ABC Classification Is Less Useful for Older Koreans Born before 1960.

Background/Aims: In the ABC classification system, group A consists of seronegative subjects without gastric corpus atrophy. This study aimed to determine the prevalence and characteristics of pseudo group A subjects. Methods: Group A subjects were identified among consecutive Korean adults who underwent a serum anti-Helicobacter pylori immunoglobulin G (IgG) test and pepsinogen (PG) assay on the day of endoscopy. Past infection was defined as the presence of either eradication history or endoscopic findings suggesting past infection (i.e., gastric xanthoma, metaplastic gastritis, or advanced atrophy >closed-type 1). Results: Among 2,620 group A subjects, 448 (17.1%) had eradication history, and 133 (5.1%) showed endoscopic findings suggesting past infection. Older age (odds ratio [OR], 1.148; 95% confidence interval [CI], 1.067 to 1.236) and earlier year of birth (OR, 1.086; 95% CI, 1.009 to 1.168) were independent risk factors for classification into pseudo group A, with cutoff points at 50.5 years and birth year of 1959.5, respectively. Positive H. pylori test findings were found in 22 subjects (3.1%) among the 715 subjects who underwent the urea breath test or Giemsa staining on the same day. Current infection was positively correlated with PG I and PG II levels (p<0.001) but not with age, anti-H. pylori IgG titer, or classification into pseudo group A. Conclusions: Among the group A subjects, 22.2% had past infection. The risk was higher in subjects older than 50 years, especially those born before 1960. Furthermore, current infection was found in 3.1% of the subjects and was correlated with increased gastric secretory ability.

TLR1 and PRKAA1 Gene Polymorphisms in the Development of Atrophic Gastritis and Gastric Cancer.

BACKGROUND AND AIMS: Previous genome-wide association studies showed that genetic polymorphisms in toll-like receptor 1 (TLR1) and protein kinase AMP-activated alpha 1 catalytic subunit (PRKAA1) genes were associated with gastric cancer (GC) or increased Helicobacter pylori (H. pylori) infection susceptibility. The aim of this study was to evaluate the association between TLR1 and PRKAA1 genes polymorphisms and H. pylori infection, atrophic gastritis (AG) or GC in the European population. METHODS: Single-nucleotide polymorphisms (SNPs) were analysed in 511 controls, 340 AG patients and 327 GC patients. TLR1 C>T (rs4833095) and PRKAA1 C>T (rs13361707) were genotyped by the real-time polymerase chain reaction. H. pylori status was determined by testing for anti-H. pylori IgG antibodies in the serum. RESULTS: The study included 697 (59.2%) H. pylori positive and 481 (40.8%) H. pylori negative cases. We observed similar distribution of TLR1 and PRKAA1 alleles and genotypes in H. pylori positive and negative cases. TLR1 and PRKAA1 SNPs were not linked with the risk of AG. TC genotype of TLR1 gene was more prevalent in GC patients compared to the control group (29.7% and 22.3% respectively, p=0.002). Carriers of TC genotype had a higher risk of GC (aOR=1.89, 95% CI: 1.26-2.83, p=0.002). A similar association was observed in a dominant inheritance model for TLR1 gene SNP, where comparison of CC+TC vs. TT genotypes showed an increased risk of GC (aOR=1.86, 95% CI: 1.26-2.75, p=0.002). No association between genetic polymorphism in PRKAA1 gene and GC was observed. CONCLUSIONS: TLR1 rs4833095 SNP was associated with an increased risk of GC in a European population, while PRKAA1 rs13361707 genetic variant was not linked with GC. Both genetic polymorphisms were not associated with H. pylori infection susceptibility or the risk of AG.

Can endoscopic atrophy predict histological atrophy? Historical study in United Kingdom and Japan.

