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Background Gastric cancer is worldwide the fourth more common cancer type by incidence, and the third by mortality. We analyzed three missense variants of TAS2R38 gene: rs713598 (A49P), rs1726866 (V262A), and rs10246939 (I296V). These variants and their combination in haplotypes (proline, alanine and valine/tasters or alanine, valine and isoleucine/nontasters) and diplotypes are responsible for individual differences in bitter perception. The single-nucleotide polymorphisms and the related phenotypes are known to be associated with susceptibility to Gram-negative bacterial infections, such as Helicobacter pylori, and with risk of various cancer types. An association between intermediate tasters (as defined by TAS2R38 diplotypes) and increased risk of gastric cancer was reported in a Korean population. Methods We analyzed 2616 individuals of Latin American origin, representing the whole spectrum of lesions from gastritis to gastric cancer. Results Comparing cancer cases vs. noncancers we observed a decrease in risk associated with heterozygous carriers of rs10246939 (P = 0.006) and rs1726866 (P = 0.003) when compared with homozygotes of the more common allele. Also, the analysis of diplotypes/phenotypes reflected the same association, with super-tasters showing a borderline increased risk of developing gastric cancer compared to medium-tasters [odds ratio (OR) = 1.63; 95% confidence interval (CI), 1.04-2.56; P = 0.033]. Also, nontasters showed an increased risk when compared to medium-tasters although not reaching statistical significance (OR = 1.58; 95% CI, 0.80-2.87; P = 0.203). We also tested the interactions between the TAS2R38 genotypes and H. pylori cagA status in a subset of samples and found no interaction. Conclusion In conclusion, our results suggest only a modest contribution of TAS2R38 gene genetic variability in gastric cancer etiology.

Gastric cancer is the fourth most common cause of cancer-linked deaths in the world. Gastric tumor cells have biological characteristics such as rapid proliferation, high invasiveness, and drug resistance, which result in recurrence and poor survival. Helicobacter pylori (H. pylori) has been proposed as a first‐class carcinogen for gastric cancer according to the 1994 world health organization (WHO) classification. One of the important mechanisms by which H. pylori affects the gastric environment and promotes carcinogenesis is triggering inflammation. H. pylori induces an inflammatory response and a plethora of different signal transduction processes, leading to gastric mucosal disturbance, chronic gastritis, and a multi-step complex pathway that initiates carcinogenesis. It seems undeniable that the interaction between various cell types, including immune cells, gastric epithelium, glands, and stem cells, is vital for the progression and development of carcinogenesis concerning H. pylori. The interactions of H. pylori with surrounding cells play a key role in cancer progression. In this review, we discuss the interplay between H. pylori and tumor-supportive cells, including mesenchymal stem cells (MSCs), cancer-associated fibroblasts (CAFs), tumor-associated macrophages (TAMs), and myeloid derived-suppressor cells (MDSCs) in gastric cancer. It is hoped that clarifying the specific mechanisms for ‘cross-talk’ between H. pylori and these cells will provide promising strategies for developing new treatments.

Objectives Despite excessive resistance of Helicobacter pylori to clarithromycin among Iranian population, unfortunately, clarithromycin-based therapy is still prescribed in Iran. Recent studies have shown high rates of H. pylori eradication in patients treated with levofloxacin. The main purpose of this study was to compare the effect of levofloxacin with clarithromycin on the eradication of H. pylori infection in Iranian population. Methods A comprehensive meta-analysis was done for the relevant cohort studies and clinical trials to compare the therapeutic effects of levofloxacin with clarithromycin in Iranian population. We pooled the data using odds ratio corresponding to 95% confidence intervals to find the clinical efficacy of levofloxacin versus clarithromycin to treat H. pylori infection. The heterogeneity and publication bias were also measured for the included studies. Results A total of 13 studies were included in the quantitative synthesis. Eradication rate in patients receiving levofloxacin and clarithromycin were 75% and 66.3%, respectively (OR: 1.76; 95% CI: 1.40-2.20). In addition, in the subgroup analysis, it was confirmed that cure rate is relatively higher in levofloxacin-treated cases. However, there is significant heterogeneity as well as publication bias, thus, the results need to be interpreted with caution. Conclusions We found that the success of levofloxacin treatment was significantly higher than that of clarithromycin. Therefore, it is suggested that clarithromycin-based triple therapy be replaced by levofloxacin-based triple therapy in countries with high resistance rate to clarithromycin such as Iran. Nevertheless, findings of the present study need to be approved with larger investigation on Iranian population.

Aims We described the presence of Helicobacter pylori (HP) and estimated the prevalence of primary and secondary resistance using molecular detection in gastric biopsies of Ecuadorian patients. Methods and Results 66.7% (238/357) of the patients demonstrated the presence of HP using CerTest qPCR. Of these, 69.79% (104/149) were without previous HP eradication treatment and 64.42% (134/208) with prior HP eradication treatment. The mutation-associated resistance rate for clarithromycin was 33.64% (primary resistance) and 32.82% (secondary resistance), whereas that in levofloxacin the primary and secondary resistance was 37.38% and 42%, respectively. For tetracycline and rifabutin, primary and secondary resistance was 0%. Primary and secondary resistance for metronidazole and amoxicillin could not be evaluated by genotypic methods (PCR and sequencing). Conclusions The analysis of mutations in gyrA, 23S rRNA and 16S rRNA is useful to detect bacterial resistance as a guide for eradication therapy following failure of the first-line regimen. Significance and Impact of the Study This study carried out in an Ecuadorian population indicates that the resistance of HP to first-line antibiotics is high, which may contribute to the high rates of treatment failure, and other treatment alternatives should be considered.

Although Helicobacter pylori infection is the most important causative factor for gastric cancer (GC), H. pylori eradication alone does not completely eliminate the GC risk. In addition to H. pylori eradication, other risk factors for GC should be identified and targeted. Diabetes mellitus (DM) confers a 20% increased risk of GC, which could be mediated via several biological mechanisms including the stimulation of cell proliferation via hyperinsulinemia and increased insulingrowth factor production, the promotion of angiogenesis, and DNA damage. With a current global prevalence of 9.3% and a predicted rise to 10.2% by 2030, DM could contribute substantially to the burden of GC cases worldwide. Emerging evidence showed that metformin possesses chemopreventive effects via both direct (e.g., adenosine monophosphate-activated protein kinase activation and subsequent inhibition of the mammalian target of rapamycin pathway) and indirect (e.g., modulation of the interaction between tumor cells and their microenvironment and gut microbiota) pathways. A recent meta-analysis of observational studies showed that metformin use was associated with 24% lower GC risk. However, many available observational studies related to metformin effects suffered from biases including the failure to adjust for the H. pylori infection status and serial glycemic control and time-related biases. Future prospective studies addressing these pitfalls are needed.

BACKGROUND AND STUDY AIM Immunohistochemistry is one of the superior methods and is regarded as the gold standard for the detection of Helicobacter pylori. We aimed to detect the presence of Helicobacter pylori in gastric biopsies among patients at the Muhimbili National Hospital from January 2012 to December 2016. Also, we determined the predictors of Helicobacter pylori infection. PATIENTS AND METHODS Retrospectively, we retrieved the tissue blocks of gastric biopsies at the Central Pathology Laboratory of the patients with different gastric pathologies at the Muhimbili National Hospital from January 2012 to December 2016. Helicobacter pylori were detected using anti-Helicobacter pylori polyclonal antibodies. Binary logistic regression analysis was done to determine the predictors of Helicobacter pylori infection. A two-tailed p

The treatment of refractory Helicobacter pylori remains challenging in clinical practice. Factors that should be considered in the treatment of refractory H. pylori infection include treatment length, dosage of antibiotics and proton pump inhibitors (PPIs), number of drugs, and the selection of appropriate antibiotics. Extending the treatment length of triple therapy and non-bismuth quadruple therapy to 14 days may increase the eradication rate compared with a shorter period (7 or 10 days). The use of a higher dose of PPIs or vonoprazan may also increase the efficacy of triple therapy. Four-drug therapy, including bismuth or non-bismuth quadruple therapies, usually achieve higher eradication rates than triple therapy. The addition of bismuth or metronidazole to levofloxacin-amoxicillin-PPI therapy may also increase the eradication rate. Therefore, four-drug therapies containing a higher dose of PPIs for 14 days are recommended in the third-line treatment setting for refractory H. pylori infection. The selection of appropriate antibiotics may be guided by susceptibility testing or empirically by medication history. Tailored therapy guided by susceptibility testing or genotypic resistance is recommended whenever possible. However, properly designed empirical therapy based on prior medication history (i.e., avoid the reuse of clarithromycin or levofloxacin empirically) is an acceptable alternative to tailored therapy after considering accessibility, cost, and the preference of the patient.

When infected by Helicobacter pylori, it often causes gastritis, gastric ulcer, or gastric cancer. Antibiotics are used to treat H. pylori infection, as they inhibit or kill H. pylori often ex-tending to reduce the incidences of gastric adenoma and cancer. However, H. pylori has developed drug resistance to many clinically used antibiotics over the years, thereby providing no warranty of successful treatment whenever H. pylori infection befalls. We report here that fucoidan from Sargassumhemiphyllum can effectively reduce infection of H. pylori without development of drug resistance. Fucoidan demonstrated a strong anti-inflammation activity in RAW264.7 cell model. Using AGS cell model, fucoidan decreased H. pylori adhesion to host cells and thus reduced its infection rate, especially in post-treatment where the infection rate was reduced to 40%. Mechanistically, fucoidan intervenes the proper functions of adhesion molecules BabA and AlpA of H. pylori. Moreover, fucoidan is able to significantly lower the total count of H. pylori and the levels of IL-6 and TNF-α in vivo. Added together, these convergent results suggest that fucoidan is an effective agent in a position to protect stomach from H. pylori infection by reducing its total count and induced inflammation.

