RESUMEN
A bibliometric analysis of studies dedicated to autoimmune gastritis (AIG) recently published demonstrated a noteworthy surge in publications over the last three years. This can be explained by numerous publications from different regions of the world reporting the results of several studies that stimulated reassessment of our view of AIG as a precancerous condition. Follow-up studies and retrospective analyses showed that the risk of gastric cancer (GC) in AIG patients is much lower than expected if the patients ever being infected with Helicobacter pylori (H. pylori) were excluded. The low prevalence of precancerous lesions, such as the incomplete type of intestinal metaplasia, may explain the low risk of GC in AIG patients because the spasmolytic polypeptide-expressing metaplasia commonly observed in AIG does not involve clonal reprogramming of the gastric gland and can be considered as an adaptive change rather than a true precancerous lesion. However, changes in gastric secretion due to the progression of gastric atrophy during the course of AIG cause changes in the gastric mic-robiome, stimulating the growth of bacterial species such as streptococci, which may promote the development of precancerous lesions and GC. Thus, Streptococcus anginosus exhibited a robust proinflammatory response and induced the gastritis-atrophy-metaplasia-dysplasia sequence in mice, reproducing the well-established process for carcinogenesis associated with H. pylori. Prospective studies in H. pylori-naïve patients evaluating gastric microbiome changes during the long-term course of AIG might provide an explanation for the enigmatic increase in GC incidence in the last decades in younger cohorts, which has been reported in economically developed countries.
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Enfermedades Autoinmunes , Bibliometría , Mucosa Gástrica , Gastritis , Infecciones por Helicobacter , Helicobacter pylori , Lesiones Precancerosas , Neoplasias Gástricas , Neoplasias Gástricas/inmunología , Neoplasias Gástricas/patología , Neoplasias Gástricas/microbiología , Neoplasias Gástricas/epidemiología , Humanos , Gastritis/inmunología , Gastritis/microbiología , Gastritis/epidemiología , Gastritis/patología , Infecciones por Helicobacter/epidemiología , Infecciones por Helicobacter/inmunología , Infecciones por Helicobacter/microbiología , Infecciones por Helicobacter/patología , Helicobacter pylori/aislamiento & purificación , Helicobacter pylori/inmunología , Helicobacter pylori/patogenicidad , Lesiones Precancerosas/inmunología , Lesiones Precancerosas/microbiología , Lesiones Precancerosas/patología , Lesiones Precancerosas/epidemiología , Animales , Enfermedades Autoinmunes/inmunología , Enfermedades Autoinmunes/epidemiología , Mucosa Gástrica/patología , Mucosa Gástrica/inmunología , Mucosa Gástrica/microbiología , Metaplasia , Factores de Riesgo , Estómago/patología , Estómago/inmunología , Estómago/microbiología , Microbioma Gastrointestinal/inmunología , RatonesRESUMEN
Helicobacter pylori is a bacterium that may colonise and proliferate in human stomachs, leading invariably to chronic inflammation and, to a lesser extent, to peptic ulcers and cancer. The main objective of this study is to describe the epidemiology surrounding H. pylori in Nunavik's Inuit population using the 2004 and 2017 Health Surveys. Estimated prevalences were 70.9% for bacterial colonisation using a stool antigens test (SAT), 72.5% for anti-H. pylori antibodies, 12.7% for faecal occult blood in participants aged ≥ 50 and respectively of 28.4%, 11.2% and 2.4% for a prior diagnosis of colonisation, gastritis and peptic ulcer in the medical charts, with under five cases of gastric cancer reported. Variables associated with higher SAT+ prevalence were the number of household members (prevalence ratio [PR] = 1.03) and age (quadratic relationship), whereas mainly drinking municipal (PR = 0.84) and natural water (PR = 0.72) compared to bottled water, and increasing alcohol consumption (PR = 0.96) were associated with reduced prevalence. Despite current regional guidelines targeting high risk individuals in the context of high prevalence, Nunavik's health authorities must remain vigilant by following gastric cancer incidence and the rapid evolution of guidelines, while considering local realities.
