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Multi-stage filtration technology (MSFT) is an alternative that reduces the risk of fecal contamination, allowing for reliable water purification in rural water supplies. MSFT is composed of two gravel filtration (GF) stages: one including dynamic gravel filters (DyGF) and up-flow gravel filters (UGF), and a final stage with slow sand filters (SSFs). However, with the purpose of reducing construction costs, this technology is partially implemented, leaving SSFs for a later construction stage and limiting its treatment potential. To evaluate the removal capabilities regarding fecal contamination (especially that by the pathogen H. pylori) of a two-stage GF system, the quality of raw and treated water and the hydraulic parameters of Los Llanos treatment system (municipality of Popayán, Cauca) were monitored for 15 weeks. This system is operated and maintained by the community. The results showed the removal efficiency regarding turbidity to be 16% (p=0,045) and 34% (p=0,030) for the DyGF and the UGF, respectively. The color removed by the DyGF reached 19% (p=0,033), and the UGF reported a value of 30% (p=0,041). The reduction of total coliforms was limited by the system’s operation and maintenance, exhibiting a tendency towards increased concentrations at the outlet. The presence or absence of H. pylori was determined via the PCR molecular technique. A greater presence was evidenced in treated water than in raw one, which may be associated with a limited operation and a low maintenance frequency of the system. The implementation of MSFT, without the complement of SSFs, is not reliable in ensuring quality of water, particularly from a perspective of microbiological control and H. pylori control., La tecnología de filtración en múltiples etapas (FIME) es una alternativa que reduce el riesgo por contaminación fecal, permitiendo la potabilización del agua de manera confiable en acueductos rurales. La tecnología FiME está compuesta por dos etapas de filtros en grava (FG): una que incluye filtros dinámicos (FGDi) y filtros gruesos ascendentes (FGAC), y una etapa final con filtros lentos en arena (FLA). Sin embargo, con el fin de reducir los costos de construcción, esta tecnología se implementa de manera parcial, dejando los FLA para una etapa posterior de construcción y limitando su potencial de tratamiento. Con el fin de evaluar la capacidad de remoción de la contaminación fecal (especialmente del patógeno H. pylori) en un sistema de FG de dos etapas, se monitoreó durante 15 semanas la calidad del agua cruda y tratada y los parámetros hidráulicos del sistema de tratamiento Los Llanos en el municipio de Popayán, Cauca, el cual es operado y mantenido por la comunidad. Los resultados mostraron que la eficiencia de remoción respecto a la turbiedad es de 16 % (p=0,045) y 34 % (p=0,030) para el FGDi y el FGAC respectivamente. El color removido por el FGDi alcanzó el 19 % (p=0,033), y el FGAC reportó un valor de 30 % (p=0,041). La reducción de los coliformes totales se vio limitada por la operación y mantenimiento del sistema, presentando una tendencia a incrementar su concentración en la salida. La presencia o ausencia del H. pylori se determinó con la técnica molecular PCR. Se evidenció una mayor presencia en agua tratada que en agua cruda, lo cual puede asociarse con una limitada operación y una baja frecuencia de mantenimiento del sistema. La implementación de la tecnología FiME, sin el complemento de FLA, es poco confiable para garantizar la calidad del agua, particularmente desde el punto de vista microbiológico y el control del H. pylori.

FUNDAMENTOS // Existen pruebas de la factibilidad de una vacuna para prevenir la infección por Helicobacter pylori. Modelizaciones en entornos de baja prevalencia informan de una muy probable coste-efectividad a largo plazo. El objetivo de este estudio fue cuantificar su eficiencia en un contexto local. MÉTODOS // Se simuló la evolución de una cohorte de nacidos a través de un modelo compartimental representativo de varios estados clínicos en relación a la infección por H. pylori. Se ejecutó dicho modelo bajo las premisas de vacunación en el periodo de lactante y de no intervención. El horizonte temporal fue equivalente a la esperanza de vida y se tuvo en cuenta la perspectiva del sistema de salud. RESULTADOS // La vacunación frente a H. pylori costaría de media 2.168 €/persona más que la no intervención. Con ello se obtendrían 0,32 años de vida ganados ajustados por calidad (AVAC), lo que implicaría una razón de coste-efectividad incremental (RCEI) media de 7.196 €/AVAC. Para una disposición a pagar de 24.506 €/AVAC, el 99,96% de las simulaciones resultaron coste-efectivas al alcanzar el horizonte temporal y se cruzó dicho umbral a partir de los treinta años de la vacunación. Las variables que más peso tuvieron para explicar la variabilidad de la RCEI fueron, en este orden, la efectividad vacunal, la incidencia de la infección en la primera infancia y el precio de la vacuna. La vacunación dejaría de ser coste-efectiva con un precio mayor de 3.634€/vial o con una cobertura poblacional efectiva menor del 11%. CONCLUSIONES // Una vacunación frente a la infección por H. pylori administrada en la infancia sería coste-efectiva a largo plazo en un entorno con las características epidemiológicas y económicas del sur de Europa.

It is estimated that more than half of the world population has been infected with Helicobacter pylori. Most newly acquired H. pylori infections occur in children before 10 years of age. We hypothesized that early life H. pylori infection could influence the composition of the microbiome at mucosal sites distant to the stomach. To test this hypothesis, we utilized the infant rhesus macaque monkey as an animal model of natural H. pylori colonization to determine the impact of infection on the lung and oral microbiome during a window of postnatal development. From a cohort of 4-7 month-old monkeys, gastric biopsy cultures identified 44% of animals infected by H. pylori. 16S ribosomal RNA gene sequencing of lung washes and buccal swabs from animals showed distinct profiles for the lung and oral microbiome, independent of H. pylori infection. In order of relative abundance, the lung microbiome was dominated by the phyla Proteobacteria, Firmicutes, Bacteroidota, Fusobacteriota, Campilobacterota and Actinobacteriota while the oral microbiome was dominated by Proteobacteria, Firmicutes, Bacteroidota, and Fusobacteriota. In comparison to the oral cavity, the lung was composed of more genera and species that significantly differed by H. pylori status, with a total of 6 genera and species that were increased in H. pylori negative infant monkey lungs. Lung, but not plasma IL-8 concentration was also associated with gastric H. pylori load and lung microbial composition. We found the infant rhesus macaque monkey lung harbors a microbiome signature that is distinct from that of the oral cavity during postnatal development. Gastric H. pylori colonization and IL-8 protein were linked to the composition of microbial communities in the lung and oral cavity. Collectively, these findings provide insight into how H. pylori infection might contribute to the gut-lung axis during early childhood and modulate future respiratory health.

UNLABELLED: Motility promotes biofilm initiation during the early steps of this process: microbial surface association and attachment. Motility is controlled in part by chemotaxis signaling, so it seems reasonable that chemotaxis may also affect biofilm formation. There is a gap, however, in our understanding of the interactions between chemotaxis and biofilm formation, partly because most studies analyzed the phenotype of only a single chemotaxis signaling mutant, e.g., cheA. Here, we addressed the role of chemotaxis in biofilm formation using a full set of chemotaxis signaling mutants in Helicobacter pylori, a class I carcinogen that infects more than half the worlds population and forms biofilms. Using mutants that lack each chemotaxis signaling protein, we found that chemotaxis signaling affected the biofilm initiation stage, but not mature biofilm formation. Surprisingly, some chemotaxis mutants elevated biofilm initiation, while others inhibited it in a manner that was not tied to chemotaxis ability or ligand input. Instead, the biofilm phenotype correlated with flagellar rotational bias. Specifically, mutants with a counterclockwise bias promoted biofilm initiation, e.g., ∆cheA, ∆cheW, or ∆cheV1; in contrast, those with a clockwise bias inhibited it, e.g., ∆cheZ, ∆chePep, or ∆cheV3. We tested this correlation using a counterclockwise bias-locked flagellum, which induced biofilm formation independent of the chemotaxis system. These CCW flagella, however, were not sufficient to induce biofilm formation, suggesting there are downstream players. Overall, our work highlights the new finding that flagellar rotational direction promotes biofilm initiation, with the chemotaxis signaling system operating as one mechanism to control flagellar rotation. IMPORTANCE: Chemotaxis signaling systems have been reported to contribute to biofilm formation in many bacteria; however, how they regulate biofilm formation remains largely unknown. Chemotaxis systems are composed of ma