MSI-78A (Pexiganan A) is one of the few antimicrobial peptides (AMPs) able to kill Helicobacter pylori, a pathogenic bacterium that colonizes the gastric mucosa of half of the world's population. Antibiotics fail in 20–40% of H. pylori-infected patients, reinforcing the need for alternative treatments. Herein, a bioengineered approach was developed. MSI-78A with a C-terminal cysteine was grafted onto chitosan microspheres (AMP-ChMic) by thiol-maleimide (Michael-addition) chemistry using a long heterobifunctional spacer (NHS-PEG113-MAL). Microspheres with ∼4 µm diameter (near H. pylori length) and stable at low pH were produced by spray drying using a chitosan solution with an incomplete genipin crosslinking. A 3 × 10−5 µg AMP/microsphere grafting was estimated/confirmed by UV/Vis and FTIR spectroscopies. AMP-ChMic were bactericidal against H. pylori J99 (highly pathogenic human strain) at lower concentrations than the free peptide (∼277 µg grafted MSI-78A-SH/mL vs 512 µg free MSI-78A-SH/mL), even after pre-incubation in simulated gastric conditions with pepsin. AMP-ChMic killed H. pylori by membrane destabilization and cytoplasm release in a ratio of ∼10 bacteria/microsphere. This can be attributed to H. pylori attraction to chitosan, facilitating the interaction of grafted AMP with bacterium membrane. Overall, it was demonstrated that the peptide-microsphere conjugation chemistry did not compromise the MSI-78A antimicrobial activity, instead it boosted its bactericidal performance against H. pylori. Statement of significance Half of the world's population is infected with Helicobacter pylori, a gastric bacterium that is responsible for 90% of non-cardia gastric cancers. Therefore, H. pylori eradication is now advocated in all infected individuals. However, available antibiotic therapies fail in up to 40% patients. Antimicrobial peptides (AMPs) are appealing alternatives to antibiotics, but their high susceptibility in vivo limits their clinical translation. AMP immobilization onto biomaterials surface will overcome this problem. Herein, we demonstrate that immobilization of MSI-78A (one of the few AMPs with activity against H. pylori) onto chitosan microspheres (AMP-ChMic) enhances its anti-H. pylori activity even at acidic pH (gastric settings). These results highlight the strong potential of AMP-ChMic as an antibiotic alternative for H. pylori eradication.

Introduction: The resistance to antibiotics of Helicobacter pylori (H. pylori) is the main factor that affects current therapeutic treatments. The main objective of this study is to describe the pattern of antibiotic resistances in children with an infection due to H. pylori. Patients and methods: An observational, retrospective study was conducted from 2014 to 2019, which included patients between 5 and 17 years old, on whom a gastroscopy, with a gastric biopsy culture positive for H. pylori, and an antibiotic sensitivity study was performed. The antibiotic sensitivity studies were performed using an epsilometer (E-test). The cut-off points to define the resistances were those proposed by the European Committee on Antimicrobial Susceptibility Testing — EUCAST. The eradication study was performed using the 13C-urea breath test or the H. pylori monoclonal test in faeces 6–8 weeks after finalising the treatment. Results: The study included 80 patients (63.8% females), with a mean age of 11.9 years (SD ± 2.7 DS). Over one-third (38.8%) of the patients had received previous treatment for H. pylori. In the endoscopy, peptic ulcer lesions were observed in 10% of patients. More than two-thirds (67.5%) had resistance to at least one drug. 16.3% presented double resistance. The primary resistances were: clarithromycin, 44.9%, metronidazole 16.3%, levofloxacine 7.9%, and amoxicillin 2%. Patients that received treatment according to the new ESPGHAN 2017 guidelines had significantly higher eradication rates compared to those that received treatment according to previous guidelines (80% vs. 55.8%, P = 0.04). Conclusions: The high rate of H. pylori resistances, and as a result, the low eradication rates, are still a very important cause for concern. The first line treatment, when this is indicated must be given following the antibiotic sensitivity studies, and in the cases where these cannot be done or are not available, at least in accordance with the regional resistance rates. The correct application of the new guidelines significantly improves the eradication rate. Resumen: Introducción: Las resistencias antibióticas de Helicobacter pylori (H. pylori) son el principal factor que afecta a la eficacia de los regímenes terapéuticos actuales. El objetivo principal del estudio es describir el patrón de resistencias antibióticas en ni˜nos con infección por H. pylori. Pacientes y métodos: Estudio observacional retrospectivo de 2014 a 2019 en el que se incluyen pacientes entre 5–17 años a los que se realizó gastroscopia, con cultivo de biopsia gástricapositivo para H. pylori y estudio de sensibilidad a antibióticos. Los estudios de sensibilidad antibiótica se realizaron mediante E-test. Los puntos de corte para definir las resistencias fueron los propuestos por el EUCAST. El estudio de erradicación se realizó con test del aliento con urea marcada con C 13 o test monoclonal de antígeno de H. pylori en heces a las 6–8 semanas de finalizar el tratamiento. Resultados: Ochenta pacientes (63,8% mujeres). Media de edad 11,9 años (±2,7 DS). Un 38,8% habían recibido tratamiento previo para H. pylori. Un 10% presentaron en la endoscopia lesiones ulcerosas pépticas. El 67,5% presentaba resistencia al menos a un fármaco. Un 16,3% presentaron doble resistencia. Las resistencias primarias fueron: claritromicina 44,9%, metronidazol 16,3%, levofloxacino 7,9% y amoxicilina 2%. Los pacientes que recibieron tratamiento acorde a las nuevas guías ESPGHAN 2017 presentaron tasas de erradicación significativamente superiores en comparación con los que recibieron tratamiento acorde a las guías previas (80% vs. 55,8% p = 0,04). Conclusiones: La alta tasa de resistencias de H. pylori y, en consecuencia, las bajas tasas de erradicación, siguen siendo una preocupación muy importante. El tratamiento de primera línea, cuando esté indicado debe hacerse guiado por estudios de sensibilidad antibiótica y en los casos en el que no se puedan realizar o no estén disponibles, al menos de acuerdo con las tasas regionales de resistencia. La aplicación correcta de las nuevas guías mejora de forma significativa el nivel de erradicación.

Background Non-bismuth containing quadruple therapy (concomitant therapy) is an alternative treatment for Helicobacter pylori (H. pylori) eradication with increasing clarithromycin-resistant strains over times. This study compared the efficacies of non-bismuth containing quadruple therapy (concomitant therapy) in the treatment of first-line anti-Helicobacter Pylori between two time intervals (January 2013 to June 2014 and June 2016 to December 2017). Methods H. pylori-infected patients were recruited in the intention-to-treat (ITT analysis) and divided into EACM-A group (enrolled from January 2013 to June 2014, N = 98) and EACM-B group (enrolled from June 2016 to December 2017, N = 99). Patients were prescribed with 7-day esomeprazole 40 mg bid., clarithromycin 500 mg bid., amoxicillin 1 g bid. and metronidazole 500 mg bid. Ninety patients and 93 patients were analyzed in the per protocol (PP) analysis (8 and 6 patients lost follow-up in each group). Urea breath tests were performed 4–8 weeks thereafter. Results The eradication rates for EACM-A and EACM-B groups were 87.8% (95% confidence interval [CI] = 79.7%–93.5%) and 84.8% (95% CI = 76.2%–91.2%) (p = 0.55) in intention-to-treat (ITT) analysis; 95.6% (95% CI = 89.1%–98.8%) and 90.3% (95% CI = 82.4%–95.5%) (p = 0.17) in per protocol (PP) analysis. The adverse event rates were 16.7% vs. 10.8% in the 2 groups (p = 0. 0.24). The antibiotic resistance rates between the 2 groups were amoxicillin (0%), tetracycline (0%); clarithromycin (11.8% vs. 17.8%, p = 0.46); metronidazole (32.4% vs. 33.3%, p = 0.93) and levofloxacin (14.7% vs. 37.8%, p = 0.02). Conclusion The success rate of 7-days concomitant therapy encountered an approximately 5% decrease across 4-year time interval (2013–2017) with the changes of clarithromycin resistance from 11.8% to 17.8% in Taiwan.

Gastric acid secretion plays a pivotal role in the physiology of gastrointestinal tract. The functioning of the system encompasses a P2 ATPase pump (which shuttles electroneutral function at low pH) along with different voltage sensitive/neutral ion channels, cytosolic proteins, acid sensor receptors as well hormonal regulators. The increased acid secretion is a pathological marker of several diseases like peptic ulcer, gastroesophageal reflux disease (GERD), chronic gastritis, and the bug Helicobacter pylori (H. pylori) has also a critical role, which altogether affects the patient's quality of life. This review comprehensively describes about the nature of potassium ion channel and its mediators, the different clinical strategy to control acid rebound, and some basic experimental observations performed to study the interplay of ion channels, pumps, as well as mediators during acid secretion. Different aspects of regulation of gastric acid secretion have been focused either in terms of physiology of secretion or molecular interactions. The importance of H pylori infection and its treatment have also been discussed. Furthermore, the relevance of calcium signaling during acid secretion has been reviewed. The entire theme will make anyone to understand in details about the gastric secretion machinery in general.

