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Gastric Atrophy (gastric + atrophy)

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Medical Sciences	100%

Selected Abstracts

Interleukin-2 Gene Polymorphisms Associated with Increased Risk of Gastric Atrophy from Helicobacter pylori Infection

HELICOBACTER, Issue 3 2005
Shozo Togawa
ABSTRACT Background., Gastric atrophy induced by Helicobacter pylori is thought to predispose patients to noncardiac gastric cancer development. However, the host genetic factors that influence the progression of gastric atrophy have not been elucidated. In this study, we examined the effects of cytokine polymorphisms on H. pylori -induced gastric atrophy. Methods., Blood samples were taken from 454 Japanese subjects. The interleukin-2 (IL-2; T-330G), IL-4 (C-33T), and IL-13 (C-1111T) polymorphisms were genotyped by polymerase chain reaction with confronting two-pair primers (PCR-CTPP). Anti- H. pylori IgG antibody and pepsinogen I and II were measured to diagnose H. pylori infection and atrophic gastritis. Results., The odds ratios (ORs) for the association between IL-2 polymorphism [OR = 2.78, 95% CI (confidence interval) = 1.26,6.17 (T/T to G/G)] or IL-4 polymorphism [OR = 2.22, 95% CI = 1.01,4.89 (T/C to C/C)] were increased significantly with gastric atrophy, whereas the corresponding OR of IL-13 polymorphism was decreased with gastric atrophy [OR = 0.61, 95% CI = 0.39,0.96 (C/T and T/T to C/C)]. There were no significant H. pylori seropositivity-related differences between these polymorphisms. We examined the relationship between these polymorphisms and gastric atrophy separately in H. pylori -seropositive and -seronegative groups. In the H. pylori -seropositive group, the IL-2 T/T (OR = 2.78, 95% CI = 1.12,6.93) had a significant association with gastric atrophy. Conclusions., These results reveal that the IL-2 gene polymorphism is associated with an increased risk of gastric atrophy induced by H. pylori infection and might predispose to gastric cancer. [source]

Impact of Helicobacter pylori on the Development of Vitamin B12 Deficiency in the Absence of Gastric Atrophy

HELICOBACTER, Issue 6 2002
Ender Serin
Abstract Background. Cobalamin (vitamin B12) deficiency is associated with Helicobacter pylori infection. This study examined how serum vitamin B12 levels relate to gastric mucosa H. pylori density and histology, and to hematological findings in patients with minimal or no gastric atrophy. A second aim was to confirm that H. pylori eradication therapy increases serum B12. Materials and Methods. Biopsies of the gastric mucosa from a population of dyspeptic patients were graded for level of chronic inflammation, neutrophil activity, atrophy, and H. pylori density. A total of 145 H. pylori -infected patients with minimal or no atrophy were included in the study. Serum cobalamin level, hemoglobin level, and mean corpuscular volume were measured in the 145 patients before eradication therapy, and in 65 of the subjects after treatment. The hematologic findings before and after eradication therapy and correlations between serum vitamin B12 level and histologic parameters, hematologic findings, and patient age were statistically analyzed. Results. There was no significant correlation between serum cobalamin level and patient age. Before treatment all the histopathological scores were inversely correlated with serum vitamin B12 level (p < .01) on univariate analysis. Only H. pylori density was significantly associated with B12 level on multivariate analysis. Serum hemoglobin and cobalamin levels were significantly increased after treatment, regardless of H. pylori eradication status (p < .001). Conclusion. The findings provide strong evidence that H. pylori infection is associated with cobalamin deficiency, and show that this is true even in patients with nonulcer dyspepsia and minimal or no gastric atrophy. [source]

Helicobacter pylori Infection and Gastroesophageal Reflux in a Population-Based Study (The HUNT Study)

HELICOBACTER, Issue 1 2007
Helena Nordenstedt
Abstract Background and Aim:, It has been suggested that Helicobacter pylori infection may prevent gastroesophageal reflux, possibly through gastric atrophy. Since, however, previous results are contradictory and no population-based studies are available, the relationship between H. pylori and reflux remains uncertain. The aim of this study was to investigate this relationship in a population-based, nested, case-control study. Methods:, From a cohort of 65,363 individuals, representing 71.2% of the adult population in the Norwegian county of Nord-Trondelag, we randomly selected 472 persons with recurrent reflux symptoms (cases) and 472 without such symptoms (controls). Occurrence of H. pylori and its virulence factor cagA was determined serologically, using an immunoblot assay. Gastric atrophy was assessed through serum levels of pepsinogen I. Odds ratios (OR) with 95% confidence intervals (CI), adjusted for potential confounding factors, represented relative risks. Results:,H. pylori infection was not associated with a decreased risk of reflux symptoms (OR 1.1, 95% CI 0.8,1.6), irrespective of positive cagA status (OR 1.1, 95% CI 0.8,1.5). Gastric atrophy reduced the risk of reflux symptoms (OR 0.2, 95% CI 0.0,0.6). Infection with H. pylori entailed a ninefold increase in the risk of gastric atrophy compared to non-infection (OR 8.9, 95% CI 2.0,39.9). Conclusions:,H. pylori infection, irrespective of cagA status, did not affect the occurrence of reflux symptoms in this population-based setting. Infected individuals are at increased risk of gastric atrophy, which in turn reduces reflux symptoms, but due to the low frequency of gastric atrophy among infected individuals overall, there was no association with reflux symptoms on a population level. [source]

