Development Of Atrophic Gastritis Research Articles

Prevalence of <i>Helicobacter pylori</i>-associated diseases in the Ural Federal District

Introduction Helicobacter pylori has the most pronounced oncogenic potential among known biological carcinogens of humans. Helicobacter positivity leads to the development of chronic gastritis and with prolonged persistence of infection in the gastric mucosa it is associated with the development of atrophic gastritis and adenocarcinoma of the stomach. According to international data, the prevalence of infection in Russia corresponds to the level of countries with low socio-economic status. The domestic literature contains data for a limited number of reggions, such as North-West Russia, Siberia and the Far East.The aim of the study was to determine the prevalence of Helicobacter pylori infection and chronic atrophic gastritis among patients residing in the Ural Federal District and to identify risk factors for these diseases using modern diagnostic methods used in clinical practice.Materials and methods Observational non-interventional anonymous cross-sectional study of 11,721 primary patients among those tested for H. pylori infection residing in the Ural Federal District. 13C-urease breath test was performed in 10,882 patients, FGDS with gastric mucosal biopsy according to OLGA and histological evaluation of biopsy specimens – in 839 patients.Results The prevalence of H. pylori infection among primary care patients by 13C-UT was 46.9 % and that of chronic atrophic gastritis by histological evaluation of a biopsy specimen was 24.9 %. The risk of chronic atrophic gastritis was higher in those infected with H. pylori (OR 1.71; 95 % CI: 1.24–2.37, p = 0.002) and in patients over 60 years old.Discussion The resulting prevalence of H. pylori infection in the Ural Federal District is below the levels reported in the current literary for Russia. The increasing prevalence of infection with age confirms the principle that the prevalence of infection depends on changing socio-economic conditions in a generation. The observed prevalence of chronic atrophic gastritis is comparable with the national data. The risk of gastric mucosal atrophy increases with age and in the presence of H. pylori infection, which prompts active screening of gastropathology in this category of individuals.Conclusion The prevalence of H. pylori infection and atrophic gastritis among primary patients, as determined by reference diagnostics, was 46.9 % and 24.9 %, respectively.

Parameters of blood short-chain peptides and digestive hydrolases in patients with chronic hepatitis B virus infection

The aim of the study was to examine specifics of changes in the level of stomach- and pancreas-released blood hydrolases in chronic viral hepatitis B and analyze the mechanisms underlying such changes. We assessed serum markers of HBV infection, liver enzymes tests as well as gastric and pancreatic hydrolase level. The patients examined were divided into three groups: control (healthy) and two study groups — HBV post-infection and chronic HBV infection. Patients with HBV post-infection had no significant deviations from normal range for blood level of gastric and pancreatic hydrolases. Patients with chronic HBV infection were found to contain increased blood level of amylase and lipase, which may evidence about increasing pancreatic functional activity and development of covert pancreatitis. At the same time, decline in the concentration of serum pepsinogen-1 below 40 μg/l could indicate about prominently decreased secretion of hydrochloric acid and development of atrophic gastritis, and it was found that the major factor contributing to development of such disorders was the short-chain peptide CCK-8, which utilization declines in patients with chronic HBV infection. CCK-8 can play a pivotal role in inhibiting stimulation of gastric acid secretion and controls gastric acid, plasma gastrin and somatostatin secretion. Cholecystokinin has been found to inhibit acid secretion by activating CCK type A receptors as well as via somatostatin-involving mechanism. The secretion of gastric somatostatin-14 increased by fivefold due to CCK-8 alone, but was blocked by the CCK-A receptor blocker loxiglumide. These data show that CCK-8 directly inhibits acid reactions by stimulating the release of gastric somatostatin indirectly through the CCK-A receptor. Thus, it can be assumed that normally CCK-8 is mainly utilized by the liver, which is altered during chronic hepatitis B resulting in elevated blood CCK-8 concentration. As a consequence, it enhances pancreatic secretion resulting in developing pancreatitis that is paralleled with inhibited gastric secretion and emerged atrophic gastritis.