BACKGROUND: The drug resistance of Helicobacter pylori in children is gaining more and more attention. METHODS: Polymerase chain reaction-reverse dot blot was used to analyze main virulence genes and drug resistance of H. pylori. RESULTS: (1) The main H. pylori vacA virulence genotypes were s1/m1 and s1/m2 in Jilin, China. There was no significant difference in H. pylori virulence genotypes between children and adults. (2) The resistance rates of H. pylori to clarithromycin, metronidazole, and levofloxacin were high, the resistance rate to tetracycline and amoxicillin were relatively low. The drug-resistance rate of clarithromycin in children was significantly higher than that in adults. The single drug-resistance rate of metronidazole in adults was significantly higher than that in children. (3) The mutation sites of clarithromycin resistance in H. pylori were mainly A2143G of 23S rRNA gene, G616A of rdxA gene in metronidazole, N81K and D91G/N/Y of gyrA gene in levofloxacin, T556S and N562D/Y of PBP1 gene in amoxicillin, AGA926-928TTC and AG926-927GT of 16S rRNA gene in tetracycline. There was significant difference in D91Y of gyrA gene in levofloxacin between children and adults. (4) In different groups, the drug-resistance rate of clarithromycin in male children was higher than that in male adults. The drug-resistance rate of clarithromycin in children with peptic ulcers was higher than that in adults. CONCLUSION: There are some differences in drug resistance of H. pylori between children and adults, which indicated us to pay attention to the infection of H. pylori in children.

Family history is an important risk factor of gastric cancer. No guidelines have been developed that target gastric cancer with a family history; only hereditary familial gastric cancer is targeted. We review the available evidence regarding the familial aggregation mechanisms of gastric cancer and a strategy of screening and surveillance for gastric cancer in individuals with a positive family history of the disease. As there is a synergic effect of Helicobacter pylori infection and family history on the increased risk of gastric cancer, Helicobacter pylori eradication should be considered in all infected individuals with a family history of gastric cancer. Currently, there is weak evidence indicating that suitable timing to initiate eradication therapy is at the age of 20, when precancerous lesions, including significant gastric atrophy and intestinal metaplasia, have not been established. Reasonable timing to initiate screening for gastric cancer in individuals with a family history of gastric cancer is 10 years prior to the age of onset of gastric cancer in affected relatives. A 2-year surveillance interval, instead of the 3-year interval recommended in the present guidelines, may be better to detect early gastric cancer in those individuals who have already developed precancerous gastric lesions.

We aimed to explore the correlation between P27 expression and Helicobacter pylori (H. pylori) infection in gastric cancer, so as to provide evidence for understanding the pathogenesis of gastric cancer caused by H. pylori infection. A total of 82 samples of gastric cancer tissues and 56 samples of tumor-adjacent normal tissues collected from the gastrectomy were enrolled in this study. Then, 14C-urease breathing test was carried out to evaluate the infection of H. pylori in gastric cancer tissues, the expression of P27 in the tissue samples was detected by the immunohistochemistry staining, and the correlation between the H. pylori infection and P27 expression in gastric cancer was analyzed. Of 82 gastric cancer patients, there were 53 patients with H. pylori infection (64.63%). Among the patients with highly or moderately differentiated gastric cancer, the expression of P27 was much higher than that of patients with poorly differentiated gastric cancer (p 0.01). Besides, comparison of the P27 expression between males and females, among different age groups, tumor sizes, TNM stages, tumor infiltration degrees, or lymph node metastasis, showed no significant differences (p 0.05). Analysis of the correlation revealed that P27 expression was negatively correlated with the infection of H. pylori (p 0.01). Multifactorial logistics regression analysis indicated that tumor differentiation was a risk factor of P27-positive expression in gastric cancer tissues (p 0.01). In addition, P27 expression in the gastric cancer tissues was lower than that in the tumor-adjacent normal tissues (p 0.01). In gastric cancer patients, expression of P27 is correlated with H. pylori infection which, via downregulating P27, can cause the cancerization of gastric mucosa, and P27, for its role in the development and progression of gastric cancer, is a potential auxiliary indicator for clinical diagnosis whether gastric cancer is complicated with H. pylori infection. So, P27 is a key indicator for diagnosis, treatment, and prognostic evaluation of disease in the advanced stage.

Objectives The Kyoto classification of gastritis was established for diagnosing Helicobacter pylori (H. pylori) infection via endoscopic findings. We investigated the role of the Kyoto classification of gastritis in the diagnosis of H. pylori infection and histological gastritis in Japanese individuals. Moreover, the histological findings of gastritis in H. pylori infection were examined based on age and sex differences. Methods We selected 561 patients aged 20-79 years who underwent gastroduodenal endoscopy at our hospital between 2010 and 2018. Endoscopic biopsy specimens from the antrum and corpus were used to investigate H. pylori infection and histology. Endoscopic findings were based on the Kyoto classification of gastritis, and histological findings were based on the updated Sydney System. Results Endoscopic findings based on the Kyoto classification of gastritis (H. pylori positive, 303 patients; H. pylori negative, 258 patients, based on endoscopic findings) had 98.7% sensitivity and 98.4% specificity for histological gastritis. In addition, endoscopic findings in the three age groups (20-39, 40-59, and 60-79 years) had high sensitivity and specificity. Atrophy and intestinal metaplasia were found only in the H. pylori-positive group and progressed with age. Histological inflammation of pyloric mucosa in the younger age group of H. pylori-positive patients was significantly higher than that in the elderly group. Significant inflammation was observed in young women. Conclusions The Kyoto classification of gastritis can not only diagnose H. pylori infection but also detect histological gastritis. Histological gastritis has varying characteristics of inflammation, atrophy, and intestinal metaplasia, depending on age and sex.

PURPOSE: Gastric cancers are classified as diffuse-type (DTGC) or intestinal-type (ITGC). DTGCs have distinct clinical and histopathologic features, and carry a worse overall prognosis compared to ITGCs. Atrophic gastritis (AG) and intestinal metaplasia (IM) are known precursors to ITGC. It is unknown if AG and IM increase risk for DTGC. METHODS: We performed a systematic review to identify studies reporting on the association of AG/IM and DTGC. We extracted the odds ratio (OR) of the association from studies, and performed pool analysis. Subgroup analysis was performed on studies reporting histologic severity (using operative link systems) to assess if histologic severity of AG/IM was associated with higher risk. RESULTS: We identified six case-control and eight cohort studies for inclusion. Both AG (pooled OR=1.9, 95% CI 1.5 to 2.4, p

Screening for gastric intestinal metaplasia (GIM) may lead to early gastric cancer detection. We developed and validated a pre-endoscopy risk prediction model for detection of GIM based on patient-level risk factors in a U.S. population. We used data from 423 GIM cases and 1796 controls from a cross-sectional study among primary care and endoscopy clinic patients at the Houston VA. We developed the model using backwards stepwise regression and assessed discrimination using area under the receiver operating characteristic (AUROC). The model was internally validated using cross-validation and bootstrapping. The final expanded model was compared to a model including H. pylori infection alone and a baseline model including remaining terms without H. pylori. Male sex, older age, non-white race/ethnicity, smoking status, and H. pylori were associated with GIM risk. The expanded model including these terms had AUROC 0.73 (95%CI 0.71–0.76) for predicting GIM and AUROC 0.82 (95%CI 0.79–0.86) for extensive GIM. This model discriminated better than a model including only H. pylori (AUROC 0.66; 95%CI 0.63–0.68) and the baseline model (AUROC 0.67; 95%CI 0.64–0.70). The expanded model performed similarly among primary care (AUROC 0.75) and endoscopy (AUROC 0.73) patients. The expanded model showed sufficient internal validity (cross-validation AUROC 0.72) with little evidence of over-fitting. We develop and validate a non-invasive risk model for GIM detection in a U.S. population that included terms for sex, age, race/ethnicity, smoking status, and H. pylori infection. Validated risk models would identify individuals with GIM who should be referred for endoscopic screening.

Vonoprazan (VPZ), a new potassium-competitive acid blocker, has been approved and used for Helicobacter pylori eradication in Japan. To date, many studies, as well as several systematic reviews and meta-analyses (MAs), have compared VPZ-based 7-day triple therapy with proton pump inhibitor (PPI)-based therapy. An MA of randomized controlled trials (RCTs) comparing first-line VPZ- with PPI-based triple therapy, the latter featuring amoxicillin (AMPC) and clarithromycin (CAM), found that approximately 30% of patients hosted CAM-resistant H. pylori; however, the reliability was poor because of high heterogeneity and a risk of selection bias. VPZ-based triple therapy is superior to PPI-based triple therapy for patients with CAM-resistant H. pylori, but not for those with CAM-susceptible H. pylori. An MA of non-RCTs found that second-line VPZ-based triple therapies were slightly (~2.6%) better than PPI-based triple therapies (with AMPC and metronidazole). However, the reliability of that MA was also low because of selection bias, confounding variables and a risk of publication bias; in addition, it is difficult to generalize the results because of a lack of data on antibiotic resistance. VPZ-based triple therapy (involving AMPC and sitafloxacin) was more effective than PPI-based triple therapy in a third-line setting, but a confirmatory RCT is needed. Non-RCT studies indicated that VPZ-based triple therapy involving CAM and metronidazole may be promising. Any further RCTs must explore the antibiotic-resistance status when evaluating the possible superiority of a potassium-competitive acid blocker.

Gastric cancer (GC) remains the fifth most common incident cancer with the highest incidence in East Asian countries and the third leading cause of cancer death worldwide. The causal association between non-cardia GC and Helicobacter pylori (H. pylori) has been firmly documented by clinical and epidemiological studies. According to the guidelines for diagnosis and treatment of H. pylori infection, eradication therapy is strongly recommended. Early detection of GC is critical and can save lives through rapid technological advancement. At present, endoscopy remains the most efficient technique. However, it is invasive and costs highly. An extensive bibliographic search was performed via PubMed/Medline, Web of Science, and EBSCO host databases to select studies conducted within the past 8 years. Forty-six relevant analyses were encompassed in this review. Several non-invasive candidate biomarkers associated with H. pylori, divided into virulence markers, transcriptome markers, genomic markers, and inflammatory markers, have been shown to be potential predictors of GC at an early stage. The discovery of non-invasive biomarkers offers new perspectives for screening, early detection, and monitoring of individuals at risk.