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Infecciones por Helicobacter , Helicobacter pylori , Inuk , Humanos , Infecciones por Helicobacter/epidemiología , Infecciones por Helicobacter/etnología , Helicobacter pylori/aislamiento & purificación , Femenino , Persona de Mediana Edad , Adulto , Masculino , Estudios Transversales , Prevalencia , Quebec/epidemiología , Adulto Joven , Adolescente , Anciano , Regiones Árticas/epidemiología , Encuestas Epidemiológicas , Niño , Neoplasias Gástricas/epidemiología , Neoplasias Gástricas/microbiología , Gastritis/microbiología , Gastritis/epidemiología , Gastritis/etnologíaRESUMEN
BACKGROUND: Helicobacter pylori infects the stomach and/or small intestines in more than half of the human population. Infection with H. pylori is the most common cause of chronic gastritis, which can lead to more severe gastroduodenal pathologies such as peptic ulcer, mucosa-associated lymphoid tissue lymphoma, and gastric cancer. H. pylori infection is particularly concerning in Colombia in South America, where > 80% of the population is estimated to be infected with H. pylori and the rate of stomach cancer is one of the highest in the continent. RESULTS: We compared the antimicrobial susceptibility profiles and short-read genome sequences of five H. pylori isolates obtained from patients diagnosed with gastritis of varying severity (chronic gastritis, antral erosive gastritis, superficial gastritis) in Pereira, Colombia sampled in 2015. Antimicrobial susceptibility tests revealed the isolates to be resistant to at least one of the five antimicrobials tested: four isolates were resistant to metronidazole, two to clarithromycin, two to levofloxacin, and one to rifampin. All isolates were susceptible to tetracycline and amoxicillin. Comparative genome analyses revealed the presence of genes associated with efflux pump, restriction modification systems, phages and insertion sequences, and virulence genes including the cytotoxin genes cagA and vacA. The five genomes represent three novel sequence types. In the context of the Colombian and global populations, the five H. pylori isolates from Pereira were phylogenetically distant to each other but were closely related to other lineages circulating in the country. CONCLUSIONS: H. pylori from gastritis of different severity varied in their antimicrobial susceptibility profiles and genome content. This knowledge will be useful in implementing appropriate eradication treatment regimens for specific types of gastritis. Understanding the genetic and phenotypic heterogeneity in H. pylori across the geographical landscape is critical in informing health policies for effective disease prevention and management that is most effective at local and country-wide scales. This is especially important in Colombia and other South American countries that are poorly represented in global genomic surveillance studies of bacterial pathogens.
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Antibacterianos , Farmacorresistencia Bacteriana , Gastritis , Genoma Bacteriano , Infecciones por Helicobacter , Helicobacter pylori , Humanos , Helicobacter pylori/genética , Helicobacter pylori/efectos de los fármacos , Helicobacter pylori/patogenicidad , Helicobacter pylori/aislamiento & purificación , Gastritis/microbiología , Colombia , Infecciones por Helicobacter/microbiología , Antibacterianos/farmacología , Virulencia/genética , Farmacorresistencia Bacteriana/genética , Genómica , Pruebas de Sensibilidad Microbiana , Filogenia , Persona de Mediana Edad , Masculino , FemeninoRESUMEN
Introduction. Cytotoxin-associated gene A (CagA) from Helicobacter pylori is highly related to chronic gastritis. Tyrosine phosphorylation of Glu-Pro-Ile-Tyr-Ala (EPIYA) motifs from CagA determines the pathogenicity of H. pylori.Gap statement. The precise amino acid variations surrounding the EPIYA motifs and their correlation with clinical outcomes have been poorly explored.Aim. The purpose of this study was to examine the CagA 3' region polymorphism of H. pylori and its association with chronic gastritis in the Chinese population.Method. A total of 86 cagA-positive H. pylori strains were isolated from patients with chronic gastritis in two different hospitals in Beijing, PR China. Genomic DNA was extracted commercial kits, and the cagA 3' variable region of H. pylori was amplified by polymerase chain reaction (PCR). The PCR products were sequenced and analysed using the CLC Sequence Viewer, BioEdit, and WebLogo 3.Results. Two hundred and fifty-nine EPIYA motifs were identified from cagA-positive H. pylori strains. Notably, EPIYA-B exhibited a higher frequency of variation in comparison to EPIYA-A, EPIYA-C, and EPIYA-D. The prevalent sequences for East-Asian-type CagA were QVNK and TIDF, while KVNK and TIDD were most commonly observed for Western-type CagA. The CRPIA motifs of East-Asian-type CagA and Western-type CagA varied at positions 4, 6, 7, 8, and 10. CagA-ABD (73.2%) was the most prevalent type, followed by CagA-ABC (18.6%) and CagA-AB (3.4%). The ratio of CagA-ABD was observed to be higher in cases of chronic non-atrophic gastritis with erosive (NAGE) or chronic atrophic gastritis (AG) compared to chronic non-atrophic gastritis (NAG), and the difference was found to be statistically significant (χ2=59.000/64.000, P<0.001).Conclusions. The EPIYA segments of Western-type CagA and East-Asian-type CagA differ significantly and the presence of CagA-ABD may be associated with severe chronic gastritis from this study.
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Antígenos Bacterianos , Proteínas Bacterianas , Gastritis , Infecciones por Helicobacter , Helicobacter pylori , Polimorfismo Genético , Humanos , Antígenos Bacterianos/genética , Helicobacter pylori/genética , Helicobacter pylori/aislamiento & purificación , Helicobacter pylori/patogenicidad , Proteínas Bacterianas/genética , Proteínas Bacterianas/metabolismo , Gastritis/microbiología , Infecciones por Helicobacter/microbiología , Infecciones por Helicobacter/epidemiología , Masculino , Femenino , China/epidemiología , Enfermedad Crónica , Persona de Mediana Edad , Adulto , Anciano , Pueblo Asiatico/genética , Secuencias de Aminoácidos , Pueblos del Este de AsiaRESUMEN
The potential role of the transient receptor potential Vanilloid 1 (TRPV1) non-selective cation channel in gastric carcinogenesis remains unclear. The main objective of this study was to evaluate TRPV1 expression in gastric cancer (GC) and precursor lesions compared with controls. Patient inclusion was based on a retrospective review of pathology records. Patients were subdivided into five groups: Helicobacter pylori (H. pylori)-associated gastritis with gastric intestinal metaplasia (GIM) (n = 12), chronic atrophic gastritis (CAG) with GIM (n = 13), H. pylori-associated gastritis without GIM (n = 19), GC (n = 6) and controls (n = 5). TRPV1 expression was determined with immunohistochemistry and was significantly higher in patients with H. pylori-associated gastritis compared with controls (p = 0.002). TRPV1 expression was even higher in the presence of GIM compared with patients without GIM and controls (p < 0.001). There was a complete loss of TRPV1 expression in patients with GC. TRPV1 expression seems to contribute to gastric-mucosal inflammation and precursors of GC, which significantly increases in cancer precursor lesions but is completely lost in GC. These findings suggest TRPV1 expression to be a potential marker for precancerous conditions and a target for individualized treatment. Longitudinal studies are necessary to further address the role of TRPV1 in gastric carcinogenesis.