Prevalence of helicobacter pylori infection in children with Vitamin B12 Deficiency - A cross-sectional observational study

Background: Vitamin B12 deficiency is common in children but under diagnosed disorder. Helicobacter pylori infection plays an important role in the development of atrophic gastritis and related malabsorption. There may be a relationship between H.Pylori infection and vitamin B12 deficiency.
 Aims and Objective: To find out prevalence of Helicobacter pylori infection by endoscopic and histopathological findings, in children aged 2-18 years, with vitamin B12 deficiency.
 Materials and Methods: Seventy-eight patients with deficient serum vitamin B12 levels were evaluated. Upper GI Endoscopy was performed in all cases and gastric biopsies were obtained for histopathological examination and evidence of H. pylori infection.
 Results: Tissue biopsy revealed chronic atrophic gastritis in 09 patients and chronic antral gastritis in 52 patients. H. pylori infection by histology was positive in 45(57.70%) patients. We found significant correlation between atrophic gastritis and H. pylori infection, as well as between H. pylori infection and B12 deficiency.
 Conclusion: H.pylori has an effect on gastric mucosa, which affects the absorption of vitamin B12. Thus individuals with B12 deficiency should be subjected for diagnostic evaluation of H.pylori infection so that appropriate therapy can be initiated.

Screening and eradication of Helicobacter pylori for gastric cancer prevention: the Taipei global consensus

ObjectiveA global consensus meeting was held to review current evidence and knowledge gaps and propose collaborative studies on population-wide screening and eradication of Helicobacter pylori for prevention of gastric cancer...

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

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. 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. 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. 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.

The Probiotic Lactobacillus rhamnosus for Alleviation of Helicobacter pylori-Associated Gastric Pathology in East Africa.

The probiotic Lactobacillus rhamnosus GG (LGG) can play a role in establishing a harmless relationship with Helicobacter pylori and reduce gastric pathology in East African populations. H. pylori has the ability to inhabit the surface of the mucous layer of the human stomach and duodenum. In the developing world, an estimated 51% of the population is carrier of H. pylori, while in some Western countries these numbers dropped below 20%, which is probably associated with improved sanitation and smaller family sizes. Colonization by H. pylori can be followed by inflammation of the gastric mucus layer, and is a risk factor in the development of atrophic gastritis, peptic ulcers and gastric cancer. Notwithstanding the higher prevalence of H. pylori carriers in developing countries, no equal overall increase in gastric pathology is found. This has been attributed to a less pro-inflammatory immune response to H. pylori in African compared to Caucasian populations. In addition, a relatively low exposure to other risk factors in certain African populations may play a role, including the use of non-steroidal anti-inflammatory drugs, smoking, and diets without certain protective factors. A novel approach to the reduction of H. pylori associated gastric pathology is found in the administration of the probiotic bacterium Lactobacillus rhamnosus yoba 2012 (LRY), the generic variant of LGG. This gastro-intestinal isolate inhibits H. pylori by competition for substrate and binding sites as well as production of antimicrobial compounds such as lactic acid. In addition, it attenuates the host’s H. pylori-induced apoptosis and inflammation responses and stimulates angiogenesis in the gastric and duodenal epithelium. The probiotic LRY is not able to eradicate H. pylori completely, but its co-supplementation in antibiotic eradication therapy has been shown to relieve side effects of this therapy. In Uganda, unlike other African countries, gastric pathology is relatively common, presumably resulting from the lack of dietary protective factors in the traditional diet. Supplementation with LRY through local production of probiotic yogurt, could be a solution to establish a harmless relationship with H. pylori and reduce gastric pathology and subsequent eradication therapy treatment.

Polymorphism rs7521584 in miR‑429 is associated with the severity of atrophic gastritis in patients with Helicobacterpylori infection.

