Effects of Helicobacterpylori eradication on atrophic gastritis and intestinal metaplasia： A 3-year follow-up study

AIM: To investigate the effect of H pylori eradication on atrophic gastritis and intestinal metaplasia (IM). METHODS: Two hundred and fifty-nine patients with atrophic gastritis in the antrum were included in the study, 154 patients were selected for H pylori eradication therapy and the remaining 105 patients served as untreated group. Gastroscopy and biopsies were performed both at the beginning and at the end of a 3-year follow-up study. Gastritis was graded according to the updated Sydney system. RESULTS: One hundred and seventy-nine patients completed the follow-up, 92 of them received H pylori eradication therapy and the remaining 87 H pylori-infected patients were in the untreated group. Chronic gastritis, active gastritis and the grade of atrophy significantly decreased in H pylori eradication group (P<0.01). However, the grade of IM increased in H pylori -infected group (P<0.05). CONCLUSION: H pylori eradication may improve gastric mucosal inflammation, atrophy and prevent the progression of IM.     

Surveillance strategies for precancerous gastric conditions after Helicobacter pylori eradication: There is still need for a tailored approach

Prevailing evidence declares that Helicobacter pylori (H. pylori) eradication therapy could shift precancerous gastric conditions (PGC) and positively confines gastric cancer (GC) risk during long-term endoscopic follow-up. Nonetheless, there is a yet unsolved controversy regarding the best-individualized surveillance strategies following H. pylori eradication, based on malignant risk stratification. This last dispute is due to the uncertainty of contemporary evidence and the role of H. pylori inflammatory changes in underestimating PGC at the index endoscopy. However, the current state of the art suggests that it is reasonable that high-quality endoscopy with histological assessment for the most accurate diagnosis of PGC may be delayed in selected high-risk patients without alarm signs for malignancy, following the eradication of H. pylori. Notwithstanding, these aspects need to be further examined in the next future to establish and optimize the most beneficial and cost-effective strategies for recognizing and managing H. pylori-positive patients with PGC in the short- and long-term follow-up. Accordingly, additional studies are yet required to sharpen the hazard stratification of patients with the greatest chance of GC evolution, also recognizing the evolving racial, ethnic, immigration factors and the necessity of novel biomarkers to limit GC development or accomplish a diagnosis of malignancy at an early stage.     

Role of magnifying narrow-band imaging endoscopy for diagnosis of Helicobacter pylori infection and gastric precancerous conditions: Few issues

Standard endoscopy with biopsy and narrow-band imaging with guided biopsy are techniques for the detection of Helicobacter pylori (H. pylori)-related gastritis and precancerous lesions. In this study, the authors compared standard endoscopy and magnified narrow-band imaging (commonly known as NBI-M) in the diagnosis of H. pylori infections, atrophic gastritis, and intestinal metaplasia. Although the sensitivity of NBI-M is better than standard endoscopy, the diagnostic accuracy did not differ substantially between the diagnostic modalities. Future prospective studies may guide endoscopists in difficult cases regarding which modality is more useful and cost-effective for the diagnosis of H. pylori-related gastritis and precancerous conditions.     

HOGG1 polymorphism in atrophic gastritis and gastric cancer after Helicobacter pylori eradication

AIM:To investigate the association between Ser326Cys human oxoguanine glycosylase 1(hOGG1) polymorphism and atrophic gastritis and gastric cancer after Helicobacter pylori(H.pylori) eradication.METHODS:A total of 488 subjects(73 patients with gastric cancer,160 with atrophic gastritis after H.pylori eradication and 255 controls) were prospectively collected.Polymerase chain reaction-restriction fragment length polymorphism analysis was performed to distinguish hOGG1 Ser326Cys polymorphism.Statistical analys...     

根除幽门螺杆菌前后对痘疹样胃炎治疗效果的比较

目的:评价痘疹样胃炎根除幽门螺杆菌(H.pylori)后的治疗效果以及病理变化情况,明确根除H.pylori对痘疹样胃炎的治疗意义.方法:325例痘疹样胃炎患者根据H.pylori检测结果分为阳性组(标准三联或四联疗法)与阴性组(单纯抑酸),比较治疗效果;阳性组根据复查胃镜H.pylori的结果再分为两组,比较病理情况...     

