The value of MG7‐Ag and COX‐2 for predicting malignancy in gastric precancerous lesions

Here we aimed to first investigate the clinical value of combined detection of MG7‐Ag and COX‐2 (cyclo‐oxygenase 2) in prediction of advances in gastric precancerous lesions. Immunohistochemical analysis was used to examine the expression of MG7‐Ag and COX‐2 in 396 cases of patients with gastric precancerous lesions, including 66 cases of atrophic gastritis, 106 cases of intestinal metaplasia, 174 cases of low‐moderate‐grade dysplasia and 50 cases of high‐grade dysplasia. The relation of MG7‐Ag and COX‐2 staining with various clinicopathological features was analysed by follow‐up study. The positive rates of MG7‐Ag and COX‐2 were increased gradually from atrophic gastritis (21.2%, 28.8%), intestinal metaplasia (36.8%, 44.3%), low‐moderate‐grade dysplasia (51.4%, 58.6%) to high‐grade dysplasia (72%, 80%). Double positive staining of MG7‐Ag and COX‐2 in gastric precancerous lesions had an increased risk of precancerous progression over 22 times, compared with negative ones. However, the expression of MG7‐Ag and COX‐2 was not significantly correlated with age and gender of patients. MG7‐Ag and COX‐2 might play an important role in the process of carcinogenesis and progression of gastric cancer. Combined detection of MG7‐Ag and COX‐2 was of value of predicting early gastric cancer from precancerous lesions.     

Optical sensory arrays for the detection of urinary bladder cancer‐related volatile organic compounds

Non‐invasive detection of urinary bladder cancer remains a significant challenge. Urinary volatile organic compounds (VOCs) are a promising alternative to cell‐based biomarkers. Herein, we demonstrate a novel diagnosis system based on an optic fluorescence sensor array for detecting urinary bladder cancer VOCs biomarkers. This study describes a fluorescence‐based VOCs sensor array detecting system in detail. The choice of VOCs for the initial part was based on an extensive systematic search of the literature and then followed up using urinary samples from patients with urinary bladder transitional cell carcinoma. Canonical discriminant analysis and partial least squares discriminant analysis (PLS‐DA) were employed and correctly detected 31/48 urinary bladder cancer VOC biomarkers and achieved an overall 77.75% sensitivity and 93.25% specificity by PLS‐DA modelling. All five urine samples from bladder cancer patients, and five healthy controls were successfully identified with the same sensor arrays. Overall, the experiments in this study describe a real‐time platform for non‐invasive bladder cancer diagnosis using fluorescence‐based gas‐sensor arrays. Pure VOCs and urine samples from the patients proved such a system to be promising; however, further research is required using a larger population sample.      

Biopsy Strategies for Endoscopic Surveillance of Pre‐malignant Gastric Lesions

Background: Endoscopic surveillance of pre‐malignant gastric lesions may add to gastric cancer prevention. However, the appropriate biopsy regimen for optimal detection of the most advanced lesions remains to be determined. Therefore, we evaluated the yield of endoscopic surveillance by standardized and targeted biopsy protocols. Materials and Methods: In a prospective, multi‐center study, patients with intestinal metaplasia (IM) or dysplasia (DYS) underwent a surveillance gastroscopy. Both targeted biopsies from macroscopic lesions and 12 non‐targeted biopsies according to a standardized protocol (antrum, angulus, corpus, cardia) were obtained. Appropriate biopsy locations and the yield of targeted versus non‐targeted biopsies were evaluated. Results: In total, 112 patients with IM (n = 101), or low‐grade (n = 5) and high‐grade DYS (n = 6) were included. Diagnosis at surveillance endoscopy was atrophic gastritis (AG) in one, IM in 77, low‐grade DYS in two, high‐grade DYS in three, and gastric cancer in one patient. The angulus (40%), antrum (35%) and lesser curvature of the corpus (33%) showed the highest prevalence of pre‐malignant conditions. Non‐targeted biopsies from the lesser curvature had a significantly higher yield as compared to the greater curvature of the corpus in diagnosing AG and IM (p = .05 and p = .03). Patients with extensive intragastric IM, which was also present at the cardia were at high risk of a concurrent diagnosis of dysplasia or gastric cancer. High‐grade DYS was detected in targeted biopsies only. Conclusions: At surveillance endoscopies, both targeted and non‐targeted biopsies are required for an appropriate diagnosis of (pre‐)malignant gastric lesions. Non‐targeted biopsies should be obtained in particular from the antrum, angulus and lesser curvature of the corpus.     