The aim of the present study was to investigate an association of genetic polymorphism (rs7521584) located in miR‑200a‑200b‑429 cluster, which has tumor suppressor and pro‑inflammatory function, with the development of gastric mucosal atrophy and metaplasia as a pre‑malignant condition. Gastric mucosa samples were obtained from the antrum of 393patients with no malignancies. The rs7521584 genotype was determined using the polymerase chain reaction‑single‑strand conformation polymorphism analysis method. The degree of gastritis was assessed histologically in all subjects and serum levels of pepsinogen (PG) I/II were quantified in 123 out of 393patients. Patients with an atrophy score ≥1 and metaplasia score ≥1 were classified into the atrophic gastritis group (AG group). The rs7521584 TT genotype was significantly associated with the development of atrophic gastritis [odds ratio (OR), 2.41; 95% confidence interval (CI), 1.10‑5.25; P=0.027), particularly in patients with H.pylori infection (OR, 3.31; 95% CI, 1.35‑8.12; P=0.0089). In addition, in patients younger than 60years of age, this genotype was associated with atrophic gastritis (OR, 3.15; 95% CI 1.03‑9.61; P=0.044)]. In patients with H.pylori infection, the metaplasia score was significantly higher in the TT homozygote compared with the GG+GT genotype. In the rs7521584 TT homozygote, serum PG I/II ratio was significantly reduced with increasing age (P=0.0084). No significant trend was identified between the GG+GT genotype and age. The results of the current study indicated that the rs7521584 minor allele homozygote was associated with the development of chronic gastritis under the influence of H.pylori‑induced inflammation, particularly with the severity of metaplastic alterations.

Mo2011 - Association of Endothelial Dysfunction with the Development of Atrophic Gastritis

Mo2011 - Association of Endothelial Dysfunction with the Development of Atrophic Gastritis

Helicobacter pylori infection and vitamin B-12 deficiency- A cross sectional study

Background: Vitamin B12 deficiency is a common, often overlooked medical problem in adult population. Diagnosis of vitamin B12 deficiency is incomplete without the evaluation of underlying cause. In majority of the cases Vitamin B12 deficiency is attributed to malnutrition. H. pylori infection plays an important role in the development of atrophic gastritis and related malabsorption. Hence it is suggested that there may be a relationship between h. pylori infection and vitamin B12 deficiency.Aims and Objective: To evaluate correlation of helicobacter pylori infection and blood levels of vitamin B12.Materials and Methods: A total of 120 patients with deficient serum vitamin B12 levels were evaluated. Upper GI Endoscopy was performed and gastric biopsies were obtained for Histopathological examination and histological evidence of H. pylori infection.Results: Tissue biopsy revealed chronic atrophic gastritis in 65 patients and chronic antral gastritis in 39 patients. H. pylori infection by histology was positive in 68 patients. There was significant correlation between atrophic gastritis and H. pylori as well as between H. pylori and B12 deficiency.Conclusion: H.pylori has an effect on gastric mucosa, which influences the absorption of vitamin B12. Thus individuals with B12 deficiency must be subjected for diagnostic evaluation of H.pylori infection and appropriate therapy must be initiatedAsian Journal of Medical Sciences Vol.8(4) 2017 16-20

Operation on Billroth-I in gastric cancer surgery: the evolution of views

In recent years almost all over the world, there is a decrease in the incidence of gastric cancer. Despite that carcinoma of the stomach annually affects on our planet about 1 million people. The prevalence of distal gastric cancer has a tendency to decrease, while the frequency of proximal cancer increases slightly. Early gastric cancer is only 10% of all new cases, and in 64,2% of patients are diagnosed at stages III-IV disease. Over the last 35 years, there has been substantial progress in the diagnosis and treatment of gastric cancer. Surgery that involves complete removal of the tumor remains the only method which gives hope for cure of the patient, despite the significant number of combined and complex treatment methods of this disease. However, many provisions of this concept have changed drastically. After surgery Billroth-I much less frequently and with less severity (than after resection Billroth-II) develops duodenogastric reflux in the absence of duodenostasis and adequate patency of the digestive tract. It is the reflux of bile and pancreatic juice plays an important role in the occurrence of cancer of the stomach stump. The basic cause of cancer is the development of atrophic gastritis as a consequence of denervation of the authority and the reflux of bile into the resected stomach. The choice of the method of restoring the integrity of digestive tract after distal gastrectomy is a topical problem, given the continuous increase in the number of patients undergoing this operation. In the review of literature shows that intervention in the modification of the Billroth-I does not increase the number of postoperative complications, no differences in long-term results of surgical treatment of gastric cancer for two methods of restoring the continuity of the digestive tract after distal resection.