AIM: To assess the diagnostic concordance between endoscopic and histological atrophy in the United Kingdom and Japan. METHODS: Using published data, a total of 252 patients, 126 in the United Kingdom and 126 in Japan, aged 20 to 80 years, were evaluated. The extent of endoscopic atrophy was classified into five subgroups according to a modified Kimura-Takemoto classification system and was compared with histological findings of atrophy at five biopsy sites according to the updated Sydney system. RESULTS: The strength of agreement of the extent of atrophy between histology and visual endoscopic inspection showed good reproducibility, with a weighted kappa value of 0.76 (P < 0.001). Multivariate analysis showed that three factors were associated with decreased concordance: Japanese ethnicity [odds ratio (OR) 0.22, 95% confidence interval (CI) 0.11-0.43], older age (OR = 0.32, 95%CI: 0.16-0.66) and endoscopic atrophy (OR = 0.10, 95%CI: 0.03-0.36). The strength of agreement between endoscopic and histological atrophy, assessed by cancer risk-oriented grading, was reproducible, with a kappa value of 0.81 (95%CI: 0.75-0.87). Only nine patients (3.6%) were endoscopically underdiagnosed with antral predominant rather than extensive atrophy and were considered false negatives. CONCLUSION: Endoscopic grading can predict histological atrophy with few false negatives, indicating that precancerous conditions can be identified during screening endoscopy, particularly in patients in western countries.

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

AIM: 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. SUBJECTS AND METHODS: 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. RESULTS: 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. CONCLUSION: 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.

High Prevalence of Gastric Preneoplastic Lesions in East Asians and Hispanics in the USA.

BACKGROUND: The prevalence of H. pylori infection and the incidence of gastric cancer differ widely around the world, but it is unclear whether these differences are mirrored in the multiethnic population of the USA. AIMS: This study tested the hypothesis that the prevalence of both H. pylori infection and gastric preneoplastic lesions in US residents of Hispanic and Asian ancestry reflects the incidence of gastric cancer in their ancestral countries. METHODS: A total of 799,075 subjects with gastric biopsies extracted from a national pathology database were stratified into the following ancestries: Indian, Hispanic, Vietnamese, Chinese, Japanese Korean, and other Americans (Caucasian and African-American US residents). The prevalence of H. pylori, intestinal metaplasia, and atrophic gastritis was compared among different ethnic groups using age- and sex-adjusted odds ratios and linear regression. RESULTS: Patients of Indian, Hispanic, Vietnamese, Chinese, Japanese, and Korean ancestry had significantly higher prevalence rates of H. pylori gastritis, intestinal metaplasia, and atrophy than other Americans. The prevalence of intestinal metaplasia and atrophy among different ethnic groups did not correlate with H. pylori prevalence, but did correlate highly significantly with gastric cancer incidence in the patients' ancestral countries. CONCLUSIONS: Various US ethnic groups have significantly different prevalence rates of H. pylori gastritis and gastric preneoplastic lesions. Patients' ethnicity needs be considered in the prevention and early detection of gastric cancer.

The value of serum pepsinogen levels for the diagnosis of gastric diseases in Chinese Han people in midsouth China.

BACKGROUND: Serum pepsinogen (PG) levels are valuable in the diagnosis of gastric diseases. However, PG levels are affected by many factors such as the area and race. This study aimed to investigate serum PG levels in patients with different gastric diseases who were Chinese Han people in Hunan Province, midsouth China. METHODS: A total of 248 gastric disease patients and 34 healthy controls were enrolled. The patients included those with non-atrophic and chronic atrophic gastritis, gastric and duodenal ulcer, early and advanced gastric cancer. Serum PG I and II levels were detected by Biohit ELISA kit (Finland), and PG I/II ratio was calculated. Differences in patients with gastric disease and healthy controls were analyzed using paired t-test. RESULTS: Compared with controls, patients with early and advanced gastric cancer had a significantly lower PG I level and PG I/II ratio (p <0.005). In contrast, patients with gastric and duodenal ulcer had a significantly higher PG I level (p <0.005). Compared with atrophic gastritis patients, patients with early and advanced carcinoma of the stomach had a significantly lower PG I/II ratio (p < 0.001). Combination of the cut-off levels of PG I (70 µg/L) and PG I/II ratio (6) provided 62.1% sensitivity of and 94.2% specificity for the diagnosis of gastric cancer. CONCLUSIONS: Decreased PG I level and PG I/II ratio are risk factors for gastric cancer. Combined use of serum PG I level and PG I/II ratio may help the early diagnosis of gastric cancer.

Gastric precancerous lesions are associated with gene variants in Helicobacter pylori-susceptible ethnic Malays.