树突状细胞对胃癌前病变的免疫保护分析

摘要 目的：探究树突状细胞(Dendritic cells,DC)对胃癌的免疫保护作用。方法：选择2016年1月至2018年1月于我院接受治疗的145例胃癌、39例慢性萎缩性胃炎、21例不典型增生、27例肠上皮化生以及20例正常对照组患者为研究对象,分别采集其胃粘膜标本进行染色,记录和比较其胃粘膜中S100⁺、CD4⁺和CD8⁺细胞的数量、平均面积以及平均吸光度,并将胃癌患者分为中分化腺癌(49例)、低分化腺癌(53例)和未分化癌(43例)进行对比。结果：(1)胃癌组、慢性萎缩性胃炎组、不典型增生、肠上皮化生组的胃粘膜S100⁺阳性细胞计数明显高于正常对照组（P<0.05）,胃癌组平均吸光度低于对照组,其他3组平均吸光度显著高于对照组,(P<0.05);胃癌组平均面积与正常对照组相比无差异(P>0.05),其他三组平均面积显著高于对照组（P<0.05）;(2)慢性萎缩性胃炎组、肠上皮化生组、不典型增生组患者CD4⁺细胞数均低于对照组(P<0.05);胃癌组、慢性萎缩性胃炎组、肠上皮化生组患者平均面积均低于对照组(P<0.05);胃癌组、慢性萎缩性胃炎组、不典型增生、肠上皮化生组平均吸光度均低于对照组(P<0.05);(3)慢性萎缩性胃炎组、肠上皮化生组、不典型增生组患者CD8⁺细胞数明显高于对照组(P<0.05),胃癌组稍低于对照组(P>0.05);胃癌组患者平均面积低于对照组(P<0.05);胃癌组患者平均吸光值低于对照组,慢性萎缩性胃炎组、肠上皮化生组患者高于对照组(P均<0.05);(4)随着胃癌分化程度的降低,胃癌患者DC细胞数有降低趋势。结论：胃癌前病变患者胃粘膜中DC数量会显著增多,免疫功能加强,DC细胞数量会随胃癌分化程度的降低而减少,分析其原因与DC细胞能够抑制癌前病变有关。     

The detection, surveillance and treatment of premalignant gastric lesions related to Helicobacter pylori infection

Gastric cancer is an important worldwide health problem and causes considerable morbidity and mortality. It represents the second leading cause of cancer-related death worldwide. A cascade of recognizable precursor lesions precedes most distal gastric carcinomas. In this multistep model of gastric carcinogenesis, Helicobacter pylori causes chronic active inflammation of the gastric mucosa, which slowly progresses through the premalignant stages of atrophic gastritis, intestinal metaplasia and dysplasia to gastric carcinoma. Detection and treatment of premalignant lesions may thus provide a basis for gastric cancer prevention. However, at present, premalignant changes of the gastric mucosa are frequently disregarded in clinical practice or result in widely varying follow-up frequency or treatment. This review provides an overview of current knowledge on detection, surveillance and treatment of patients with premalignant gastric lesions, and identifies the uncertainties that require further research.     