Leptin receptor signaling is required for high-fat diet-induced atrophic gastritis in mice.

BackgroundObesity increases the risk for malignancies in various tissues including the stomach. Atrophic gastritis with precancerous lesions is an obesity-associated disease; however, the mechanisms that underlie the development of obesity-associated atrophic gastritis are unknown. Leptin is a hormone derived from stomach as well as adipose tissue and gastric leptin is involved in the development of gastric cancer. The aim of the current study is to investigate the involvement of leptin receptor signaling in the development of atrophic gastritis during diet-induced obesity.MethodsMale C57BL/6, ob/ob and db/db mice were fed a high-fat diet (HFD) or a control diet (CD) from 1 week to 5 months. Pathological changes of the gastric mucosa and the expression of molecules associated with atrophic gastritis were evaluated in these mice.ResultsHFD feeding induced gastric mucosal hyperplasia with increased gastric leptin expression. Mucosal hyperplasia was accompanied by a higher frequency of Ki67-positive proliferating cells and atrophy of the gastric glands in the presence of inflammation, which increased following HFD feeding. Activation of ObR signaling-associated molecules such as ObR, STAT3, Akt, and ERK was detected in the gastric mucosa of mice fed the HFD for 1 week. The morphological alterations associated with gastric mucosal atrophy and the expression of Muc2 and Cdx2 resemble those associated with human intestinal metaplasia. In contrast to wild-type mice, leptin-deficient ob/ob mice and leptin receptor-mutated db/db mice did not show increased Cdx2 expression in response to HFD feeding.ConclusionTogether, these results suggest that activation of the leptin signaling pathway in the stomach is required to develop obesity-associated atrophic gastritis.Electronic supplementary materialThe online version of this article (doi:10.1186/s12986-016-0066-1) contains supplementary material, which is available to authorized users.

Gastric-and-Intestinal Mixed Intestinal Metaplasia Is Irreversible Point with Eradication of <i>Helicobacter pylori</i>

Helicobacter pylori (H. pylori) represents an important factor in the development of atrophic gastritis, intestinal metaplasia (IM), and gastric cancer. Eradication of H. pylori has been reported to prevent gastric cancer only in cases without atrophy or IM. However, histological changes with eradication have yet to be fully clarified. We evaluated 38 H. pylori-positive cases before and after eradication at the gland level; pyloric glands were classified as showing gastric proper (G) and IM gland types, with the latter including gastric-and-intestinal mixed IM (GI-IM) and solely intestinal IM (I-IM), depending on the remaining gastric phenotypes. On eradication, acute and chronic inflammation attenuated rapidly and gradually, respectively, whereas levels of MUC5AC and MUC6 expression were not markedly altered. Gland width, size of nuclei and cytoplasm and their ratio in surface foveolar epithelium, the number of Ki-67-positive cells and the length of the proliferating zone in each gland were significantly decreased in G glands after eradication compared with those in GI-IM and I-IM. The number of mitotic phase cells, positive for phosphorylated histone H3 at serine 28, was increased in both types of IM compared to that in G glands in the H. pylori-infected state, but unexpectedly remained unchanged with eradication. These results suggest that GI-IM, as the beginning of IM, could represent a histological irreversible point with eradication and be considered as a “histological point of no return”.