AIM: To identify genes associated with gastric precancerous lesions in Helicobacter pylori (H. pylori)-susceptible ethnic Malays. METHODS: Twenty-three Malay subjects with H. pylori infection and gastric precancerous lesions identified during endoscopy were included as "cases". Thirty-seven Malay subjects who were H. pylori negative and had no precancerous lesions were included as "controls". Venous blood was collected for genotyping with Affymetrix 50K Xba1 kit. Genotypes with call rates < 90% for autosomal single nucleotide polymorphisms (SNPs) were excluded. For each precancerous lesion, associated SNPs were identified from Manhattan plots, and only SNPs with a χ² P value < 0.05 and Hardy Weinberg Equilibrium P value > 0.5 was considered as significant markers. RESULTS: Of the 23 H. pylori-positive subjects recruited, one sample was excluded from further analysis due to a low genotyping call rate. Of the 22 H. pylori-positive samples, atrophic gastritis only was present in 50.0%, complete intestinal metaplasia was present in 18.25%, both incomplete intestinal metaplasia and dysplasia was present in 22.7%, and dysplasia only was present in 9.1%. SNPs rs9315542 (UFM1 gene), rs6878265 (THBS4 gene), rs1042194 (CYP2C19 gene) and rs10505799 (MGST1 gene) were significantly associated with atrophic gastritis, complete intestinal metaplasia, incomplete metaplasia with foci of dysplasia and dysplasia, respectively. Allele frequencies in "cases" vs "controls" for rs9315542, rs6878265, rs1042194 and rs10505799 were 0.4 vs 0.06, 0.6 vs 0.01, 0.6 vs 0.01 and 0.5 vs 0.02, respectively. CONCLUSION: Genetic variants possibly related to gastric precancerous lesions in ethnic Malays susceptible to H. pylori infection were identified for testing in subsequent trials.

Gastric intestinal metaplasia with basal gland atypia: a morphological and biologic evaluation in a large Chinese cohort.

Gastric intestinal metaplasia can display cytoarchitectural atypia that falls short of qualifying for dysplasia but can be classified as indefinite for dysplasia. Yet few studies have evaluated the prevalence, the morphologic, and biologic characteristics of this variant. Out of a cohort of 554 biopsies with chronic atrophic gastritis and/or dysplasia, we categorized the cases as either (1) simple intestinal metaplasia; (2) intestinal metaplasia with hyperplasia; (3) intestinal metaplasia with basal gland atypia; and (4) gastric dysplasia. The relationship between the subtypes and various clinicopathologic features, mucin immunophenotypes, and biologic characteristics was evaluated. The final cohort consisted of 424 cases of simple intestinal metaplasia, 93 intestinal metaplasia with hyperplasia, 16 intestinal metaplasia with basal gland atypia, and 21 gastric dysplasia. Intestinal metaplasia with basal gland atypia had a prevalence of 2.8% and similar to gastric dysplasia, 3.7%. Both of these lesions were similar in body/fundus distribution (12.5%) and paucity of goblet cells (68.8%). Intestinal metaplasia with basal gland atypia and gastric dysplasia seem to share some biologic similarities but with a lower frequency of alpha-methylacyl-CoA racemase expression (25% versus 62%), p53 expression (6.3% versus 47.6%), and increased Ki-67 index on surface/pit and isthmus in intestinal metaplasia with basal gland atypia. Alternatively, simple intestinal metaplasia and intestinal metaplasia with hyperplasia did not differ statistically with regard to the various characteristics evaluated. We concluded that gastric intestinal metaplasia can be divided into 2 broad categories that are readily defined by cytoarchitectural and biologic characteristics. Based on the characteristics of intestinal metaplasia with basal gland atypia and in keeping with others, we confirm that this subtype could represent a preneoplastic lesion that needs further evaluation.

Surveillance strategy of atrophic gastritis and intestinal metaplasia in a country with a high prevalence of gastric cancer.

BACKGROUND: It is not clear which screening examinations are best suited for gastric cancer prevention, especially in patients with atrophic gastritis and intestinal metaplasia. Therefore, we investigated the gastric cancer screening methods and intervals that are performed in clinical practice in an area with a high prevalence of gastric cancer. METHODS: Eighty-seven physicians voted by keypad and discussed the consistency of endoscopic diagnosis of atrophic gastritis and intestinal metaplasia at the Annual Symposium of the Korean College of Helicobacter and Upper Gastrointestinal Research. Additionally, 100 core members of this academic society were asked via e-mail to complete the questionnaires related to screening strategies for gastric cancer. RESULTS: The most common recommendation for the subjects with intestinal metaplasia was an annual endoscopic follow-up (95.5% vs. 80.4% in the expert and non-expert groups, respectively; P = 0.118). Annual endoscopic follow-up was also the most predominant recommendation for atrophic gastritis (95.5% vs. 76.5%; P = 0.092), regardless of the physicians' endoscopic experience, position, and degree of the hospital. However, the correct answer rate for the diagnosis of normal endoscopic findings was only 16.7 and 14.1% in the expert and non-expert groups, respectively (P = 0.883). CONCLUSIONS: The most common practical screening strategy for patients with atrophic gastritis and intestinal metaplasia in Korea was annual endoscopic examination. However, a new program estimating individualized gastric cancer risk might be needed because of the low inter-observer agreement in the endoscopic diagnosis of atrophic gastritis and intestinal metaplasia.