Currently, gastric cancer is one of the leading death-related cancer globally. The etiopathogenesis of gastric cancer is multifactorial and includes among others dysbiotic alterations of gastric microbiota. Molecular techniques revealed that stomach is not a sterile organ and it is resides with ecosystem of microbes. Due to the fact that the role of Helicobacter pylori infection in development of gastric cancer is established and well-studied, this paper is mainly focused on the role of other bacterial as well as viral and fungal gut microbiota imbalance in gastric carcinogenesis. Notably, not only the composition of gastric microbiota may play an important role in development of gastric cancer, but also its activity. Microbial metabolites, such as short-chain fatty acids, polyamines, N-nitroso compounds, and lactate, may significantly affect gastric carcinogenesis. Therefore, this paper discussed aforementioned aspects with the interdisciplinary insights (regarding also immunological point of view) into the association between gut microbiome and gastric carcinogenesis based on up-to-date studies.

Reliable diagnostics are a major challenge for the detection and treatment of Helicobacter pylori (H. pylori) infection. Currently at the forefront are non-invasive urea breath test (UBT) and stool antigen test (SAT). Polymerase chain reaction (PCR) is not endorsed due to nonspecific primers and the threat of false-positives. The specificity of DNA amplification can be achieved by nested PCR (NPCR), which involves two rounds of PCR. If the primers are properly designed for the variable regions of the 16S rRNA gene, it is not difficult to develop an NPCR assay for the unambiguous identification of H. pylori. Elaborate NPCR for a 454 bp amplicon was validated on 81 clinical biopsy, stool, and saliva samples, each from the same individuals, and compared with available H. pylori assays, namely histology, rapid urease test, SAT, and 13C-UBT. The assay was much more sensitive than simple PCR, and it was equally sensitive in biopsy samples as the 13C-UBT test, which is considered the gold standard. In addition, it is sufficiently specific because sequencing of the PCR products exclusively confirmed the presence of H. pylori-specific DNA. However, due to the threshold and lower abundance, the sensitivity was much lower in amplifications from stool or saliva. Reliable detection in saliva also complicates the ability of H. pylori to survive in the oral cavity aside from and independent of the stomach. The reason for the lower sensitivity in stool is DNA degradation; therefore, a new NPCR assay was developed to obtain a shorter 148 bp 16S rRNA amplicon. The assay was validated on stool samples from 208 gastroenterological patients and compared to SAT results. Surprisingly, this NPCR revealed the presence of H. pylori in twice the number of samples as SAT, indicating that many patients are misdiagnosed, not treated by antibiotics, and their problems are interpreted as chronic. Thus, it is unclear how to properly diagnose H. pylori in practice. In the first approach, SAT or UBT is sufficient. If samples are negative, the 148 bp amplicon NPCR assay should be performed. If problems persist, patients should not be considered negative, but due to threshold H. pylori abundance, they should be periodically tested. The advantage of NPCR over UBT is that it can be used universally, including questionable samples taken from patients with achlorhydria, receiving proton pump inhibitors, antibiotics, bismuth compound, intestinal metaplasia, or gastric ulcer bleeding.

Objective Helicobacter pyloriinfection is mostly a family-based infectious disease. To facilitate its prevention and management, a national consensus meeting was held to review current evidence and propose strategies for population-wide and family-basedH. pyloriinfection control and management to reduce the related disease burden. Methods Fifty-seven experts from 41 major universities and institutions in 20 provinces/regions of mainland China were invited to review evidence and modify statements using Delphi process and grading of recommendations assessment, development and evaluation system. The consensus level was defined as ≥80% for agreement on the proposed statements. Results Experts discussed and modified the original 23 statements on family-basedH. pyloriinfection transmission, control and management, and reached consensus on 16 statements. The final report consists of three parts: (1)H. pyloriinfection and transmission among family members, (2) prevention and management ofH. pyloriinfection in children and elderly people within households, and (3) strategies for prevention and management ofH. pyloriinfection for family members. In addition to the ‘test-and-treat’ and ‘screen-and-treat’ strategies, this consensus also introduced a novel third ‘family-basedH. pyloriinfection control and management’ strategy to prevent its intrafamilial transmission and development of related diseases. Conclusion H. pyloriis transmissible from person to person, and among family members. A family-basedH. pyloriprevention and eradication strategy would be a suitable approach to prevent its intra-familial transmission and related diseases. The notion and practice would be beneficial not only for Chinese residents but also valuable as a reference for other highly infected areas.

Background The progression to gastric cancer has been linked to chronic infection with Helicobacter pylori (H. pylori). Immune checkpoint inhibitors (programmed cell death -1, PD-1; programmed cell death –ligand 1, PD-L1) have a role in cancer immune escape. The relationship between H. pylori virulence factors with PD-1, PD-L1 T helper 1 (Th1), T helper 17 (Th17), and regulatory T cell (Treg) response genes, has not been thoroughly investigated in the development of gastric cancer. Therefore, we evaluated how H. pylori virulence factors influence the expression levels of immune-related genes in the development of gastric immunopathology. Methods A total of 92 gastric tissues of normal controls and patients with gastritis, gastric ulcer, and gastric cancer were examined for the expression of immune-checkpoint inhibitor genes (PD-1 PD-L1), Th1 (interferon- γ, IFN-γ), Th17 (interleukin- 17, IL-17, Retinoic-acid-receptor- related orphan nuclear receptor gamma t, RORγ-t), and Treg (Forkhead box P3, FOXP3) response genes with quantitative real-time PCR (qRT-PCR). Furthermore, correlation of H. pylori virulence factors’ (cytotoxin-associated gene A, cagA; vacuolating cytotoxin gene A, vacA (s1,s2,m1,m2); blood group antigen-binding adhesin gene A, babA, duodenal ulcer promoting gene A, dupA; the putative neuraminyllactose-binding hemagglutinin homolog, hpaA; neutrophil-activating protein A napA; outer inflammatory protein A, oipA; urease A, ureA; and urease B, ureB) genotypes with a degree of inflammation and density of H. pylori were investigated. Next, the relationship between H. pylori virulence factors and immune-checkpoint inhibitor genes, and T-cell response genes was evaluated. Eventually, a decision tree model was developed to determine the clinical outcome of patients using expression data. Results The intensity of PD-1 and PD-L1 mRNA expression was increased significantly in gastric tissue of patients with gastric ulcer (PD-1: 2.3 fold, p=0.01; PD-L1: 2.1 fold, p=0.004), and gastric cancer (PD-1: 2 fold, p= 0.04; PD-L1: 1.8 fold, p=0.05) compared with control subjects. Also, PD-1: PD-L1 expression was significantly higher in patients with gastritis, who were infected with a marked density of H. pylori compared with its mildly infected counterparts. Furthermore, a novel negative correlation was found between PD-1 (r= -0.43) and PD-L1 (r= -0.42) with FOXP3 in patients with gastritis. CagA-positive H. pylori strain's negative association with PD-L1 expression (r=-0.34) was detected in patients with gastritis. Interestingly, PD-1 mRNA expression correlated positively with vacA s2/m2, in gastritis (r=0.43) and ulcer (r=0.43) patients. Furthermore, PD-1: PDL1 expression negatively correlated with vacA m1/m2 (r=-0.43 for PD-1; r=-0.38 for PD-L1) in gastritis patients. Moreover, an inverse correlation of PDL1 was present with vacA m1 (r=0.52) and vacA s1/m1 (r=0.46) versus vacA m2 (r=-0.44) and vacA m1 (r=0.52) and vacA s1/m2 (r=-0.14) in ulcer patients, respectively. Also, a correlation of vacA m2 (r=-0.47) and vacA s1/s2 (r= 0.45) with PD-1 was detected in ulcer patients. In addition, a novel negative correlation between FOXP3 mRNA levels and napA was shown in patients with gastritis and ulcer (r=-0.59). Finally, a computer-based model that was developed showed that knowing the expression levels of PD-L1, RORγ-t, and vacA s1/m2 would be useful to detect the clinical outcome of a patient. Conclusion Our results suggested that PD-1:PD-L1 immune checkpoint inhibitors were increased in gastric pre-cancerous lesions that progress to gastric cancer. Herein, we report the relationship between H. pylori virulence factors and expression of host immune checkpoint inhibitors for diagnostic prediction of gastric malignancies using computer-based models.

Globally, prevalence of Helicobacter pylori is around 50%, and it has a directly proportional relationship with gastric cancer. Screening and treatment of Helicobacter pylori could reduce gastric cancer by 35%. Drawing on the scarce resources, it is reasonable to use the most cost-effectiveness Helicobacter pylori screening procedure. The purpose of this study was to evaluate Helicobacter pylori screening techniques and to specify the efficient technique from a cost-effectiveness perspective. This systematic review was conducted via searching electronic databases including Scopus, Embase, PubMed, Web of Science, and Cochrane Reviews. Our search retrieved 904 articles, of which, 606 full-text studies have been selected after duplicate removal. Next, the 25 articles were sorted based on eligibility criteria and quality appraisal; eventually, only eight studies have been included for analysis. We reported the incremental cost-effectiveness ratio (ICER) screening compared to non-screening and different screening strategies. Eight studies were identified and retained for the final analysis. In this study, when screening techniques were compared to no-screening, serology screening techniques showed to be cost-effective. The lowest ICER calculated was US$$1230 cost per life-year gained (LYG) and US$1500 cost per quality-adjusted life-year (QALY). However, determining the optimal strategy compared to other strategies was depended on parameters such as context-specific, type of cost, threshold, and perspective, and also, it influenced by the framework of the cost-effectiveness analysis.

