Treatment of Helicobacter pylori infection 2011

This article reviews the literature published pertaining to Helicobacter pylori eradication over the last year. The general perception among clinicians and academics engaged in research on H. pylori has been that eradication rates for first-line therapies are falling, although some data published this year have cast doubt on this. The studies published this year have therefore focussed on developing alternative strategies for the first-line eradication of H. pylori. In this regard, clear evidence now exists that both levofloxacin and bismuth are viable options for first-line therapy. The sequential and "concomitant" regimes have also been studied in new settings and may have a role in future algorithms also. In addition, data have emerged that the probiotic Saccharomyces boulardii may be a useful adjunct to antibiotic therapy. Other studies promote individualized therapies based on host polymorphisms, age, and other such demographic factors.     

Helicobacter pylori arginase inhibits T cell proliferation and reduces the expression of the TCR zeta-chain (CD3zeta)

Helicobacter pylori infects approximately half the human population. The outcomes of the infection range from gastritis to gastric cancer and appear to be associated with the immunity to H. pylori. Patients developing nonatrophic gastritis present a Th1 response without developing protective immunity, suggesting that this bacterium may have mechanisms to evade the immune response of the host. Several H. pylori proteins can impair macrophage and T cell function in vitro through mechanisms that are poorly understood. We tested the effect of H. pylori extracts and live H. pylori on Jurkat cells and freshly isolated human normal T lymphocytes to identify possible mechanisms by which the bacteria might impair T cell function. Jurkat cells or activated T lymphocytes cultured with an H. pylori sonicate had a reduced proliferation that was not caused by T cell apoptosis or impairment in the early T cell signaling events. Instead, both the H. pylori sonicate and live H. pylori induced a decreased expression of the CD3zeta-chain of the TCR. Coculture of live H. pylori with T cells demonstrated that the wild-type strain, but not the arginase mutant rocF(-), depleted L-arginine and caused a decrease in CD3zeta expression. Furthermore, arginase inhibitors reversed these events. These results suggest that H. pylori arginase is not only important for urea production, but may also impair T cell function during infection.     

2-week triple therapy for Helicobacter pylori infection is better than 1-week in clinical practice: a large prospective single-center randomized study

BACKGROUND: Proton pump inhibitor (PPI)-based triple therapies are considered the standard regimens for Helicobacter pylori eradication, but the optimal duration of these regimens is still controversial. The aim of this study was to compare the efficacy of 1-week versus 2-week triple therapies in H. pylori-positive patients. MATERIALS AND METHODS: A total of 486 consecutive H. pylori-positive patients were randomized to receive omeprazole, 20 mg b.i.d., clarithromycin 500 mg b.i.d., and either amoxicillin 1 g b.i.d. or metronidazole 500 mg b.i.d. for 1 or 2 weeks. Upper gastrointestinal endoscopy and histology were performed at entry and 2 months after the end of therapy. H. pylori status was defined according to histology and urea breath test. RESULTS: At intention-to-treat analysis, 2-week therapy with omeprazole, amoxicillin, and clarithromycin achieved a significantly higher eradication rate than 1- or 2-week regimens with metronidazole (70% versus 52%, p = .003, versus 56%, p < .01) and the same therapy for 1-week (70% versus 57%, p = .05). At per-protocol analysis, 2-week therapy with omeprazole, amoxicillin, and clarithromycin showed a significantly higher eradication rate than 1-week of amoxicillin and metronidazole (77% versus 62%; p = .03) but no difference with 1-week same regimen (66%) or 2-week metronidazole and clarithromycin regimen (72%). Compliance and tolerability were good for all regimens. CONCLUSIONS: Two-week therapies, independently of antibiotic combination, lead to a significant increase of H. pylori eradication rate compared to 1-week therapies, with same compliance and tolerability, even if, taking account of low-eradication rates, one must question whether the triple therapy should still be used.     