[Peculiarities of relationship between atrophic gastritis and stomach cancer in the population of Eastern Siberia].

The authors studied the prevalence of atrophic gastritis, H.pylori strains carrying the CagA gene, seeding and apoptosis indices of gastric mucosa in indigenous and newcomer residents of Evenkia. A total of 136 Evenks and 159 newcomers were examined using fibrogastroscopy and biopsy of antral gastric mucosa. Morphological study included light microscopy of hematoxylin and eosin-stained biopsies and their analysis using a visual-analog scale to reveal signs of inflammation, apoptosis, intestinal metaplasia and the degree of insemination by P. pylori. Urease and morphological tests were used to identify H. pylori and the TUNEL technique (Mebstain Apoptosis kit direct, France) to determine apoptosis index; serum anti-Helicobacter and CagA antibodies were detected by an immunoenzyme assay in 22 Evenks and 24 newcomers with chronic H. pylori-associated gastritis. The prevalence of atrophic gastritis in these groups was estimated at 13.2 and 23.9% respectively, seeding density 45.37 +/- 2.01 and 214 +/- 8.75 (p < 0.001). H. pylori strains carrying the CagA gene were identified in 59.6 and 43.6% of the newcomers and Evenks (p = 0.01), total apoptosis index in greater curvature mucosa was 4.99 +/- 0.23 and 3.19 +/- 0.28 (p < 0.01) respectively. These ethnic difference in the prevalence of atrophic gastritis appear to be attributable to different intensity of apoptosis in greater curvature mucosa.

Helicobacter pylori infection and gastritis: the Systematic Investigation of gastrointestinaL diseases in China (SILC).

BACKGROUND AND AIM: Helicobacter pylori infection remains common in East Asia, though its prevalence is decreasing in Western countries. H. pylori-related atrophic gastritis (AG) may reduce the likelihood of gastroesophageal reflux disease (GERD). We investigated the prevalence of H. pylori infection and AG and their association with endoscopic findings and symptom-defined GERD in Shanghai. METHODS: A representative random sample of 3600 Shanghai residents aged 18-80 years was invited to complete a general information questionnaire and a Chinese version of the Reflux Disease Questionnaire, to provide blood samples for H. pylori serology and pepsinogen (PG) I/II assay (to detect AG, defined as PGI < 70 µg/L and/or PGI/PGII < 7), and to undergo endoscopy. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by multivariate logistic regression. RESULTS: A total of 1022 Shanghai residents underwent endoscopy and were valid for inclusion in the study. Of these, 71.7% tested positive for H. pylori, 63.8% had AG and 30.5% had moderate/severe AG (PGI < 50 µg/L and/or PGI/PGII < 5). Helicobacter pylori infection was equally common in all age groups. Severity of AG increased with age in women. Reflux esophagitis was inversely associated with AG (OR, 0.23 [CI, 0.09-0.55] for moderate/severe AG compared with no H. pylori or gastritis). However, symptom-defined GERD showed no clear association with AG. CONCLUSIONS: Helicobacter pylori infection and AG are very common in Shanghai, and the infection is acquired early in life. Atrophic gastritis is inversely associated with reflux esophagitis but is not significantly associated with symptom-defined GERD.

[Peculiarities of relationship between atrophic gastritis and stomach cancer in the population of East Siberia].