BACKGROUND AND AIM Vonoprazan has more potent and sustained acid inhibitory effects than proton pump inhibitors; therefore, Helicobacter pylori eradication rates are expected to improve with the use of vonoprazan-based regimens. To date, no randomized trial has compared the efficacy of 7-day vonoprazan-based triple therapy (7-VAC) with 14-day omeprazole-based triple therapy (14-OAC). This study aimed to compare the H. pylori eradication rates of 7-VAC and 14-OAC. METHODS This randomized clinical trial was performed at a tertiary hospital in Bangkok. Patients with active H. pylori infection who were naive to treatment were included and randomized (1:1) into either a 7-VAC group (vonoprazan 20 mg bid. pc., amoxicillin 1000 mg bid. pc., and clarithromycin 500 mg bid. pc.) or a 14-OAC group (omeprazole 20 mg bid. ac., amoxicillin 1000 mg bid. pc., and clarithromycin 500 mg bid. pc.). Eradication success was evaluated by urea breath test 4-6 weeks after completion of treatment. RESULTS A total of 122 subjects were randomized to receive 7-VAC (n = 61) or 14-OAC (n = 61). The H. pylori eradication rates of the 7-VAC and 14-OAC groups were 96.7% and 88.5% (P = 0.083), respectively, by intention-to-treat analysis and 98.3% and 93.1% (P = 0.159), respectively, by per-protocol analysis. All treatment-related adverse events were mild and not significantly different between the two groups. Common side effects included bitter taste, nausea, and dizziness. CONCLUSIONS The 7-VAC regimen was well tolerated and achieved similar eradication rates and side effects to those of 14-OAC; therefore, 7-VAC may be considered an alternative regimen for H. pylori treatment with the benefit of shorter duration.

The inflammatory spectrum of gastric diseases includes different clinico-pathological entities, the etiology of which was recently established in the international Kyoto classification. A diagnosis of gastritis combines the information resulting form the gross examination (endoscopy) and histology (microscopy). It is important to consider the anatomical/functional heterogeneity of the gastric mucosa when obtaining representative mucosal biopsy samples. Gastritis includes self-limiting and non-self-limiting (long-standing) inflammatory diseases, and the latter are epidemiologically, biologically and clinically linked to the onset of gastric cancer (i.e. "inflammation-associated cancer"). Different biological models of inflammation-associated gastric oncogenesis have been proposed. Helicobacter pylori (H. pylori) gastritis is the most prevalent worldwide, and H. pylori is classified as a first-class carcinogen. On these bases, eradicating H. pylori is mandatory for the primary prevention of gastric cancer. Non-self-limiting gastritis may also be triggered by the immune-mediated destruction of gastric parietal cells, resulting in autoimmune gastritis. In both H. pylori-related and autoimmune gastritis, the non-self-limiting inflammation results in atrophy of the gastric mucosa, which is the main factor promoting gastric cancer. Long-term follow-up studies consistently demonstrate the prognostic impact of the histological staging of gastritis in gastric cancer secondary prevention strategies.

A meta-analysis was conducted to examine the correlation between Helicobacter pylori infection and chronic urticaria.We searched Chinese and English databases, including CNKI, Wanfang, and Weipu, using search terms such as Helicobacter pylori infection, and chronic urticaria for articles published from the establishment of the databases to February 2021 examining the correlation between Helicobacter pylori infection and chronic urticaria. The retrieved articles contained data on Helicobacter pylori infection rates in chronic urticaria cases in different regions of the north and south in China. The retrieved articles underwent strict screenings according to inclusion and exclusion criteria. Revman5.3 software was used to perform a meta-analysis on the data of the included articles.A total of 39 documents were retrieved following the searches. According to the inclusion and exclusion criteria, a total of 6 articles on 6 studies, comprising a total of 1,320 patients, were finally included in the meta-analysis. The results showed that the heterogeneity was high (I2=58%). A random-effects model was performed. An analysis of the correlation between Helicobacter pylori infection and chronic urticaria revealed significant differences between the study group and the control group [odds ratio (OR) =3.00; 95% confidence interval (CI): 1.98-4.55; P0.00001]. The infection rate of Helicobacter pylori among chronic urticaria cases in the northern population was 16.1% (95% CI: 15.6-16.6%); of these patients 12.2% were male and 21.4% were female. The infection rate of Helicobacter pylori among chronic urticaria cases in the southern population was 18.0% (95% CI: 17.5-18.5%); of these patients, 12.3% were male and 23.1% were female. There was no significant difference in the prevalence between the male population, the female population, and the general population in the north and the south (P0.05).Helicobacter pylori infection is correlated with the occurrence of chronic urticaria. There is no significant difference in the infection rate of Helicobacter pylori in chronic urticaria cases in different regions of the north and south. This study had some limitations. First, the number of patients included in each study was low, which may affect the accuracy of the results. Second, the detection methods were not uniform; thus, further research is required to support the conclusions drawn.

Background Helicobacter pylori (H. pylori) is the causative agent of stomach diseases such as duodenal ulcer and gastric cancer, in this regard incomplete eradication of this bacterium has become to a serious concern. Probiotics are a group of the beneficial bacteria which increase the cure rate of H. pylori infections through various mechanisms such as competitive inhibition, co-aggregation ability, enhancing mucus production, production of bacteriocins, and modulating immune response. Result In this study, according to the received articles, the anti-H. pylori activities of probiotics were reviewed. Based on studies, administration of standard antibiotic therapy combined with probiotics plays an important role in the effective treatment of H. pylori infection. According to the literature, Lactobacillus casei, Lactobacillus reuteri, Lactobacillus rhamnosus GG, and Saccharomyces boulardii can effectively eradicate H. pylori infection. Our results showed that in addition to decrease gastrointestinal symptoms, probiotics can reduce the side effects of antibiotics (especially diarrhea) by altering the intestinal microbiome. Conclusion Nevertheless, antagonist activities of probiotics are H. pylori strain-specific. In general, these bacteria can be used for therapeutic purposes such as adjuvant therapy, drug-delivery system, as well as enhancing immune system against H. pylori infection.

The increasing resistance of Helicobacter pylori (H. pylori) to antibiotics has limited the efficacy of antibiotic therapy in the treatment of H. pylori-associated gastric diseases. The vaccine as an alternative method is becoming a safe and effective way to address this problem. In previous studies, live vector vaccines have proved to be effective in controlling H. pylori infection. Attenuated Listeria monocytogenes (L. monocytogenes) is a potential candidate vector applied in clinical trials, which can deliver foreign antigens and induce a broad immune response. To further explore the effectiveness of L. monocytogenes as a vaccine vector against H. pylori, attenuated L. monocytogenes-based vaccine EGDeΔactA/inlB(EGDeAB)-MECU was constructed to secrete a multi-epitope chimeric antigen (MECU) containing multiple B cell epitopes from H. pylori antigens. EGDeAB-MECU could secrete MECU stably. After immunized by gavage and intravenous injection, both EGDeAB and EGDeAB-MECU could significantly decrease gastric H. pylori colonization and induce a high level of specific antibodies against H. pylori. In conclusion, attenuated L. monocytogenes had an immunotherapeutic effect on H. pylori-infected mice, indicating its further development as a promising candidate vaccine vector for the H. pylori vaccine.

Purpose Helicobacter pylori (H. pylori) is a major risk factor for gastric cancer and may affect androgen activity in men. The association between H. pylori and androgen deprivation therapy (ADT) in patients with prostate cancer (PCa) remains unclear. Methods This retrospective cohort study linked National Health Insurance (NHI) data to Taiwan Cancer Registry (TCR) and Taiwan Death Registry (TDR) between 1995 and 2016. PCa patients who received ADT were classified into H. pylori infection and non‐H. pylori infection groups. The outcomes were overall mortality, prostate cancer‐specific mortality, and castration‐resistant prostate cancer (CRPC). Propensity score matching was adopted for the primary analysis and inverse probability of treatment weighting (IPTW) was used for the sensitivity analysis. Results Of the 62,014 selected PCa patients, 23,701 received ADT, of whom 3516 had H. pylori infections and 20,185 did not. After matching, there were 3022 patients in the H. pylori infection group and 6044 patients in the non‐H. pylori infection group. The mean follow‐up period for the matched cohort was 4.8 years. Compared to the non‐H. pylori group, the H. pylori group was significantly associated with decreased risks of all‐cause mortality (hazard ratio [HR] 0.90; 95% confidence interval [CI] 0.84–0.96) and prostate cancer‐specific mortality (HR 0.88; 95% CI 0.81–0.95) in the matched analysis. Conclusions H. pylori infection was associated with a reduced risk of mortality in PCa patients receiving ADT.

BACKGROUND: Bovine lactoferrin addition to regimens of Helicobacter pylori treatment has been tried, with conflicting results. AIM: To assess the effect of bovine lactoferrin in addition to the anti-H. pylori treatment. METHODS: We enrolled 400 H. pylori-infected patients who were randomized into 4 equal groups: (A): proton-pump-based triple therapy (PpTT) for 2 weeks, (B): sequential therapy for 2 weeks, (C): proton-pump-based triple therapy plus bovine lactoferrin for 2 weeks, and (D): sequential therapy plus bovine lactoferrin for 2 weeks. RESULTS: In the per-protocol analysis, the success in groups A, B, C, and D were 70.3%, 82.8%, 85.6%, and 94.5%, respectively (P < .001). The treatment success rate for the sequential therapy plus bovine lactoferrin regimen was significantly higher than that with sequential therapy alone (94.5% vs. 82.8%, P = .013). The same applied for proton-pump-based triple therapy (85.6% vs. 70.3%, P = .014). The addition of bovine lactoferrin and the presence of endoscopic corpus gastritis were independent predictors for successful eradication of H. pylori. CONCLUSION: Bovine lactoferrin could hasten the effectiveness of the proton-pump-based triple therapy or sequential therapy for H. pylori eradication.

