Prevalence of Chronic Atrophic Gastritis in Different Parts of the World

Weck, Melanie N.; Brenner, Hermann

doi:10.1158/1055-9965.epi-05-0931

Cited by 132 publications

(98 citation statements)

References 80 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Taking the short follow-up into account, this finding could partly be due to impaired cobalamin status in atrophic gastritis (58) that often precedes gastric cancer (57). Our data support this hypothesis as the associations between cobalamin and its marker MMA and gastric cancer were confined to the cancer cases with serologic evidence of severe chronic atrophic gastritis.…”

Section: Discussionsupporting

confidence: 65%

The Association of Gastric Cancer Risk with Plasma Folate, Cobalamin, and Methylenetetrahydrofolate Reductase Polymorphisms in the European Prospective Investigation into Cancer and Nutrition

Vollset

Igland

Jenab³

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

View full text Add to dashboard Cite

Previous studies have shown inconsistent associations of folate intake and polymorphisms of the methylenetetrahydrofolate reductase (MTHFR) gene with gastric cancer risk. Our nested case-control study within the European Prospective Investigation into Cancer and Nutrition cohort is the first prospective study of blood folate levels and gastric cancer. Gastric cancer cases (n = 247) and controls (n = 631) were matched for study center, age, sex, and time of blood donation. Two common single nucleotide polymorphisms of the MTHFR gene were determined, as were plasma concentrations of folate, cobalamin (vitamin B12), total homocysteine, and methylmalonic acid (cobalamin deficiency marker) in prediagnostic plasma. Risk measures were calculated with conditional logistic regression. Although no relations were observed between plasma folate or total homocysteine concentrations and gastric cancer, we observed a trend toward lower risk of gastric cancer with increasing cobalamin concentrations (odds ratio, 0.79 per SD increase in cobalamin; P = 0.01). Further analyses showed that the inverse association between cobalamin and gastric cancer was confined to cancer cases with low pepsinogen A levels (marker of severe chronic atrophic gastritis) at the time of blood sampling. The 677 C!T MTHFR polymorphism was not associated with gastric cancer, but we observed an increased risk with the variant genotype of the 1298 A!C polymorphism (odds ratio, 1.47 for CC versus AA; P = 0.04). In conclusion, we found no evidence of a role of folate in gastric cancer etiology. However, we observed increased gastric cancer risk at low cobalamin levels that was most likely due to compromised cobalamin status in atrophic gastritis preceding gastric cancer. (Cancer Epidemiol Biomarkers Prev 2007;16(11):2416 -24)

show abstract

Section: Discussionsupporting

confidence: 65%

The Association of Gastric Cancer Risk with Plasma Folate, Cobalamin, and Methylenetetrahydrofolate Reductase Polymorphisms in the European Prospective Investigation into Cancer and Nutrition

Vollset

Igland

Jenab³

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

View full text Add to dashboard Cite

show abstract

“…The highest percentage of cases were diagnosed at advanced stages (stage III and IV) due to non-specific symptoms and an inadequate screening program. Gastric carcinogenesis is a continuous process from non-atrophic gastritis leading to chronic atrophic gastritis (CAG), to intestinal metaplasia (IM) and dysplasia, and finally to intestinal-type gastric adenocarcinoma (2)(3)(4). A prospective 10-year follow-up study in Japan demonstrated that patients with Helicobacter pylori (H. pylori)-induced chronic active gastritis developed atrophic gastritis, which was observed endoscopically and histologically (5).…”

Section: Introductionmentioning

confidence: 99%

“…Serum PG concentrations measured in certain areas of Asia appear to be higher than those in Western countries. For example, the median PGI levels were >90 µg/l in Shandong, China (25), the mean PGI was >100 µg/l in Hunan, China (17) and Yazd, Iran (24), whereas values were usually <70 µg/l in European countries (4,26). However, a Japanese study by Inoue et al (19) involving 200 patients and a Korean study involving 2,558 patients by Lee et al (27) reported a mean serum PGI:I level of <70 µg/l (56.0 and 63.5 µg/l, respectively).…”