The authors studied the relationship between atrophic gastritis and gastric cancer in Europeoid and Mongoloid populations of East Siberia. Screening for atrophic gastritis was carried out in parallel in Evenkia, Khakassia, and Tyva. 1492 Europeoids, 533 Khakasses, 493 Evenks, and 414 Tuvinians were examined by oesogastroduodenoscopy with simultaneous biopsy sampling. Morphological studies of gastric mucosa were performed by light microscopy of hematoxylin/eosin stained samples with evaluation of results based on the visual analogous scale. H.pylori was identified in Giemsa stain preparations. Immunoenzyme assay was used to detect IgG and IgG of H.pylori CagA. Gastric cancer morbidity was estimated using materials of local oncological dispensaries and autopsy data. The prevalence of antral atrophic gastritis was 25.8% in Europeoids, 15.2% in Khakasses, 14% in Evenks, and 25.8% in Tuvinians. The incidence of gastric cancer was 33.2 in Europeoids, 20.2 in Khakasses, and 50.7in Tuvinians per 100,000. The occurrence of H.pylori was similar in all these populations (roughly 90%). CagA strains were identified in 61.2% Europeoids, in 44% Khakasses, in 36.44% Evenks, and in 60% Tuvinians. The study revealed ethnic differences in the association between gastritis cancer and H.pylori CagA-related gastritis among populations of different regions of East Siberia.

Gastric lesions in patients with autoimmune metaplastic atrophic gastritis (AMAG) in a tertiary care setting.

Autoimmune metaplastic atrophic gastritis (AMAG) is an early manifestation of pernicious anemia that precedes the hematologic changes by years to decades. It is associated with metaplastic changes and neoplasms, including pyloric gland adenomas (PGAs). We investigated the frequency of PGAs and other lesions in all nonconsultation gastric biopsies and resections (1988 to 2008) diagnosed as AMAG. We further selected cases confirmed as AMAG by immunohistochemical identification of the gastric body (negative gastrin) and linear and nodular enterochromaffin-like cell hyperplasia (chromogranin). From this subset, all polyps and neoplasms were reviewed. We identified a total of 41,245 patients with gastric biopsies or resections from 46.7% males and 53.3% females comprising patients self-identified as 67.0% white, 23.6% African-American, 1.4% Asian, 0.8% non-White Hispanic, and 7.2% other or unknown. AMAG was diagnosed in 461 patients (1.1%), and had the following percentages based on race: 1.1% White, 1.3% African-American, 1.4% Asian, and 2.7% non-White Hispanic. The female:male ratio was 2:1 with an overall median age at presentation of 67.0 years. Of the 461 patients with AMAG, 143 had endoscopically identifiable lesions. These lesions (n=240) consisted of 179 polyps (138 hyperplastic polyps, 20 oxyntic mucosa pseudopolyps, 18 intestinal-type gastric adenomas, and 3 PGAs), 46 well-differentiated neuroendocrine neoplasms (carcinoid), 1 gastrointestinal stromal tumor, 3 lymphomas, and 11 adenocarcinomas. In summary, AMAG occurred with similar frequency across all racial groups. Although PGAs are associated with AMAG, they remain rare in the setting of AMAG.

Interleukin-1B and interleukin-1 receptor antagonist gene polymorphisms are not associated with premalignant gastric conditions: a combined haplotype analysis.

OBJECTIVE: Contradictory results have been reported about the role of interleukin-1B (IL1B) and IL1 receptor antagonist (IL1RN) alleles in gastric carcinogenesis. Here, IL1B and IL1RN polymorphisms were analyzed as genotypes and haplotypes in relation to the presence of atrophic gastritis (AG) and intestinal metaplasia in the stomach. METHODS: Two hundred and seventy-eight patients (212 Caucasians and 66 Asians) aged 50 years and above, referred for upper endoscopy because of dyspeptic symptoms, were included in the study. Gastric biopsies were histologically assessed according to the updated Sydney classification. Genomic DNA was typed for polymorphisms at position -3737, -1464, -511, -31 for the IL1B gene and the allele 2 of IL1RN using restriction fragment length polymorphism of amplified PCR fragments and intron-spanning PCR analysis, respectively. RESULTS: IL1B-1464-C/C genotype was associated with higher presence of AG in antrum of the stomach in Caucasians [odds ratio: 4.8 (95% confidence interval=1.7-14.3); P=0.028]. IL1B-1464-G/C genotype was associated with lower incidence of AG in corpus of the stomach in Asians [odds ratio: 0.7 (95% confidence interval=0.5-0.8); P=0.02]. IL1RN*2 allele was not linked with AG or intestinal metaplasia in all parts of the stomach both among Asians and Caucasians. Overall, data show that none of the major four IL1B polymorphisms (IL1B-3737C>T, -1464G>C, -511C>T, -31T>C) and the IL1RN*2 is individually, or in its haplotype configuration, linked to the presence of premalignant lesions in Caucasians. CONCLUSION: The determination of these IL1-related loci does not have any predictive value for stratification of subgroups with respect to gastric cancer risk.