Helicobacter pylori is a Gram-negative bacterium found on the luminal surface of the gastric mucosa in at least 50% of the world's human population. The protective effect of breastfeeding against H. pylori infection has been extensively reported; however, the mechanisms behind this protection remain poorly understood. Human IgA from colostrum has reactivity against H. pylori antigens. Despite that IgA1 and IgA2 display structural and functional differences, their reactivity against H. pylori had not been previously determined. We attested titers and reactivity of human colostrum-IgA subclasses by ELISA, immunoblot, and flow cytometry. Colostrum samples from healthy mothers had higher titers of IgA; and IgA1 mostly recognized H. pylori antigens. Moreover, we found a correlation between IgA1 reactivity and their neutralizing effect determined by inhibition of cytoskeletal changes in AGS cells infected with H. pylori. In conclusion, colostrum-IgA reduces H. pylori infection of epithelial gastric cells, suggesting an important role in preventing the bacteria establishment during the first months of life. As a whole, these results suggest that IgA1 from human colostrum provides protection that may help in the development of the mucosal immune system of newborn children.

Background: The global epidemiological situation of gastric cancer has changed considerably over time, and it is essential to understand the epidemiological trends and future perspectives of gastric cancer. Summary: Although gastric cancer was common in the United States less than a century previously, it is no longer common in this country. Currently, over 60% of gastric cancers are found in Eastern Asia. In some Eastern Asian countries such as Japan and Korea, population-based gastric cancer screening has been conducted using upper gastrointestinal endoscopy or radiography to lower gastric cancer mortality. Due to earlier detection of gastric cancer, the survival of patients with gastric cancer is more favorable in these countries than in other Western countries. Even in Eastern Asia, a remarkable decrease in the age-standardized incidence and mortality of gastric cancer has been observed. This downward trend is mainly due to the reduced Helicobacter pylori infection, and this trend is considered to continue. Nevertheless, both the absolute number of incident cases and deaths of gastric cancer are still increasing at present due to the aging population. For the time being, the management of gastric cancer in elderly population is a critical issue in Eastern Asia. The absolute numbers of gastric cancer cases and deaths are believed to peak in the near future, following the decreasing age-standardized incidence and mortality. Key Messages: After a long period, gastric cancer may become a rare cancer even in Eastern Asia, and new efficient approaches for its prevention, screening, and treatment are warranted.

H. pylori (H. pylori) infection is considered the leading cause of gastric cancer. Gastric cancer is currently a common cancer with high incidence and mortality rates, but it is expected that the incidence rate will gradually decrease as the H. pylori infection prevalence decreases in the future. When evaluating the effectiveness of gastric cancer prevention strategies, it is essential to note the differences in long-term cumulative risks between H. pylori-infected and uninfected populations, but this has not yet been precisely evaluated. In this study, we aimed to estimate the cumulative incidence risks of developing gastric cancer from birth to 85 years among H. pylori-infected and uninfected populations by using population-based cancer registry data and birth year-specific H. pylori infection prevalence rates. Death from gastric cancer and other causes of death were considered in the estimations of the adjusted cumulative incidence risks stratified by sex and H. pylori infection status. After performing 5000 Monte Carlo simulations with repeated random sampling using observed cancer incidence in selected three prefectures (Fukui, Nagasaki, Yamagata) of prefectural population-based cancer registry in Japan, the mean adjusted cumulative incidence risk for gastric cancer in the H. pylori-infected population was 17.0% for males and 7.7% for females and 1.0% for males and 0.5% for females in the uninfected population. These results calculated with Japanese cancer registry data may be useful in considering and evaluating future prevention strategies for gastric cancer in Japan. This article is protected by copyright. All rights reserved.

This review focuses on the efficacy of herbal medicines for managing dyspepsia in humans and animals. Searches were conducted on the PubMed, Science Direct, and Medline databases, for publications in the last 3 years. In each database, the search terms used consisted of the 2 key terms describing the disorder and subtypes plus each of the terms relating to the therapy. The key terms used were “natural product” and “medicinal plant” in a cross-over with “dyspepsia” and “functional dyspepsia” (i.e., gastroprotection, Helicobacter pylori infection, prokinetic). We included all human and animal studies on the effects of herbal medicines reporting the key outcome of dyspepsia symptoms. Preclinical studies using critically validated models showed that most medicinal plants with gastroprotective action had antioxidant, anti-inflammatory, anti-apoptotic, and antisecretory effects. Moreover, several species displayed anti Helicobacter pylori and prokinetic efficacy. The data availability of controlled clinical studies is currently minimal. The use of different methodologies and the minimal number of patients raise doubts about the effects of these preparations. Only adequate clinical trials with scientifically validated methods can determine whether different herbal medicines can be used as viable alternatives to the conventional pharmacological treatments used to control dyspepsia symptoms.

Helicobacter pylori is a causative pathogen of many gastric and extra-gastric diseases. It has infected about half of the global population. There were no genome-wide association studies (GWAS) for H. pylori infection conducted in Chinese population, who carried different and relatively homogenous strain of H. pylori. In this work, we performed SNP (single nucleotide polymorphism)-based, gene-based and pathway-based genome-wide association analyses to investigate the genetic basis of host susceptibility to H. pylori infection in 480 Chinese individuals. We also profiled the composition and function of the gut microbiota between H. pylori infection cases and controls. We found several genes and pathways associated with H. pylori infection (P TLR1 gene region (P = 0.02). We also found that glycosaminoglycan biosynthesis related pathway was associated with both onset and progression of H. pylori infection. In the gut microbiome association study, we identified 2 species, 3 genera and several pathways had differential abundance between H. pylori infected cases and controls. This paper is the first GWAS for H. pylori infection in Chinese population, and we combined the genetic and microbial data to comprehensively discuss the basis of host susceptibility to H. pylori infection.

Objective To investigate the effect of Helicobacter pylori (H. pylori) eradication on the prognosis of postoperative early gastric cancer (EGC). Methods This is a retrospective study based on data from 6 hospitals. We identified 429 patients with EGC who underwent curative gastrectomy from January 2010 to December 2016. All of the patients were tested for H. pylori. Patients were divided into two groups, the successful H. pylori eradication group (group A, 268 patients) and the non-H. pylori eradication group (group B, 161 patients), for calculating the disease-free survival (DFS) and overall survival (OS) of each group. Result Positive node metastasis (hazard ratio (HR), 3.13; 95% confidence interval (CI), 1.84–5.32; P P H. pylori eradication (HR, 1.73; 95% CI, 1.08–2.77; P = 0.023) were statistically significantly independent risk factors of recurrence. Patient’s age ≥60 years old (HR, 3.32; 95% CI, 2.00–5.53; P P P H. pylori eradication (HR, 1.83; 95% CI, 1.11–3.02; P = 0.018) were statistically significantly independent risk factors of overall survival. Conclusion H. pylori eradication treatment could prevent the recurrence of postoperative EGC to prolong the overall survival of patients with EGC.

BACKGROUND: The Prex2 protein is a member of the Rac family proteins that belongs to small G proteins with a critical role in cell migration, cell proliferation, and apoptosis through its effects on PI3K cell signaling pathway and phosphatase activity of PTEN protein. The effect of PREX2 gene expression has been shown in some cancer cells. A survey of PREX2 gene expression in gastric antral epithelial cells of gastric cancer patients with Helicobacter pylori various genotypes infection can conduct to better understanding H. pylori infection’s carcinogenesis. METHODS: In a case-control study, PREX2 gene expression was evaluated in gastric antral biopsy samples on four groups of patients referred to Sanandaj hospitals, including gastritis with (n=23) and without (n=27) H. pylori infection and gastric cancer with (n=21) and without (n=32) H. pylori infection. Each gastric biopsy sample’s total RNA was extracted and cDNA synthesized by using Kits (Takara Company). The PREX2 gene expression was measured using the relative quantitative real-time RT-PCR method and ΔΔCt formula. RESULTS: The PREX2 gene expression increased in gastric antral biopsy samples of gastritis and gastric cancer patients with H. pylori infection (case groups) than patients without H. pylori infection (control groups) 2.38 and 2.27 times, respectively. The patients with H. pylori vacA s1m1 and sabB genotypes infection showed a significant increase of PREX2 gene expression in gastric cancer antral epithelial cells. CONCLUSION: H. pylori vacA s1m1 and sabB genotypes have the positive correlations with PREX2 gene expression in gastric antral epithelial cells of gastritis and gastric cancer patients. RESUMO CONTEXTO: A proteína Prex2 é membro das proteínas da família Rac que pertencem a pequenas proteínas G com um papel crítico na migração celular, na proliferação celular e na apoptose através de seus efeitos na via de sinalização celular PI3K e atividade fosfatase da proteína PTEN. O efeito da expressão genética PREX2 tem sido mostrada em algumas células cancerosas. Um levantamento da expressão genética PREX2 em células epiteliais antrais gástricas de pacientes infectados com vários genótipos de Helicobacter pylori pode conduzir a um melhor entendimento da carcinogênese da infecção por H. pylori. MÉTODOS: Em estudo de caso-controle, a expressão genética PREX2 foi avaliada em amostras de biópsia antral gástrica em quatro grupos de pacientes encaminhados aos hospitais de Sanandaj, incluindo gastrite com (n=23) e sem (n=27) infecção por H. pylori e de câncer gástrico com (n=21) e sem (n=32) infecção por H. pylori. O RNA total de cada amostra de biópsia gástrica foi extraído e cDNA sintetizado por meio de kits (Takara Company). A expressão genética PREX2 foi medida utilizando-se o método RT-PCR em tempo real quantitativo relativo e a fórmula ΔΔCt. RESULTADOS: A expressão genética PREX2 aumentou em amostras de biópsia antral gástrica de pacientes com gastrite e câncer gástrico com infecção por H. pylori (grupos de casos) em relação aos sem infecção por H. pylori (grupos de controle) 2,38 e 2,27 vezes, respectivamente. Os pacientes com infecção por genótipos H. pylori vacA s1m1 e sabB apresentaram um aumento significativo da expressão genética PREX2 em células epiteliais antrais de câncer gástrico. CONCLUSÃO: Os genótipos H. pylori vacA s1m1 e sabB têm correlações positivas com a expressão genética PREX2 em células epiteliais antrais gástricas de pacientes com câncer gástrico e gastrites.

