori histology of biopsy specimens from the stomach. The extent of atrophic gastritis was endoscopically graded from 0 to 6. RESULTS: There were no differences in age, sex, or traditional coronary risk factors between the two groups. Atrophy scores of the stomach were greater in patients with H. pylori infection than in patients without (3.9 ± 1.4 vs 2.2 ± 1.8, p < 0.0001). Patients with H. pylori infection had lower levels of vitamin B 12 (630 ± 222 vs 747 ± 259 pg/ml, p = 0.02) and folate (6.2 ± 2.1 vs 7.4 ± 2.8, p = 0.046), as well as higher levels of homocysteine (11 ± 4.9 vs 8.3 ± 2.1 nmol/ml, p = 0.01), than did patients without H. pylori infection. Plasma homocysteine levels correlated inversely with plasma vitamin B 12 and folate levels and positively with atrophic scores. CONCLUSIONS: This study suggests that H. pylori-induced chronic atrophic gastritis decreases plasma vitamin B 12 and folic acid levels, thereby increasing homocysteine levels. However, this effect does not seem to be strong.

Gastric cancer: pathogenesis, risks, and prevention.

Intestinal (IGCA) and diffuse (DGCA) gastric adenocarcinomas, the two main microscopic subtypes, are dissimilar regarding their epidemiological and demographic characteristics. Both tumor types comprise approximately 40% of all gastric adenocarcinomas. The DGCAs more often occur in young age groups, more often affect the corpus, and are less infrequently associated with atrophic gastritis and intestinal metaplasia than the IGCAs. The risk of both DGCA and IGCA is increased in the presence of Helicobacter pylori infection, and the risk rises with increases in grade and extent of atrophic gastritis and intestinal metaplasia. It is likely that the development of up to 80% of the DGCAs and IGCAs can be prevented with early eradication of the H. pylori infection. The pathogenesis and morphogenesis of DGCAs are unknown, but the morphogenesis of IGCAs includes identifiable precancerous conditions such as atrophic gastritis and intestinal metaplasia as well as identifiable precancerous lesions (adenomas, dysplasias). Atrophic gastritis is a direct result of the H. pylori infestation. Atrophic gastritis, for unknown reasons, appears in more than half of the infected subjects during their lifetime. H. pylori gastritis triggers a variety of reactions, with the reaction cascades resulting in errors of the cell genome and ending up as neoplastic tumors.

Most Gastric Cancer Occurs on the Distal Side of the Endoscopic Atrophic Border

Background: The endoscopic atrophic border indicates the extent of atrophic gastritis. The aims of this study were to examine the relation of intestinal and diffuse types of gastric cancer to the atrophic border and to study the pathologic condition of the atrophic border. Methods: In 83 patients with gastric cancer the extent of atrophic gastritis was assessed macroscopically. In 46 patients gastric biopsy specimens were also taken, to compare the histologic features of gastritis proximal and distal to the atrophic border. Results: Eighty-five per cent of gastric cancers (including 93% of intestinal type) occurred on the distal side of the atrophic border. Early diffuse gastric cancer arose closer to the atrophic border than intestinal-type cancer and was more likely to be sited proximal to it. Histologically, the grade of polymorphonuclear cell infiltration (inflammatory activity) and Helicobacter pylori density were significantly greater on the proximal side (P < 0.05), whereas the grades of glandular atrophy and intestinal metaplasia were significantly greater distally (P < 0.001). Conclusions: The atrophic border delineates the area of atrophic gastritis and intestinal metaplasia, and it is within the distal part of the stomach that gastric cancer occurs most frequently. Endoscopists should observe the distal side particularly carefully to identify early gastric cancer. The relationship of the two histologic types of cancer to areas of intestinal metaplasia and 'active' inflammation may have implications for the pathogenesis of cancer and, if so, for the potential protective effect of H. pylori eradication.

Relationship between the presence of serum anti-Helicobacter pylori antibody and the extent of atrophic gastritis

Relationship between the presence of serum anti-Helicobacter pylori antibody and the extent of atrophic gastritis

加齢による胃の形態的変化と機能的変化の関連 胃排出を中心に

The authors investigated the relationship between morphological changes and functional changes of the stomach with ageing, especially in term of change of gastric emptying in 92 healthy subjects. We checked the difference in chronological age and the stomach age in these subjects (in order to assess these subjects). The morphological change was evaluated by extent of atrophic gastritis in endoscopical atrophic border and histological findings of biopsy specimens, and the functional change was evaluated by maximal acid output in gastric secretion. Atrophic gastritis was expanded and maximal acid output was significantly reduced with ageing. From these results we confirmed that there was no difference between the chronological age and the stomach age and the quality of these subjects was very good. Gastric emptying was investigated by the acetaminophen method. In spite of ageing, gastric emptying was almost constant in these healthy subjects.

慢性萎縮性胃炎における組織性カリクレインの消長

We measured amount of tissue kallikrein of gastric mucosa in 39 patients of chronic gastritis by sandwich type enzyme linked immunosorbent assay (S-ELISA) . Amount of tissue kallikrein was 9.1±4.4 ng/g tissue (mean±S.E.) in gastric mucosa of gastric glands, and was about twenty five times as much as it in the parts of atrophic gastric mucosa of them. The quantity of kallikrein was in proportion to age and the extent of atrophic gastritis. It was speculated that tissue kallikrein would participate in inflammatory atrophic change of gastric mucosa in chronic gastritis.