RESUMO
OBJECTIVE: To investigate the clinical potential and safety of Moluodan to reverse gastric precancerous lesions. METHODS: Patients aged 18-70 years diagnosed with moderate-to-severe atrophy and/or moderate-to-severe intestinal metaplasia, with or without low-grade dysplasia, and negative for Helicobacter pylori were recruited in this randomized, double-blind, parallel-controlled trial. The primary outcome was the improvement of global histological diagnosis at 1-year follow-up endoscopy using the operative link for gastritis assessment, the operative link for gastric intestinal metaplasia assessment, and the disappearance rate of dysplasia. RESULTS: Between November 3, 2017 and January 27, 2021, 166 subjects were randomly assigned to the Moluodan group, 168 to the folic acid group, 84 to the combination group, and 84 to the high-dose Moluodan group. The improvement in global histological diagnosis was achieved in 60 (39.5%) subjects receiving Moluodan, 59 (37.8%) receiving folic acid, 26 (32.1%) receiving the combined drugs, and 36 (47.4%) receiving high-dose Moluodan. Moluodan was non-inferior to folic acid (95% confidence interval: -9.2 to 12.5; P = 0.02). High-dose Moluodan had a trend for better protective efficacy, though there was no statistical significance. The disappearance rate of dysplasia was 82.8% in the Moluodan group, which was superior to folic acid (53.9%; P = 0.006). No drug-related serious adverse events were observed. CONCLUSIONS: One pack of Moluodan three times daily for 1 year was safe and effective in reversing gastric precancerous lesions, especially dysplasia. Doubling its dose showed a better efficacy trend.
Assuntos
Medicamentos de Ervas Chinesas , Gastrite Atrófica , Infecções por Helicobacter , Helicobacter pylori , Lesões Pré-Cancerosas , Neoplasias Gástricas , Humanos , Neoplasias Gástricas/tratamento farmacológico , Neoplasias Gástricas/patologia , Gastrite Atrófica/tratamento farmacológico , Gastrite Atrófica/patologia , Infecções por Helicobacter/complicações , Infecções por Helicobacter/tratamento farmacológico , Lesões Pré-Cancerosas/tratamento farmacológico , Lesões Pré-Cancerosas/patologia , Metaplasia , Ácido Fólico/uso terapêutico , Mucosa Gástrica/patologiaRESUMO
BACKGROUND & AIMS: Potassium-competitive acid blockers (PCABs) have been increasingly used to treat upper gastrointestinal disorders, replacing proton pump inhibitors (PPIs). Whereas PPIs are associated with an increased risk of gastric cancer (GC) after Helicobacter pylori (Hp) eradication, it is uncertain whether PCABs carry the same risk. METHODS: Using a population-based claims database in Japan, we identified patients who were prescribed a clarithromycin-based first regimen of Hp eradication between 2015 and 2018. Patients who failed this regimen and those diagnosed with GC before or within 1 year after Hp eradication were excluded. We compared GC incidence between PCAB users and histamine type-2 receptor antagonist (H2RA) users, matching them on the basis of propensity scores calculated with considerations for age, sex, smoking, alcohol consumption, comorbidities, and co-administered medications. PCABs included only vonoprazan in this study. RESULTS: Among 54,055 patients, 568 (1.05%) developed GC during the follow-up period (mean, 3.65 years). The cumulative incidence of GC was 1.64% at 3 years, 2.02% at 4 years, and 2.36% at 5 years in PCAB users and 0.71% at 3 years, 1.04% at 4 years, and 1.22% at 5 years in H2RA users. The use of PCABs was associated with a higher GC risk (matched hazard ratio, 1.92; 95% confidence interval, 1.13-3.25; P = .016). Longer PCAB use and high-dose PCAB use were significantly associated with higher incidence of GC. Sensitivity analyses showed the risk of GC incidence among PCAB users was comparable with that of PPI users. CONCLUSIONS: The use of PCABs was associated with an increased risk of GC among Hp-eradicated patients, with duration/dose response effects.