Background: Infection with multiple pathogens may play a key role in the pathogenesis of dementia. Whether Helicobacter pylori (H. pylori) infection is associated causally with dementia is controversial. Objective: We conduct a meta-analysis of case-control and cohort studies on the association between H. pylori infection and the risk for all-cause and Alzheimer’s disease (AD) dementia. Methods: Two independent reviewers searched the PubMed, Cochrane Library, and Embase databases with English language restrictions from the date of conception to September 18, 2020. The primary analysis was as follows: the exposure variable was H. pylori infection, and the outcome was incident all-cause and AD dementia. Pooled odds ratios (OR), relative risk (RR), and corresponding 95% confidence intervals (CI) were obtained using the fixed-or random-effect model. Forest plots were generated to summarize the results. Results: Ten studies involving 96,561 participants were included in the meta-analysis: 5 case-control studies and 5 cohort studies. The overall pooled cohort studies showed a significant positive association between H. pylori infection and all-cause dementia with pooled RR of 1.36 (95% CI, 1.11-1.67). There was no association between H. pylori infection and risk for developing AD: RR of 1.33 (95% CI, 0.86-2.05) in cohort studies, and OR of 1.72 (95% CI, 0.97-3.04) in case-control studies. Significant heterogeneity was showed in each comparison group. Conclusion: This meta-analysis supports a positive association between H. pylori infection and the risk of all-cause dementia, but not AD dementia. Due to the interference of confounding factors, randomized controlled trials are needed to prove their causality.

Epstein‐Barr virus (EBV)‐associated gastric cancer belongs to 1 of the 4 subtypes of gastric cancer and accounts for 10% of total gastric cancers. However, most cases of gastric cancer have a history of Helicobacter pylori infection. Therefore, we investigated the possibility that H. pylori infection promotes the development of EBV‐associated gastric cancer. H. pylori was exposed to principal EBV receptor, CD21, negative gastric epithelial cells, and then infected with EBV recombinant expressing enhanced green fluorescent protein. Changes in EBV infectivity due to prior H. pylori exposure were analyzed using flow cytometry. The treatment of gastric epithelial cells with H. pylori increased the efficiency of EBV infection. An increase was also observed when CagA‐deficient, VacA‐deficient, and FlaA‐deficient H. pylori strains were used, but not when cag pathogenicity island‐deficient H. pylori was used. The treatment of epithelial cells with H. pylori induced the expression of accessory EBV receptors, EphA2 and NMHC‐IIA, and increased the efficiency of EBV infection depending on their expression levels. When gastric epithelial cells were treated with EPHA2 or NMHC‐IIA siRNA, EBV infection via H. pylori attachment was decreased. The adhesion of H. pylori induced the expression of accessory EBV receptors in gastric epithelial cells and increased the efficiency of EBV infection., We investigated the possibility that H. pylori infection promotes the development of EBV‐associated gastric cancer (EBVaGC). H. pylori adheres to gastric epithelial cells and induces low‐affinity EBV receptor expression in epithelial cells. A continuous increase in the number of EBV‐infected cells is expected during life‐long gastric inflammation caused by H. pylori. Therefore, H. pylori infection is thought to increase the incidence of EBVaGC by increasing the efficiency of EBV infection.

Helicobacter pylori is a bacterium that causes infections in the gastrointestinal tract. This type of bacterium is very common and contagious at the same time. H. pylori enters the mouth and continues its course along the gastrointestinal tract. H. pylori infection induces an inflammatory response that leads to the activity of neutrophils, lymphocytes, plasma cells, and macrophages. In addition to the bacterial role in gastric mucosa, the host's inflammatory response may also play a role in disease outcome. In inflammation, the risk of carcinogenesis increases due to DNA damage increased proliferation and the creation of an environment rich in cytokines and growth factors. Genetic methods and diagnosis of H. pylori genes are used to identify healthy and healthy gastric cancer patients infected with H. pylori. In relation to the genes associated with H. pylori pathogenesis, the presence of genes such as cagA, hopQI, hopQII and so on is used, and PCR of a part of these genes amplified fragments of different lengths. One of the less-studied cases is the association of two or more pathogenic genes simultaneously with H. pylori. In this research, the frequency of disease and healthy individuals who are infected with H. pylori and have two genotypes cagA and hopQI at the same time, was examined. In order to diagnose H. pylori-infected individuals in healthy and gastric cancer patients, after PCR of glmM gene, PCR product electrophoresis on agarose gel was used. For this purpose, gastric tissue biopsy was used in patients and saliva was used in healthy individuals. For this purpose, 100 gastric biopsy samples were collected from patients with gastric cancer and 100 saliva samples from healthy individuals. According to the data, there is a significant relationship between the simultaneous presence of two genes cagA and hopQI and gastric cancer. In patients, 45.3% showed both genotypes, while in healthy individuals only 10.5% have this genotype and other healthy but infected with H. pylori (90.8%) do not have this genotype. To be. No report was observed on the simultaneous study of cagA and hopQI genes. No report was observed regarding the simultaneous study of cagA and hopQI genes.

INTRODUCTION Although the incidence and prevalence of duodenal and gastric ulcers have been declining, it remains challenging for health care systems. Based on the underlying cause, history, and characteristics of ulcers, management is generally provided by administering proton pump inhibitors (PPIs) or antibiotics. AREAS COVERED This article is based on global guidelines and English language literature from the past decade obtained through searches using PubMed, Clinicaltrials.gov, the US FDA, and the Cochrane library. Using a stepwise approach, dose and duration of treatment, drug interactions, warnings and contraindications, adverse effects, and administration points were specified. New drug candidates that may get American and European approvals were also introduced. EXPERT OPINION Despite the wide use of PPIs, their development lags behind the clinical need. There is an absolute requirement to develop third-generation PPIs with higher potency and improved pharmacokinetic and safety profiles. Regarding the antibiotic resistance crisis, including those used against H. pylori, conducting more clinical trials and investigating regional antibiotic resistance are warranted. Potassium competitive acid blockers, ilaprazole, and an H. pylori vaccine all show promise for the future.

Background: Conflicting results exist on the association between Helicobacter pylori infection and gastro-oesophageal reflux (GOR), and its complications, such as erosive oesophagitis (EO) and Barrett's oesophagus (BO). Aims: To explore the association of H. pylori infection with GOR symptoms and their complications. Methods: We searched Embase, PubMed, Web of Science and Scopus databases through December 2020 for relevant articles. Regarding the association between H. pylori and GOR symptoms (heartburn, regurgitation or reflux), we included observational studies comparing the prevalence of GOR symptoms between H. pylori-positive and -negative individuals. Concerning the association between H. pylori and complications of GOR, we included studies comparing the prevalence of EO or BO between H. pylori-positive and -negative individuals. Results: In total, 36 papers were eligible. Based on seven cross-sectional surveys, H. pylori infection was associated with a lower odds of GOR symptoms (odds ratio [OR] 0.74, 95% confidence interval [CI] 0.61-0.90). However, in four case-control studies, H. pylori infection was not associated with odds of GOR symptoms (OR 1.10, 95% CI 0.85-0.1.43). In 26 cross-sectional studies in patients with GOR symptoms, the OR for EO was 0.70 (95% CI 0.58-0.84) in H. pylori-positive vs -negative cases. Based on nine cross-sectional studies in subjects with GOR complications, no significant association was found between H. pylori infection and either endoscopically-diagnosed (OR 1.84, 95% CI 0.67-5.02) or histologically confirmed (OR 0.85, 95% CI 0.60-1.20) BO. Conclusions: Helicobacter pylori infection appears to be associated with a decreased odds of GOR symptoms and EO. In contrast, H. pylori infection did not seem to affect the odds of BO in patients with GER complications.

Helicobacter pylori, the most frequent pathogen worldwide that colonizes around 50% of the world’s population, causes important diseases such as gastric adenocarcinoma, chronic gastritis, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. In recent years, various studies have reported that H. pylori biofilm may be one of the critical barriers to the eradication of this bacterial infection. Biofilms inhibit the penetration of antibiotics, increase the expression of efflux pumps and mutations, multiple therapeutic failures, and chronic infections. Nanoparticles and natural products can demolish H. pylori biofilm by destroying the outer layers and inhibiting the initial binding of bacteria. Also, the use of combination therapies destroying extracellular polymeric substances decreases coccoid forms of bacteria and degrading polysaccharides in the outer matrix that lead to an increase in the permeability and performance of antibiotics. Different probiotics, antimicrobial peptides, chemical substances, and polysaccharides by inhibiting adhesion and colonization of H. pylori can prevent biofilm formation by this bacterium. Of note, many of the above are applicable to acidic pH and can be used to treat gastritis. Therefore, H. pylori biofilm may be one of the major causes of failure to eradication of infections caused by this bacterium, and antibiotics are not capable of destroying the biofilm. Thus, it is necessary to use new strategies to prevent recurrent and chronic infections by inhibiting biofilm formation.