Association of the human leukocyte antigen class II alleles with chronic atrophic gastritis and gastric carcinoma in Koreans.

OBJECTIVE: Gastric carcinogenesis is a multi-step process and is influenced by several etiological agents, including the host's genetic factors. Since whether a patient remains with chronic superficial gastritis (CSG) or progresses to either chronic atrophic gastritis (CAG) or gastric carcinoma (GC) could be a genetic predisposition unique in each population, we hypothesized that host human leukocyte antigen (HLA) alleles could be discriminative in predicting the risk of CSG progression to precancerous CAG and GC in Koreans. METHODS: A total of 165 patients with gastric disorders (CSG, 62; CAG, 69 and GC, 34), were selected to investigate the association of HLA class II alleles with the progression of CSG to CAG or GC. HLA genotypes were obtained by the polymerase chain reaction-sequence based typing method. RESULTS: The phenotypic frequencies of DRB1*1101 and DQA1*0505 were significantly higher in the CAG group compared to those in the CSG group. In the subjects with Helicobacter pylori (H. pypori) (+), the frequencies of DRB1*1501 and DQB1*0602 were significantly lower in the CAG compared to those in the CSG. Further analysis showed that sex (P < 0.05, OR = 0.41-0.42) and age (P < 0.05, OR = 1.05) also affected the risk of progression from CSG to CAG in H. pylori (+) patients carrying the DRB1*1501 or DQB1*0602 allele. Additionally, the frequency of DRB1*0404 in the GC group was significantly higher than that in the gastritis group. CONCLUSION: Our findings strongly imply an association between HLA class II alleles and the risk of CAG development and GC progression in Koreans.

Helicobacter pylori infection and gastropathy: a comparison between Indonesian and Japanese patients.

AIM: To compare the effects of Helicobacter pylori (H. pylori) infection on gastropathy between Indonesian and Japanese patients. METHODS: Biopsy specimens were obtained during upper gastrointestinal endoscopy from 167 subjects (125 Indonesians and 42 Japanese) with uninvestigated symptoms of dyspepsia. The specimens were analyzed for the presence of H. pylori using urease analysis, histopathology, and cell culture. The grade and activity of gastritis was assessed using the updated Sydney system. RESULTS: The percentages of Indonesian and Japanese patients who were H. pylori-positive at the antrum or body of the stomach were similar (68% and 59.5%, respectively; P = 0.316). Of those who were H. pylori-positive, more Japanese patients than Indonesian patients had high levels of polymorphonuclear cells (P = 0.001), mononuclear cells (P = 0.013), glandular atrophy (P = 0.000), and intestinal metaplasia (P = 0.011) in both the antrum and body of the stomach. CONCLUSION: The grade of gastritis and prevalence of mucosal atrophy and intestinal metaplasia were higher in Japanese patients. The difference between Indonesian and Japanese patients was significant.

Study of association between atrophic gastritis and body mass index: a cross-sectional study in 10,197 Japanese subjects.

OBJECTIVES: The aim of this study was to elucidate the association between body mass index (BMI) and both Helicobacter pylori and atrophic gastritis. METHODS: The study involved 10,197 subjects participating in a Japanese mass endoscopic gastric cancer screening program. Atrophic gastritis was assessed by pepsinogen I to II ratio. RESULTS: In logistic regression models, BMI had an inverse association with atrophic gastritis, with the odds ratios (OR) decreasing progressively to 0.67 (95% confidence interval [CI] 0.57-0.79, P<0.0001) in the highest BMI quintiles (BMI >or=25.66) group compared with the lowest BMI quintiles (BMI <20.97) group. In linear regression models, atrophic gastritis predicted BMI (regression coefficient -0.326, 95% CI -0.469, -0.184, P<0.0001), whereas H. pylori antibody was not a predictor (regression coefficient 0.072, 95% CI -0.053, 0.198, P=0.3). CONCLUSIONS: A small, inverse association between BMI and atrophic gastritis was found in the general population. In contrast, no association was observed between H. pylori seropositivity and BMI.

Atrophic gastritis, but not antibody to Helicobacter pylori, is associated with body mass index in a Japanese population.