14 EBI3 Regulates the Development of Atrophic Gastritis and Progression to Gastric Cancer by Regulating IL-17A/IL-22 Production by CD4+ T-Cells

14 EBI3 Regulates the Development of Atrophic Gastritis and Progression to Gastric Cancer by Regulating IL-17A/IL-22 Production by CD4+ T-Cells

Differences of mutation of helicobacter pylori cagA gene isolated from duodenal ulcer and gastric cancer.

69 Background: H. pylori is the pathogen of both duodenal ulcer and gastric carcinoma. However, they are markedly different in terms of its physiologic and pathologic basis. CagA is 120-145-kDa protein of H. pylori and located one end of Cag PAI encoding components of type IV secretion system. H. pylori expressing CagA are associated with development of atrophic gastritis, peptic ulcer, and gastric carcinoma. This study was aimed to examine the differences of cagA mutations of H. pylori isolated from duodenal ulcer and gastric carcinoma. Methods: Isolated H. pylori from 29 patients with gastric carcinoma and 31 patients with duodenal ulcer were compared the frequency of mutations after cloning of cagA of H. pylori. Results: Even there were diverse mutations scattered on whole sequence of cagA, mutations were more frequent in amino acid sequence 200-400 and 850-1100. Amino acid loci G311, D371, M393, T899, and S1068 were mutated in more than half of patients regardless of diseases. The mutations of CagA in C-terminal area, especially Q889, T899, R952, A968, R997, K1034, Q1067, and S1068, were 20% or more frequent in H. pylorifrom duodenal ulcer than those from gastric carcinoma. EPIYA type was not different between the duodenal ulcer and gastric carcinoma. Conclusions: These results suggest that the mutations of cagA of H. pylori, especially in C-terminus are distinguishable between duodenal ulcer and gastric carcinoma.

Relation between bile acid reflux into the stomach and the risk of atrophic gastritis and intestinal metaplasia: A multicenter study of 2283 cases

The relationship between bile acid reflux into the stomach and the risk of atrophic gastritis and intestinal metaplasia is still not well understood. Towards obtaining a better understanding, concentrations of bile acids were measured. This study was carried out with the participation of 14 facilities in Japan, and 2283 samples were collected. The subjects with bile acid concentrations equal to or higher than the limit of detection were divided into four groups of equal size (group A: 0-25%, group B: 26-50%, group C: 51-75%, and group D: 76-100%). Thus, including the control group, there were five groups in total. The odds that the control group would develop atrophic gastritis and intestinal metaplasia was set as 1,and the odds ratios (OR) in groups A, B, C and D were calculated based on the odds in the control group. Regarding the development of atrophic gastritis, no increased risk was observed in either the Helicobacter pylori (H. pylori)-positive or -negative cases. The OR for the development of intestinal metaplasia were significantly higher, for both cases with and without H. pylori infection, in group D. High concentrations of bile acid seem to be associated with an elevated risk of intestinal metaplasia.

CagA Helicobacter pylori Seropositivity in Asymptomatic, Apparently Healthy, Young Adult Egyptian Food Handlers

Background/Aim: Infection with CagA Helicobacter pylori(H. pylori) positive strain is a risk factor for the development ofatrophic gastritis and gastric adenocarcinoma. This studyinvestigated the seroprevalence of H. pylori and its virulentstrains CagA in Egyptian food handlers.Subjects and methods: A total of 365 eligible male subjectsparticipated in the initial study. Venous blood samples werecollected from all participants for assessment of H. pylori specificIgG and serum CagA antibodies.Results: Out of 365 subjects, 310 were reactive to H. pylori.Out of them, CagA was detected in 143 H. pylori-infectedsubjects. CagA antibodies were more common in cigarettesmokers (< 0.001), living in high crowding index (< 0.001), withlow family income (< 0.01) and sharing their bedrooms duringchildhood (< 0.001).Conclusion: Our data revealed a high prevalence of CagAvirulent strains among asymptomatic apparent food handlersof Egypt. Emergency surveillance mechanisms should bedeveloped for containment of H. pylori infection in Egypt.Abbreviations: H. pylori: Helicobacter pylori; CagA: Cytotoxinassociated gene A.