Anti-Helicobacter pylori activities of six Iranian plants

BACKGROUND: Helicobacter pylori is the major worldwide cause of bacterial gastrointestinal infections in adults and children. Antibiotic therapy and a combination of two or three drugs have been widely used to eradicate these infections. However, development of drug resistance in bacteria calls for new sources of drugs, and plants seem to be a logical source of new antibacterial compounds. METHODS: The anti-H. pylori activities of six native Iranian plants (Glycyrrhiza aspera, Juglans regia, Ligustrum vulgare, Thymus kotschyanus, Trachyspermum copticum and Xanthium brasilicum) and seven antibiotics were determined against 70 clinical isolates from children using the disk susceptibility assay. Minimum inhibitory concentrations were also measured for the biologically active extracts. One extract with the best anti-H. pylori activity was fractionated by silica gel and thin layer chromatography and the active compounds were identified by hydrogen nuclear magnetic resonance ((1)HNMR) spectroscopy. RESULTS: All plant extracts showed anti-H. pylori activity by the disk sensitivity method, but the most active extracts were those from X. brasilicum and T. copticum. In fact, the anti-H. pylori activities of the two extracts were superior to the disk antibiotic susceptibility profile. Minimum inhibitory concentrations were within the range of 31.25-250 micro g/ml. Fractionation and chemical identification of the extract from X. brasilicum showed the presence of two substances, a flavonoid and a xanthanolide. CONCLUSIONS: Due to the rise in antibiotic resistance, new sources of anti-H. pylori drugs are needed. The use of medicinal plants and/or their chemical components may have potential benefit in eradicating such problems.     

Immediate endoscopy or initial Helicobacter pylori serological testing for suspected peptic ulcer disease: estimating cost-effectiveness using decision analysis.

OBJECTIVE: To compare the clinical and economic effects of a strategy using immediate endoscopy to a non-invasive strategy utilizing a serologic test for Helicobacter pylori infection for individuals with symptoms suggestive of peptic ulcer disease. DESIGN: Cost-effectiveness analysis evaluating the clinical and economic effects of alternative management strategies of hypothetical patients with suspected peptic ulcer disease in a computer simulation model. INTERVENTION: Two strategies for hypothetical patients with suspected ulcer disease were evaluated: 1) Immediate endoscopy and biopsy for H. pylori, using antisecretory treatment in all patients with documented ulcers and adding antibiotic eradication therapy for those patients with ulcers whose biopsies were positive for H. pylori. 2) Empiric treatment with antisecretory therapy and serologic testing for H. pylori for all patients, using antibiotic eradication therapy only in patients testing positive for H. pylori. MEASUREMENTS: Cost per ulcer cured over a one-year study period. RESULTS: The more cost-effective strategy was the test-and-treat strategy (Strategy 2) with $4481 cost per ulcer cured. The immediate endoscopy strategy resulted in $8045 cost per ulcer cured. The cost-effectiveness advantage of the non-invasive strategy diminished as the cost of endoscopy fell or as the probability of recurrent symptoms rose in patients initially managed without endoscopy. CONCLUSION: Endoscopy, though costly, precisely guided diagnosis and treatment and, thus, potentially reduced the number of patients inappropriately treated. However, cost-effectiveness analysis supports the continued practice of initial non-invasive management of patients with symptoms suggestive of peptic ulcer disease, achieving the benefits of H. pylori eradication through the use of serologic testing to guide antibiotic use.     

Progress in vaccine development against Helicobacter pylori

Based on the very high prevalence of diseases caused by Helicobacter pylori, particularly in the developing world, and the rapid emergence of antibiotic resistance among clinical isolates, there is a strong rationale for an effective vaccine against H. pylori. In this review we describe recent promising candidate vaccines and prophylactic or therapeutic immunization strategies for use against H. pylori, as well as studies to identify immune responses that are related to protection in experimental animals. We also describe identification of different types of immune responses that may be related to protection against symptoms based on comparisons of H. pylori-infected patients with duodenal ulcers or gastric cancer and asymptomatic carriers. We conclude that there is still a strong need to clarify the main protective immune mechanisms against H. pylori as well as to identify a cocktail of strong protective antigens, or recombinant bacterial strains that express such antigens, that could be administered by a regimen that gives rise to effective immune responses in humans.     