BACKGROUND/AIMS: While DNA methylation and gastric microbiome are each associated with gastric cancer (GC), their combined role in predicting GC remains unclear. This study investigated the potential of a combined DNA methylation and gastric microbiome signature to predict Helicobacter pylori-negative GC. METHODS: In this case-control study, we conducted quantitative methylation-specific polymerase chain reaction to measure the methylation levels of DKK3, SFRP1, EMX1, NKX6-1, MIR124-3, and TWIST1 in the gastric mucosa from 75 H. pylori-negative patients, including chronic gastritis (CG), intestinal metaplasia (IM), and GC. A combined analysis of DNA methylation and gastric microbiome, using 16S rRNA gene sequencing, was performed in 30 of 75 patients. RESULTS: The methylation levels of DKK3, SFRP1, EMX1, MIR124-3, and TWIST1 were significantly higher in patients with GC than in controls (all q<0.05). MIR124-3 and TWIST1 methylation levels were higher in patients with IM than those with CG and also in those with GC than in those with IM (all q<0.05). A higher methylation level of TWIST1 was an independent predictor for H. pylori-negative GC after adjusting for age, sex, and atrophy (odds ratio [OR], 15.15; 95% confidence interval [CI], 1.58 to 145.46; p=0.018). The combination of TWIST1 methylation and GC microbiome index (a microbiome marker) was significantly associated with H. pylori-negative GC after adjusting for age, sex, and atrophy (OR, 50.00; 95% CI, 1.69 to 1,476; p=0.024). CONCLUSIONS: The combination of TWIST1 methylation and GC microbiome index may offer potential as a biomarker for predicting H. pylori-negative GC.

Background: Special antibiotics are prescribed against Helicobacter (H.) pylori . However, sometimes the bacteria are not completely eliminated, or they are recurrent. Unlike most infections, it is very difficult to eliminate a H. pylori infection. Heteroresistance is defined as the phenomenon in which subpopulations of the same colony of bacteria exhibit a range of susceptibilities to a particular antibiotic. Because of heteroresistant cells, antibiotic failure and chronic infection can occur; thus, the current research aimed to investigate presence of heteroresistant cells in H. pylori collected from patients reffering to clinic in Ilam, Iran. Subsequently, patients who were infected with heteroresistant H. p ylori were treated with antibiotics effective against heteroresistant subpopulations.Methods: In this cross-sectional descriptive study, 100 patients with clinical symptoms and suspected of being infected with H. pylori were studied in private clinics in Ilam, Iran. Fiftyisolates of H. pylori accompanied by patients' information were obtained from Ilam clinics. We cultured the bacteria to identify heteroresistance and to find the cause of recurrent infection in these patients. Results: Out of a total of 50 samples, 3 were heteroresistant to clarithromycin (6%). Levofloxacin was applied in cases of heteroresistant samples, and the effectiveness was determined after one month of follow-up of patients. Conclusion: Patients with heteroresistance showed sensitivity to levofloxacin. After one month of follow-up, it was found that the effectiveness of this antibiotic was good. Therefore, this antibiotic was introduced as a more effective drug in patients with heteroresistant H. pylori ., Zur Eradikation von Helicobacter (H.) pylori werden spezielle Antibiotika verschrieben. Manchmal werden nicht alle Bakterien abgetötet oder sie treten wieder auf. Anders als bei den meisten Infektionen ist es sehr schwierig, eine H. pylori -Infektion zu beseitigen. Heteroresistenz ist definiert als ein Phänomen, bei dem Subpopulationen derselben Species eine unterschiedliche Empfindlichkeit gegenüber einem bestimmten Antibiotikum aufweisen. Aufgrund der Heteroresistenz kann es zum Versagen des Antibiotikums und zu einer chronischen Infektion kommen. Daher sollte das Vorhandensein heteroresistenter Zellen von Patienten aus Ilam, Iran, von H. pylori untersucht werden. Die Patienten mit Vorkommen heteroresistenter H. pylori Subpopulationen wurden mit gegen diese Erreger wirksamen Antibiotika behandelt.

Bakgrund: Helicobacter pylori är en viktig bakterie som kan leda till magcancerutveckling, då den ökar risken för magcancer med 4–6 gånger. År 2020 rapporterades över en miljon Helicobacter pylori-relaterade magcancer och runt 800 000 dödsfall. Från 2014 har världshälsoorganisationen rekommenderat att Helicobacter pylori ska utrotas för att minska antal dödsfall av magcancer över hela världen. Behandling av Helicobacter pylori består oftast av två olika antibiotika och protonpumpshämmare. Flera kliniska studier visade att probiotika som komplement till standard eradikeringsbehandling av Helicobacter pylori ökar eradikeringsfrekvens och minskar biverkningar till följd av antibiotikabehandling. Syfte: Studien syftar till att granska och analysera publicerade kliniska prövningar för att studera effekten av probiotika som komplement till standardterapi på eradikering av Helicobacter pylori.Metod: Fem randomiserade, placebo-kontrollerade kliniska prövningar granskades. Sökningen av studier gjordes i januari 2024 med hjälp av PubMed och Google Scholar databaser. Resultat: Fyra av fem studier visade statistiskt signifikant skillnad i Helicobacterpylori eradikeringsfrekvens hos patienter som behandlades med probiotika, som komplement till eradikeringsbehandling, jämfört med placebo. Två av fem studier visade statistiskt signifikant skillnad i antibiotikaassocierade biverkningar hos interventiongruppen jämfört med placebo.Slutsats: Probiotika som komplement till standarderadikeringsbehandling är effektiv på att öka Helicobacter pylori eliminering och utrotningshastigheten.

Background: The influence of indications for Helicobacter pylori investigation on prescriptions and effectiveness is unknown. The aim of the study was to assess the impact of indications for H. pylori investigation on prescriptions, effectiveness, compliance, and tolerance. Methods: International, prospective, non-interventional registry of the management of H. pylori infection by European gastroenterologists (Hp-EuReg). Treatment-näive patients registered from 2013 to 2023 at e-CRF AEG-REDCap were analyzed. The effectiveness was assessed by modified intention-to-treat analysis. Results: Overall, 53,636 treatment-naïve cases from 34 countries were included. Most frequent indications were: dyspepsia with normal endoscopy (49%), non-investigated dyspepsia (20%), duodenal ulcer (11%), gastric ulcer (7.7%), and gastroesophageal reflux disease (GERD) (2.6%). Therapy effectiveness varied by indication: duodenal ulcer (91%), gastric ulcer (90%), preneoplastic lesions (90%), dyspepsia with normal endoscopy (89%), GERD (88%), and non-investigated dyspepsia (87%). Bismuth-metronidazole-tetracycline and clarithromycin-amoxicillin-bismuth quadruple therapies achieved 90% effectiveness in all indications except GERD. Concomitant clarithromycin-amoxicillin-tinidazole/metronidazole reached 90% cure rates except in patients with non-investigated dyspepsia; whereas sequential clarithromycin-amoxicillin-tinidazole/metronidazole proved optimal (≥90%) in patients with gastric ulcer only. Adverse events were higher in patients treated for dyspepsia with normal endoscopy and duodenal ulcer compared with the remaining indications (23% and 28%, p < 0.001). Therapeutic compliance was higher in patients with duodenal ulcer and preneoplastic lesions (98% and 99%, p < 0.001). Conclusion: In Europe, patients with gastric or duodenal ulcers and preneoplastic lesions showed higher H. pylori treatment effectiveness. Bismuth and non-bismuth quadruple therapies achieved optimal results in almost all

Prophages can have major clinical implications through their ability to change pathogenic bacterial traits. There is limited understanding of the prophage role in ecological, evolutionary, adaptive processes and pathogenicity of Helicobacter pylori, a widespread bacterium causally associated with gastric cancer. Inferring the exact prophage genomic location and completeness requires complete genomes. The international Helicobacter pylori Genome Project (HpGP) dataset comprises 1011 H. pylori complete clinical genomes enriched with epigenetic data. We thoroughly evaluated the H. pylori prophage genomic content in the HpGP dataset. We investigated population evolutionary dynamics through phylogenetic and pangenome analyses. Additionally, we identified genome rearrangements and assessed the impact of prophage presence on bacterial gene disruption and methylome. We found that 29.5% (298) of the HpGP genomes contain prophages, of which only 32.2% (96) were complete, minimizing the burden of prophage carriage. The prevalence of H. pylori prophage sequences was variable by geography and ancestry, but not by disease status of the human host. Prophage insertion occasionally results in gene disruption that can change the global bacterial epigenome. Gene function prediction allowed the development of the first model for lysogenic-lytic cycle regulation in H. pylori. We have disclosed new prophage inactivation mechanisms that appear to occur by genome rearrangement, merger with other mobile elements, and pseudogene accumulation. Our analysis provides a comprehensive framework for H. pylori prophage biological and genomics, offering insights into lysogeny regulation and bacterial adaptation to prophages.