Helicobacter pylori infection‐induced H3Ser10 phosphorylation in stepwise gastric carcinogenesis and its clinical implications

Background

Our previous works have demonstrated that Helicobacter pylori (Hp) infection can alter histone H3 serine 10 phosphorylation status in gastric epithelial cells. However, whether Helicobacter pylori‐induced histone H3 serine 10 phosphorylation participates in gastric carcinogenesis is unknown. We investigate the expression of histone H3 serine 10 phosphorylation in various stages of gastric disease and explore its clinical implication.

Materials and Methods

Stomach biopsy samples from 129 patients were collected and stained with histone H3 serine 10 phosphorylation, Ki67, and Helicobacter pylori by immunohistochemistry staining, expressed as labeling index. They were categorized into nonatrophic gastritis, chronic atrophic gastritis, intestinal metaplasia, low‐grade intraepithelial neoplasia, high‐grade intraepithelial neoplasia, and intestinal‐type gastric cancer groups. Helicobacter pylori infection was determined by either ¹³C‐urea breath test or immunohistochemistry staining.

Results

In Helicobacter pylori‐negative patients, labeling index of histone H3 serine 10 phosphorylation was gradually increased in nonatrophic gastritis, chronic atrophic gastritis, intestinal metaplasia groups, peaked at low‐grade intraepithelial neoplasia, and declined in high‐grade intraepithelial neoplasia and gastric cancer groups. In Helicobacter pylori‐infected patients, labeling index of histone H3 serine 10 phosphorylation followed the similar pattern as above, with increased expression over the corresponding Helicobacter pylori‐negative controls except in nonatrophic gastritis patient whose labeling index was decreased when compared with Helicobacter pylori‐negative control. Labeling index of Ki67 in Helicobacter pylori‐negative groups was higher in gastric cancer than chronic atrophic gastritis and low‐grade intraepithelial neoplasia groups, and higher in intestinal metaplasia group compared with chronic atrophic gastritis group. In Helicobacter pylori‐positive groups, Ki67 labeling index was increased stepwise from nonatrophic gastritis to gastric cancer except slightly decrease in chronic atrophic gastritis group. In addition, we noted that histone H3 serine 10 phosphorylation staining is accompanied with its location changes from gastric gland bottom expanded to whole gland as disease stage progress.

Conclusions

These results indicate that stepwise gastric carcinogenesis is associated with altered histone H3 serine 10 phosphorylation, Helicobacter pylori infection enhances histone H3 serine 10 phosphorylation expression in these processes; it is also accompanied with histone H3 serine 10 phosphorylation location change from gland bottom staining expand to whole gland expression. The results suggest that epigenetic dysregulation may play important roles in Helicobacter pylori‐induced gastric cancer.     

PGI、PGⅡ在胃癌组织中的表达及意义

目的：研究胃蛋白酶原I(PGI)、胃蛋白酶原Ⅱ(PGⅡ)在胃癌组织中的表达及意义。方法：将我院2011 年5 月至2013年10月 收治的上消化道疾病患者243 例纳入研究,根据胃镜及病理组织学结果,按照胃癌、慢性萎缩性胃炎、慢性非萎缩性胃炎、不典型 增生以及胃溃疡分为5 组,对照组为57 名来我院检查的健康的人群。应用酶联免疫法测定各组血清PGI、PGⅡ的含量并计算胃 蛋白酶原比值(PGR),比较胃癌患者手术前后血清PGI、PGⅡ的含量以及PGR,并通过ROC曲线下面积评价血清PGI、PGⅡ以及 PGR 诊断胃癌的效能。结果：与对照组比较,胃溃疡组PG I、PG II均明显升高,PGR 降低(P<0.05),慢性萎缩性胃炎组、不典型增生 组及胃癌组PGI、PGR均明显降低(P<0.05);与慢性萎缩性胃炎组比较,不典型增生组和胃癌组PGR 显著降低(P<0.05)。手术治疗 后,胃癌患者血清PGⅠ、PGⅡ含量较手术前明显下降(P＜0.05)。血清PGⅠ、PGⅡ以及PGR含量诊断胃癌的ROC 曲线下面积依 次为0.779、0.920 以及0.991。结论：胃癌患者血清PGI、PGR均明显降低,二者可用于初步筛查胃癌。     