Helicobacter pylori eradication to prevent gastric cancer： underlying molecular and cellular mechanisms

Numerous cellular and molecular events have been described in development of gastric cancer. In this article, we overviewed roles of Helicobacter pylori (H pylori) infection on some of the important events in gastric car-cinogenesis and discussed whether these cellular and molecular events are reversible after cure of the infection. There are several bacterial components affecting gastric epithelial kinetics and promotion of gastric carci-nogenesis. The bacterium also increases risks of genetic instability and mutations due to NO and other reactive oxygen species. Epigenetic silencing of tumor suppressor genes such as RUNX3 may alter the frequency of phe-notype change of gastric glands to those with intestinal metaplasia. Host factors such as increased expression of growth factors, cytokines and COX-2 have been also reported in non-cancerous tissue in H py/ori-positive subjects. It is noteworthy that most of the above phenomena are reversed after the cure of the infection. However, some of them including overexpression of COX-2 continue to exist and may increase risks for carcinogenesis in metaplastic or dysplastic mucosa even after successful H pylori eradication. Thus, H pylori eradication may not completely abolish the risk for gastric carcinogenesis. Efficiency of the cure of the infection in suppressing gastric cancer depends on the timing and the target population, and warrant further investigation.     

根除幽门螺杆菌对胃黏膜及肠化、不典型增生的影响

目的探讨根除幽门螺杆菌（Hp）后慢性胃炎的胃黏膜炎症及肠上皮化生、不典型增生的变化。方法选择172例伴有Hp感豢的慢性活动性胃炎病人分为两组：阴性组（68例）和阳性组（104例），观察阴性组治疗后的变化并与阳性组进行比较，并观察阴性组肠上皮化生和不典型增生在治疗前后的变化。结果阴性组的胃黏膜炎症有28例（41．2％）好转，2例（2．9％）治愈，明显高于阳性组（P〈0.01），其伴有的肠上皮化生有2例（25％）治愈，4例（50％）好转，不典型增生有7例（38．9％）好转，6例（33．3%）治愈。结论Hp感染阴转后慢性胃炎的治疗效果明显优于阳性者，其伴有的肠化和不典型增生亦能好转或治愈。因此，根除Hp是治疗Hp相关性胃炎和防止发生胃癌的重要措施。     

Helicobacter pylori eradication for preventing gastric cancer

Helicobacter pylori(H.pylori)infection is a major riskfactor for gastric cancer(GC)development,which isone of the most challenging malignant diseases worldwide with limited treatments.In the multistep pathogenesis of GC,H.pylori infection slowly induces chronicactive gastritis,which progresses through the premalignant stages of atrophic gastritis,intestinal metaplasia,and dysplasia,and then finally to GC.Although eradication of H.pylori is a reasonable approach for the prevention of GC,there have been some contradictory reports,with only some long-term follow-up data showingefficacy of this approach.The inconsistencies are likely due to the insufficient number of participants,relatively short follow-up periods,poor quality of study designs,and the degree and extent of preneoplastic changes atthe time of H.pylori eradication.This review analyzesrecent high-quality studies to resolve the discrepancies regarding the eradication of H.pylori for GC prevention.The relationship between H.pylori eradication and GC/precancerous lesions/metachronous GC is examined,and the cost-effectiveness of this strategy in the prevention of GC is assessed.Although it is assumed that eradication of H.pylori has the potential to prevent GC,the feasibility and appropriate timing of this strategy for cancer prevention remain to be determined.As a result,additional well-designed trials with longer followup periods are needed to clarify this issue.     

Endoscopic surveillance of gastric cancers after Helicobacter pylori eradication

The incidence and mortality of gastric cancer remains high in East Asian countries. Current data suggest that Helicobacter pylori(H. pylori) eradication might be more effective for preventing gastric cancer in young people before they develop atrophic gastritis and intestinal metaplasia. However, the long-term effect of H. pylori eradication on metachronous cancer prevention after endoscopic resection(ER) of early gastric cancer remains controversial, with some discordance between results published for Japanese and Korean studies.The detection ability of synchronous lesions before ER and eradication of H. pylori directly influences these results. After eradication, some gastric cancers are more difficult to diagnose by endoscopy because of morphologic changes that lead to a flat or depressed appearance. Narrow-band imaging with magnifying endoscopy(NBI-ME) is expected to be useful for identifying metachronous cancers. However, some gastric cancers after eradication show a "gastritislike"appearance under NBI-ME. The gastritis-like appearance correlates with the histological surface differentiation of the cancer tubules and superficial non-neoplastic epithelium atop or interspersed with the cancer. Till date, it remains unclear whether H.pylori eradication could prevent progression of gastric cancer. Until we can establish more useful endoscopic examination methodologies, regular endoscopic surveillance of high-risk groups is expected to be the most beneficial approach for detection.     