Role of Sonic Hedgehog signaling during progression from inflammation to cancer in the stomach

Despite advances in treatment and the declining incidence, gastric cancer remains the second leading cause of cancer-related deaths in the world. Understanding the progression from inflammation to cancer in the stomach is crucial in the development of novel therapies and strategies for treating this disease. Chronic inflammation of the stomach is typically caused by Helicobacter pylori (H. pylori) and resulting lesions may lead to gastric cancer. During the progression from inflammation to cancer, the stomach epithelium changes with evidence of the disruption of normal epithelial cell differentiation and infiltrating inflammatory cells. Coincident with the development of atrophic gastritis and metaplasia, is the loss of the gastric morphogen Sonic Hedgehog (Shh). Given its critical role as a regulator of gastric tissue homeostasis, the disruption of Shh expression during inflammation correlates with the loss of normal epithelial cell differentiation, but this has only recently been rigorously tested in vivo using a unique mouse model of targeted gastric Shh deletion. While pre-neoplastic lesions such as atrophic gastritis and intestinal metaplasia are associated with the loss of Shh within the acid-secreting glands of the stomach, there is a clear link between elevated Shh and signaling to gastric cancers. The current review focuses on the effects of aberrant Shh expression and its role in the development of gastric cancer, specifically in response to H. pylori infection.

The Regenerating Gene IαIs Overexpressed in Atrophic Gastritis Rats with Hypergastrinemia

The role of gastrin on the development of atrophic gastritis (AG) and its relationship with the expression of RegIα in vivo remain unclear. We established experimental AG in rats by combination administration with sodium salicylate, alcohol, and deoxycholate sodium. The mean score of inflammation in gastric antrum in AG rats was significantly elevated (P < 0.05), while the number of glands dramatically decreased (P < 0.05). In addition, the cell proliferation in gastric glands was increased in experimental AG rats, as determined by immunohistochemistry staining of PCNA and GS II. The level of serum gastrin in AG rats was significantly elevated relative to that of normal rats (P < 0.01). Moreover, the expression of RegIα protein and its receptor mRNA was increased in gastric tissues in AG rats (P < 0.05). Taken together, we demonstrated that the overexpression of Reglα is related with hypergastrinemia in AG rats.

Clinical relevance ofHelicobacter pylori babA2andbabA2/Bin Costa Rica and Japan

To evaluate the prevalence of Helicobacter pylori (H. pylori) babA2, babB and a recombinant gene between babA2 and babB (babA2/B), and their role in the development of atrophic gastritis in Costa Rican and Japanese clinical isolates. A total of 95 continuous H. pylori-positive Costa Rican (41 males and 54 females; mean age, 50.65 years; SD, +/- 13.04 years) and 95 continuous H. pylori-positive Japanese (50 males and 45 females; mean age, 63.43; SD, +/- 13.21 years) patients underwent upper endoscopy from October 2005 to July 2006. They were enrolled for the polymerase chain reaction (PCR)-based genotyping of the H. pylori babA2, babB and babA2/B genes. Statistical analysis was performed using the chi(2) test and the Fisher's exact probability test and multivariate analysis was performed by logistic regression adjusting for gender and age. P < 0.05 was regarded as statistically significant. The PCR-based genotyping of 95 Costa Rican and 95 Japanese isolates showed a higher prevalence of babA2 in Japan (96.8%) than in Costa Rica (73.7%), while that of babA2/B was higher in Costa Rica (11.6%) than in Japan (1.1%). In Costa Rican isolates only, babA2 was significantly associated with atrophic gastritis (P = 0.01). These results suggest that the status of babA2 and babA2/B shows geographic differences, and that babA2 has clinical relevance in Costa Rica.

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

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. 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. 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. 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.