Section: Introductionmentioning

confidence: 99%

Serum pepsinogen and gastrin-17 as potential biomarkers for pre-malignant lesions in the gastric corpus

et al. 2017

View full text Add to dashboard Cite

Abstract. There is a lack of non-invasive screening modalities to diagnose chronic atrophic gastritis (CAG) and intestinal metaplasia (IM). Thus, the aim of the present study was to determine the sensitivity and specificity of serum pepsinogen I (PGI), PGI:II, the PGI:II ratio and gastrin-17 (G-17) in diagnosing CAG and IM, and the correlations between these serum biomarkers and pre-malignant gastric lesions. A cross-sectional study of 72 patients (82% of the calculated sample size) who underwent oesophageal-gastro-duodenoscopy for dyspepsia was performed in the present study. The mean age of the participants was 56.2±16.2 years. Serum PGI:I, PGI:II, G-17 and Helicobacter pylori antibody levels were measured by enzyme-linked immunosorbent assay. Median levels of PGI:I, PGI:II, the PGI:II ratio and G-17 for were 129.9 µg/l, 10.3 µg/l, 14.7 and 4.4 pmol/l, respectively. Subjects with corpus CAG/IM exhibited a significantly lower PGI:II ratio (7.2) compared with the control group (15.7; P<0.001). Histological CAG and IM correlated well with the serum PGI:II ratio (r=-0.417; P<0.001). The cut-off value of the PGI:II ratio of ≤10.0 demonstrated high sensitivity (83.3%), specificity (77.9%) and area under the receiver operating characteristic curve of 0.902 in detecting the two conditions. However, the sensitivity was particularly low at a ratio of ≤3.0. The serum PGI:II ratio is a sensitive and specific marker to diagnose corpus CAG/IM, but at a high cut-off value. This ratio may potentially be used as an outpatient, non-invasive biomarker for detecting corpus CAG/IM.

show abstract

“…However, the majority of epidemiological studies on CAG and its risk factors have been cross-sectional [4]. Infection with the gastric bacterium Helicobacter pylori was shown to be strongly associated with CAG in a recently published meta-analysis that relied on cross-sectional data [5].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2010

Self Cite

View full text Add to dashboard Cite

Chronic atrophic gastritis (CAG) is an important precursor lesion of intestinal gastric cancer. As it is typically asymptomatic, epidemiological data on the incidence of CAG are sparse. We aimed to provide an overview of published data on CAG incidence (overall and according to risk factors) from follow-up studies. Articles with information on incidence of CAG published in English until 26th of July 2009 were identified through a systematic MEDLINE and EMBASE search. Data extracted include study characteristics and key findings regarding the incidence of CAG. A meta-analysis was performed on the association between Helicobacter pylori infection and CAG incidence. Overall, data on CAG incidence were available from 14 studies, in 7 studies incidence could be estimated according to H. pylori infection. Most studies were conducted in symptomatic or high risk populations and the maximum number of incident cases was 284. Incidence estimates ranged from 0 to 11% per year and were consistently below 1% in patients not infected with H. pylori. The highest incidence was observed in a special study conducted on ulcer patients treated by proximal gastric vagotomy. Rate ratios for the association between H. pylori infection and CAG incidence ranged from 2.4 to 7.6 with a summary estimate of 5.0 (95% confidence interval: 3.1-8.3). Incidence of CAG is very low in the absence of H. pylori infection. There is a need for more population-based studies to provide comparable estimates of incidence and the impact of risk factors in the development of CAG.

show abstract

Prevalence of Chronic Atrophic Gastritis in Different Parts of the World

Cited by 132 publications

References 80 publications

The Association of Gastric Cancer Risk with Plasma Folate, Cobalamin, and Methylenetetrahydrofolate Reductase Polymorphisms in the European Prospective Investigation into Cancer and Nutrition

The Association of Gastric Cancer Risk with Plasma Folate, Cobalamin, and Methylenetetrahydrofolate Reductase Polymorphisms in the European Prospective Investigation into Cancer and Nutrition

Serum pepsinogen and gastrin-17 as potential biomarkers for pre-malignant lesions in the gastric corpus

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

Contact Info

Product

Resources

About