Objectives:To describe the clinical features and the risk of developing gastric tumors in patients with autoimmune gastritis (AIG).Methods:This was a retrospective, longitudinal, multicenter study conducted at eight Italian tertiary referral centers. We retrieved clinical data from all histologically proven AIG patients. Differences between H. pylori-exposed vs H. pylori-naïve, and anti-parietal cell antibody (PCA)-positive vs PCA-negative patients were investigated. The rate of gastric adenocarcinoma and type 1 gastric neuroendocrine neoplasm (gNEN) was assessed. A multivariable model for factors associated to gNEN was fitted.Results:1598 patients with AIG (median age 58 years, IQR 46-68; F:M ratio 2.7:1) were included. H. pylori-naïve patients were more likely to have a first-degree family history of AIG (14.7% vs 8.9%; p=0.012), type 1 diabetes mellitus (4.9% vs 2.3%; p=0.025), and pernicious anemia (30.9% vs 21.1%; p=0.003). PCA-positive patients had significantly more associated autoimmune diseases (59.0% vs 42.9%; p<0.001) and were more likely to have been diagnosed by a case-finding strategy (15.3% vs 2.6%; p<0.001). Overall, 15 cases (0.9%) of gastric adenocarcinoma and 153 cases (9.6%) of gNEN occurred, with a global rate of 0.12 (95% CI 0.07-0.20) and 1.22 (95% CI 1.03-1.42) per 100 person/year, respectively. Having a vitamin B12/iron deficiency manifestation at AIG diagnosis was associated with an 16.44 (95% CI 9.94-27.20 p<0.001) hazard ratio of gNEN.Conclusions:The "pure"AIG pattern has typical features of an autoimmune disease and seems to be unrelated to H. pylori. In a tertiary referral setting, the risk of developing overt gastric adenocarcinoma is low, while patients with vitamin B12 deficiency complications at onset may benefit from a more intense endoscopic follow-up for early gNEN detection.

Introduction and Aim: Helicobacter pylori is a gram-negative bacterium that affects up to half of the world's population, particularly in poorer nations. It is the leading cause of chronic gastritis, ulcers, gastric lymphoma, and gastric cancer, with more frequent cases in children and adolescents. Transmission can occur through fecal-oral, gastro-oral, oral-oral, or sexual means. The infection is caused by H. pylori's urease activity, invasion of host gastric epithelial cells, and adherence to host cell receptors. Early treatment can enhance gastric protection. Materials and Methods: Between November 2022 and July 2023, 103 samples were collected from patients at Mihrabani Surgical Hospital in Erbil City to identify Helicobacter pylori infection. Blood samples and stool samples were used to test for antibodies. Results: The study found a relatively equal gender representation in the patient and control groups, with 48.48% of men in the patient group and 48.64% in the control group. However, there are significant differences in age distribution, with G3 of age (<35) having the highest prevalence of H.pylori (48.48%). Additionally, 62.12% of patients are rural residents, while 97.29% of the control group are urban residents. Finally, 56.07% of patients are married, indicating a significant difference. Conclusion: The study found equal gender representation in patient and control groups but significant age differences, rural residency, and marital status, with G3 under 35 having the highest H.pylori prevalence.

UNLABELLED: The bacterial chemotaxis system is a well-understood signaling pathway that promotes bacterial success. Chemotaxis systems comprise chemoreceptors and the CheA kinase, linked by CheW or CheV scaffold proteins. Scaffold proteins provide connections between chemoreceptors and CheA and also between chemoreceptors to create macromolecular arrays. Chemotaxis is required for host colonization by many microbes, including the stomach pathogen Helicobacter pylori. This bacterium builds chemoreceptor-CheA contacts with two distinct scaffold proteins, CheW and CheV1. H. pylori cheW or cheV1 deletion mutants both lose chemoreceptor array formation, but show differing semisolid agar chemotaxis assay behaviors: ∆cheW mutants exhibit total migration failure, whereas ∆cheV1::cat mutants display a 50% reduction. On investigating these varied responses, we found that both mutants initially struggle with migration. However, over time, ∆cheV1::cat mutants develop a stable, enhanced migration capability, termed migration-able (Mig+). Whole-genome sequencing analysis of four distinct ∆cheV1::cat Mig+ strains identified single-nucleotide polymorphisms (SNPs) in hpg27_252 (hp0273) that were predicted to truncate the encoded protein. Computational analysis of the hpg27_252-encoded protein revealed it encoded a hypothetical protein that was a remote homolog of the PilO Type IV filament membrane alignment complex protein. Although H. pylori lacks Type IV filaments, our analysis showed it retains an operon of genes for homologs of PilO, PilN, and PilM. Deleting hpg27_252 in the ∆cheV1::cat or wild type strain resulted in enhanced migration in semisolid agar. Our study thus reveals that while cheV1 mutants initially have significant migration defects, they can recover the migration ability through genetic suppressors, highlighting a complex regulatory mechanism in bacterial migration. IMPORTANCE: Chemotactic motility, present in over half of bacteria, depends on chemotaxis signaling

The antimicrobial resistance of Helicobacter pylori (Hp) currently poses a threat to available treatment regimens. Developing antimicrobial drugs targeting new bacterial targets is crucial, and one such class of drugs includes Hp-flavodoxin (Hp-fld) inhibitors that target an essential metabolic pathway in Hp. Our study demonstrated that combining these new drugs with conventional antibiotics used for Hp infection treatment prevented the regrowth observed with drugs used alone. Hp-fld inhibitors show promise as new drugs to be incorporated into the treatment of Hp infection, potentially reducing the development of resistance and shortening the treatment duration.

This study aims at providing an accurate and up-to-date quantification of the dose–response association between cigarette smoking and gastric cancer (GC) risk, overall and by subsite. We conducted a systematic review and meta-analysis of case–control and cohort studies on the association between cigarette smoking and GC risk published up to January 2023. We estimated pooled relative risks (RR) of GC and its subsites according to smoking status, intensity, duration, and time since quitting. Among 271 eligible articles, 205 original studies were included in this meta-analysis. Compared with never smokers, the pooled RR for GC was 1.53 (95% confidence interval; CI 1.44–1.62; n = 92) for current and 1.30 (95% CI 1.23–1.37; n = 82) for former smokers. The RR for current compared with never smokers was 2.08 (95% CI 1.66–2.61; n = 21) for gastric cardia and 1.48 (95% CI 1.33–1.66; n = 8) for distal stomach cancer. GC risk nonlinearly increased with smoking intensity up to 20 cigarettes/day (RR:1.69; 95% CI 1.55–1.84) and levelled thereafter. GC risk significantly increased linearly with increasing smoking duration (RR: 1.31; 95% CI 1.25–1.37 for 20 years) and significantly decreased linearly with increasing time since quitting (RR: 0.65; 95% CI 0.44–0.95 for 30 years since cessation). The present meta-analysis confirms that cigarette smoking is an independent risk factor for GC, particularly for gastric cardia. GC risk increases with a low number of cigarettes up to 20 cigarettes/day and increases in a dose-dependent manner with smoking duration.

Myocardial infarction (MI) with obstructive coronary artery disease (MI-CAD) and MI in the absence of obstructive coronary artery disease (MINOCA) affect different populations and may have separate pathophysiological mechanisms, with greater inflammatory activity in MINOCA compared to MI-CAD. Helicobacter pylori (Hp) can cause systemic inflammation and has been associated with cardiovascular disease (CVD). We aimed to investigate whether Hp infection is associated with concentrations of protein biomarkers of inflammation and CVD. In a case-control study, patients with MINOCA (n = 99) in Sweden were included, complemented by matched subjects with MI-CAD (n = 99) and controls (n = 100). Protein biomarkers were measured with a proximity extension assay in plasma samples collected 3 months after MI. The seroprevalence of Hp and cytotoxin-associated gene A (CagA) was determined using ELISA. The associations between protein levels and Hp status were studied with linear regression. The prevalence of Hp was 20.2%, 19.2%, and 16.0% for MINOCA, MI-CAD, and controls, respectively (p = 0.73). Seven proteins were associated with Hp in an adjusted model: tissue plasminogen activator (tPA), interleukin-6 (IL-6), myeloperoxidase (MPO), TNF-related activation-induced cytokine (TRANCE), pappalysin-1 (PAPPA), soluble urokinase plasminogen activator receptor (suPAR), and P-selectin glycoprotein ligand 1 (PSGL-1). Hp infection was present in one in five patients with MI, irrespective of the presence of obstructive CAD. Inflammatory proteins were elevated in Hp-positive subjects, thus not ruling out that Hp may promote an inflammatory response and potentially contribute to the development of CVD.

