Incidence of chronic atrophic gastritis: systematic review and meta-analysis of follow-up studies

Adamu, Mariam; Weck, Melanie N.; Gao, Lei; Brenner, Hermann

doi:10.1007/s10654-010-9482-0

Cited by 113 publications

(87 citation statements)

References 32 publications

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“…In addition, because HP infection is a well-established risk factor for GC and the inflammation caused by HP infection is thought to cause atrophic gastritis (AG) and GC (13)(14)(15)(16), we also assessed the difference among ABO genotypes in AG prevalence and HP infection.…”

Section: Introductionmentioning

confidence: 99%

ABO Genotype and the Risk of Gastric Cancer, Atrophic Gastritis, and Helicobacter pylori Infection

Nakao

Matsuo

Ito

et al. 2011

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: Although several studies have investigated the association between ABO blood type and risk of gastric cancer (GC), atrophic gastritis (AG), and Helicobacter pylori (HP) infection, no study has investigated these associations by using ABO genotype.Methods: We conducted a case-control study in 703 patients with GC and 1,465 noncancer patients. We also conducted a cross-sectional study by using 1,406 of these 1,465 controls, who were examined for pepsinogens and anti-HP IgG antibody levels in serum. ABO genotype was determined from single nucleotide polymorphisms in ABO gene. We used rs8176719 to mark the O allele, and rs8176746 and rs8176747 to mark the B allele. ORs and 95% CIs were calculated by a multivariate logistic model.Results: We observed significant associations between ABO genotype and GC, AG, and HP infection. ORs (95% CIs) of GC were 0.70 (0.50-0.99) for OO and 0.53 (0.36-0.77) for BO relative to AA genotype. An increased risk of GC was observed with addition of the A allele (P trend < 0.001), and a decreased risk with that of the B allele (P trend ¼ 0.023). An OR of AG was 0.73 (95% CI, 0.53-0.99) for blood type B relative to blood type A, and an OR of HP infection was 0.39 (95% CI, 0.17-0.87) for BB relative to AA genotype.Conclusion: This study identified a statistically significant association between ABO genotype and GC risk. In addition, ABO gene locus may influence AG prevalence and HP infection.Impact: Further studies are necessary to confirm these findings. Cancer Epidemiol Biomarkers Prev; 20(8); 1665-72. Ó2011 AACR.

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Section: Introductionmentioning

confidence: 99%

ABO Genotype and the Risk of Gastric Cancer, Atrophic Gastritis, and Helicobacter pylori Infection

Nakao

Matsuo

Ito

et al. 2011

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…Hp infection is a risk factor for occurrence of AG. A metaanalysis showed that the relative risk of Hp positive patients for AG was 5.0 compared to Hp negative patients (16). However, it is unclear whether Hp infection increases the risk for disease progression in AG patients with or without intestinal metaplasia and dysplasia and whether anti-Hp therapy is necessary under this condition.…”

Section: Discussionmentioning

confidence: 99%

Analysis of alarming signals for the progression of atrophic gastritis to dysplasia

Qiang

Zhou

Wang

et al. 2012

Rev. esp. enferm. dig.

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Background and aims: atrophic gastritis (AG) and dysplasia are precancerous lesions, with which early surveillance of disease progression is particularly important for patients. The present study aimed to explore potential alarming signals for atrophic gastritis progression towards dysplasia.Methods: clinical data for patients with AG in the Digestive Endoscopy Center of Guangzhou Nanfang Hospital between 2001 and 2011 were retrospectively reviewed. Survival analysis, dichotomous logistic regression analysis and rank correlation analysis were carried out.Results: in 234 patients with atrophic gastritis, after follow up of 0.5, 1, 2, 5 and 10 years, the occurrence rates of dysplasia were respectively 2. 3, 4.4, 9.6, 19.3, and 42.4%. Patients with AG combined with antral ulcer or gastric angle ulcer, had a higher risk for dysplasia than patients with simple AG (OR = 2.427, 95%Cl 1.069 5.511, p = 0.034; OR = 2.961, 95%Cl 1.336 ~ 6.564, p = 0.008). The constituent ratios of moderate to severe dysplasia were respectively 8.6, 2.7 and 1.2% (p = 0.000) in three patient groups: AG combined with antral ulcer/gastric angle ulcer (n = 255), antral ulcer/gastric angle ulcer alone (n = 1,389), and AG alone (n = 3,106). The Spearman correlation coefficients between a) Hp infection; and b) atrophy, intestinal metaplasia and dysplasia were -0.114 (p = 0.078), -0.169 (p = 0.009) and 0.064 (p > 0.05), respectively.Conclusions: long follow-up interval and gastric ulcer may be alarming signals for the progression of AG to dysplasia. But in patients with atrophy, intestinal metaplasia or dysplasia, Hp infection may not be a risk factor for these lesions aggravated, further studies are required to confirm it.Key words: Atrophic gastritis. Dysplasia. Helicobacter pylori. Gastric ulcer. Follow-up. INTRODUCTIONAtrophic gastritis (AG) is a recognized precancerous lesion. AG-related lesions (such as intestinal metaplasia and dysplasia) are risk factors for gastric cancer (GC). Studies reported that during 5-year follow-up, the annual incidence rates of GC, intestinal metaplasia, mild to moderate dysplasia and severe dysplasia were, respectively, 0.1, 0.25, 0.6 and 6% in patients with AG in Western countries (1). With the wide application of endoscopy and the improvement of health awareness, the rate of detection of AG in clinical practice is increasing. This means that an increasing number of patients with AG will bear the psychological pressure to have follow-up exams and their financial burden. Currently, no effective preventative strategies have been developed; there is only symptomatic therapy and Helicobacter pylori (Hp) eradication. During follow-up, timely and accurate assessment of disease condition and monitoring of risk factors for dysplasia are critically important for these patients. In the present study, clinical data for patients with AG treated at the Digestive Endoscopy Center of the Guangzhou Nanfang Hospital in the past 11 years were retrospectively analyzed and some valuable characteristics were identified. Our ...