Difluoromethylornithine is a novel inhibitor of Helicobacter pylori growth, CagA translocation, and interleukin-8 induction

Helicobacter pylori infects half the world's population, and carriage is lifelong without antibiotic therapy. Current regimens prescribed to prevent infection-associated diseases such as gastroduodenal ulcers and gastric cancer can be thwarted by antibiotic resistance. We reported that administration of 1% D,L-α-difluoromethylornithine (DFMO) to mice infected with H. pylori reduces gastritis and colonization, which we attributed to enhanced host immune response due to inhibition of macrophage ornithine decarboxylase (ODC), the rate-limiting enzyme in polyamine biosynthesis. Although no ODC has been identified in any H. pylori genome, we sought to determine if DFMO has direct effects on the bacterium. We found that DFMO significantly reduced the growth rate of H. pylori in a polyamine-independent manner. Two other gram-negative pathogens possessing ODC, Escherichia coli and Citrobacter rodentium, were resistant to the DFMO effect. The effect of DFMO on H. pylori required continuous exposure to the drug and was reversible when removed, with recovery of growth rate in vitro and the ability to colonize mice. H. pylori exposed to DFMO were significantly shorter in length than those untreated and they contained greater internal levels of ATP, suggesting severe effects on bacterial metabolism. DFMO inhibited expression of the H. pylori virulence factor cytotoxin associated gene A, and its translocation and phosphorylation in gastric epithelial cells, which was associated with a reduction in interleukin-8 expression. These findings suggest that DFMO has effects on H. pylori that may contribute to its effectiveness in reducing gastritis and colonization and may be a useful addition to anti-H. pylori therapies.     

Helicobacter pylori as a class I carcinogen: physiopathology and management strategies

The gram-negative bacterium Helicobacter pylori is known as a persistent colonizer of the human stomach, and probably less known is that it is also involved in extraintestinal diseases. Public awareness of its contribution in the development of gastric cancer is less than 15 years old. The efficacy of the current therapies based on antibiotics against H. pylori has been limited by difficulties such as antibiotic resistance and recurrence. As a consequence, the development of promising vaccines was prompted as the best preventive measure. Unfortunately, so far vaccines failed the transition from animal models to human trials. This keynote presentation is to provide a bird's eye view of H. pylori-related gastric diseases, including gastric cancer, with a synthesis of the molecular mechanisms involved, and an exhaustive presentation and discussion of the current therapeutic guidelines and future strategies for prevention or therapy.     

Impact of Quadruple Regimen of Clarithromycin Added to Metronidazole-Containing Triple Therapy Against Helicobacter pylori Infection Following Clarithromycin-Containing Triple-Therapy Failure

Background: The establishment of an optimal second-line regimen for Helicobacter pylori infection is required. Although quadruple therapy should overcome resistance to either clarithromycin or metronidazole, the effects of a quadruple regimen in second-line therapy are unknown. This study aims to evaluate the efficacy of triple therapy composed of proton pump inhibitor/amoxicillin plus metronidazole with the combined additive effects of clarithromycin as a second-line quadruple therapy against H. pylori infection.
Materials and Methods: Participants were 104 patients in whom first-line therapy containing proton pump inhibitor-amoxicillin-clarithromycin failed. Before starting second-line therapy, patients underwent endoscopy to obtain H. pylori strain for antibiotic susceptibility tests. Patients were randomized to receive rabeprazole (10 mg), amoxicillin (750 mg), and metronidazole (250 mg), either with clarithromycin (200 mg; RAMC group) or without (RAM group); all treatments were administered twice daily for 7 days. H. pylori eradication was confirmed by ¹³C-urea breath tests performed 2 to 3 months post-therapy.
Results: As shown by intention-to-treat/per-protocol analyses, the cure rates for H. pylori infection were 88.5%/93.9% and 82.7%/84.3% for the RAMC and RAM groups. Although the study probably had an insufficient power to show a significant difference between the cure rates of the two regimens, the eradication rates showed a clear trend in favor of the RAMC group. There were no severe side-effects in any group.
Conclusions: In Japan, the RAMC regimen is thought to be a promising alternative strategy for second-line eradication of H. pylori infection.     