Treatment of Helicobacter pylori infection in atrophic gastritis

Helicobacter pylori(Hp) is a major human pathogen causing chronic, progressive gastric mucosal damage and is linked to gastric atrophy and cancer. Hp-positive individuals constitute the major reservoir for transmission of infection. There is no ideal treatment for Hp. Hp infection is not cured by a single antibiotic, and sometimes, a combined treatment with three or more antibiotics is ineffective. Atrophic gastritis(AG) is a chronic disease whose main features are atrophy and/or intestinal metaplasia of the gastric glands, which arise from long-standing Hp infection. AG is reportedly linked to an increased risk for gastric cancer, particularly when extensive intestinal metaplasia is present. Active or past Hp infection may be detected by conventional methods in about two-thirds of AG patients. By immunoblotting of sera against Hp whole-cell protein lysates, a previous exposure to Hp infection is detected in all AG patients. According to guidelines, AG patients with Hp positivity should receive eradication treatment. The goals of treatment are as follows:(1) Cure of infection, resolution of inflammation and normalization of gastric functions;(2) possible reversal of atrophic and metaplastic changes of the gastric mucosa; and(3) prevention of gastric cancer. An ideal antibiotic regimen for Hp should achieve eradication rates of approximately 90%, and complex multidrug regimens are required to reach this goal. Amongst the factors associated with treatment failure are high bacterial load, high gastric acidity, Hp strain, smoking, low compliance, overweight, and increasing antibiotic resistance. AG, when involving the corporal mucosa, is linked to reduced gastric acid secretion. At a non-acidic intra-gastric p H, the efficacy of the common treatment regimens combining proton pump inhibitors with one or more antibiotics may not be the same as that observed in patients with Hp gastritis in an acid-producing stomach. Although the efficacy of these therapeutic regimens has been thoroughly tested in subjects with Hp infection, there is a paucity of evidence in the subgroupof patients with AG. Bismuth-based therapy may be an attractive treatment in the specific setting of AG, and specific studies on the efficacy of bismuth-based therapies are needed in patients with AG.     

Histological characteristics of gastric mucosa prior to Helicobacter pylori eradication may predict gastric cancer

Abstract

Objective. Although Helicobacter pylori (H. pylori) eradication has been shown to inhibit gastric cancer, it does not completely suppress it. Therefore, risk factors of gastric cancer development following H. pylori eradication were examined. Material and methods. A total of 2355 patients (1501 males and 824 females) underwent successful eradication of H. pylori. Endoscopic atrophy, histological gastritis, atrophy, intestinal metaplasia (IM), and operative link for gastritis assessment (OLGA) staging were subsequently evaluated. Results. Following eradication, 33/2355 patients (25 males and 8 females) developed gastric cancer. Compared to a nongastric cancer group that was matched according to gender and age, the incidence of endoscopic atrophy (3.52 ± 1.45 vs. 4.85 ± 1.18, p < 0.001), histological atrophy at the greater curvature of the antrum (1.42 ± 0.80 vs. 1.95 ± 0.86, p = 0.0059), inflammation (2.05 ± 0.59 vs. 2.33 ± 0.66, p = 0.031), IM at the greater curvature of the corpus (0.06 ± 0.30 vs. 0.24 ± 0.54, p = 0.029), the ratio of OLGA-stage 0–II/III, IV (13/8 vs. 55/11, p = 0.038) were significantly higher for the gastric cancer group. Multivariate analysis also showed the highest odds ratio (6.26, 95% confidence interval or CI, 1.28–30.60, p = 0.023) for IM at the greater curvature of the corpus. Conclusions. Severe endoscopical atrophy, OLGA staging, histological atrophy at the antrum, inflammation, and particularly IM at the corpus, were identified as risk factors for gastric cancer development following H. pylori eradication. Therefore, eradication should be performed before these predictors develop.     