BACKGROUND Antibiotic resistance to Helicobacter pylori (H. pylori) infection, which ultimately results in eradication failure, has been an emerging issue in the clinical field. Recently, to overcome this problem, an antibiotic sensitivity-based tailored therapy (TT) for H. pylori infection has received attention. AIM To investigate the efficacy and safety profiles of TT for H. pylori infection treatment compared to a non-bismuth quadruple therapy, concomitant therapy (CT) regimen. METHODS We included patients (> 18 years) with an H. pylori infection and without a history of Helicobacter eradication who visited the Gil Medical Center between March 2016 and October 2020. After being randomly assigned to either the TT or CT treatment group in 1 to 1 manner, patient compliance, eradication success rate (ESR), and patient-reported side effects profiles were assessed and compared between the two groups. H. pylori infection was diagnosed using a rapid urease test, Giemsa stain, or dual priming oligonucleotide polymerase chain reaction (DPO-PCR). Tailored eradication strategy based through the presence of a 23S ribosomal RNA point mutation. For the TT group, a DPO-PCR test, which detected A2142G and/or A2143G point mutations, and a clarithromycin resistance test were performed. Patients in the clarithromycin-resistant group were treated with a bismuth-containing quadruple combination therapy, while those with sensitive results were treated with the standard triple regimen. RESULTS Of the 217 patients with a treatment naive H. pylori infection, 110 patients [mean age: 58.66 ± 13.03, men, n = 55 (50%)] were treated with TT, and 107 patients [mean age: 56.67 ± 10.88, men, n = 52 (48.60%)] were treated with CT. The compliance (TT vs CT, 100% vs 98.13%, P = 0.30), and follow-up loss rates (8.18% vs 9.35%, P = 0.95) were not significantly different between the groups. The ESR after treatment was also not statistically different between the groups (TT vs CT, 82.73% vs 82.24%, P = 0.95). However, the treatment-related and patient-reported side effects were significantly lower in the TT group than in the CT group (22.77% vs 50.52%, P < 0.001). CONCLUSION The DPO-based TT regimen shows promising results in efficacy and safety profiles as a first-line Helicobacter eradication regimen in Korea, especially when physicians are confronted with increased antibiotic resistance rates.

Purpose of review Gastric cancer remains one of the most common causes of death globally. Increasing evidence suggests that many gastric cancer cases can be prevented by eradicating its most important etiological agent, Helicobacter pylori. Using the search terms 'H. pylori' and 'gastric cancer' we reviewed the scientific literature regarding the association between H. pylori and gastric cancer published from 1 January 2020 to 30 May 2021. We review the most important articles relevant to the clinical issues regarding H. pylori eradication for gastric cancer prevention. Recent findings In randomized trials, eradication of H. pylori is associated with an approximately 50% reduction in sporadic gastric cancer. A similar benefit was observed when screening first-degree relatives of gastric cancer cases, after resection of early gastric cancer to prevent metachronous neoplasia, and in population-based screen and treatment programs in areas of high H. pylori and gastric cancer prevalence. Even in relatively low gastric cancer countries such as the United States, gastric cancer may potentially be avoided by screening for H. pylori, especially among minority groups who are at greatest risk. Summary Gastric cancer is preventable, at least in part, by H. pylori eradication. Ongoing screening trials will help determine whether population-based H. pylori screening programs are feasible and cost-effective. Their results are likely to differ according to H. pylori and gastric cancer prevalence rates.

Helicobacter pylori plays a consequential role in gastric inflammations and ulceration. The cure for the same was researched and identified to be the triple therapy regime. Intensive research in the field also proved that altering the food habits during ulcers will be a major factor in the time period that is required for cure. Fermented foods usage dates back to ancient civilizations, but their role in maintaining gastric health are slowly being uncovered. One such major role reported will be the bacterial check that the probiotics in fermented food do in human gastrointestinal tract. Various species of bacteria present in the fermented products will lead to reduction of the H. Pylori infection in the GI tract.Key teaching pointsMicrobes that are active in fermented foods reduce inflammation and improve histological conditions of ulcers caused due to H. pylori.Microbes such as Lactobacillus that were in fermented products when tested showed inhibitory effects, decreasing infection density and reducing mucus depletion.Lactic fermented products showed a decrease in urease activity and reduces H. pylori adhesion through various organic acid secretions.Organisms in fermented products involve various mechanisms like lowering gut pH, improving immunological responses, scavenging free radicals and so on.Fermented foods have many modulatory effects that help fighting and curing gastric ulcers.

Background BM-MSCs contribute to Helicobacter pylori (H. pylori)-induced gastric cancer, but their mechanism is still unclear. The aim of our study was to investigate the specific role and mechanism of BM-MSCs in H. pylori-induced gastric cancer. Main methods Mice received total bone marrow transplants and were then infected with H. pylori. BM-MSCs were extracted and transplanted into the gastric serosal layer of mice chronically infected with H. pylori. Hematoxylin and eosin staining, immunohistochemistry staining and immunofluorescence were performed to detect tumor growth and angiogenesis in mouse stomach tissues. Chicken chorioallantoic membrane assays, xenograft tumor models, and human umbilical vein endothelial cell tube formation assays were used for in vivo and in vitro angiogenesis studies. THBS4 was screened from RNA-seq analysis of gastric tissues of BM-MSCs transplanted into H. pylori-infected mice. Results BM-MSCs can migrate to the site of chronic mucosal injury and promote tumor angiogenesis associated with chronic H. pylori infection. Migration of BM-MSCs to the site of chronic mucosal injury induced the upregulation of THBS4, which was also evident in human gastric cancer and correlated with increased blood vessel formation and worse outcome. The THBS4/integrin α2 axis promoted angiogenesis by facilitating the PI3K/AKT pathway in endothelial cells. Conclusions Our results revealed a novel proangiogenic effect of BM-MSCs in the chronic H. pylori infection microenvironment, primarily mediated by the THBS4/integrin α2 axis, which activates the PI3K/AKT pathway in endothelial cells and eventually induces the formation of new tumor vessels.

Összefoglaló. A Helicobacter pylori továbbra is a világ legelterjedtebb fertőzése: prevalenciája a fejlődő országokban 70–80%, a fejlett országokban csökkenő tendenciát mutat. A dél-magyarországi véradókban a prevalencia 32%-ra csökkent. A migráció a befogadó ország számára a fertőzés fokozott kockázatával jár. A szövettani diagnózisban az immunhisztokémiai vizsgálat pontosabb a hagyományos Giemsa-festésnél. A mesterséges intelligencia érzékenysége a hagyományos endoszkópiáéval összehasonlítva 87%, pontossága 86%. Az újgenerációs szekvenálással lehetséges egy biopsziás mintából több antibiotikumérzékenység meghatározása. A Helicobacter pylori kezelésének európai regisztere kimutatta, hogy 2013 és 2018 között a bizmutalapú négyes vagy a 14 napos egyidejű négyes kezelések hatásosabbak, mint a hagyományos hármas kezelés, de elterjedésük igen lassú folyamat, jelentős földrajzi különbségekkel. Az új típusú koronavírus (SARS-CoV-2) felléphet Helicobacter pylori fertőzésben is, egymás kóros hatását felerősítve. A diagnosztikai módszerek korlátozottak. Protonpumpagátlók szedése növeli a COVID–19-fertőzés kockázatát és annak súlyos kimenetelét. Előzetesen ismert peptikus fekély, vérzés, illetve antikoguláns kezelés előtt az eradikáció a vírusos fertőzés lezajlása után indokolt. A probiotikumoknak az eradikációra gyakorolt hatásáról 20, közepes minőségű metaanalízis született, így a konszenzusokban foglalt álláspontok sem egyértelműek: a jövőben ezt tisztázni kell. Orv Hetil. 2021; 162(32): 1275–1282. Summary. Helicobacter pylori is still the most widespread infection in the world: its overall prevalence is 70–80% in developing regions, but fortunately it is decreasing in the Western world. The prevalence in blood donors from South-Eastern Hungary decreased from 63% in the 1990’s to 32% in 2019. Migration constitutes an increased risk of infection for the destination countries. Immunohistochemistry has proven to be more accurate in histological diagnosis than the conventional Giemsa stain. The sensitivity and accuracy of artificial intelligence as compared to videoendoscopy were 87% and 86%, respectively. The European Register on the management of Helicobacter pylori infection revealed that concomitant quadruple and 14-day bismuth-based therapies are more efficient than triple combinations, although their incorporation in practice is a long-lasting process, with large geographical variations. The novel type of coronavirus (SARS-CoV-2) can also occur in Helicobacter pylori-infected patients, mutually enhancing their pathogenetic effects. Diagnostic possibilities are limited in this setting. The use of proton pump inhibitors increases the risk of viral infection and the severity of the disease. Eradication treatment seems justified in patients with previously known peptic ulcers or gastrointestinal bleeding, or before starting anticoagulant treatment, but must be postponed after resolution of viral infection. The effect of probiotics on eradication was addressed by 20, medium-to-low quality meta-analyses and so, the recommendations of the guidelines are equivocal, which must be clarified in the future with higher quality studies. Orv Hetil. 2021; 162(32): 1275–1282.