Effect of Helicobacter pylori Eradication on Incidence of Gastric Cancer in Human and Animal Models: Underlying Biochemical and Molecular Events

Background:  Gastric cancer remains one of the most common cancers worldwide. A strong association exists between Helicobacter pylori infection and the risk of developing noncardia gastric cancer. H. pylori eradication by antibiotic treatment is regarded as a primary chemoprevention strategy to reduce gastric cancer incidence.
Aim:  To analyze the efficacy of H. pylori eradication in preventing gastric cancer in human and animal models, and to discuss whether biochemical, genetic, and epigenetic changes associated with H. pylori infection are reversible after curing the infection.
Results:  Several intervention trials have indicated that in some patients, H. pylori eradication leads to regression and prevents the progression of precancerous lesions. The eradication therapy reduces gastric cancer incidence in patients without any precancerous lesions at the baseline and is most effective before the development of atrophic gastritis. A few recent intervention studies in Japan have demonstrated significant prophylactic effects of eradication therapy on the development of gastric cancer, suggesting the use of eradication therapy in high-risk populations as a gastric cancer reduction strategy. However, gastric cancer may still develop despite successful eradication therapy. Studies in animal models have confirmed the use of eradication therapy at an early point of infection to prevent gastric cancer development.
Conclusion:  H. pylori eradication may not completely abolish the risk of gastric cancer. However, eradication therapy may be used in high-risk populations to reduce gastric cancer incidence. It can reverse many biochemical, genetic, and epigenetic changes that H. pylori infection induces in the stomach.     

胃癌与萎缩性胃炎的血清拉曼光谱数据分析

利用激光诱导拉曼光谱技术,测定了萎缩性胃炎患者、胃癌患者血清的拉曼光谱。采用主成分分析法和判别分析法对拉曼光谱数据进行了分析和处理,得到辨别胃癌和萎缩性胃炎的准确率为92％。     

Autofluorescence imaging identifies tumor cell‐cycle status on a single‐cell level

The goal of this study is to validate fluorescence intensity and lifetime imaging of metabolic co‐enzymes NAD(P)H and FAD (optical metabolic imaging, or OMI) as a method to quantify cell‐cycle status of tumor cells. Heterogeneity in tumor cell‐cycle status (e. g. proliferation, quiescence, apoptosis) increases drug resistance and tumor recurrence. Cell‐cycle status is closely linked to cellular metabolism. Thus, this study applies cell‐level metabolic imaging to distinguish proliferating, quiescent, and apoptotic populations. Two‐photon microscopy and time‐correlated single photon counting are used to measure optical redox ratio (NAD(P)H fluorescence intensity divided by FAD intensity), NAD(P)H and FAD fluorescence lifetime parameters. Redox ratio, NAD(P)H and FAD lifetime parameters alone exhibit significant differences (p<0.05) between population means. To improve separation between populations, linear combination models derived from partial least squares ‐ discriminant analysis (PLS‐DA) are used to exploit all measurements together. Leave‐one‐out cross validation of the model yielded high classification accuracies (92.4 and 90.1 % for two and three populations, respectively). OMI and PLS‐DA also identifies each sub‐population within heterogeneous samples. These results establish single‐cell analysis with OMI and PLS‐DA as a label‐free method to distinguish cell‐cycle status within intact samples. This approach could be used to incorporate cell‐level tumor heterogeneity in cancer drug development.