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“…Chronic atrophic gastritis (CAG) is the long-term inflammation of epithelial lining of the stomach mucosa, leading to the loss of gastric glands and replacement by fibrous and intestinal tissues [7] . According to one recent meta-analysis, which included 14 studies and was published in 2010, the incidence rates of CAG ranged from 0% to 10.9% per year [8] . H. pylori infection has been identified as the most important risk factor (cause) of CAG [7] .…”

Section: Mpe In H Pylori Infection and Risk Of Cagmentioning

confidence: 99%

Molecular Pathological Epidemiology in Helicobacter Pylori Infection and Risk of Chronic Atrophic Gastritis

Gao

2017

Journal of Gastroenterology and Hepatology Research

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and multidisciplinary study field, which has emerged as an integrated approach of molecular pathology and epidemiology, and investigates the relationships between molecular characteristics or molecular changes, exogenous and endogenous exposure factors, and initiation, evolution, progression, and response to treatment of diseases. According to the principle and methods, MPE may be a promising approach to achieve our purpose. Moreover, the MPE can provide some very important insights on the molecular mechanisms, personalized prevention and treatment for the study field of H. pylori infection and CAG. HELICOBACTER PYLORI (H. PYLORI) INFECTION AND CHRONIC ATROPHIC GASTRITIS (CAG)Helicobacter pylori (H. pylori), which was isolated for the first time in the year of 1982 by Australian scientists Marshall and Warren [1] , infects more than 50% of the global population [2] . In developing countries, the prevalence of H. pylori infection is very high and it has been found in the stomachs of 70 to 90% of the total population, whereas in developed countries, 25 to 50% of the people carries H. pylori and the prevalence is relatively lower [3] . As early as 1984, it had been very clear that the infection of H. pylori was strongly associated with the inflammation of gastric mucosa tissues, especially the polymorphonuclear cell infiltration [4] . Until now, it is well known that H. pylori infection plays an important etiologic role in many of the most common gastroduodenal diseases, including chronic ABSTRACTHelicobacter pylori (H. pylori) infects more than 50% of the global population and has been identified as the most important risk factor (cause) of chronic atrophic gastritis (CAG), the main precursor lesion of gastric cancer (GC). Regular endoscopic examination and worry of development of GC bring these CAG patients serious physical, psychological and economic burden. However, most of the H. pyloriinfected patients will not progress to the development of CAG, not to speak of GC, through their lives. Therefore, if we can classify all the H. pylori-infected patients according to the risk of CAG, most of them would be relieved from their burden. Molecular pathological epidemiology (MPE) is a new interdisciplinary, transdisciplinary

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Incidence of chronic atrophic gastritis: systematic review and meta-analysis of follow-up studies

Cited by 113 publications

References 32 publications

ABO Genotype and the Risk of Gastric Cancer, Atrophic Gastritis, and Helicobacter pylori Infection

ABO Genotype and the Risk of Gastric Cancer, Atrophic Gastritis, and Helicobacter pylori Infection

Analysis of alarming signals for the progression of atrophic gastritis to dysplasia

Molecular Pathological Epidemiology in Helicobacter Pylori Infection and Risk of Chronic Atrophic Gastritis

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