Assuntos
Infecções por Helicobacter , Inibidores da Bomba de Prótons , Pirróis , Neoplasias Gástricas , Sulfonamidas , Humanos , Masculino , Feminino , Neoplasias Gástricas/epidemiologia , Infecções por Helicobacter/complicações , Pessoa de Meia-Idade , Japão/epidemiologia , Sulfonamidas/efeitos adversos , Sulfonamidas/uso terapêutico , Idoso , Incidência , Pirróis/efeitos adversos , Pirróis/uso terapêutico , Inibidores da Bomba de Prótons/efeitos adversos , Inibidores da Bomba de Prótons/administração & dosagem , Helicobacter pylori , Antagonistas dos Receptores H2 da Histamina/efeitos adversos , Antagonistas dos Receptores H2 da Histamina/uso terapêutico , Antagonistas dos Receptores H2 da Histamina/administração & dosagem , Estudos Retrospectivos , Adulto , Medição de Risco , Fatores de Risco , Antibacterianos/efeitos adversos , Antibacterianos/uso terapêuticoRESUMO
Objective: To study the association of H. pylori infection with colorectal adenomas. Methods: Web searches of PubMed, Embase, and Scopus databases for randomized controlled trials, class-experimental studies, and cohort studies on the association between H. pylori and colorectal adenomas were performed from May 2000 to May 2023. Literature was screened based on inclusion and exclusion criteria, data were extracted and evaluated for quality, and statistical analyses were performed using RevMan 5.2 software. Results: A total of 15 studies were included, and meta-analysis showed a statistically significant difference between colorectal neoplastic polyp cases in the H. pylori-positive and H. pylori-negative groups [OR=1.80, 95%CI: (1.31, 2.47), P < .01, I2 = 95%]. Analysis based on subgroups of different H. pylori detection methods showed that the correlation between H. pylori infection and colorectal polyp incidence is not affected by their detection methods, with serological detection subgroup: [OR=0.13, 95%CI: (0.05, 0.21), P < .01, I2 = 88%], and non-serological detection subgroup: [OR=0.13, 95%CI: (0.04, 0.22), P < .01, I2 = 95%]. Subgroup analysis of pathological types showed that H. pylori infection is not significantly associated with the development of non-neoplastic polyps [OR=1.47, 95%CI: 0.98-2.22, P = .06], whereas it is correlated with the development of neoplastic polyps [95%CI: 1.69-3.22, P < .01]. In the subgroup analysis of geographic differences in the population, H. pylori infection was correlated with the development of colorectal polyps in different geographic populations (P < .01). Conclusion: H. pylori infection is a risk factor for colorectal polyp neoplasia, its infection is associated with colorectal neoplasia, and the correlation is not affected by the different methods of H. pylori detection and the different geographic regions of the population.
Assuntos
Neoplasias Colorretais , Infecções por Helicobacter , Helicobacter pylori , Humanos , Infecções por Helicobacter/complicações , Infecções por Helicobacter/epidemiologia , Neoplasias Colorretais/microbiologia , Neoplasias Colorretais/epidemiologia , Helicobacter pylori/patogenicidade , Fatores de Risco , Adenoma/epidemiologia , Adenoma/microbiologiaRESUMO
BACKGROUND/AIMS: Upper gastrointestinal bleeding (UGIB) is a frequent medical issue. The primary risk factors for bleeding peptic ulcers are Helicobacter pylori infection and non-steroidal anti-inflammatory drugs. The association between acute gastric/duodenal ulcer and opium use has been previously proposed; however, there is no available data on endoscopic findings of patients with acute UGIB who use opium. MATERIALS AND METHODS: In the present descriptive cross-sectional study, endoscopic data of 50 consecutive patients with oral opium use and 50 consecutive patients without any opium use who were admitted for UGIB were recorded. The size (5-10 mm, 11-20 mm, or more than 20 mm), number (single, double, or multiple), and location of the ulcers (esophagus, gastric corpus including the fundus and body, antrum, angulus, or duodenum) were examined by endoscopy in both groups. RESULTS: Three or more ulcers were observed in 46% and 16% of patients with oral opium use and without opium use, respectively (P-value = 0.001). The rate of giant ulcers (> 20 mm) was significantly higher in patients who used oral opium (40% vs. 12%; P-value = 0.007). Esophageal ulcers were also more common in oral opium users (30%) than non-users (8%) with UGIB (P-value = 0.01). Nevertheless, the location of the ulcers between the two groups generally was not statistically different. CONCLUSIONS: This study has demonstrated that multiple, large peptic ulcers in GIB are potential complications of oral opium use. This could aid the needed modifications in the treatment protocol for these patients.