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Infecciones por Helicobacter , Neoplasias Gástricas , Canales Catiónicos TRPV , Humanos , Canales Catiónicos TRPV/metabolismo , Canales Catiónicos TRPV/genética , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patología , Masculino , Femenino , Persona de Mediana Edad , Anciano , Infecciones por Helicobacter/metabolismo , Infecciones por Helicobacter/complicaciones , Infecciones por Helicobacter/patología , Carcinogénesis/metabolismo , Carcinogénesis/patología , Estudios Retrospectivos , Lesiones Precancerosas/metabolismo , Lesiones Precancerosas/patología , Helicobacter pylori/patogenicidad , Metaplasia/metabolismo , Metaplasia/patología , Gastritis/metabolismo , Gastritis/patología , Gastritis/microbiología , Adulto , Inmunohistoquímica , Mucosa Gástrica/metabolismo , Mucosa Gástrica/patología , Gastritis Atrófica/metabolismo , Gastritis Atrófica/patologíaRESUMEN
BACKGROUND: Helicobacter pylori infection is one of the most common chronic bacterial infections, especially in developing countries. MicroRNA-148a is involved in the regulation of various genes, including Rock1, which is altered in gastric cancer. Decreased expression of mir-148a leads to tumor metastasis and increased Rock1 gene expression in gastric cancer. This study aimed to investigate the expression of these genes in biopsies collected from patients with H. pylori induced gastritis. METHODS: Informed consent forms were gotten from the studied patients with gastritis who needed endoscopy. Gastric biopsies were taken by a gastroenterologist from patients with inflammation. Rapid urease test, stool antigen detection, and histopathological staining were used to determine the H. pylori infected patients. Real time PCR was used to evaluate the miRNA and Rock1 expression levels. RESULTS: The Rock1 expression level in biopsies that were positive for H. pylori was significantly increased compared to our control gastritis group that were H. pylori-negative, but the results were not statistically significant. Moreover, the mir-148a expression level in H. pylori-positive patients with gastritis was increased compared to our control group. However, the results were not statistically significant. We did not find a significant relation between the expression levels of Rock1 and mir-148a in samples with gastritis infected or uninfected by H. pylori. This result may be due to the small sample size. CONCLUSION: We suggest that this test should be carried out with more samples, and the comparison should be done between biopsies with inflammation and no inflammation in a patient.
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Gastritis , Infecciones por Helicobacter , Helicobacter pylori , MicroARNs , Quinasas Asociadas a rho , Humanos , Gastritis/microbiología , Gastritis/patología , Gastritis/metabolismo , MicroARNs/metabolismo , MicroARNs/genética , Infecciones por Helicobacter/patología , Quinasas Asociadas a rho/metabolismo , Quinasas Asociadas a rho/genética , Helicobacter pylori/aislamiento & purificación , Biopsia , Masculino , Femenino , Persona de Mediana Edad , Adulto , Mucosa Gástrica/patología , Mucosa Gástrica/microbiología , AncianoRESUMEN
INTRODUCTION: Helicobacter pylori is a major risk factor for gastric cancer. In addition to eradication therapy, early-phase detection of gastric cancer through screening programs using high-vision endoscopy is also widely known to reduce mortality. Although European and US guidelines recommend evaluation of atrophy and intestinal metaplasia by high-vision endoscopy and pathological findings, the guideline used in Japan - the Kyoto classification of gastritis - is based on endoscopic evaluation, and recommends the grading of risk factors. This system requires classification into three endoscopic groups: H. pylori-negative, previous H. pylori infection (inactive gastritis), and current H. pylori infection (active gastritis). Major endoscopic findings in active gastritis are diffuse redness, enlarged folds, nodularity, mucosal swelling, and sticky mucus, while those in H pylori-related gastritis - irrespective of active or inactive status - are atrophy, intestinal metaplasia, and xanthoma. AREAS COVERED: This review describes the endoscopic characteristics of current H. pylori infection, and how characteristic endoscopic findings should be evaluated. EXPERT OPINION: Although the correct evaluation of endoscopic findings related to H. pylori remains necessary, if findings of possible infection are observed, it is important to diagnose infection by detection methods with high sensitivity and specificity, including the stool antigen test and urea breath test.