     

血清胃蛋白酶原联合G-17对萎缩性胃炎及胃癌早期诊断价值

目的:探索检测血清胃蛋白酶原Ⅰ(PGⅠ)、胃蛋白酶原Ⅱ(PGⅡ)、胃泌素-17(G-17)在萎缩性胃炎及胃癌中的诊断价值。方法:收集医院2015年2月至12月门诊及住院的慢性非萎缩性胃炎44例(非萎缩性胃炎组),慢性萎缩性胃炎47例(萎缩性胃炎组),早期胃癌42例(胃癌组)。采用酶联免疫吸附试验(ELISA)测定各组血清PGⅠ、PGⅡ、G-17的水平,同时计算PGⅠ/PGⅡ的比值(PGR),比较各组指标间的差异,同时绘制各指标筛查萎缩性胃炎及胃癌的受试者工作曲线(ROC)曲线,分别评价其诊断价值。结果:胃癌组及萎缩性胃炎组的血清PGⅠ、PGR水平较非萎缩性胃炎组明显下降,且胃癌组下降更明显,差异均具有统计学意义(P0.05),萎缩性胃炎组血清PGⅡ显著低于非萎缩性胃炎组,差异均具有统计学意义(P0.05);胃癌组的血清G-17水平较非萎缩性胃炎组及萎缩性胃炎组均升高,差异有统计学意义(P0.05)。血清PGⅠ筛查萎缩性胃炎的最佳界值为PGⅠ90 ng/m L,其灵敏度和特异度分别为71.5%和51.0%,血清PGR筛查萎缩性胃炎的最佳界值为PGR8,其灵敏度和特异度分别为71.9%和54.0%,血清G-17筛查萎缩性胃炎的最佳界值为G-175 pmol/L,其灵敏度和特异度分别为66.1%和64.0%。血清PGⅠ筛查胃癌的最佳界值为PGⅠ73 ng/m L,其灵敏度和特异度分别为86.0%和74.9%;血清PGR筛查胃癌的最佳界值为PGR3,其灵敏度和特异度分别为90.2%和62.5%;血清G-17筛查胃癌的最佳界值为G-174 pmol/L,其灵敏度和特异度分别为62.5%和61.3%。结论:胃癌及萎缩性胃炎患者血清PGⅠ、PGR水平下降明显,且胃癌患者的血清G-17异常升高,血清PG联合GS-17测定可用于萎缩性胃炎及胃癌的早期筛查。     

血清Hcy，叶酸和维生素B12在胃癌及其癌前疾病中的作用

目的:探讨血清同型半胱氨酸(Hcy)、叶酸以及维生素B12在胃癌及癌前疾病中的水平及临床意义。方法:收集2014年1月至2016年8月我院收治的100例胃癌患者(胃癌组),及100例胃良性病变患者包括41例胃炎、34例胃溃疡、25例胃息肉(癌前病变组),并于同期随机选择200例健康体检者为对照组,采用循环酶法测定三组的血清Hcy,电化学发光免疫分析法测定叶酸及维生素B12水平,并分析各指标与胃癌临床病理特征的关系。结果:胃癌组、癌前病变组血清Hcy水平均高于对照组,叶酸及维生素B12水平均低于对照组,并且胃癌组血清Hcy水平高于癌前病变组,叶酸及维生素B12水平低于癌前病变组,差异有统计学意义(P0.05)。Ⅲ+Ⅳ期胃癌患者Hcy水平高于Ⅰ+Ⅱ期,进展期患者Hcy水平高于早期,有淋巴结转移患者Hcy水平高于无转移者,差异有统计学意义(P0.05);Hcy表达与性别、年龄、病变位置以及分化程度无关,差异无统计学意义(P0.05)。叶酸、维生素B12的表达在胃癌患者中与各临床病理特征(性别、年龄、TNM分期、肿瘤浸润深度、病变位置、有无淋巴结转移、分化程度)无明显关系,差异无统计学意义(P0.05)。结论:血清Hcy在胃癌患者中呈高水平表达,而叶酸及维生素B12呈低水平表达,联合检测三种指标有助于早期区分胃癌及癌前病变,同时血清Hcy还可能参与了胃癌的发生发展过程。Hcy、叶酸及维生素B12可作为早期鉴别诊断胃癌及其癌前病变的重要指标。     