根除幽门螺杆菌对胃黏膜肠化的影响

目的　幽门螺杆菌 (Hp)感染可导致慢性活动性胃炎进一步发展为慢性萎缩性胃炎、胃黏膜肠化、最终发展成肠型胃癌。通过 5年随访 ,探讨根除Hp是否对胃黏膜肠化逆转、发生及发展有影响。方法　将 1996年快速尿素酶试验及组织学方法检测Hp均为阳性的 398例病人随机分为治疗组和对照组。治疗组 2 0 1例 ,进行根除Hp治疗 ;对照组 197例 ,给予安慰剂 ;服药前及 5年后分别从胃窦部及胃体部取材检测胃炎、胃炎活动性及肠化。结果　 5年后治疗组中 15 1/2 0 1例Hp为阴性 ,对照组中 16 1/197例Hp为阳性 ;治疗组中Hp被根除的病人胃炎活动性的检出率明显减少 ,与对照组持续Hp感染者比较 ,差异有显著性 (P <0 .0 0 0 1) ;对照组中持续Hp感染者 5年后肠化检出率与自身 5年前、治疗组成功根除Hp者 5年前和 5年后比较均增高 ,差异有显著性 (P均 <0 .0 0 1) ,治疗组根除Hp的病人 5年前后比较差异无显著性 ;对照组中持续Hp感染者胃窦部 5年后肠化检出率与自身 5年前、治疗组根除Hp者 5年前和 5年后比较均增高 ,差异有显著性 (分别为P <0 .0 0 1,P <0 .0 0 1和P<0 .0 1) ,治疗组根除Hp感染的病人 5年前后比较差异无显著性 ;对照组持续Hp感染的病人与治疗组根除Hp感染的病人胃窦部肠化新增及新减情况比较无差异。 结论　 5年     

Kyoto classification in patients who developed multiple gastric carcinomas after Helicobacter pylori eradication

BACKGROUND Endoscopic Kyoto classification predicts gastric cancer risk; however, the score in the patients with primary gastric cancer after Helicobacter pylori(H. pylori) eradication therapy is unknown.AIM To elucidate the Kyoto classification score in patients with both single gastric cancer and multiple gastric cancers developed after H. pylori eradication.METHODS The endoscopist recorded the Kyoto classification at the endoscope and the Kyoto classification score at the time of the first diagnosis of gastric cancer after H. pylori eradication. The score was compared between single gastric cancer group and multiple gastric cancers group.RESULTS The Kyoto score at the time of diagnosis of 45 cases of gastric cancer after H. pylori eradication was 4.0 points in average. The score was 3.8 points in the single gastric cancer group, and 5.1 points in the multiple gastric cancers group. The multiple group had a significantly higher score than the single group(P = 0.016). In the multiple gastric cancers group, all the patients(7/7) had 5 or higher Kyoto score, while in single gastric cancer group, the proportion of patients with a score of 5 or higher was less than half, or 44.7%(17/38).CONCLUSION Patients diagnosed with gastric cancer after H. pylori eradication tended to have advanced gastritis. In particular, in cases of multiple gastric cancers developed after H. pylori eradication, the endoscopic Kyoto classification score tended to be 5 or higher in patients with an open type atrophic gastritis and the intestinal metaplasia extended to the corpus.     

Comparison of the improvement in gastric mucosal tissue after Helicobacter pylori eradication between young and elderly people

Background and study aimsHelicobacter pylori (H. pylori) infection has been clearly shown to be a cause of gastric cancer, and the incidence of gastric cancer has been shown to decrease with eradication. However, few reports have described the utility of eradication therapy in elderly people. Thus, an investigation focusing on how much actual histological improvement is obtained with eradication therapy in elderly people was conducted.Patients and methodsThis was a retrospective study conducted using medical information of patients diagnosed with H. pylori-associated gastritis and who underwent eradication therapy. The histological improvement was assessed based on changes in the atrophy and intestinal metaplasia scores of the Updated Sydney system from before to after eradication. We investigated the rates of histological improvement in atrophy and intestinal metaplasia one year after and long term more than five years after H. pylori eradication in an elderly group and a younger group.ResultsThis study included 221 patients (elderly group 123, younger group 98). In histological atrophy, higher rates of improvement were seen in the corpus than in the antrum, and the rates of cure in the antrum were lower in elderly group than in younger group (p = 0.0282). With regard to intestinal metaplasia, the rates of improvement in the antrum were lower in elderly group than in younger. In long term observation, although the rates of cure in the antrum were lower in elderly, improvements were seen in atrophy scores in most of the patients and intestinal metaplasia scores in about half of patients.ConclusionThough there is more obvious improvement in the gastric mucosa when H. pylori eradication therapy is performed at a young age, some mucosal improvement can be expected in about half of patients after eradication, even in elderly people.     