BACKGROUND: The relationship between Helicobacter pylori (HP) infection and body mass index (BMI) is controversial. Several reports have indicated that eradication of HP infection induces an increase in BMI. In contrast, epidemiological case-control studies have failed to show an association between HP infection and BMI. Therefore, we investigated whether HP and atrophic gastritis (AG) were associated with BMI. METHODS: A total of 617 individuals were recruited for the measurements of BMI, serum leptin, pepsinogens (PGs) I and II, and IgG antibody to HP (HP-IgG). BMI and leptin of the subjects were compared when the subjects were stratified by HP-IgG and PGs. RESULTS: The subjects were divided into AG-positive and AG-negative groups according to PGs (AG-positive: PG I < or = 70 ng/ml and PG I/II ratio < or =3.0). BMI after adjusting for sex and age was significantly lower in the AG-positive group than in the AG-negative group (23.47 +/- 3.05 vs. 24.18 +/- 3.25, P = 0.010). When the subjects were divided into two groups according to HP-IgG, BMI tended to be lower in the HP-IgG-positive group, though the difference was not large. When the subjects were divided into four groups for different combinations of AG and HP-IgG, BMI was the lowest in the AG-positive and HP-IgG-negative group. CONCLUSIONS: BMI was associated with AG, as diagnosed by PGs, but not with HP infection status. These results mean that HP infection affects BMI via atrophic gastritis.

Nodular gastritis in Japanese young adults: endoscopic and histological observations.

BACKGROUND: Endoscopic findings of nodular gastritis (NG) are characterized by the presence of Helicobacter pylori infection and follicular gastritis. A possible association with diffuse-type gastric cancer has recently been suggested from observations in Japanese. Our aim was to analyze antral nodularity and histological scores in young adults. METHODS: Subjects (55 men and 45 women; age range, 18-25 years) with upper gastrointestinal (GI) symptoms or positive H. pylori antibodies underwent endoscopy. One specimen each was obtained from the greater and lesser curvatures (curves) of the corpus and from those of the antrum. Endoscopic appearance was assessed using 0.2% indigo carmine, and histopathological grading was evaluated by the updated Sydney System. RESULTS: Antral nodularity was identified in none of 17 H. pylori-negative subjects and in 55 of 83 (66.3%) H. pylori-positive subjects. By the distribution of nodular or granular elevated lesions in the antrum, NG was divided into diffuse (n = 27) or nondiffuse (n = 28) types. The diffuse-type NG predominantly affected women (odds ratio, 3.9; 95% confidence interval, 1.5-10). The atrophy scores in the lesser curve of the antrum were significantly higher in the nondiffuse than in the diffuse group. However, the scores for activity, inflammation, and H. pylori density were not significantly different among the three groups. CONCLUSIONS: Diffuse-type NG depended on sex, and antral nodularity seemed to change from the diffuse to the nondiffuse type in association with atrophy.

Associations of TNF-A-1031TT and -857TT genotypes with Helicobacter pylori seropositivity and gastric atrophy among Japanese Brazilians.

BACKGROUND: Our previous study in a Japanese population showed elevated Helicobacter pylori seropositivity in those with tumor necrosis factor (TNF) A -1031TT and -857TT genotypes. This study examined the associations of this seropositivity and serum pepsinogen (PG) levels with these genotypes in Japanese Brazilians. METHODS: The subjects were 963 individuals (399 males and 564 females), aged 33 to 69 years, from four regions (Sao Paulo, Curitiba, Mogi das Cruzes, and Mirandopolis) in Brazil. Gastric atrophy was evaluated with serum pepsinogens (PGI < 70 ng/dl and PGI/II < 3), and TNF T-1031C and C-857T were genotyped by polymerase chain reaction with confronting two-pair primers (PCR-CTPP). RESULTS: The frequency of TNF-A T-1031C was 68.4% TT, 28.4% TC, and 3.3% CC, and that of C-857T was 64.5% CC, 31.7% CT, and 3.8% TT, whose distributions were in Hardy-Weinberg equilibrium. No significant associations of the genotypes with H. pylori seropositivity or gastric atrophy were found. However, male participants with TNF-A -1031CC and -857CC showed the lowest seropositivity (43.8% out of 16), and males with TNF-A -1031TT and -857TT showed the highest (61.5% out of 13). CONCLUSION: This study demonstrated that the associations between H. pylori seropositivity and TNF-A genotypes were not marked for Japanese Brazilians. The genotypes were not associated with gastric atrophy among the seropositive individuals.