Review ‐ Helicobacter pylori and non‐malignant upper gastro‐intestinal diseases

This review takes into account recent publications focusing on the relationship between Helicobacter pylori infection and non‐malignant diseases of the upper gastro‐intestinal tract. The authors have summarized current knowledge on associations between the H pylori infection and non‐malignant upper GI conditions including gastroesophageal reflux disease (GERD), Barrett's esophagus, eosinophilic esophagitis (EOE), peptic ulcer disease (PUD), H pylori gastritis, celiac disease and functional dyspepsia. In the field of GERD, current data focusing on different locations of H pylori infection detect significant differences between antrum‐ and corpus predominant gastritis explainable by different changes in acid secretion in different gastric niches. High volume studies from Sweden and Brazil underline the safety of H pylori eradication concerning the risk of Barret's esophagus or adenocarcinoma. The relationship betweenH pylori infection and EOE remains uncertain, but current data supports the concept of expected positive and protective effects of H pylori exposure reducing the risk of EOE. Analyzing biomarkers might be helpful to identify subjects under risk for the development of precancerous lesions after H pylori infection, where microRNAs, IL‐9 and IL‐4, and also Tc17/9 and Th17/9 and microbiota profiles showed promising results to identify subgroups under risk.     

Chronic injury as a major factor in susceptibility to gastric cancer

The etiology of gastric cancer is still unclear. The lesser curvature of stomach is more susceptible to chronic injury due to the anatomical characteristics. Many previous studies demonstrated that the lesser curvature is the most frequent tumor site in gastric cancer. And, precancerous gastric lesions, such as atrophic and intestinal metaplasia were also typically located in the lesser curvature. The lesser curvature is the first part of the stomach to be infected with Helicobacter pylori (H. pylori) infection which was associated with precancerous gastric lesions and gastric cancer. So, chronic injury of the stomach may lead to gastric cancer have hypothesized.     

TFF2在胃癌中的表达及与幽门螺杆菌感染关系的研究

目的探讨三叶因子Ⅱ(Trefoil factors2,TFF2)在胃癌和癌前病变中的表达及与幽门螺杆菌感染(Helicobacter pylori,H.pylori)的关系。方法选取经病理证实的慢性浅表性胃炎、胃溃疡、慢性萎缩性胃炎和胃癌4种不同胃黏膜病变的标本140例,用免疫组化法检测标本中TFF2的表达及H.pylori的感染情况,并分析TFF2的表达与H.pylori的感染的关系。结果在慢性浅表性胃炎、胃溃疡、慢性萎缩性胃炎和胃癌中,TFF2和H.pylori的表达率依序呈逐渐增加的趋势,但TFF2在胃癌组织中表达降低。H.pylori阳性组TFF2的表达率低于阴性组,TFF2的阳性率与H.pylori感染率之间呈负相关(r=-0.335,P<0.05)。结论 TFF2的表达和H.pylori的感染与肿瘤的发生密切相关,检测该指标可为胃癌诊断、判断预后和指导治疗提供理论依据。     

CEA levels in gastric juice in precancerous conditions and cancer

First described in 1965 as a specific antigen for cancer of the colon, CEA is now considered to be an antigen associated with many types of malignant neoplasia, although the CEA-Test's role in clinical routine has yet to be clearly defined. In the present study CEA levels in gastric juice were measured in subjects with gastric carcinoma (n = 25) and with benign gastric lesions (n = 171). CEA was significantly (p less than 0.05) higher in patients with gastric carcinoma (GC) than in subjects with benign gastric lesions, other than chronic atrophic gastritis (CAG) associated with intestinal metaplasia (IM). In this latter condition CEA levels were similar to those in patients with GC. These results suggest that the assay of CEA in gastric juice could be included in the diagnostic program for gastric cancer and its precursors with the aim of assessing its utility as risk indicator in the management of precancerous conditions and lesion.     