The eradication of Helicobacter pylori to prevent gastric cancer: a critical appraisal

Introduction: Gastric cancer is one of the top causes of cancer-related death worldwide. How to eliminate gastric cancer is an urgent public-health issue.

Areas covered: In this review, we present up-to-date results of studies on gastric cancer prevention through the eradication of Helicobacter pylori and discuss strategies and obstacles for the implementation of population-wide screening and treatment of this pathogen to prevent gastric cancer.

Expert commentary: Gastric cancer is an inflammation-associated cancer with multistep carcinogenesis. The process consists of H. pylori infection, ongoing inflammation, development of metaplastic epithelia and genetic instability eventuating in gastric cancer. H. pylori infection is critical for development of the disease and studies have consistently shown that H. pylori eradication results in a reduction in (a) gastric mucosal inflammation, (b) progression of histologic damage, (c) risk of peptic ulcers and ulcer recurrence, and (d) risk of gastric cancer. Compared with a large number of clinical trials evaluating chemopreventive approaches, studies of population-wide screening, and eradication of H. pylori have only recently begun and only in high-risk populations. To eliminate gastric cancer requires information on how to implement an effective program for screening and treatment of H. pylori taking into consideration the other health priorities in any specific population.     

Eradication rate and histological changes after Helicobacter pylori eradication treatment in gastric cancer patients following subtotal gastrectomy

AIM: To investigate the eradication rate and histological changes after Helicobacter pylori(H. pylori) eradication treatment following subtotal gastrectomy for gastric cancer.METHODS: A total of 610 patients with H. pylori infection who had undergone surgery for either early or advanced gastric adenocarcinoma between May 2004 and December 2010 were retrospectively studied. A total of 584 patients with proven H. pylori infection after surgery for gastric cancer were enrolled in this study. Patients received a seven day standard triple regimen as first-line therapy and a 10 d bismuthcontaining quadruple regimen as second-line therapy in cases of eradication failure. The patients underwent an esophagogastroduodenoscopy(EGD) between six and 12 mo after surgery, followed by annual EGDs. A further EGD was conducted 12 mo after confirming the result of the eradication and the histological changes. A gastric biopsy specimen for histological examination and Campylobacter-like organism testing was obtained from the lesser and greater curvature of the corpus of the remnant stomach. Histological changes in the gastric mucosa were assessed using the updated Sydney system before eradication therapy and at follow-up after 12 mo.RESULTS: Eradication rates with the first-line and second-line therapies were 78.4%(458/584) and 90%(36/40), respectively, by intention-to-treat analysis and 85.3%(458/530) and 92.3%(36/39), respectively, by per-protocol analysis. The univariate and multivariate analyses revealed that Billroth Ⅱ surgery was an independent factor predictive of eradication success in the eradication success group(OR = 1.53, 95%CI: 1.41-1.65, P = 0.021). The atrophy and intestinal metaplasia(IM) scores 12 mo after eradication were significantly lower in the eradication success group than in the eradication failure group(0.25 ± 0.04 vs 0.47 ± 0.12, P = 0.023; 0.27 ± 0.04 vs 0.51 ± 0.12, P = 0.015, respectively). The atrophy and IM scores 12 mo after successful eradication were significantly lower in the Billroth Ⅱ group than in the Billroth I group(0.13 ± 0.09 vs 0.31 ± 0.12, P = 0.029; 0.32 ± 0.24 vs 0.37 ± 0.13, P = 0.034, respectively).CONCLUSION: Patients with H. pylori following subtotal gastrectomy had a similar eradication rate to patients with an intact stomach. H. pylori eradication is recommended after subtotal gastrectomy.     

Non-microbial approach for Helicobacter pylori as faster track to prevent gastric cancer than simple eradication

Although the International Agency for Research on Cancer declared Helicobacter pylori(H.pylori)as a definite human carcinogen in 1994,the Japanese Society for Helicobacter Research only recently(February 2013)adopted the position that H.pylori infection should be considered as an indication for either amelioration of chronic gastritis or for decreasing gastric cancer mortality.Japanese researchers have found that H.pylori eradication halts progressive mucosal damage and that successful eradication in patients with non-atrophic gastritis most likely prevents subsequent development of gastric cancer.However,those who have already developed atrophic gastritis/gastric atrophy retain potential risk factors for gastric cancer.Because chronic perpetuated progression of H.pylori-associated gastric inflammation is associated with increased morbidity culminating in gastric carcinogenesis,a non-microbial approach to treatment that provides long-term control of gastric inflammation through nutrients and other interventions may be an effective way to decrease this morbidity.This non-microbial approach might represent a new form of prerequisite"rescue"therapy that provides a quicker path to the prevention of gastric cancer as compared to simple eradication.     