Assuntos
Úlcera Duodenal , Infecções por Helicobacter , Helicobacter pylori , Dependência de Ópio , Úlcera Péptica , Úlcera Gástrica , Humanos , Ópio/efeitos adversos , Úlcera , Estudos Transversais , Infecções por Helicobacter/complicações , Úlcera Péptica/complicações , Hemorragia Gastrointestinal/induzido quimicamente , Úlcera Duodenal/complicações , Úlcera Gástrica/complicaçõesRESUMO
The progression of any disease and its outcomes depend on the complicated interaction between pathogens, host and environmental factors. Thus, complete knowledge of bacterial toxins involved in pathogenesis is necessary to develop diagnostic methods and alternative therapies, including vaccines. This review summarizes recently employed biomarkers to diagnose the presence of Helicobacter pylori bacteria. The authors review distinct types of disease-associated biomarkers such as urease, DNA, miRNA, aptamers and bacteriophages that can be utilized as targets to detect Helicobacter pylori and, moreover, gastric cancer in its early stage. A detailed explanation is also given in the context of the recent utilization of these biomarkers in the development of a highly specific and sensitive biosensing platform.
Assuntos
Infecções por Helicobacter , Helicobacter pylori , Neoplasias Gástricas , Humanos , Helicobacter pylori/genética , Neoplasias Gástricas/diagnóstico , Infecções por Helicobacter/diagnóstico , Infecções por Helicobacter/complicações , BiomarcadoresRESUMO
OBJECTIVE: The aim of this study was to determine whether serum vitamin D levels are associated with H. pylori infection and whether low serum vitamin D levels are an independent risk factor for H. pylori infection. METHODS: We conducted a retrospective analysis of a multicenter cohort study from 2017 to 2019. A total of 415 H. pylori+ patients and 257 H. pylori- patients aged between 18 and 75 years with both 13 C-urea breath test and serum vitamin D level results were included from four hospitals. A questionnaire was used to collect information on potential factors influencing H. pylori infection. RESULTS: Serum vitamin D levels were significantly lower in the H. pylori+ group than in the H. pylori- group (16.7 ± 6.6 ng/ml vs. 19.2 ± 8.0 ng/ml, p < 0.05). Using a cutoff value of 20 ng/ml, the H. pylori infection rate was significantly higher in the vitamin D-deficient group (< 20 ng/ml) than in the vitamin D-nondeficiency group (≥ 20 ng/ml) (66.5% vs. 51.0%, p < 0.001). Ordered logistic regression analysis showed that serum vitamin D levels < 20 ng/ml (OR: 1.652, 95% CI: 1.160-2.351, p = 0.005), higher education levels (OR: 1.774, 95% CI: 1.483-2.119, p < 0.001), family size ≥ 4 (OR: 1.516, 95% CI: 1.081-2.123, p = 0.016), and lower annual income (OR: 1.508, 95% CI: 1.289-1.766, p < 0.001) were independent risk factors for H. pylori infection. CONCLUSION: Lower serum vitamin D levels may be associated with an increased risk of H. pylori infection, and lower serum vitamin D levels are an independent risk factor for increasing H. pylori infection rates. Randomized controlled trials are needed to determine whether supplementation with vitamin D can reduce H. pylori infection rates.
Assuntos
Infecções por Helicobacter , Helicobacter pylori , Adolescente , Adulto , Idoso , Humanos , Pessoa de Meia-Idade , Adulto Jovem , Estudos de Coortes , Infecções por Helicobacter/complicações , Estudos Retrospectivos , Vitamina D , Estudos Multicêntricos como AssuntoRESUMO
Observational studies have reported a correlation between Helicobacter pylori infection and colorectal cancer (CRC); however, the underlying cause has remained unclear. This research was aimed at determining whether there is a correlation between H. pylori infection and CRC by measuring the prevalence of H. pylori CagA antibodies and VacA antibodies. Using data from many genome-wide association studies (GWAS), we conducted a Mendelian randomization (MR) study with two sample GWAS. Then, we used bidirectional MR to evaluate the association between H. pylori infection and CRC for identifying causation. The most common method of analysis was the inverse variance-weighted technique. In addition, we performed supplementary analyses using the weighted median technique and MR-Egger regression. Horizontal pleiotropic outliers were identified and corrected using the MR Pleiotropy RESidual Sum and Outlier (MR-PRESSO) method. Genetically predicted anti-H. pylori IgG seropositivity was not causally associated with CRC [odds ratio (OR): 1.12; 95% confidence interval (CI): 0.98-1.27, P = 0.08] and neither were H. pylori VacA antibody levels (OR = 0.96, 95% CI: 0.90-1.02, P = 0.25) or H. pylori CagA antibody levels (OR = 1.00, 95% CI: 0.93-1.07, P = 0.92). Furthermore, reverse MR analysis did not reveal evidence for a causal effect of CRC on H. pylori infection. The weighted median, the MR-Egger method, and MR-PRESSO yielded identical results. Using genetic data, MR analysis showed there was no evidence for a causal association between seroprevalence of H. pylori infection and CRC. The relationship between H. pylori infection and CRC requires further research.