Las infecciones por Helicobacter pylori son muy comunes en nuestro entorno, en muchos casos se presentan como asintomáticas o con afecciones gastrointestinales, pero no se deben tomar a la ligera, es una infección que puede llevar a graves consecuencias, desde gastritis hasta cáncer gástrico. Su tratamiento se ha estado modificando por casos de resistencia a los medicamentos de primera línea en distintos países. Se realizó una recopilación de datos a través de PubMed, HINARI, SciELO, SCOPUS y Cochrane Library. Los probióticos se utilizan para incrementar el rango de erradicación de la bacteria, la disminución de la bacteria, pero esto acompañado de un tratamiento adecuado, mejora de dieta, sistema inmune del paciente. Debido a que reduce los efectos secundarios en pacientes, promueve un restablecimiento microbiota gastrointestinal, la cual es afectada ante agentes patógenos como el H. pylori.

Introducción: En las dos últimas décadas, se ha explorado el rol de la infección por Helicobacter pylori en la génesis de las enfermedades alérgicas, obteniéndose datos que apoyan la idea de que podría jugar un papel importante en el desarrollo de la alergia. Objetivo: Identificar la asociación entre Helicobacter pylori y enfermedades alérgicas. Materiales y métodos: Estudio de casos y controles prospectivo realizado en la Clínica “Santa Cruz” (Barquisimeto, Estado Lara, Venezuela), entre junio 2022 y junio 2023, donde se compararon 65 niños con enfermedades alérgicas con 130 controles sanos, con edades entre 2 y 15 años, que acudieron a consulta ambulatoria de rutina. Fueron comparadas variables demográficas, parto por cesárea, antecedentes familiares de alergias, tiempo de lactancia materna, exposición al humo de tabaco, mascotas, obesidad, porcentaje de eosinófilos y test de Helicobacter pylori positivo en heces con la presencia de enfermedades alérgicas como variable dependiente. Se utilizó: análisis bivariable y regresión logística binaria. Resultados: Los factores asociados significativamente a enfermedades alérgicas fueron: antecedentes familiares de alergia, tiempo de lactancia materna menor a 12 meses, y test de Helicobacter pylori positivo en heces. Fueron identificados como predictores independientes asociados a enfermedades alérgicas: antecedentes familiares de alergia (RO=2,345; IC95%: 1,245 – 4,416; p = 0,008) y test de Helicobacter pylori positivo en heces (RO=2,072; IC95%: 1,090 – 3,939; p = 0,026). Conclusión: La presencia de antecedentes familiares de alergia y test de Helicobacter pylori positivo en heces fueron identificados como variables independientes asociadas a enfermedades alérgicas.

Introduction: Adding probiotics to triple and quadruple therapies has been proposed to improve their effectiveness in the eradication of Helicobacter pylori, but there is controversy about their usefulness. Objective: To assess the effectiveness and safety of probiotics as adjuvants in triple or quadruple therapies for H. pylori eradication in adults. Materials and methods: Systematic review and meta-analysis. Randomized clinical trials (RCTs) assessing the effectiveness and safety of probiotics as adjuvant therapy in combination with triple and quadruple therapies for the eradication of H. pylori in adults and published in English or Spanish between January 2010 and May 2020 were searched in the Embase, Ovid Medline, Cochrane Library, and LILACS databases. Regarding the meta-analysis, a fixed-effects model was used to calculate the pooled measure (OR and RR) of the effectiveness and safety of using adjuvant probiotics in triple and quadruple therapy. Results: Twelve RCTs were included (1 091 patients in total): 9 assessed triple therapy, 2 assessed quadruple therapy, and 1 assessed both triple and quadruple therapy. In the case of triple therapy, the use of adjuvant probiotics was more effective than placebo: 79.4% vs. 71.1%, (OR=1.42; 95%CI: 1.05-2.09), but in the case of quadruple therapy, their use did not increase effectiveness. The most widely used probiotic was Lactobacillus reuteri, with an eradication rate of 77.9% (95%CI: 70.5-84.19) versus 66.8% (95%CI: 58.8-74.2) for placebo. Probiotics decreased the occurrence of adverse effects in both triple therapy (OR=0.50; 95%CI: 0.28-0.90) and quadruple therapy (OR=0.26; 95%CI: 0.09-0.74). Conclusions: Adjuvant probiotics improve the effectiveness of triple therapy to eradicate H. Pylori by 8.5%, but the final effectiveness is <90%. Furthermore, their use does not increase the effectiveness of quadruple therapy. However, the use of these microorganisms reduces the adverse effects of these therapies., Introducción. Se ha propuesto agregar probióticos a las terapias triples y cuádruples para mejorar su efectividad en la erradicación de Helicobacter pylori, pero existe controversia sobre su utilidad. Objetivo. Evaluar la efectividad y seguridad del uso adyuvante de probióticos en la terapia triple o cuádruple para la erradicación de H. pylori en adultos. Materiales y métodos. Revisión sistemática y metaanálisis. Se realizó una búsqueda en Embase, Ovid Medline, Cochrane Library y LILACS de ensayos clínicos aleatorizados (ECA) publicados en inglés o español entre enero de 2010 y mayo de 2020 que evalúan la efectividad y seguridad de usar probióticos como terapia coadyuvante en combinación con la terapia triple o cuádruple en la erradicación de H. pylori en adultos. En el metaanálisis se utilizó un modelo de efectos fijos para calcular la medida combinada (OR y RR) de efectividad y seguridad de los probióticos coadyuvantes en terapia triple y cuádruple. Resultados: Se incluyeron 12 ECA (1 091 pacientes en total): 9 evaluaron terapia triple; 2, terapia cuádruple, y 1, terapia triple y cuádruple. En la terapia triple el uso coadyuvante de probióticos fue más efectivo que el uso de placebo: 79.4% vs. 71.1% (OR=1.42; IC95%: 1.05-2.09), pero en la terapia cuádruple, su uso no aumentó la efectividad. El probiótico más utilizado fue Lactobacillus reuteri, con una tasa de curación de 77.9% (IC95%: 70.5-84.19) versus 66.8% (IC95%: 58.8-74.2) del placebo. Los probióticos disminuyeron la ocurrencia de efectos adversos tanto en terapia triple (OR=0.50; IC95%: 0.28-0.90) como en cuádruple (OR=0.26; IC95%: 0.09-0.74). Conclusiones. El uso coadyuvante de probióticos mejora la efectividad de la terapia triple para erradicar H. Pylori en un 8.5%, pero la efectividad final es <90%. Además, su uso no aumenta la efectividad de la terapia cuádruple. No obstante, el uso de estos microorganismos disminuye los efectos adversos de estas terapias.

BACKGROUND & AIMS: Practice guidelines promote a routine noninvasive, non-endoscopic initial approach to investigating dyspepsia without alarm features in young patients, yet many patients undergo prompt upper endoscopy. We aimed to assess tradeoffs among costs, patient satisfaction, and clinical outcomes to inform discrepancy between guidelines and practice. METHODS: We constructed a decision-analytic model and performed cost-effectiveness/cost-satisfaction analysis over a 1-year time horizon on patients with uninvestigated dyspepsia without alarm features referred to gastroenterology. A RAND/UCLA expert panel informed model design. Four competing diagnostic/management strategies were evaluated: prompt endoscopy, testing for Helicobacter pylori and eradicating if present (test-and-treat), testing for H pylori and performing endoscopy if present (test-and-scope), and empiric acid suppression. Outcomes were derived from systematic reviews of clinical trials. Costs were informed by prospective observational cohort studies and national commercial/federal cost databases. Health gains were represented using quality-adjusted life years. RESULTS: From the patient perspective, costs and outcomes were similar for all strategies (maximum out-of-pocket difference of $30 and <0.01 quality-adjusted life years gained/year regardless of strategy). Prompt endoscopy maximized cost-satisfaction and health system reimbursement. Test-and-scope maximized cost-effectiveness from insurer and patient perspectives. Results remained robust on multiple one-way sensitivity analyses on model inputs and across most willingness-to-pay thresholds. CONCLUSIONS: Noninvasive management strategies appear to result in inferior cost-effectiveness and patient satisfaction outcomes compared with strategies promoting up-front endoscopy. Therefore, additional studies are needed to evaluate the drivers of patient satisfaction to facilitate inclusion in value-based healthcare transformation efforts.