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Infecciones por Helicobacter , Helicobacter pylori , Humanos , Infecciones por Helicobacter/diagnóstico , Infecciones por Helicobacter/microbiología , Helicobacter pylori/aislamiento & purificación , Gastritis/microbiología , Gastritis/diagnóstico , Mucosa Gástrica/patología , Mucosa Gástrica/microbiología , Pruebas Respiratorias , Metaplasia , Gastroscopía , Valor Predictivo de las Pruebas , Neoplasias Gástricas/microbiología , Neoplasias Gástricas/diagnóstico , Neoplasias Gástricas/patologíaRESUMEN
A wealth of research indicates that superficial gastritis (SG) and atrophic gastritis (AG) are precursors to gastric cancer (GC). While Helicobacter pylori (H. pylori) has long been recognized as a key player in GC development, recent findings by Fu et al. have identified Streptococcus anginosus (S. anginosus) as an emerging pathogen that can trigger SG, AG and GC. S. anginosus, a gram-positive coccus, leverages its surface protein T. pallidum membrane protein C (TMPC) to engage with the annexin A2 (ANXA2) receptor of gastric epithelial cells, facilitating its colonization and invasion in the gastric mucosa. This leads to an upregulation of proinflammatory chemokines Ccl20 and Ccl8, causing prolonged effects on gastric barrier function and microbiota homeostasis, leading to SG. Moreover, these bacteria activate the mitogen-activated protein kinase (MAPK) signaling pathway, which is associated with the development of AG and GC. Importantly, inhibiting TMPC or knocking down ANXA2 can reduce S. anginosus colonization and invasion, lowering the chances of SG, AG, and GC. This paper highlights the molecular mechanisms of S. anginosus in SG, AG and GC, emphasizing the importance of a multi-pathogen strategy in gastric disease management and the need for further investigation into the role of S. anginosus in GC progression.
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Gastritis Atrófica , Neoplasias Gástricas , Streptococcus anginosus , Humanos , Neoplasias Gástricas/microbiología , Neoplasias Gástricas/patología , Gastritis Atrófica/microbiología , Gastritis Atrófica/patología , Anexina A2/metabolismo , Infecciones Estreptocócicas/inmunología , Infecciones Estreptocócicas/microbiología , Mucosa Gástrica/microbiología , Mucosa Gástrica/patología , Mucosa Gástrica/metabolismo , Gastritis/microbiología , Gastritis/patología , Gastritis/inmunología , AnimalesRESUMEN
INTRODUCTION: Cytokeratins (CKs) have been associated with precancerous and cancerous gastric lesions in patients with Helicobacter pylori-associated chronic gastritis, making them useful for diagnosing epithelial tumors. METHODOLOGY: A retrospective study was conducted utilizing 200 formalin-fixed paraffin-embedded gastric biopsy samples collected from the lesser curvature of the stomach. Samples from the control group, patients with H. pylori infection, and patients with H. pylori-associated gastritis, with complete and incomplete intestinal metaplasia (IM) were immunostained. Monoclonal antibodies were utilized to determine the expression of CK7, CK20, and Ki-67. RESULTS: Patients infected with H. pylori had strong CK20 expression on the surface, and weak CK7 expression on the surface and deep glands; while non-specific chronic gastritis patients had weak focal CK7 expression and strong CK20 expression. The normal gastric mucosa of patients in the control group had relatively weak CK7 expression, restricted to a few cells in the neck and deep glands. CK20 showed diffuse strong reactivity on the surface. On the other hand, patients with complete IM showed a CK7 staining pattern that was either negative or weakly focal on the surface and crypts associated with diffuse surface CK20 and focal crypt staining corresponding to gastric type IM. The Ki67 proliferating index was low (≤ 15%) in H. pylori infected patients, high (> 30%) in patients with incomplete IM, and intermediate (16-30%) in patients with complete IM. CONCLUSIONS: These results indicate a significant link between the expressions of CK7/CK20 and Ki67 in patients afflicted with H. pylori and IM.