Assuntos
Neoplasias Colorretais , Infecções por Helicobacter , Helicobacter pylori , Humanos , Infecções por Helicobacter/complicações , Estudo de Associação Genômica Ampla , Análise da Randomização Mendeliana , Estudos Soroepidemiológicos , Anticorpos Antibacterianos , Calgranulina A , Neoplasias Colorretais/genéticaRESUMO
Functional dyspepsia is defined by epigastric pain/burning, postprandial fullness and/or early satiety that have been present for at least six months before diagnosis, including three consecutive months, without evidence of an organic cause likely to explain these symptoms. The pathogenesis is complex and incompletely understood. The initial assessment includes a thorough history, physical examination, blood work, celiac disease serology and ruling out Helicobacter pylori infection. Most patients will undergo upper gastrointestinal endoscopy and abdominal ultrasound to exclude organic differential diagnoses. The therapy is multi-facetted and includes, among others, proton pump inhibitors, Helicobacter pylori eradication, herbal agents, and neuromodulators.
La dyspepsie fonctionnelle est définie par la présence d'un ou plusieurs des symptômes suivants : douleur/brûlure épigastrique, plénitude postprandiale, satiété précoce qui doivent être présents depuis au moins six mois avant le diagnostic, dont trois mois consécutifs, sans qu'il y ait de preuve d'une cause organique. La physiopathologie est complexe et mal comprise. Le bilan initial comprend une anamnèse approfondie, un examen physique, un bilan sanguin, une sérologie de la maladie cÅliaque et écarter une infection à Helicobacter pylori. Une gastroscopie et un ultrason abdominal sont indiqués chez la majorité des patients afin d'exclure les diagnostics différentiels organiques. Le traitement est multiple et comprend les inhibiteurs de la pompe à proton, l'éradication d'Helicobacter pylori, la phytothérapie et les neuromodulateurs.
Assuntos
Doença Celíaca , Dispepsia , Infecções por Helicobacter , Helicobacter pylori , Humanos , Dispepsia/diagnóstico , Dispepsia/etiologia , Dispepsia/terapia , Infecções por Helicobacter/complicações , Infecções por Helicobacter/diagnóstico , Infecções por Helicobacter/tratamento farmacológico , Dor AbdominalRESUMO
INTRODUCTION: Helicobacter pylori colonizes the human stomach. Infection causes chronic gastritis and increases the risk of gastroduodenal ulcer and gastric cancer. Its chronic colonization in the stomach triggers aberrant epithelial and inflammatory signals that are also associated with systemic alterations. METHODS: Using a PheWAS analysis in more than 8,000 participants in the community-based UK Biobank, we explored the association of H. pylori positivity with gastric and extragastric disease and mortality in a European country. RESULTS: Along with well-established gastric diseases, we dominantly found overrepresented cardiovascular, respiratory, and metabolic disorders. Using multivariate analysis, the overall mortality of H. pylori -positive participants was not altered, while the respiratory and Coronovirus 2019-associated mortality increased. Lipidomic analysis for H. pylori -positive participants revealed a dyslipidemic profile with reduced high-density lipoprotein cholesterol and omega-3 fatty acids, which may represent a causative link between infection, systemic inflammation, and disease. DISCUSSION: Our study of H. pylori positivity demonstrates that it plays an organ- and disease entity-specific role in the development of human disease and highlights the importance of further research into the systemic effects of H. pylori infection.