Lower prevalence of Helicobacter pylori infection in patients with inflammatory bowel disease but not with chronic obstructive pulmonary disease - antibiotic use in the history does not play a significant role

BACKGROUND: Patients with inflammatory bowel disease have lower prevalence of Helicobacter pylori infection, but the exact reason for this is not yet clear. AIM: To examine whether the antibiotics frequently used in inflammatory bowel disease are responsible for the lower prevalence of H. pylori infection. Patients with chronic obstructive pulmonary disease on prolonged previous antibiotic therapy were used for comparison. METHODS: Presence/absence of H. pylori infection was detected by a (13)C-urea breath test in 133 patients with inflammatory bowel disease (82 ulcerative colitis, and 51 Crohn's disease) and compared with that of 135 patients with chronic obstructive pulmonary disease and with two age-matched control groups (200 patients each). Primary disease location, duration of disease and detailed analysis of previous and current medication (dose and duration of antibiotics, steroids, 5-aminosalicylic acid) were analysed in each cases. RESULTS: Seventeen of the 133 patients with inflammatory bowel disease [12.2% (10/82) of ulcerative colitis and 13.7% (7/51) of Crohn's disease] and 90/135 patients with chronic obstructive pulmonary disease (66.7%) were positive for H. pylori. A total of 78/200 (39%) for the inflammatory-bowel-disease-group-matched controls and 110/210 (55%) for the chronic-obstructive-pulmonary-disease-matched controls were positive for H. pylori. The history of any antibiotic or steroid therapy had no influence on H. pylori status of patients with inflammatory bowel disease. CONCLUSION: The prevalence of H. pylori compared to the age-matched controls is significantly lower in patients with inflammatory bowel disease but not in those with chronic obstructive pulmonary disease. Antibiotic use is not responsible for the lower prevalence of H. pylori infection in patients with inflammatory bowel disease.     

Helicobacter pylori and peptic ulcer disease.

Medical therapy for duodenal or gastric ulcer disease has traditionally involved gastric acid antisecretory therapy for 4 to 8 weeks to promote initial healing and indefinitely to prevent recurrences of ulcer. The discovery of Helicobacter pylori in most patients with peptic ulcer disease has led to a change in this approach. Therapy designed to eradicate H pylori may facilitate ulcer healing with acid antisecretory agents and, more important, may greatly reduce the incidence of ulcer recurrence, obviating the need for maintenance antisecretory therapy. Regimens designed to eradicate H pylori are difficult to comply with, however, and are associated with adverse effects in some patients. In this article we review the diagnosis and treatment of H pylori infection in patients with peptic ulcer disease and make recommendations regarding the use of conventional ulcer therapies and therapies designed to eradicate H pylori.     

Helicobacter pylori therapy demystified

We discuss the role of comparators in Helicobacter pylori treatment trials and why anti-H. pylori therapeutic trials (an infectious disease) are fundamentally different from common gastrointestinal diseases (e.g., the absence of a placebo response, the expectation that cure rates in excess of 95%, and the ability to understand why treatment fails). No comparator is absolutely required other than to 100% success and comparison trials should be limited to comparisons between therapies that reliably achieve 90% or greater success (i.e., good therapies). Comparisons with known low success regimens (i.e., bad therapies) are unethical as is withholding information from the subject regarding current effectiveness of a regimen even if that information would reduce the likelihood that the subject would volunteer. We also discuss how it is possible to predict the outcome of a published but locally untried new regimen. The reason for different outcomes of typical gastrointestinal therapies is shrouded in mystery. In contrast, treatment success for H. pylori should be predictable and treatment failures explainable. For too long expectations and analyses of H. pylori therapy has been confused with what is appropriate for gastrointestinal disease such as constipation or irritable bowel syndrome rather than for infectious diseases such as pneumonia.     

Helicobacter pylori "rescue" therapy after failure of two eradication treatments

Nowadays, apart from having to know well first-line eradication regimens, we must also be prepared to face Helicobacter pylori treatment failures. Therefore, in designing a treatment strategy we should not focus on the results of primary therapy alone, but also on the final--overall--eradication rate. After failure of a combination of proton pump inhibitor (PPI), amoxicillin, and clarithromycin, the use of empirical quadruple therapy (PPI-bismuth-tetracycline-metronidazole), has been generally used as the optimal second-line therapy. Even after two consecutive failures, several studies have demonstrated that H. pylori eradication can finally be achieved in almost all patients if several "rescue" therapies are consecutively given. It seems that performing culture even after a second eradication failure may not be necessary, as it is possible to construct an overall strategy to maximize H. pylori eradication, based on the different possibilities of empirical treatment (when antibiotic susceptibilities are unknown). Thus, if one does not want to perform culture before the administration of the third treatment after failure of the first two, different empirical treatments exist, including regimens based on: 1, amoxicillin (amoxicillin-PPI at high doses); 2, amoxicillin plus tetracycline (PPI-bismuth-tetracycline-amoxicillin, or ranitidine-bismuth-citrate-tetracyline-amoxicillin); 3, rifabutin (rifabutin-amoxicillin-PPI); 4, levofloxacin (levofloxacin-amoxicillin-PPI); and 5, furazolidone (furazolidone-bismuth-tetracycline-PPI).     