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Gastritis , Infecciones por Helicobacter , Helicobacter pylori , Queratina-20 , Queratina-7 , Antígeno Ki-67 , Metaplasia , Adulto , Anciano , Femenino , Humanos , Masculino , Persona de Mediana Edad , Biopsia , Mucosa Gástrica/patología , Mucosa Gástrica/microbiología , Mucosa Gástrica/metabolismo , Gastritis/microbiología , Gastritis/patología , Infecciones por Helicobacter/patología , Infecciones por Helicobacter/microbiología , Inmunohistoquímica , Queratina-20/metabolismo , Queratina-7/metabolismo , Antígeno Ki-67/metabolismo , Metaplasia/patología , Metaplasia/microbiología , Estudios RetrospectivosRESUMEN
The changes in tongue coating metabolites in patients with chronic gastritis (CG) under different gastroscopy indicators were analyzed, and these metabolites were screened for potential non-invasive biomarkers to assist in the diagnosis of chronic gastritis. The technology of gas chromatography and liquid chromatography combined with mass spectrometry has been used to more comprehensively detect tongue coating metabolites of 350 CG patients. Spearman correlation analysis and random forest algorithm were used to screen metabolites that can serve as potential biomarkers. Compared with healthy individuals, CG group showed significant changes in the content of 101 metabolites, with an increase in the content of 54 metabolites and a decrease in the content of 47 metabolites. These differential metabolites are mainly composed of 47 lipids and lipid like substances. 1 metabolite was associated with bile reflux, 1 metabolite was associated with gastric mucosal erosion, 10 metabolites were associated with atrophy, 10 metabolites were associated with intestinal metaplasia, and 3 metabolites were associated with Helicobacter pylori infection. The ROC model composed of 5 metabolites can distinguish between CG group and healthy individuals, with an accuracy of 95.4%. The ROC model composed of 5,6-Dihydroxyindole can distinguish between chronic superficial gastritis group and chronic atrophic gastritis group, with an accuracy of 75.3%. The lipids and lipid like metabolites were the main abnormal metabolites in patients with chronic gastritis. It was worth noting that the content of Sphinganine 1-phase, 4-Ipomenol, and Nervonic acid in tongue coating increased, and the content of 1-Methyladenosine and 3-Hydroxycapric acid decreased, which helped to identify CG patients. The decrease in the content of 5,6-dihydroxyindole reminded patients that the development trend of CG was shifting from superficial to atrophic or even intestinal metaplasia. The detection of these metabolic markers of tongue coating was expected to be developed as a non-invasive and convenient technology in the future to assist us in monitoring and diagnosing the occurrence and development of CG.
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Biomarcadores , Gastritis , Lípidos , Lengua , Humanos , Gastritis/metabolismo , Gastritis/diagnóstico , Gastritis/microbiología , Biomarcadores/metabolismo , Biomarcadores/análisis , Masculino , Femenino , Lengua/metabolismo , Lengua/patología , Persona de Mediana Edad , Adulto , Lípidos/análisis , Enfermedad Crónica , Anciano , Infecciones por Helicobacter/metabolismo , Infecciones por Helicobacter/diagnósticoRESUMEN
BACKGROUND: Chronic gastritis caused by Helicobacter pylori (Hp) infection is a common gastrointestinal disorder. Despite the high prevalence of Hp infection and chronic gastritis in the Tibetan Plateau, there is a lack of studies elucidating the influence of plateau hypoxia on Hp-induced gastritis. This study aimed to investigate the impact of high-altitude hypoxia on Hp-induced gastritis, particularly focusing on pathological manifestations and inflammatory responses. METHODS: This study was conducted from July 2023 to March 2024 at the Department of Gastroenterology, Affiliated Hospital of Qinghai University. Ninety patients diagnosed with chronic gastritis were enrolled in the study and divided into four groups based on their residential altitude and Hp infection status. Data on endoscopic and pathological characteristics were collected, along with serum oxidative stress and inflammatory markers. RESULTS: Patients with Hp gastritis exhibit distinctive features in the gastric mucosa, including diffuse erythema, enlarged folds, and white turbid mucus during endoscopy. Notably, individuals with Hp gastritis at high altitudes show a higher prevalence of diffuse erythema and enlarged folds. Pathological analysis reveals that these patients have elevated gastric mucosal inflammation scores and increased chronic and active inflammation. Furthermore, individuals with Hp gastritis at high altitudes demonstrate elevated levels of serum TNF-α, IL-1ß, IL-6, and MDA, as well as reduced serum SOD and GSH-Px activities. CONCLUSIONS: High-altitude hypoxia may exacerbate gastric mucosal damage by enhancing oxidative stress and inflammatory response induced by Hp infection.
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Altitud , Gastritis , Infecciones por Helicobacter , Helicobacter pylori , Estrés Oxidativo , Humanos , Gastritis/microbiología , Gastritis/patología , Masculino , Infecciones por Helicobacter/complicaciones , Infecciones por Helicobacter/patología , Femenino , Adulto , Persona de Mediana Edad , Hipoxia , Inflamación , Adulto Joven , Mucosa Gástrica/patología , Mucosa Gástrica/microbiología , Tibet/epidemiologíaRESUMEN
BACKGROUND: Map-like redness is a newly identified endoscopic risk factor for gastric cancer in patients who received Helicobacter pylori eradication therapy. However, the incidence rate of map-like redness in patients who received eradication, and the risk factors for the development of map-like redness remain unclear. We hence aimed to investigate the incidence rate of map-like redness at 1-year post H. pylori eradication, and evaluated its associations with map-like redness and gastric cancer in relation with gastric condition. MATERIALS AND METHODS: Endoscopic severity of gastritis and map-like redness were retrospectively evaluated according to the Kyoto Classification of Gastritis in patients who had undergone endoscopy before and after H. pylori eradication therapy. RESULTS: The incidence rate of map-like redness for all 328 patients at a mean of 1.2 ± 0.6 years after eradication was 25.3% (95% confidence interval [CI]: 20.7%-30.4%). Patients who developed map-like redness were older, had more severe atrophy and intestinal metaplasia, a higher total score of the Kyoto Classification of Gastritis both before and after eradication, and a higher rate of gastric cancer history than patients who did not have map-like redness. On multivariate analysis, risk of map-like redness was increased in patients with intestinal metaplasia (odds ratio [OR]: 2.794, 95% CI: 1.155-6.757) and taking acid inhibitors (OR: 1.948, 95% CI: 1.070-3.547). Characteristics of H. pylori-positive patients with gastric cancer history were patients who were older (OR: 1.033, 95% CI: 1.001-1.066), taking acid inhibitors (OR: 4.456, 95% CI: 2.340-8.484), and with occurrence of map-like redness after eradication therapy (OR: 2.432, 95% CI: 1.264-4.679). CONCLUSIONS: Map-like redness is observed in one fourth of patients at 1-year post eradication. Patients who developed map-like redness were found to have severe intestinal metaplasia and taking acid inhibitors, and hence such patients require increased attention at surveillance endoscopy.