Previous Helicobacter pylori infection–induced atrophic gastritis: A distinct disease entity in an understudied population without a history of eradication

Individuals with chronic atrophic gastritis who are negative for active H. pylori infection with no history of eradication therapy have been identified in clinical practice. By excluding false‐negative and autoimmune gastritis cases, it can be surmised that most of these patients have experienced unintentional eradication of H. pylori after antibiotic treatment for other infectious disease, unreported successful eradication, or H. pylori that spontaneously disappeared. These patients are considered to have previous H. pylori infection–induced atrophic gastritis. In this work, we define these cases based on the following criteria: absence of previous H. pylori eradication; atrophic changes on endoscopy or histologic confirmation of glandular atrophy; negative for a current H. pylori infection diagnosed in the absence of proton‐pump inhibitors or antibiotics; and absence of localized corpus atrophy, positivity for autoantibodies, or characteristic histologic findings suggestive of autoimmune gastritis. The risk of developing gastric cancer depends on the atrophic grade. The reported rate of developing gastric cancer is 0.31%‐0.62% per year for successfully eradicated severely atrophic cases (pathophysiologically equal to unintentionally eradicated cases and unreported eradicated cases), and 0.53%‐0.87% per year for spontaneously resolved cases due to severe atrophy. Therefore, for previous H. pylori infection–induced atrophic gastritis cases, we recommend endoscopic surveillance every 3 years for high‐risk patients, including those with endoscopically severe atrophy or intestinal metaplasia. Because of the difficulty involved in the endoscopic diagnosis of gastric cancer in cases of previous infection, appropriate monitoring of the high‐risk subgroup of this understudied population is especially important.     

Associated Factors of Atrophic Gastritis Diagnosed by Double-Contrast Upper Gastrointestinal Barium X-Ray Radiography: A Cross-Sectional Study Analyzing 6,901 Healthy Subjects in Japan

Background

Double-contrast upper gastrointestinal barium X-ray radiography (UGI-XR) is one of the most widely conducted gastric cancer screening methods. It has been executed to find gastric cancer, but has not been usually executed to detect premalignant atrophic mucosa of stomach. To understand the meaning of UGI-XR-based atrophic gastritis, we analyzed its association with several causative factors including Helicobacter pylori (HP) infection.

Methods

We evaluated 6,901 healthy adults in Japan. UGI-XR-based atrophic gastritis was diagnosed based on the irregular shape of areae gastricae and its expansion in the stomach.

Results

Of the 6,433 subjects with no history of HP eradication and free from gastric acid suppressants, 1,936 were diagnosed as UGI-XR-based atrophic gastritis (mild: 234, moderate: 822, severe: 880). These were univariately associated with serum HP IgG and serum pepsinogen I/II ratio with statistical significance. The multiple logistic analysis calculating standardized coefficients (β) and odds ratio (OR) demonstrated that serum HP IgG (β = 1.499, OR = 4.48), current smoking (β = 0.526, OR = 1.69), age (β = 0.401, OR = 1.49), low serum pepsinogen I/II ratio (β = 0.339, OR = 1.40), and male gender (β = 0.306, OR = 1.36) showed significant positive association with UGI-XR-based atrophic gastritis whereas drinking and body mass index did not. Among the age/sex/smoking/drinking-matched 227 pairs derived from chronically HP-infected and successfully HP-eradicated subjects, UGI-XR-based atrophic gastritis was detected in 99.1% of the former but in only 59.5% of the latter subjects (p<0.0001). Contrastively, UGI-XR-based atrophic gastritis was detected in 13 of 14 HP-positive proton pump inhibitor users (92.9%) and 33 of 34 HP-positive histamine H₂-receptor antagonist users (97.1%), which are not significantly different from gastric acid suppressant-free subjects.

Conclusions

The presence of UGI-XR-based atrophic gastritis is positively associated with Helicobacter pylori infection, current smoking, age, decreased serum pepsinogen I/II ratio, and male gender. Eradication of Helicobacter pylori seems to superficially improve UGI-XR-based atrophic gastritis whereas intake of gastric acid suppressants does not.