Risk of gastric cancer in Helicobacter pylori infection in a 15-year follow-up

Objective: We investigated the risk of gastric cancer among men with Helicobacter pylori (H. pylori) infection or atrophic gastritis (AG) in a 15-year follow-up.

Materials and methods: Study population consists of 12,016 men aged 50–65 years at the beginning of the follow-up in 1994–1996. Serum levels of pepsinogen I (SPGI) and antibodies (IgG) to H. pylori (HpAb) were assayed from serums collected in 1994–1996. Incidence of gastric cancer in the study population was assessed in follow-up from 1994 to 2011 by data from the nationwide cancer registry. Based on SPGI and HpAb values, standardized incidence ratios (SIRs) of gastric cancer were calculated in three subgroups, that is, in those with a healthy stomach, those with H. pylori infection but without AG and those with AG. Risk ratios (RR) of gastric cancer were calculated using SIR of subgroups.

Results: During 15 years, seven gastric cancers appeared per 79,928 person years among men with healthy stomachs, 50 cancers per 92,533 person years in men with H. pylori infection but without AG, and 8 per 8658 person years in men with AG. Risk ratio (RR) of stomach cancer in men with H. pylori infection was 5.8 (95%CI: 2.7–15.3) compared to men with healthy stomachs, and 9.1 (95%CI: 2.9–30.0) in men with AG. There were no differences in cancer risk between cardia and distal stomach.

Conclusions: Risk of gastric cancer is low in men with healthy stomachs. It is significantly increased in those with H. pylori infection and more in those with AG.     

Long-term follow-up of gastric histology after Helicobacter pylori eradication

Helicobacter pylori causes chronic active gastritis and is thought to be associated with the development of gastric atrophy, intestinal metaplasia and carcinoma. As the effect of H. pylori eradication on this process is poorly understood, we sought to determine the long-term effects of H. pylori eradication on gastric histology. Fifty-four patients with duodenal ulceration associated with H. pylori infection received H. pylori eradication therapy in 1985/86 and either remained infected (n= 22) or had the infection eradicated (n= 32); patients were followed up by endoscopy with gastric antral biopsy for 7.1 years (mean). Histopathological analysis of gastric antral mucosa from patients rendered H. pylori-negative revealed a marked decrease in both inflammatory cells within the lamina propria and intraepithelial neutrophils and an increase in epithelial mucinogenesis. Gland atrophy remained unchanged in both H. pylori-positive and -negative patients. When examined for the presence and severity of intestinal metaplasia, there was neither a difference between the two patient groups nor a change with time. These data demonstrate that significant long-term improvements in gastric histology accompany H. pylori eradication when compared with histology in patients with persistent infection. Whether this confers a protective effect by reducing the risk of gastric carcinoma remains unknown.     

Progression of Atrophic Gastritis and Intestinal Metaplasia Drives Helicobacter pylori Out of the Gastric Mucosa

This study was performed to evaluate the implication of anti-H. pylori IgG positivity when CLOtest, histological test, and culture in the antrum and body are all negative, and to find out the specific disease category that is more affected by the hostile relationship of atrophic gastritis and intestinal metaplasia (IM) with H. pylori. Four hundred thirty-six patients (84 controls, 69 with duodenal ulcer, 96 with benign gastric ulcer, 43 with dysplasia, 144 with gastric cancer), who had not received any eradication therapy, were divided into three groups according to H. pylori test: CLOtest or histological H. pylori-positive group (group A; 294 cases), only anti-H. pylori IgG-positive group (group B; 62 cases), and anti-H. pylori IgG-negative group (group C; 80 cases). The grade of neutrophil and monocyte infiltration, atrophic gastritis, and IM was compared according to the updated Sydney system classification. Neutrophil and monocyte infiltrations were significantly severe in the group A. In contrast, the grade of atrophic gastritis and IM in the antrum was significantly higher in group B than the other two groups, A or C. When patients were divided according to the disease outcome in each group, the grade of IM in the body was statistically higher only in the patients with cancer or dysplasia in group B. These results suggest that anti-H. pylori IgG positivity with all negative invasive H. pylori tests represents past infection with H. pylori rather than a false negative, especially in the case of dysplasia and gastric cancer.