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Gastritis , Infecciones por Helicobacter , Helicobacter pylori , Humanos , Infecciones por Helicobacter/tratamiento farmacológico , Infecciones por Helicobacter/microbiología , Infecciones por Helicobacter/complicaciones , Masculino , Femenino , Persona de Mediana Edad , Estudios Retrospectivos , Factores de Riesgo , Anciano , Gastritis/microbiología , Gastritis/tratamiento farmacológico , Helicobacter pylori/efectos de los fármacos , Adulto , Neoplasias Gástricas/tratamiento farmacológico , Neoplasias Gástricas/epidemiología , Incidencia , Antibacterianos/uso terapéutico , Antibacterianos/efectos adversosRESUMEN
BACKGROUND: Africa has consistently had the highest prevalence (70.1%) of H. pylori, and this has led to significant cases of dyspepsia, gastric cancers, and upper gastrointestinal bleeding. However, most studies have used sero-prevalence, which might not give the current state of the infection. Among the tests, the stool antigen test is simple, quick, and effective. The study aimed to determine the feco-prevalence, endoscopic pattern, and associated factors of H. pylori infection among symptomatic adult patients in Northern Tanzania. MATERIALS AND METHODS: A hospital-based, cross-sectional study was conducted from October 2022 to April 2023 among adults attending the gastroenterology clinic at Kilimanjaro Chistian Medical Centre. A systematic random sampling was used to select the participants with indications of undergoing esophagogastroduodenoscopy. Questionnaires, stool and blood samples, and endoscopy were used to collect variable data. Numerical and categorical variables were summarized into narrations and tables. Logistic regression was used to assess the factors associated with H. pylori. RESULTS: The feco-prevalence of H. pylori was 43.4%. Chronic gastritis (51.1%) was the most common endoscopic pattern, whereas duodenal ulcers and gastric ulcers were significantly associated with H. pylori infection. Increasing in age (p <0.001) and blood group (p <0.001) were significantly associated with H. pylori infection in the adjusted analysis. CONCLUSION: The feco-prevalence of H. pylori is high in this setting. H. pylori stool antigen can be used as the initial workup for symptomatic patients before the initiation of proton pump inhibitors. Additionally, due to other causes of dyspepsia, it is advised that H. pylori stool antigen testing be part of the initial evaluation and esophagogastroduodenoscopy be considered in the absence of other alarm symptoms if symptoms persist despite an appropriate trial of medical therapy.
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Heces , Infecciones por Helicobacter , Helicobacter pylori , Humanos , Infecciones por Helicobacter/epidemiología , Infecciones por Helicobacter/diagnóstico , Tanzanía/epidemiología , Masculino , Femenino , Adulto , Persona de Mediana Edad , Prevalencia , Estudios Transversales , Heces/microbiología , Anciano , Endoscopía del Sistema Digestivo , Gastritis/epidemiología , Gastritis/microbiología , Adulto Joven , Dispepsia/epidemiología , Dispepsia/microbiologíaRESUMEN
Objective To investigate whether vitamin D3 (VD3) can alleviate Helicobacter pylori (Hp) infection by reducing blood lipids and inhibiting the Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) signaling pathway. Methods High-cholesterol mouse model and Hp infected mouse model were established. Each was treated with VD3 via oral administration for 8 weeks. Real-time quantitative PCR was used to detect the expression of vitamin D receptor (VDR), insulin-induced gene 2 (Insig-2), and gastrin mRNA. Western blot analysis was used to examine the expression of JAK, STAT3, and cyclooxygenase-2 (COX2) proteins in gastric tissues. Biochemical analyses were performed to measure serum cholesterol levels, and ELISA was utilized to evaluate serum gastrin, interleukin 6 (IL-6), and IL-8 levels, along with histopathological examination of liver and gastric tissues using HE staining. Results After oral administration of VD3, the levels of VDR and Insig-2 in mouse liver tissue significantly increased in the high cholesterol group and the high cholesterol combined with Hp infection group. And the expression of serum gastrin decreased. The expression of JAK, STAT3 in gastric tissues reduced, as did the expression of COX2. Serum cholesterol levels decreased, with no significant changes in IL-6 levels, but a reduction in IL-8 levels. Compared to the control group, the high cholesterol combined with Hp infection group showed reduced hepatic ballooning degeneration and alleviated gastric tissue inflammation. In addition, inflammation in gastric tissue was also reduced in the cholesterol group and the Hp infection group. Conclusion VD3 alleviates gastritis by enhancing the activity of VDR in liver tissues, blocking the JAK/STAT3 signaling pathway, and inhibiting the expression of inflammatory factors.