Interleukin-2 Gene Polymorphisms Associated with Increased Risk of Gastric Atrophy from Helicobacter pylori Infection

Fundal gastritis as a potential cause of reflux oesophagitis

DISEASES OF THE ESOPHAGUS, Issue 1 2000
M. Newton
The transient lower oesophageal sphincter relaxations which allow reflux may be due to altered afferent pathways from the fundus. We aimed to determine whether fundal inflammation is the underlying cause. Two endoscopic biopsies were taken from each of the gastric antrum and fundus in 25 asymptomatic controls with a normal endoscopy (median age 54 range 13,83 years), and 33 patients with erosive oesophagitis (median age 52, 11,78 years). No patient had taken acid suppression therapy or antibiotics for at least 1 month. Sections were stained with haematoxylin and eosin and Giemsa stain and examined in a blinded fashion by one pathologist for the presence of gastritis (Sydney classification) and Helicobacter pylori. Chronic gastritis was common in both groups, but was usually mild. In Helicobacter pylori -negative subjects, there was significantly less chronic gastritis in the antrum and the fundus in oesophagitis patients than in controls (p < 0.05). When present, gastric atrophy was usually antral and mild in severity. There was no difference in the incidence of gastric atrophy in patients with oesophagitis compared with controls (24% compared with 40%; p > 0.05). Chronic gastritis is not more common in patients with oesophagitis, and is unlikely to play a part in the pathogenesis of this disease. [source]

Helicobacter pylori Infection and Gastroesophageal Reflux in a Population-Based Study (The HUNT Study)

Interleukin-2 Gene Polymorphisms Associated with Increased Risk of Gastric Atrophy from Helicobacter pylori Infection

Geographic Pathology of Helicobacter pylori Gastritis

HELICOBACTER, Issue 2 2005
Yi Liu
ABSTRACT Background and aim.,Helicobacter pylori is etiologically associated with gastritis and gastric cancer. There are significant geographical differences between the clinical manifestation of H. pylori infections. The aim of this study was to compare gastric mucosal histology in relation to age among H. pylori -infected patients from different geographical areas using the same grading system. The prevalence of atrophy and intestinal metaplasia were also compared with the respective gastric cancer incidence in the different countries. Methods., A total of 1906 patients infected with H. pylori from seven countries were evaluated. Entry criteria included H. pylori positive cases with antral and corpus biopsies between the ages of 18 and 75 years. The minimum number of cases required from a country was 100. Hematoxylin-eosin stained biopsies from antrum and corpus were scored semiquantitatively using the parameters suggested by the Sydney Classification System. Statistical evaluation was performed using Krusakal-Wallis test and Spearman's rank correlation test. Results., The severity of gastric atrophy varied among the different groups with the highest scores being present in Japan. The lowest scores were found in four European countries and in Thailand. The scores for intestinal metaplasia were low in general except for Xi-an, Japan, and Shanghai. For all the countries, the presence of atrophy in the antrum correlated well (r = 0.891) with the incidence of gastric cancer. Conclusion., Using a standardized grading system in a large study of H. pylori -related geographic pathology, we found major differences in the overall prevalence and severity of H. pylori gastritis in relation to age. These differences mirrored the respective incidences of gastric cancer in those geographical areas. [source]

Impact of Helicobacter pylori on the Development of Vitamin B12 Deficiency in the Absence of Gastric Atrophy

Mucosal Production of Antigastric Autoantibodies in Helicobacter pylori Gastritis