Efficacy of Clostridium butyricum preparation concomitantly with Helicobacter pylori eradication therapy in relation to changes in the intestinal microbiota

Antibiotic associated diarrhea due to human intestinal microbiota abnormalities is a side effect of H. pylori eradication therapy. We examined intestinal microbiota changes during H. pylori eradication therapy and the preventive effect of CBM588 as a probiotic agent. Nineteen patients with gastro-duodenal ulcer were randomly divided into three groups: group A (without probiotics), group B (with regular doses of CBM588) and group C (with double doses of CBM588). The incidence of diarrhea and soft stools during H. pylori eradication therapy was 43% in group A and 14% in group B, while none of the patients in group C reported diarrhea or soft stools. Both bacterial counts and detection rates of bifidobacteria and/or obligate anaerobe were decreased by eradication therapy. However, bacterial counts of obligate anaerobes in group C were significantly higher than in group A ( P  < 0.05). Additionally, during eradication therapy C. difficile toxin A was detected in both group A and group B but not in group C.
In conclusion, these results indicate that H. pylori eradication therapy induces antibiotic associated diarrhea due to abnormalities in intestinal microbiota and/or C. difficile . However, these side effects might be prevented by probiotics.     

Treatment of Helicobacter pylori infection 2012

Helicobacter pylori resistance rates to antibiotics vary in different countries and even in different regions of the same country. Choice of treatment is strongly dependent on antibiotic resistance rates. In some countries, triple therapy with a proton-pump inhibitor, amoxicillin, and clarithromycin is still the best option, but eradication results fall short of what would be desired (90-95%) in countries with clarithromycin resistance >20%, bismuth-containing quadruple therapy, or nonbismuth sequential or concomitant therapies may then be the preferred option. Newer antibiotic regimens are awaited. Vaccination would be the best option, especially for developing countries, but little progress has been made in designing a vaccine.     

Characterization and Therapy for Experimental Infection by Helicobacter mustelae in Ferrets

Background. Numerous clinical trials evaluating the efficacy of various antimicrobial compounds against Helicobacter pylori infection have been performed in humans. A convenient animal model for Helicobacter infection would facilitate the evaluation of novel therapies. These experiments were performed to evaluate the use of ferrets as a model of Helicobacter infection.
Materials and Methods. Ferrets were infected experimentally with Helicobacter mustelae and subsequently treated with bismuth subsalicylate (BSS) triple therapy (BSS, metronidazole, and amoxicillin), or left untreated. The status of infection and serology was assessed during treatment and for 8 weeks posttreatment. Seven ferrets successfully treated with triple therapy were challenged with H. mustelae and monitored for infection for an additional 5 weeks.
Results. Infection of ferrets by H. mustelae was accompanied by gastritis and a specific antibody response. Treatment of H. mustelae -infected ferrets with BSS suppressed bacterial growth in four of nine animals but did not eradicate infection. Triple therapy eradicated infection in all nine ferrets with a reduction in gastric inflammation. No relapse of infection occurred up to 8 weeks posttherapy. Challenge with H. mustelae of ferrets successfully treated with triple therapy resulted in a 100% rate of reinfection.
Conclusions. H. mustelae infection can be eliminated by triple therapy, but this does not result in protective immunity against reinfection by H. mustelae. This model, using a strain of Helicobacter indigenous to the host, may be useful for assessing therapeutic efficacy of novel therapies for the treatment of human infection by H. pylori.     

Is Antrum or Corpus the Best Site for Culture of Helicobacter pylori?