Assuntos
Gastrite Atrófica , Gastrite , Infecções por Helicobacter , Helicobacter pylori , Úlcera Péptica , Neoplasias Gástricas , Humanos , Gastrite/complicações , Neoplasias Gástricas/complicações , Infecções por Helicobacter/complicações , Infecções por Helicobacter/epidemiologiaRESUMO
INTRODUCTION: Refractory peptic ulcer is now a rare disease since most peptic ulcers heal with appropriate treatment with proton pump inhibitors (PPIs) and/or Helicobacter pylori eradication. AREAS COVERED: The most frequent cause of apparent refractoriness is lack of adherence to treatment. Persistence of H. pylori infection, use or abuse (often surreptitious) of high dose non-steroidal anti-inflammatory drugs (NSAIDs) or aspirin (ASA) are the two major causes of true refractory ulcers. There is a growing number of peptic ulcers which are not linked to either NSAIDs or H. pylori infection. Refractoriness in these ulcers can be linked to gastric acid hypersecretion, rapid PPI metabolization, ischemia, chemo-radiotherapy, immune diseases, more rarely to other drugs or be fully idiopathic. Treatment of the cause of the ulcer, if known, is essential. This review is based on pertinent publications retrieved by a selective search in PubMed, with particular attention to refractory peptic ulcer. EXPERT OPINION: High-dose PPI or the new potassium competitive acid blocker or the combination of PPIs with misoprostol can be recommended in these cases. Other more experimental treatments such the topical application of platelet-rich plasma or mesenchymal stem cells have also been suggested. Surgery is the last option, but there is no guarantee of success, especially in NSAID or ASA abusers.
Assuntos
Infecções por Helicobacter , Helicobacter pylori , Úlcera Péptica , Humanos , Úlcera/complicações , Úlcera/tratamento farmacológico , Úlcera Péptica/tratamento farmacológico , Anti-Inflamatórios não Esteroides/uso terapêutico , Aspirina/uso terapêutico , Inibidores da Bomba de Prótons/uso terapêutico , Infecções por Helicobacter/complicações , Infecções por Helicobacter/tratamento farmacológicoRESUMO
The Hippo pathway plays an important role in cell proliferation, apoptosis, and differentiation; it is a crucial regulatory pathway in organ development and tumor growth. Infection with Helicobacter pylori (H. pylori) increases the risk of developing gastric cancer. In recent years, significant progress has been made in understanding the mechanisms by which H. pylori infection promotes the development and progression of gastric cancer via the Hippo pathway. Exploring the Hippo pathway molecules may yield new diagnostic and therapeutic targets for H. pylori-induced gastric cancer. The current article reviews the composition and regulatory mechanism of the Hippo pathway, as well as the research progress of the Hippo pathway in the occurrence and development of H. pylori-related gastric cancer, in order to provide a broader perspective for the study and prevention of gastric cancer.
Assuntos
Infecções por Helicobacter , Helicobacter pylori , Neoplasias Gástricas , Humanos , Neoplasias Gástricas/patologia , Via de Sinalização Hippo , Proliferação de Células , Infecções por Helicobacter/complicações , Infecções por Helicobacter/tratamento farmacológico , Infecções por Helicobacter/metabolismoRESUMO
Helicobacter pylori modulates the host inflammatory response, resulting in chronic gastritis, which contributes to gastric cancer pathogenesis. We verified the effect of Cudrania tricuspidata on H. pylori infection by inhibiting H. pylori-induced inflammatory activity. Five-week-old C57BL/6 mice (n = 8) were administered C. tricuspidata leaf extract (10 or 20 mg/kg per day) for 6 weeks. An invasive test (campylobacter-like organism [CLO]) and noninvasive tests (stool antigen test [SAT] and H. pylori antibody enzyme-linked immunosorbent assay) were performed to confirm the eradication of H. pylori. To evaluate the anti-inflammatory effect of C. tricuspidata, pro-inflammatory cytokines levels and inflammation scores were measured in mouse gastric tissue. C. tricuspidata significantly decreased the CLO score and H. pylori immunoglobulin G antibody optical density levels at both 10 and 20 mg/kg per day doses (P < .05). C. tricuspidata decreased the H. pylori antibody levels in a concentration-dependent manner, increased negative responses to SAT by up to 37.5%, and inhibited the pro-inflammatory cytokines interleukin (IL; IL-1ß, IL-6, 1L-8, and tumor necrosis factor alpha). C. tricuspidata also relieved gastric erosions and ulcers and significantly reduced the inflammation score (P < .05). We measured rutin in C. tricuspidata extract as a standard for high-performance liquid chromatography. C. tricuspidata leaf extract showed anti-H. pylori activity through the inhibition of inflammation. Our findings suggest that C. tricuspidata leaf extract is potentially an effective functional food material against H. pylori.