Levodopa is the gold standard for the symptomatic treatment of Parkinson's disease (PD). There are well documented motor and non-motor fluctuations, however, that occur almost inevitably once levodopa is started after a variable period in people with PD. Whilst brain neurodegenerative processes play a part in the pathogenesis of these fluctuations, a range of barriers across the gastrointestinal (GI) tract can alter levodopa pharmacokinetics, ultimately contributing to non-optimal levodopa response and symptoms fluctuations. GI barriers to levodopa transport and absorption include dysphagia, delayed gastric emptying, constipation, Helicobacter pylori infection, small intestinal bacterial overgrowth and gut dysbiosis. In addition, a protein-rich diet and concomitant medication intake can further alter levodopa pharmacokinetics. This can result in unpredictable or sub-optimal levodopa response, 'delayed on' or 'no on' phenomena. In this narrative review, we provided an overview on the plethora of GI obstacles to levodopa transport and absorption in PD and their implications on levodopa pharmacokinetics and development of motor fluctuations. In addition, management strategies to address GI dysfunction in PD are highlighted, including use of non-oral therapies to bypass the GI tract.

Background: Long-term Helicobacter pylori infection increases the risk of gastric malignancies. Since the symptoms for H. pylori gastritis, as well as for several malignancies, may be nonexisting or highly unspecific, even H. pylori-positive subjects with underlying malignancies may receive eradication therapy. The aim was to assess the incidence of gastrointestinal and various other malignancies in individuals after eradication therapy for H. pylori infection. Materials and Methods: A cohort of 217,554 subjects (120,344 women and 97,210 men), who had purchased specific combinations of drugs for H. pylori eradication therapy in 1994-2004, was identified by the Finnish National Prescription Registry and followed for cancer incidence until the end of 2008 (1.89 million person-years at risk). Results: A total of 22,398 malignancies were identified in the cohort. In both genders, for the first 6 months after drug prescription, the standardized incidence ratios (SIRs) were between 5 and 32 for gastric, colorectal, and pancreatic cancers, and 2 and 3 for several other malignancies. Although later on the SIRs of most malignancies fell rapidly, those of gastric noncardia and lung cancers remained elevated up to 5 years of follow-up. The only SIRs below unity were seen in men for gastric cancers (cardia 0.61, 95% CI: 0.37-0.95; intestinal noncardia 0.74, 95% CI: 0.56-0.97) during the post-therapy period covering years 5-15. Conclusion: Incidence levels significantly above the population rates were detected for many malignancies. Although eradication of H. pylori may have a long-lasting protective effect against gastric cancer, H. pylori therapy may postpone the detection of malignancies possibly underlying unspecific gastrointestinal symptoms. Therefore, it should be emphasized that the diagnostic work-up for malignancies should not be stopped in case of detection and treatment of H. pylori infection.

Helicobacter pylori is a significant risk factor for chronic gastritis, gastric ulcers, and gastric cancer. The purpose of this article is to investigate the potential impact of fifty herbal compounds derived from Ginger and Parsley plants, known for their antibacterial properties on the Oxygen-insensitive NADPH nitro reductase enzyme of metronidazole-resistant H. pylori. In the present study, the information on the structure of compounds, the H. pylori resistant to metronidazole enzyme, myristicin, and shogaol derivatives were obtained from databases such as ZINC15, RCSB (Protein Data Bank), and PubChem, respectively. Finally, molecular docking was performed with iGemdock2.1 and Molegro Virtual Docker. After molecular docking, four out of the fifty phytocompounds showed the lowest energy and the highest number of interactions with the amino acids at the binding sites. Among these four phytocompounds, the best phytocompound was N-Vanillyloctanamide derived from Ginger. Our molecular docking study suggests that ginger can be introduced as a potential candidate to inhibit the growth of H. pylori.

Helicobacter pylori colonizes half of the world's population and is responsible for a significant disease burden by causing gastritis, peptic ulcers, and gastric cancer. The development of host inflammation drives these diseases, but there are still open questions in the field about how H. pylori controls this process. We characterized H. pylori inflammation using an 8-month mouse infection time course and comparison of the wild type (WT) and a previously identified mutant lacking the TlpA chemoreceptor that causes elevated inflammation. Our work shows that H. pylori chronic-stage corpus inflammation undergoes surprising fluctuations, with changes in Th17 and eosinophil numbers. The H. pylori tlpA mutant changed the inflammation temporal characteristics, resulting in different inflammation from the wild type at some time points. tlpA mutants have equivalent total and gland colonization in late-stage infections. During early infection, in contrast, they show elevated gland and total colonization compared to those by WT. Our results suggest the chronic inflammation setting is dynamic and may be influenced by colonization properties of early infection.

The flagellar motor protein FliL is conserved across many microbes, but its exact role has been obscured by varying fliL mutant phenotypes. We reanalyzed results from fliL studies and found they utilized alleles that differed in the amount of N- and C-terminal regions that were retained. Alleles that retain the N-terminal cytoplasmic and transmembrane helix (TM) regions in the absence of the C-terminal periplasmic domain result in loss of motility, while alleles that completely lack the N-terminal region, independent of the periplasmic domain, retain motility. We then tested this prediction in Helicobacter pylori fliL and found support for the idea. This analysis suggests that FliL function may be more conserved across bacteria than previously thought, that it is not essential for motility, and that the N-terminal region has the negative ability to regulate motor function. IMPORTANCE FliL is a protein found in the flagellar motor of bacteria, but what it does was not clear. To study FliL function, scientists often remove it and see what happens. Loss of FliL was thought to have different effects depending on the microbe. We uncovered, however, that part of the confusion arose because scientists inadvertently removed different parts of the protein. Our analysis and data suggest that leaving the N-terminal regions blocks motility, while fully removing FliL allows normal motility. This finding will help scientists understand FliL because it clarifies what needs to be removed to fully eliminate the protein, and also that the N-terminal region can block motility.

The complement system has long been appreciated for its role in bloodborne infections, but its activities in other places, including the gastrointestinal tract, remain elusive. Here, we report that complement restricts gastric infection by the pathogen Helicobacter pylori. This bacterium colonized complement-deficient mice to higher levels than wild-type counterparts, particularly in the gastric corpus region. H. pylori uses uptake of the host molecule L-lactate to create a complement-resistant state that relies on blocking the deposition of the active complement C4b component on H. pylori's surface. H. pylori mutants unable to achieve this complement-resistant state have a significant mouse colonization defect that is largely corrected by mutational removal of complement. This work highlights a previously unknown role for complement in the stomach, and has revealed an unrecognized mechanism for microbial-derived complement resistance.