HELICOBACTER, Issue 3 2000
Gerhard Faller
Background. Apart form bacterial virulence factors of Helicobacter pylori, certain host factors influence the pathogenesis of H. pylori gastritis. In particular, antigastric autoantibodies that are detectable in the sera of a substantial proportion of H. pylori were shown to correlate with the development of gastric atrophy. The aim of this study was to analyze the possible antigastric autoimmune response in H. pylori gastritis at the site where the action is, i.e., in the gastric mucosa. Material and Methods. Gastric biopsy specimens from antrum and corpus mucosa of 24 H. pylori,infected and of 33 noninfected patients were cultured for 3 days, and tissue culture supernatants were analyzed for the amount of locally produced IgA and IgG. Antigastric autoantibodies were screened in the sera and in the supernatants by means of immunohistochemistry. Results. The infected patients had significantly higher concentrations of locally produced IgA, whereas the IgG concentrations were virtually the same in infected and noninfected patients. IgG or IgA antigastric autoantibodies, or both, were detectable only in the sera (38%) and supernatants (17%) of infected patients. Interestingly, the patient with the strongest local autoimmune response showed body-predominant H. pylori gastritis, with destruction of gastric glands and atrophy of the body mucosa. Conclusions. These results demonstrate that antigastric autoimmune reactions are detectable at the site of the disease and might be relevant for the pathogenesis of gastric mucosa atrophy in H. pylori gastritis. [source]

High incidence of newly-developed gastroesophageal reflux disease in the Japanese community: A 6-year follow-up study

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 3 2008
Masaki Miyamoto
Abstract Background and Aim:, We conducted a community-based study to assess the incidence of newly-developed gastroesophageal reflux disease (GERD). We also analyzed the risk factors of GERD occurrence. Methods:, A total of 322 patients without acid suppression therapy (135 men, mean age: 59.8 years), who lived in the Japanese community, took a QUEST questionnaire (a self-administered questionnaire for the screening of GERD) in 1998. Blood samples were taken for the measurement of an anti- Helicobacter pylori antibody and pepsinogen (PG) I/II to assess the grade of gastric atrophy. Of these patients, 289 scored less than six points and were diagnosed as non-GERD. Two-hundred-and-forty-one patients (95 men, mean age: 67.0 years) took the QUEST questionnaire again in 2004 (after 6 years). The incidence of newly-developed GERD was analyzed. These patients were categorized into three groups based on their initial PG I/II (group A: less than three, group B: three to six, and group C: more than six). The risk factors of GERD occurrence were evaluated. Results:, Of the 241 non-GERD patients, 37 patients (15.4%) developed GERD after 6 years. The incidence of newly-developed GERD in group C was significantly higher than both groups A and B (group A: 3.8% [three of 79], group B: 11.8% (11/93), group C: 33.3% (26/69), P < 0.01, respectively). The prevalence of H. pylori negativity, constipation, and medication of Ca antagonists in newly-developed GERD were significantly higher than in those who did not develop GERD. [Correction added after online publication on 1 July 2007: the preceding sentence has replaced one that read ,The prevalence of H. pylori negativity, constipation, and medication of Ca antagonists in newly-developed GERD were significantly higher than in those who did develop GERD.'] Conclusion:, The incidence of newly-developed GERD in the Japanese community was 16.5% for 6 years. The incidence of newly-developed GERD patients who scored a PG I/II over six was significantly higher than those who scored lower. H. pylori negativity, constipation, and medication of Ca antagonists might be risk factors of GERD occurrence. [source]

Genetic factors involved in the development of Helicobacter pylori -related gastric cancer

CANCER SCIENCE, Issue 11 2006
Nobuyuki Hamajima
Developmental process to gastric cancer by Helicobacter pylori infection consists of three steps: (1) H. pylori infection; (2) gastric atrophy development; and (3) carcinogenesis. In each step, genetic traits may influence the process, interacting with lifestyle. In the step of H. pylori infection, two lines of genetic polymorphisms were assumed: one influencing gastric acid inhibition interacting with smoking, and the other concerning innate immune response attenuation. The former includes functional polymorphisms of IL-1B (C-31T or tightly linked T-511C), and TNF-A (T-1031C and C-857T), and the latter possibly includes NQO1 C609T. In the step to gastric atrophy, polymorphisms pertaining to the signal transduction from cytotoxin-associated gene A (PTPN11 A/G at intron 3) and to T-cell responses (IL-2 T-330G and IL-13 C-1111T) were hypothesized. There are a limited number of epidemiological genotype studies on the final step of literal carcinogenesis, potentially interacting with smoking, a low vegetable and fruit intake, and salty foods, the well-documented risk factors. In past case-control studies on the associations between genotype and gastric cancer risk, the cases consisted of H. pylori -related and unrelated gastric cancer patients and the controls consisted of individuals including the uninfected (H. pylori unexposed and exposed) and the infected with and without gastric atrophy. Accordingly, it was not clear whether the observed risk was for H. pylori -related or -unrelated gastric cancer, nor which step was involved in the observed associations even when nearly all cases were H. pylori -related. In order to elucidate the genetic traits of H. pylori -related gastric cancer, stepwise evaluation will be required. (Cancer Sci 2006; 97: 1129,1138) [source]