Assuntos
Gastrite , Infecções por Helicobacter , Helicobacter pylori , Moraceae , Animais , Camundongos , Gastrite/tratamento farmacológico , Camundongos Endogâmicos C57BL , Inflamação , Citocinas , Extratos Vegetais/farmacologia , Infecções por Helicobacter/complicações , Infecções por Helicobacter/tratamento farmacológico , Mucosa GástricaRESUMO
BACKGROUND: An ulcer is a condition characterized by inflammation, irritation, or erosion in the mucosal lining of the stomach or duodenum. Hence, peptic ulcer is the ulcer of both the stomach and the duodenum. 10% of the world's population is affected by chronic peptic ulcers. The formation of peptic ulcers depends on gastric juice pH and the decrease in mucosal defenses. Nonsteroidal antiinflammatory drugs (NSAIDs) and Helicobacter pylori (H. pylori) infection are the two significant factors disrupting mucosal resistance to injury. Indian herbal plants are exceptional for their ethnic, ethnobotanical, and ethno-pharmaceutical use. In this review, attempts have been made to gain information regarding some plants that may be used to treat or prevent peptic ulcers. The ultimate goal of peptic ulcer disease treatment is to reduce pain, cure ulcers, and prevent recurrence. OBJECTIVE: The aim of the study was to gain knowledge about several common medicinal plants employed in Ayurveda or contemporary science for the treatment or prevention of peptic ulcers and some natural and simple approaches to cure ulcers using readily available herbs. METHODS: The literature search was carried out using search engines, like Google Scholar, Scopus, PubMed, Medline, Springer, etc. Results: The extensive literature search showed natural herbs to have potential anti-ulcer activity, including cabbage, bananas, liquorice, fenugreek, garlic, Terminalia chebula, Acacia arabica, Aegle marmelos, Aloe vera, Allium sativum, Plantago ispagula, Mimosa pudica, Annona squamosa, Azadirachta indica, and Galega purpurea. CONCLUSION: This study concluded several medicinal plants to effectively prevent or cure peptic ulcers caused by a variety of factors, including H. pylori, aspirin, indomethacin, alcohol, and others.
Assuntos
Infecções por Helicobacter , Úlcera Péptica , Plantas Medicinais , Humanos , Úlcera Péptica/tratamento farmacológico , Úlcera Péptica/epidemiologia , Úlcera Péptica/etiologia , Aspirina , Anti-Inflamatórios não Esteroides/uso terapêutico , Infecções por Helicobacter/complicações , Infecções por Helicobacter/tratamento farmacológico , Inflamação/tratamento farmacológicoRESUMO
Background: Cannabis plant extracts suppress gastric acid secretion and inflammation, and promote gastroduodenal ulcer healing, all of which are triggered by Helicobacter Pylori infection (HPI). Here, we evaluate the association between cannabis use and HPI among a representative community sample. Materials and Methods: We identified respondents who completed cannabis use questions and were tested for HPI (H. pylori IgG antibody seropositivity) from the National Health and Nutrition Examination Survey III dataset (n=4556). Cannabis usage was categorized as ever-use (ever, never), cumulative lifetime use (>10-times, 1-10-times, never), or recent use (>31-days-ago, within-31-days, never). We calculated the crude and adjusted risk (prevalence rate ratio, cPRR and aPRR) of having HPI with cannabis use using generalized Poisson models (SAS 9.4). The models were adjusted for demographics and risk factors for HPI. Results: The prevalence of HPI was lower among ever versus never cannabis users (18.6% vs. 33%, p<0.0001). Cannabis use was associated with a decreased risk of HPI (cPRR: 0.56 confidence interval [95% CI: 0.47-0.67]; p<0.0001), which persisted after adjusting for demographics (aPRR: 0.75 [95% CI: 0.63-0.90]; p=0.0016) and comorbidities (aPRR: 0.79 [95% CI: 0.66-0.95]; p=0.0145). Further, individuals with >10-times lifetime cannabis use had a decreased risk of HPI compared with those with 1-10-times lifetime use (aPRR: 0.70 [95% CI: 0.55-0.89]; p=0.0011) and never-users (aPRR: 0.65 [95% CI: 0.50-0.84]; p=0.0002). Conclusion: Recreational cannabis use is associated with diminished risk of HPI. These observations suggest the need for additional research assessing the effects of medical cannabis formulations on HPI.