Aim: The main objective of this study is to determine the response to the firstline treatment regimen with triple standard therapy (amoxicillin, clarithromycin, omeprazole), to eradicate Helicobacter pylori in a certain population. The goal is to determine if the proposed regimen in international guidelines services is still a suitable option for patients in a certain region of Costa Rica.Methods: The study took place in San Francisco de Asís Hospital, Grecia, Alajuela, Costa Rica. All patients with a Helicobacter pylori infection that were given first- line treatment with triple therapy (amoxicillin, clarithromycin and omeprazole) for its eradication for 14 days, in the period between February of 2017 and February of 2019, were included in the study. Results: A total of 369 cases were identified. The diagnosis was made with biopsy in 96.4% of patients. Response to first-line treatment was achieved in 90.5% corroborated by fecal antigen in 92.1% of all cases.Conclusions: This study shows that triple therapy with amoxicillin, clarithromycin and omeprazole for 14 days maintains an adequate level of efficacy. However, it must be considered that these results are from a specific area and may not reflect the reality of the entire country., Objetivo: Este estudio tiene como objetivo principal determinar la respuesta al esquema de tratamiento de primera línea con triple terapia estándar (amoxicilina, claritromicina, omeprazol), para erradicación de Helicobacter pylori en una determinada población, para determinar si este esquema propuesto en guías internacionales es aún una opción adecuada para pacientes en una determinada región de Costa Rica.Métodos: Se realizó una búsqueda en el servicio de gastroenterología del Hospital San Francisco de Asís, Grecia, Alajuela, Costa Rica; de todos los pacientes con infección por Helicobacter pylori y que recibieron tratamiento de primera línea con triple terapia (amoxicilina, claritromicina y omeprazol) por 14 días, en el periodo comprendido entre febrero 2017 a febrero 2019, incluyendo para el análisis solamente en los que se contaba con una prueba confirmatoria posterior a tratamiento, ya fuera por antígeno fecal de H. pylori o biopsia convencional.Resultados: Se identificaron un total de 369 casos. El diagnóstico se realizó con biopsiaen el 96,4% de los pacientes. La respuesta al tratamiento de primera línea se alcanzó enun 90.5% corroborada por antígeno fecal en el 92.1% de los casos.Conclusiones: Este estudio muestra que la terapia triple con amoxicilina, claritromicina e Inhibidor de bomba de protones por 14 días mantiene un adecuado nivel de eficacia. Sin embargo, hay que tomar en cuenta que estos datos son únicamente de un área de atracción determinada y puede que no reflejen la realidad de todo el país.

An increase in resistance to key antibiotics has made the need for novel treatments for the gastric colonization of Helicobacter pylori (H. pylori) a matter of the utmost urgency. Recent studies tackling this topic have focused either on the discovery of new compounds to ameliorate therapeutic regimes (such as vonoprazan) or the synthesis of gastroretentive drug delivery systems (GRDDSs) to improve the pharmacokinetics of oral formulations. The use of semi-interpenetrating polymer networks (semi-IPNs) that can act as super-porous hydrogels for this purpose is proposed in the present work, specifically those displaying low ecological footprint, easy synthesis, self-floating properties, high encapsulation efficiency for drugs such as amoxicillin (AMOX), great mucoadhesiveness, and optimal mechanical strength when exposed to stomach-like fluids. To achieve such systems, biodegradable synthetic copolymers containing acid-labile monomers were prepared and interpenetrated with guar gum (GG) in a one-pot polymerization process based on thiol-ene click reactions. The resulting matrices were characterized by SEM, GPC, TGA, NMR, and rheology studies, and the acidic hydrolysis of the acid-sensitive polymers was also studied. Results confirm that some of the obtained matrices are expected to perform optimally as GRDDSs for the sustained release of active pharmaceutical ingredients at the gastrointestinal level, being a priori facilitated by its disaggregation. Therefore, the optimal performance of these systems is assessed by varying the molar ratio of the labile monomer in the matrices.

Approximately 36% of the United States (US) population is infected with Helicobacter pylori (HP), a known major risk factor for peptic ulcer disease and gastric cancer. HP eradication reduces the rate of complications; however, the benefits are undermined by rising rates of HP eradication treatment failure. This real-world observational cohort analysis aims to describe HP diagnostic and treatment patterns among insured patients in the US. Using diagnoses, lab results, and treatment patterns, we identified adults (18+) with new diagnoses of HP in the Veradigm Health Insights EHR Database linked to Komodo claims data (1/1/2016-12/31/2019). Patients were required to have ≥ 12 months of data pre-/post-index. We captured patient characteristics, HP-related diagnostic testing, and the use of US guideline-recommended HP eradication regimens. HP eradication rates following first-line eradication treatment were measured among patients with available lab results. Overall, 31.8% of the 60,593 included patients did not receive guideline-recommended treatment. Among the 68.2% (41,340) with first-line treatment, 80.2% received clarithromycin-based triple therapy, and 6.6% received bismuth quadruple therapy. Of the 4569 patients with a repeated course of eradication therapy, 53.4% received the same regimen as their first-line, the majority (90.7%) of whom received two rounds of clarithromycin-based triple therapy. Among the 2455 patients with results of HP non-serology testing following first-line treatment, the 180-day eradication rate was 80.2% overall, with differences based on treatments and demographics. This study highlights gaps between guideline-recommended HP management and real-world patterns, underscoring the need to improve HP testing, treatment, and follow-up practices.

Helicobacter pylori, first described in 1983 (1), is one of the most common chronic bacterial infections worldwide (2). It is mainly acquired in childhood, persists for life if left untreated, and can cause chronic gastritis, peptic ulcers and, in some cases, contribute to the development of gastric cancer later in adulthood (3–5). Vietnam has a high prevalence of H. pylori infection in adults and children (70%) (2). The incidence of peptic ulcer disease in children is on the rise (6–8), while the eradication effectiveness is decreasing mainly due to high antibiotic resistance (6,9,10). The important questions in H. pylori research remain what is the true burden of H. pylori infection in terms of its prevalence, the incidence of H. pylori-associated gastroduodenal complications, its antibiotic resistance patterns, and the effectiveness of treatment in Vietnamese symptomatic children?In this context, a prospective multicenter clinical series study was conducted at the two tertiary Children’s Hospitals in Ho Chi Minh City, Vietnam’s largest city to investigate the burden of H. pylori infection among Vietnamese children. Between October 2019 and May 2021, a total of 394 children were included with a mean age of 9.4 ± 2.5 years and 217 were girls (55%). Five gastric biopsies were obtained during endoscopy to perform H. pylori culture, histological examination, polymerase chain reaction (PCR) to detect urease gene (ureA), virulence genes (cytotoxin-associated gene A (cagA), vacuolating cytotoxin A (vacA genotypes)), and point mutations on 23S rRNA gene conferring clarithromycin resistance. Diagnosis of H. pylori infection was based on a positive culture or histological evidence in combination with a positive rapid urease test or a positive PCR assay of ureA according to internationally recognized criteria. An eradication treatment was prescribed for patients with confirmed H. pylori infection. After completion of therapy, a monoclonal stool antigen test was performed to, Doctorat en Sciences médicales (Médecine), info:eu-repo/semantics/nonPublished

Objectives Helicobacter pylori gastritis is considered an infectious disease, regardless of symptoms and stage of disease. Most consensus documents recommend empirical therapy based on local antimicrobial susceptibility patterns. We aimed to provide clinically useful information about primary and secondary antimicrobial resistance to antimicrobials commonly prescribed for H. pylori. Methods Overall, 31,406 gastroduodenal biopsies and 2,641 string tests from patients over 15 years of age were plated on selective media, isolating H. pylori in 36.7% of biopsies and 50.7% of string tests. Susceptibility testing could be performed in 96.6% (12,399/12,835) of H. pylori isolates. Polymerase chain reaction (PCR) was also used to detect H. pylori and its resistance to clarithromycin, providing susceptibility data for 112 patients with negative culture results. Results Resistance to amoxicillin and tetracycline was unusual (0.6% and 0.2%, respectively). Rates of primary resistance to clarithromycin and metronidazole remained steady over the 22-year study period, at around 14% for clarithromycin and 30% for metronidazole, while primary resistance to levofloxacin tripled (from 7.6% in 2000 to 21.7% in 2021, P < 0.001) and increased with patient age. Notably, 1.8% of isolates were multiresistant to clarithromycin, metronidazole, and levofloxacin. Overall, secondary resistance rates were higher (P < 0.0001) than primary resistance rates for clarithromycin (42.5% vs 14.1%), metronidazole (40.9% vs 32%), and levofloxacin (21.5% vs 17.1%). Conclusion Determination of susceptibility for H. pylori by culture and/or PCR in patients undergoing endoscopy could facilitate the implementation of tailored therapy and guide the choice of empirical therapy when susceptibility testing cannot be performed, potentially helping limit the emergence of antimicrobial resistance.