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Colecalciferol , Gastritis , Infecciones por Helicobacter , Helicobacter pylori , Hipercolesterolemia , Quinasas Janus , Hígado , Receptores de Calcitriol , Factor de Transcripción STAT3 , Transducción de Señal , Animales , Infecciones por Helicobacter/tratamiento farmacológico , Infecciones por Helicobacter/metabolismo , Factor de Transcripción STAT3/metabolismo , Colecalciferol/farmacología , Colecalciferol/administración & dosificación , Receptores de Calcitriol/metabolismo , Receptores de Calcitriol/genética , Transducción de Señal/efectos de los fármacos , Hígado/metabolismo , Hígado/efectos de los fármacos , Hígado/patología , Ratones , Quinasas Janus/metabolismo , Gastritis/tratamiento farmacológico , Gastritis/metabolismo , Gastritis/microbiología , Masculino , Hipercolesterolemia/metabolismo , Hipercolesterolemia/tratamiento farmacológicoRESUMEN
BACKGROUND: Helicobacter pylori eradication therapy based on antimicrobial susceptibility in Vietnamese children currently get low efficiency. There are causes of treatment failure, among host genetic factors namely MDR1 C3435T and CYP2C19 affect the absorption and metabolism of proton pump inhibitors - a crucial component of eradication therapy. The study aimed to investigate the effect of MDR1 C3435T and CYP2C19 genetic polymorphisms on the cure rate. METHODS: 207 pediatric patients with gastritis and peptic ulcer infecting Helicobacter pylori completed the eradication therapy based on antimicrobial susceptibility with proton pump inhibitor esomeprazole. Eradication efficacy was assessed after at least 4 weeks by the urease breath test. MDR1 C3435T genetic polymorphism and CYP2C19 genotype were determined using a sequencing method based on Sanger's principle. RESULTS: Among 207 children recruited in this study, the ratio of CYP2C19 EM, IM, and PM phenotypes was 40.1%, 46.4%, and 16.9%, respectively. The patient with MDR1 3435 C/C polymorphism accounted for 43.0%, MDR1 3435 C/T was 40.1%, and MDR1 3435T/T was 16.9%. The cure rate of Helicobacter pylori infection in patients with CYP2C19 EM genotype was 78.3%; 83.3% of those with the IM genotype, and PM genotype was 96,4% (p = 0.07). Successful eradication rates for Helicobacter pylori were 85.4%, 86.7%, and 68.6% in patients with the MDR1 3435 C/C, C/T, and T/T, respectively (p = 0.02). Multiple logistic regression analysis found that MDR1 C3435T genetic polymorphisms of patients were significant independent risk factors for treatment failure, and CYP2C19 genotype did not affect Helicobacter pylori eradication. CONCLUSIONS: The Helicobacter pylori eradication rates by regimens based on antibiotic susceptibility and esomeprazole were not significantly different between the CYP2C19 phenotypes. The MDR1 C3435T polymorphism is one of the factors impacting Helicobacter pylori eradication results in children.
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Subfamilia B de Transportador de Casetes de Unión a ATP , Citocromo P-450 CYP2C19 , Gastritis , Infecciones por Helicobacter , Helicobacter pylori , Úlcera Péptica , Inhibidores de la Bomba de Protones , Humanos , Citocromo P-450 CYP2C19/genética , Infecciones por Helicobacter/tratamiento farmacológico , Infecciones por Helicobacter/genética , Helicobacter pylori/efectos de los fármacos , Niño , Masculino , Femenino , Vietnam , Gastritis/tratamiento farmacológico , Gastritis/microbiología , Gastritis/genética , Úlcera Péptica/tratamiento farmacológico , Úlcera Péptica/genética , Úlcera Péptica/microbiología , Subfamilia B de Transportador de Casetes de Unión a ATP/genética , Inhibidores de la Bomba de Protones/uso terapéutico , Adolescente , Preescolar , Genotipo , Polimorfismo Genético , Resultado del Tratamiento , Esomeprazol/uso terapéutico , Antibacterianos/uso terapéuticoRESUMEN
BACKGROUND: The requirement for routine biopsy sampling in esophagogastroduodenoscopy (EGD) with normal endoscopic findings is a subject of debate. In this study, patients who had normal endoscopic findings in EGD and underwent biopsy sampling were retrospectively analyzed. METHODS: This single-center retrospective cohort study included 671 patients who underwent EGD between 2021 and 2023 in the Sisli Hamidiye Etfal Training and Research Hospital Surgical Endoscopy Unit. All patients had normal endoscopic findings and a sampling biopsy was performed on all patients included. Patients were evaluated based on demographic and clinicopathologic findings. This study was registered to ClinicalTrials.gov (NCT06269380). RESULTS: Two hundred sixty patients (38.7%) have abnormal histopathologic findings. Helicobacter pylori positivity was detected in 200 (29.8%) patients. Intestinal metaplasia (IM) was present in 80 of 260 patients (30.8%). The frequency of IM was higher in older age groups and cases with mild gastritis ( P <0.001). The frequency and severity of gastritis were associated with increased H. pylori positivity and density ( P <0.001). CONCLUSIONS: The biopsy sampling may contribute to the diagnosis and treatment process in cases where normal endoscopic findings are observed during EGD.