Assuntos
Cannabis , Infecções por Helicobacter , Helicobacter pylori , Humanos , Cannabis/efeitos adversos , Infecções por Helicobacter/epidemiologia , Infecções por Helicobacter/complicações , Infecções por Helicobacter/diagnóstico , Inquéritos Nutricionais , Fatores de RiscoRESUMO
Gastric carcinoma (GC) is a complex multifactorial disease occurring as sequential events commonly referred to as the Correa's cascade, a stepwise progression from non-active or chronic active gastritis, to gastric precancerous lesions, and finally, adenocarcinoma. Therefore, the identification of novel agents with multi-step actions on the Correa's cascade and those functioning as multiple phenotypic regulators are the future direction for drug discovery. Recently, berberine (BBR) has gained traction owing to its pharmacological properties, including anti-inflammatory, anti-cancer, anti-ulcer, antibacterial, and immunopotentiation activities. In this article, we investigated and summarized the multi-step actions of BBR on Correa's cascade and its underlying regulatory mechanism in gastric carcinogenesis for the first time, along with a discussion on the strength of BBR to prevent and treat GC. BBR was found to suppress H. pylori infection, control mucosal inflammation, and promote ulcer healing. In the gastric precancerous lesion phase, BBR could reverse mucosal atrophy and prevent lesions in intestinal metaplasia and dysplasia by regulating inflammatory cytokines, promoting cell apoptosis, regulating macrophage polarization, and regulating autophagy. Additionally, the therapeutic action of BBR on GC was partly realized through the inhibition of cell proliferation, migration, and angiogenesis; induction of apoptosis and autophagy, and enhancement of chemotherapeutic drug sensitivity. BBR exerted multi-step actions on the Correa's cascade, thereby halting and even reversing gastric carcinogenesis in some cases. Thus, BBR could be used to prevent and treat GC. In conclusion, the therapeutic strategy underlying BBR's multi-step action in the trilogy of Correa's cascade may include "prevention of gastric mucosal inflammation (Phase 1); reversal of gastric precancerous lesions (Phase 2), and rescue of GC (Phase 3)". The NF-κB, PI3K/Akt, and MAPK signaling pathways may be the key signaling transduction pathways underlying the treatment of gastric carcinogenesis using BBR. The advantage of BBR over conventional drugs is its multifaceted and long-term effects. This review is expected to provide preclinical evidence for using BBR to prevent gastric carcinogenesis and treat gastric cancer.
Assuntos
Berberina , Gastrite Atrófica , Gastrite , Infecções por Helicobacter , Lesões Pré-Cancerosas , Neoplasias Gástricas , Antibacterianos/uso terapêutico , Berberina/farmacologia , Berberina/uso terapêutico , Carcinogênese , Citocinas/uso terapêutico , Gastrite Atrófica/patologia , Infecções por Helicobacter/complicações , Infecções por Helicobacter/tratamento farmacológico , Infecções por Helicobacter/microbiologia , Humanos , Inflamação , NF-kappa B , Fosfatidilinositol 3-Quinases , Lesões Pré-Cancerosas/patologia , Proteínas Proto-Oncogênicas c-akt , Neoplasias Gástricas/tratamento farmacológico , Neoplasias Gástricas/patologia , Neoplasias Gástricas/prevenção & controleRESUMO
OBJECTIVES: To explore the effect of Helicobacter pylori (Hp ) infection on zinc, copper, calcium, magnesium, phosphorus, and iodine status in the pediatric population. METHODS: A protocol was registered on PROSPERO. A literature search was conducted on Embase, PubMed MEDLINE, and Web of Science, from inception to September 2020, including all studies in English, Spanish, and Portuguese languages. Reference lists were manually searched. Primary studies describing at least one micronutrient status in Hp -positive and Hp -negative or control children were included. PRISMA recommendations were applied. Pooled mean differences (MDs) and 95% confidence intervals were estimated using a random-effects model. A total of 1011 citations were screened. Six cross- sectional studies were included. No publications regarding phosphorus and iodine were identified. RESULTS: Included studies in meta-analyses comprised an overall age range of 4-18 years, with Hp positivity ranging between 29.5% and 72.3%. These meta-analyses demonstrated a lack of evidence of an association between Hp -positive and Hp -negative or control children regarding serum zinc (vs Hp -negative: MD -1.36 µg/dL; vs control: MD 326.22 µg/dL), copper (MD -0.83 µg/dL), and calcium (MD 0.09 mg/dL) status. Considerable heterogeneity was recognized, except for calcium analysis (I 2 = 0%). Meta-analysis for magnesium was not performed. Five studies presented a low risk of bias. CONCLUSIONS: The study demonstrated a lack of evidence of an effect of Hp infection on serum zinc, copper, and calcium status. Studies concerning magnesium, phosphorus, and iodine status are warranted. Furthermore, larger and well-controlled studies are recommended.