Introduction. The OLGA system has been proved to be useful in Asia and Europe as a risk marker of gastric cancer. However, its usefulness in high-risk populations in Colombia is still unknown.Objective. To assess potential associations between the OLGA staging system and an increased risk of gastric cancer and dysplasia in a high-risk Colombian population and to establish diagnostic capacity of the scale to assess the risk.Materials and methods. We carried out a multicenter study including patients with cancer and dysplasia (cases) and patients with atrophy and intestinal metaplasia (controls). A total of 506 patients were recruited from three centers in an area with a high risk population in Colombia. The endoscopic and histopathologic studies were evaluated according to the Sydney system and the OLGA staging system proposed by Rugge. The effect of each variable on the disease (gastric cancer and dysplasia) was evaluated using bivariate and multivariate models. Statistical significance was set considering a p value inferior to 0.05. Results. Advanced stages of the OLGA system (III-IV) were associated with a higher risk of dysplasia and gastric cancer (adjusted OR = 8.71; CI95% = 5.09-14.9; p=0.001), sensitivity=54.9%, specificity=89.3% and positive likelihood ratio=5.17.Conclusions. The OLGA staging system is a risk marker for gastric cancer and dysplasia in the studied population. We recommend its implementation to improve the timelydiagnosis and follow-up of patients with the highest cancer risk., Introducción. En Asia y Europa, el sistema OLGA ha sido útil como marcador de riesgo de cáncer gástrico. Sin embargo, su utilidad en poblaciones de alto riesgo en Colombia aún se desconoce.Objetivo. Establecer si los estadios OLGA se asocian con un mayor riesgo de cáncer y displasia en una población de alto riesgo en Colombia y determinar la capacidad diagnóstica de la escala para evaluar dicho riesgo. Materiales y métodos. Se realizó un estudio multicéntrico con pacientes con cáncer gástrico y displasia (casos), y pacientes con atrofia y metaplasia intestinal (controles), provenientes de tres centros de una zona de alto riesgo de cáncer gástrico en Colombia. Se incluyeron 506 pacientes cuyo estudio endoscópico e histopatológico fue realizado mediante el sistema de Sydney y la estadificación de OLGA propuesta por Rugge. El efecto de cada variable de interés sobre la enfermedad (cáncer gástrico y displasia) se evaluó mediante modelos bivariados y multivariados. Un valor de p menor de 0,05 se consideró estadísticamente significativo.Resultados. Los estadios elevados del sistema OLGA (III-IV) se asociaron con un mayor riesgo de displasia y cáncer gástrico (OR ajustado = 8,71; IC95 % = 5,09-14,9; p=0,001) con una sensibilidad del 54,9 %, especificidad del 89,3 % y una razón de probabilidad positiva de 5,17.Conclusiones. El estadio OLGA es un marcador de riesgo de cáncer gástrico y displasia en la población de estudio. Se recomienda su implementación como estrategia para optimizar el diagnóstico oportuno y el seguimiento de pacientes con mayor riesgo.

[ES] Introducción: Helicobacter pylori es una bacteria Gram-negativa gástrica que se estima que infecta al 50% de la población mundial. La infección por H. pylori es generalmente asintomática, pero puede provocar la aparición de patología digestiva como úlcera péptica o adenocarcinoma gástrico. Durante los últimos años, además, se ha planteado la existencia de una posible relación entre enfermedades extra-gastrointestinales y la infección por H. pylori. Objetivos: Realizar una revisión bibliográfica actualizada sobre la evidencia existente entre la asociación de la infección por H. pylori y manifestaciones extra-gastrointestinales e identificar la prevalencia y factores de virulencia posiblemente asociados a las mismas. Metodología: Se realizó una revisión bibliográfica en la base de datos Pubmed de las publicaciones comprendidas entre los años 2016 y 2021 que analizaban la relación entre H. pylori y diferentes manifestaciones extra-gastrointestinales. Resultados: Cuatro grupos de enfermedades fueron asociadas a la infección por H. pylori: enfermedades hematológicas, neurológicas, metabólicas y dermatológicas. La anemia ferropénica, fue la enfermedad que presentó con mayor frecuencia asociación significativa con la infección por H. pylori sobre la cual se obtuvo mayor evidencia científica. Aunque con menor cantidad de evidencia científica, otras manifestaciones que también se asociaron significativamente a la infección por H. pylori fueron: trombocitopenia inmune primaria y déficit de vitamina B12 entre las enfermedades hematológicas, enfermedad de Parkinson, hipertensión arterial, síndrome metabólico y urticaria crónica idiopática. La hipertensión arterial fue la manifestación extra-gastrointestinal que mostró una mayor prevalencia entre los pacientes infectados por H. pylori. Se observó un posible papel de la proteína CagA en el desarrollo de trombocitopenia inmune primaria, déficit de vitamina B12 y Diabetes Mellitus. Conclusiones: Se debe considerar a H. pylori

Gastritis is a disease that produces changes at the gastric mucosa and alteration in the immune system, is caused mostly by the Helicobacter pylori bacteria. he taxonomic classification of this microorganism corresponds to Proteobacteria, Spirillaceae family, Helicobacter genus and pylori species, it is a Gram negative, curved and microarophilic bacillus, it measures 2.5 microns long by approximately 0.5 to 1 micron in diameter, has 2 to 6 flagella, It is a glucose non-fermenter and is also oxidase and catalase positive. The isolation of Helicobacter pylori in a culture medium is very complex, due to the different requirements of the medium for its ideal growth (blood, serum and antibiotics), which is why it has currently been determined that the best diagnostic method is detection of deterioration by immunochromatographic assay in feces. Helicobacter pylori is a pathogen associated to gastritis, peptic ulcers and gastric cancer, being gastritis as the principal manifestation. This disease can be related with certain factors like age, sex, socioeconomic status and demographics. Through the years prevalence has been increasing through all countries of Latin America. Therefore, an early diagnosis is essential.

Objective: Helicobacter pylori and human immunodeficiency virus (HIV) are both pandemic infections with variable geographic prevalence rates. H. pylori–HIV co-infection at the regional and sub-regional levels with a perspective on gastric cancer incidence is discussed. Design: Based on PRISMA guidelines, national data for H. pylori, HIV, and H. pylori–HIV co-infection were collected for the general population through December 2019. Joint temporal and geographical data for H. pylori and HIV infections in 48 countries were available and used to generate H. pylori–HIV co-infection estimates by cross-sectional analysis. These data were compared with gastric carcinoma statistics for the same countries. Results: The estimated global prevalence rate of H. pylori–HIV co-infection was 1.7 per 1000 people, representing 12.6 million people. Prevalence according to region was, in decreasing order, sub-Saharan Africa 21.9‰, Eastern Europe/Central Asia 4.3‰, Latin America/Caribbean 2.0 ‰, North America/Western/Southern/Northern Europe 1.1‰, Asia/Pacific 0.8‰, and North Africa/Middle East 0.1 ‰. The incidence and mortality rates for gastric carcinoma were higher in East/Pacific Asia, Southern/Andean Latin America, and Eastern Europe regions, and the incidence appeared to be 1.8-fold greater in H. pylori–HIV-infected people in East Asia. Conclusions: The population at risk of H. pylori–HIV co-infection is estimated to be 12.6 million people (2015 reference year). The heterogeneity of H. pylori–HIV co-infection across regions and sub-regions does not show a clear association with gastric carcinoma. Other methodological approaches with analytical studies (cohort, case–control) are required to measure the potential effect of H. pylori infection and its treatment on the incidence of gastric carcinoma in the large HIV–H. pylori-positive cohort., SCOPUS: ar.j, SCOPUS: ar.j, info:eu-repo/semantics/published

In this course we will explore the new emerging field of pathogen-induced chronic diseases. Work in this field has redefined the causes of some major disorders, such as ulcers. By reading the primary research literature we will learn about the molecular mechanisms through which pathogens cause disease. The diseases that we cover will be introduced with a short patient case study. We will discuss the bacterium Helicobacter pylori and gastric disease, HPV and cervical cancer, hepatitis C virus and liver disease, Epstein-Barr virus and lymphoma, Cytomegalovirus and atherosclerosis, as well as diabetes and multiple sclerosis. We will study technical advances in the fight against microbes and explore future directions for new treatment strategies of chronic infections and inflammation. This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored for students with an interest in using primary research literature to discuss and learn about current biological research in a highly interactive setting. Many instructors of the Advanced Undergraduate Seminars are postdoctoral scientists with a strong interest in teaching.