Background Isolating Helicobacter pylori on culture media and performing antibiotic susceptibility testing is potentially the most useful tool for guiding antibiotic therapy, especially when antimicrobial resistance is suspected. The aim of this study was to determine whether the yield of H. pylori culture was related to the site from which the gastric specimen was obtained either before or after therapy.
Methods. Gastric mucosal biopsies from the antrum and the corpus of the stomach were cultured. H. pylori status was determined by histological assessment using the Genta stain.
Results. Fifty-two patients with documented H. pylori infection were studied: Twenty-three were tested before antibiotic therapy and 29 after therapy had failed. In 47 patients (90%), both antral and corpus culture specimens were positive. In 5 patients (10%), only one site was positive, with three false-negative antral and two false negative corpus cultures. The overall sensitivity of culture in detecting H. pylori infection was 95% (95% confidence interval = 89–98%) and was not significantly different for the antrum or corpus, either before or after therapy.
Conclusion. Culture of gastric biopsies from either the antrum or the corpus has an excellent diagnostic yield even in patients who failed antimicrobial therapy.     

Double-blind comparison of absorbable colloidal bismuth subcitrate and nonabsorbable bismuth subnitrate in the eradication of Helicobacter pylori and the relief of nonulcer dyspepsia

Background. Bismuth is widely used for the eradication of H. pylori , especially in developing countries, although there are concerns over its neurotoxicity. Whether bismuth has to be absorbed in humans to act against H. pylori is not known. In this study, we compared "absorbable" (colloidal bismuth subcitrate) and "nonabsorbable" (bismuth subnitrate) bismuth as part of triple therapy in the eradication of H. pylori.
Materials and Methods. A double-blind, randomized, placebo-controlled trial was carried out with 120 H. pylori –positive patients with nonulcer dyspepsia. Group CBS + Ab (n = 35) received colloidal bismuth subcitrate (one tablet qds), amoxicillin (500 mg qds), and metronidazole (400 mg tds). Group BSN + Ab (n = 35) received bismuth subnitrate (two tablets tds) and the same antibiotics. Group Ab (n = 35) received placebo bismuth (two tablets tds) and the antibiotics. Group BSN (n = 15) received bismuth subnitrate (two tablets tds) and placebo antibiotics. Bismuth was taken for 4 weeks and the antibiotics for the first 2 weeks. H. pylori eradication, side effects, compliance, pre- and post-treatment symptom scores, and bismuth absorption were assessed.
Results. H. pylori eradication was 69%, 83%, 31%, and 0% in CBS + Ab, BSN + Ab, Ab, and BSN, respectively. Side effects, compliance, and symptom relief were similar in all groups, but blood bismuth levels were significantly greater in CBS + Ab than the other three groups.
Conclusion. The efficacy of bismuth-based therapies as part of triple therapy in the eradication of H. pylori is unrelated to absorption. Hence, the use of effective but poorly absorbed bismuth preparations should be encouraged for bismuth-based eradication therapies.     

Role of Probiotics in Pediatric Patients with Helicobacter pylori Infection: A Comprehensive Review of the Literature

Background: The current guidelines suggest the use of triple therapy as first choice treatment of Helicobacter pylori infection, although the eradication failure rate is more than 30%. Current interest in probiotics as therapeutic agents against H. pylori is stimulated not only by the clinical data showing efficacy of some probiotics in different gastrointestinal diseases but also by the increasing resistance of pathogenic bacteria to antibiotics, thus the interest for alternative therapies is a real actual topic. Aim: To review in vitro and in vivo studies on the role of probiotics in H. pylori infection focusing on the paediatric literature. Materials and methods: Pre‐clinical and clinical paediatric studies in English assessing the role of probiotics in H. pylori infection identified by MEDLINE search (1950–2009) were reviewed. Results: In vitro studies demonstrated an inhibitory activity of probiotics on H. pylori growth and that this effect is extremely strain specific. Available data in children indicate that probiotics seems to be efficacious for the prevention of antibiotic associated side‐effects, and might be of help for the prevention of H. pylori complications by decreasing H. pylori density and gastritis, and for the prevention of H. pylori colonization or re‐infection by inhibiting adhesion to gastric epithelial cells. There is no clear evidence that probiotics may increase the H. pylori eradication rate. Conclusion: Both in vitro and in vivo studies provide evidence that probiotics may represent a novel approach to the management of H. pylori infection.     

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.