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Endoscopía del Sistema Digestivo , Gastritis , Infecciones por Helicobacter , Helicobacter pylori , Humanos , Estudios Retrospectivos , Femenino , Masculino , Persona de Mediana Edad , Biopsia/métodos , Endoscopía del Sistema Digestivo/métodos , Infecciones por Helicobacter/patología , Infecciones por Helicobacter/diagnóstico , Helicobacter pylori/aislamiento & purificación , Adulto , Gastritis/patología , Gastritis/microbiología , Gastritis/diagnóstico , Anciano , Antro Pilórico/patología , Antro Pilórico/microbiología , Metaplasia/patología , Adulto JovenRESUMEN
Immune-related adverse events (irAEs) are complications of the use of immune checkpoint inhibitors (ICIs). ICI-associated gastritis is one of the main irAEs. The gastric microbiota is often related to the occurrence and development of many gastric diseases. Gastric microbiota adjustment may be used to treat gastric disorders in the future. Faecal microbiota transplantation can alter the gut microbiota of patients and has been used for treating ICI-associated colitis. Therefore, we propose gastric microbiota transplantation as a supplementary treatment for patients with ICI-associated gastritis who do not respond well to conventional therapy.
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Trasplante de Microbiota Fecal , Gastritis , Microbioma Gastrointestinal , Inhibidores de Puntos de Control Inmunológico , Humanos , Trasplante de Microbiota Fecal/métodos , Trasplante de Microbiota Fecal/efectos adversos , Mucosa Gástrica/microbiología , Mucosa Gástrica/inmunología , Mucosa Gástrica/patología , Mucosa Gástrica/efectos de los fármacos , Gastritis/microbiología , Gastritis/inmunología , Gastritis/terapia , Gastritis/inducido químicamente , Microbioma Gastrointestinal/inmunología , Microbioma Gastrointestinal/efectos de los fármacos , Inhibidores de Puntos de Control Inmunológico/efectos adversos , Estómago/microbiología , Estómago/inmunología , Estómago/cirugía , Resultado del TratamientoRESUMEN
Aim: Understanding molecular mechanisms of Helicobacter pylori (H. pylori)-induced inflammation is important for developing new therapeutic strategies for gastrointestinal diseases.Materials & methods: We designed an H. pylori-neutrophil infection model and explored the effects of H. pylori infection on neutrophils.Results: H. pylori infected neutrophils showed a low level of apoptosis. H. pylori stimulation activated the NACHT/LRR/PYD domain-containing protein 3 (NLRP3)-gasdermin-D (GSDMD) pathway for interleukin (IL)-1ß secretion. However, IL-1ß secretion was not completely dependent on GSDMD, as inhibition of autophagy significantly reduced IL-1ß release, and autophagy-related molecules were significantly upregulated in H. pylori-infected neutrophils.Conclusion: Therefore, H. pylori infection inhibits neutrophils apoptosis and induces IL-1ß secretion through autophagy. These findings may be utilized to formulate therapeutic strategies against H. pylori mediated chronic gastritis.
[Box: see text].
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Apoptosis , Autofagia , Infecciones por Helicobacter , Helicobacter pylori , Inflamación , Interleucina-1beta , Neutrófilos , Neutrófilos/inmunología , Neutrófilos/metabolismo , Infecciones por Helicobacter/microbiología , Infecciones por Helicobacter/inmunología , Infecciones por Helicobacter/patología , Interleucina-1beta/metabolismo , Humanos , Inflamación/metabolismo , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismo , Proteínas de Unión a Fosfato/metabolismo , Proteínas de Unión a Fosfato/genética , Péptidos y Proteínas de Señalización Intracelular/metabolismo , Péptidos y Proteínas de Señalización Intracelular/genética , Gastritis/microbiología , Gastritis/patología , Gastritis/inmunología , AnimalesRESUMEN
Trained immunity is a concept in immunology in which innate immune cells, such as monocytes and macrophages, exhibit enhanced responsiveness and memory-like characteristics following initial contact with a pathogenic stimulus that may promote a more effective immune defense following subsequent contact with the same pathogen. Helicobacter pylori, a bacterium that colonizes the stomach lining, is etiologically associated with various gastrointestinal diseases, including gastritis, peptic ulcer, gastric adenocarcinoma, MALT lymphoma, and extra gastric disorders. It has been demonstrated that repeated exposure to H. pylori can induce trained immunity in the innate immune cells of the gastric mucosa, which become more responsive and better able to respond to subsequent H. pylori infections. However, interactions between H. pylori and trained immunity are intricate and produce both beneficial and detrimental effects. H. pylori infection is characterized histologically as the presence of both an acute and chronic inflammatory response called acute-on-chronic inflammation, or gastritis. The clinical outcomes of ongoing inflammation include intestinal metaplasia, gastric atrophy, and dysplasia. These same mechanisms may also reduce immunotolerance and trigger autoimmune pathologies in the host. This review focuses on the relationship between trained immunity and H. pylori and underscores the dynamic interplay between the immune system and the pathogen in the context of gastric colonization and inflammation.