The oral cavity with periodontal disease is considered as an extragastric reservoir of Helicobacter pylori, this gram negative bacillus is found in approximately 50% of the population worldwide and it is also mentioned as the main etiological agent of chronic gastritis. The present investigation was carried out with the objective of analyzing the relationship between chronic gastritis and periodontal disease. Through a review of the literature, it was determined that there is a correlation between the two disorders, which share an inflammatory state that can intervene in the pathogenesis, being necessary a simultaneous treatment to avoid reinfections or aggravations either in the gastrointestinal tract or in the supporting tissue of the teeth., La cavidad oral con afección periodontal es considerada como un reservorio extragástrico de Helicobacter pylori, este bacilo gram negativo se encuentra en aproximadamente el 50% de la población a nivel mundial y además es mencionado como el agente etiológico principal de la gastritis crónica. La presente investigación fue realizada con el objetivo de analizar la relación entre la gastritis crónica con la enfermedad periodontal. Mediante la revisión de la literatura se determinó que si existe correlación entre las dos alteraciones las mismas que comparten un estado inflamatorio el cual puede intervenir en la patogenia, siendo necesario un tratamiento simultáneo para evitar reinfecciones o agudizaciones ya sea en el tracto gastrointestinal o en el tejido de soporte de los dientes.

Gastric cancer (GC) is one of the leading causes of cancer-related deaths worldwide. The gastric microbiota plays a critical role in the development of GC. First, Helicobacter pylori (H. pylori) infection is considered a major risk factor for GC. However, recent studies based on microbiota sequencing technology have found that non-H. pylori microbes also exert effects on gastric carcinogenesis. Following the infection of H. pylori, gastric microbiota dysbiosis could be observed; the stomach is dominated by H. pylori and the abundances of non-H. pylori microbes reduce substantially. Additionally, decreased microbial diversity, alterations in the microbial community structure, negative interactions between H. pylori and other microbes, etc. occur, as well. With the progression of gastric lesions, the number of H. pylori decreases and the number of non-H. pylori microbes increases correspondingly. Notably, H. pylori and non-H. pylori microbes show different roles in different stages of gastric carcinogenesis. In the present mini-review, we provide an overview of the recent findings regarding the role of the gastric microbiota, including the H. pylori and non-H. pylori microbes, in the development of GC. Copyright © 2023 Guo, Cao, Zhou and Yu.

Background: Helicobacter pylori (H. pylori) remains a major cause of gastroduodenal diseases. We aimed to evaluate the burden of this infection, particularly peptic ulcer disease in Vietnamese children. Methods: We enrolled consecutive children referred for esophagogastroduodenoscopy at two tertiary children’s hospitals in Ho Chi Minh City, from October 2019 to May 2021. Children treated with proton pump inhibitors during the last two weeks or antibiotics for four weeks, and those having a previous or interventional endoscopy were excluded. H. pylori infection was diagnosed with either a positive culture or positive histopathology combined with a rapid urease test, or with a polymerase chain reaction of the urease gene. The study was approved by the Ethics Committee and written informed consent/assent was obtained. Results: Among 336 enrolled children aged 4–16 (mean: 9.1 ± 2.4 years; 55.4% girls), H. pylori infection was positive in 80%. Peptic ulcers were detected in 65 (19%), increasing with age, and 25% with anemia. cagA+ strains were detected at a higher rate in children with ulcers. Conclusions: Prevalence of H. pylori and peptic ulcers is high among symptomatic Vietnamese children. It is crucial to have a program for early detection of H. pylori to reduce ulcer risk and gastric cancer later., SCOPUS: ar.j, info:eu-repo/semantics/published

Helicobacter pylori is a Gram-negative bacterium that is able to colonize the human stomach, whose high prevalence has a major impact on human health, due to its association with several gastric and extra-gastric disorders, including gastric cancer. The gastric microenvironment is deeply affected by H. pylori colonization, with consequent effects on the gastrointestinal microbiota, exerted via the regulation of various factors, including gastric acidity, host immune responses, antimicrobial peptides, and virulence factors. The eradication therapy required to treat H. pylori infection can also have detrimental consequences for the gut microbiota, leading to a decreased alpha diversity. Notably, therapy regimens integrated with probiotics have been shown to reduce the negative effects of antibiotic therapy on the gut microbiota. These eradication therapies combined with probiotics have also higher rates of eradication, when compared to standard treatments, and are associated with reduced side effects, improving the patient's compliance. In light of the deep impact of gut microbiota alterations on human health, the present article aims to provide an overview of the complex interaction between H. pylori and the gastrointestinal microbiota, focusing also on the consequences of eradication therapies and the effects of probiotic supplementation.

Helicobacter pylori is a type of gram-negative bacteria that causes various gastric infections, which are acquired in the first years of life. The manifestation of this disease is determined by different factors like socioeconomic status, poor hygienic conditions, and overcrowding, among others. In 2021, tha Pan American Health Organization (PAHO) reported that over half of the world's population is infected by this bacterium, and 15-20% of those cases are related to the development of peptic ulcers, mucosa-associated lymphoid, and gastric cancer. The purpose of this study was to determine the frequency of Helicobacter pylori through the immunochromatographic fecal antigen test in patients of Hospital Universitario del Río, 2018-2021. It was a descriptive, retrospective, and cross-sectional study. Data was collected from the anonymized database of the results of the immunochromatographic fecal antigen test of the hospital clinical laboratory. Those results were recorded in a digital form and interpreted through simple and/or cross tabulation using the IBM SPSS Statistics Version 25 software, Microsoft Excel, and Microsoft Word. The results show that the frequency of Helicobacter pylori infection was 42%; with a predominance of the female gender (63%). Participants aged over 61 were the ones with the highest positivity rate (18%). The province of Azuay reported the highest number of positive cases (64%) and the most frequently demanded hospital services was that of outpatient care (87%).

Gastric cancer (GC) is a relevant public health issue as its incidence and mortality rates are growing worldwide. There are recognized carcinogen agents, such as obesity, tobacco, meat, alcohol consumption and some dietary protective factors. Strategies of early diagnosis through population-based surveillance programs have been demonstrated to be effective in lowering the morbidity and mortality related to GC in some countries. Indeed, the detection of early lesions is very important in order to offer minimally invasive treatments. Endoscopic resection is the gold standard for lesions with a low risk of lymph node metastasis, whereas surgical mini-invasive approaches can be considered in early lesions when endoscopy is not curative. This review outlines the role of lifestyle and prevention strategies for GC, in order to reduce the patients’ risk factors, implement the surveillance of precancerous conditions and, therefore, improve the diagnosis of early lesions. Furthermore, we summarize the available treatments for early gastric cancer.

Helicobacter pylori eradication is characterized by decreasing successful eradication rates. Although treatment failure is primarily associated with resistance to antibiotics, other unknown factors may influence the eradication outcome. This study aimed to assess the presence of the antibiotics resistance genes in H. pylori and the presence of Candida spp., which are proposed to be endosymbiotic hosts of H. pylori, in gastric biopsies of H. pylori-positive patients while simultaneously assessing their relationship. The detection and identification of Candida yeasts and the detection of mutations specific for clarithromycin and fluoroquinolones were performed by using the real-time PCR (RT-PCR) method on DNA extracted from 110 gastric biopsy samples of H. pylori-positive participants. Resistance rate to clarithromycin and fluoroquinolone was 52% and 47%, respectively. Antibiotic resistance was associated with more eradication attempts (p < 0.05). Candida species were detected in nine (8.18%) patients. Candida presence was associated with older age (p < 0.05). A high rate of antibiotic resistance was observed, while Candida presence was scarce, suggesting that endosymbiosis between H. pylori and Candida may not be a major contributing factor to the eradication failure. However, the older age favored Candida gastric mucosa colonization, which could contribute to gastric pathologies and microbiome dysbiosis.

Purpose: This cohort description presents the Nordic Helicobacter Pylori Eradication Project (NordHePEP), a population-based cohort of patients having received eradication treatment for Helicobacter pylori (HP). The cohort is created with the main purpose of examining whether and to what extent HP eradication treatment influences the risk of gastrointestinal cancer. Participants: NordHePEP includes all adults (aged ≥18 years) having been prescribed and dispensed HP eradication treatment according to the nationwide complete drug registries in any of the five Nordic countries (Denmark, Finland, Iceland, Norway, or Sweden) between 1994 and 2020 (start and end year varies between countries). We have retrieved and merged individual-level data from multiple national registries, including drug, patient, cancer, population, and death registries. Findings: The cohort includes 674,771 patients having received HP eradication treatment. During up to 23 years of follow-up, 59,292 (8.8%) participants were diagnosed with cancer (non-melanoma skin cancer excluded), whereof 15,496 (2.3%) in the gastrointestinal tract. Future plans: We will analyse HP eradication treatment in relation to gastrointestinal cancer risk. Standardised incidence ratios will be calculated as the observed cancer incidence in the cohort divided by the expected cancer incidence, derived from the background population of the corresponding age, sex, and calendar year.