Assuntos
Infecções por Helicobacter , Helicobacter pylori , Iodo , Oligoelementos , Criança , Humanos , Pré-Escolar , Adolescente , Infecções por Helicobacter/complicações , Infecções por Helicobacter/epidemiologia , Cobre , Cálcio , Zinco , FósforoRESUMO
BACKGROUND: Evidence from epidemiological studies on the role of tea drinking in gastric cancer risk remains inconsistent. We aimed to investigate and quantify the relationship between tea consumption and gastric cancer in the Stomach cancer Pooling (StoP) Project consortium. METHODS: A total of 9438 cases and 20,451 controls from 22 studies worldwide were included. Odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) of gastric cancer for regular versus non-regular tea drinkers were estimated by one and two-stage modelling analyses, including terms for sex, age and the main recognised risk factors for gastric cancer. RESULTS: Compared to non-regular drinkers, the estimated adjusted pooled OR for regular tea drinkers was 0.91 (95% CI: 0.85-0.97). When the amount of tea consumed was considered, the OR for consumption of 1-2 cups/day was 1.01 (95% CI: 0.94-1.09) and for >3 cups/day was 0.91 (95% CI: 0.80-1.03). Stronger inverse associations emerged among regular drinkers in China and Japan (OR: 0.67, 95% CI: 0.49-0.91) where green tea is consumed, in subjects with H. pylori infection (OR: 0.68, 95% CI: 0.58-0.80), and for gastric cardia cancer (OR: 0.64, 95% CI: 0.49-0.84). CONCLUSION: Our results indicate a weak inverse association between tea consumption and gastric cancer.
Assuntos
Infecções por Helicobacter , Neoplasias Gástricas , Estudos de Casos e Controles , Infecções por Helicobacter/complicações , Infecções por Helicobacter/epidemiologia , Humanos , Razão de Chances , Fatores de Risco , Neoplasias Gástricas/epidemiologia , Neoplasias Gástricas/etiologia , CháRESUMO
OBJECTIVE: To investigate the enrichment of Helicobacter pylori (Hp) in adenoma tissue of patients with colorectal adenoma, and analyze the correlation between the enrichment and the clinical and pathological characteristics of colorectal adenoma. METHODS: The data of 1,622 patients undergoing gastrointestinal endoscopy in the Endoscopy Center of Wenzhou Integrated Traditional Chinese and Western Medicine Hospital affiliated to Zhejiang University of Traditional Chinese Medicine from January 2019 to June 2021 were retrospectively collected. The general data, gastric Hp infection, clinical and pathological features of colorectal adenoma, methylene blue staining of adenoma Hp, immunohistochemistry of adenoma Hp and immunofluorescence staining of adenoma TLR5 protein. were compared between the colorectal adenoma group (743 cases) and the control group (879 cases). RESULTS: There were 361 gastric Hp positive cases in the colorectal adenoma group, with a positive rate of 48.59%, and 331 gastric Hp positive cases in the control group, with a positive rate of 37.66%, and the difference was statistically significant (P < 0.001). Gastric Hp infection significantly correlates with the Hp enrichment in colorectal adenomas (OR: 28.449; 95%CI: 18.188-44.500; P < 0.001). Moreover, we found that Hp enrichment in colorectal adenomas was correlated with the diameter, pathological type, and malignancy of adenoma (OR: 3.536; 3.652; 2.833; all P < 0.001). Expression TLR5 protein was also increased in Hp-enriched adenoma tissue. CONCLUSION: There is a correlation between gastric Hp infection and intestinal Hp enrichment. The intestinal Hp enrichment significantly correlates with the clinical and pathological characteristics of colorectal adenomas, and its tumor-promoting effect may be related to the up-regulation of mucosal TLR5 expression.
Assuntos
Adenoma , Neoplasias Colorretais , Infecções por Helicobacter , Helicobacter pylori , Adenoma/patologia , Neoplasias Colorretais/patologia , Mucosa Gástrica/patologia , Infecções por Helicobacter/complicações , Infecções por Helicobacter/metabolismo , Humanos , Estudos Retrospectivos , Receptor 5 Toll-LikeRESUMO
Gastritis is a common inflammation of stomach with multiple pathogenesis. This study was designed to investigate the protective effects of oral octreotide (OCT) against ethanol-induced acute gastric injury and H. pylori-induced chronic gastritis via promoting gastric mucosa restoration, reducing gastric acid secretion and inflammation. Male C57BL/6J mice were randomly divided and treated with three doses of OCT (0.5, 2.5, 10 mg/kg) alone or combined respectively with 10 mg/kg omeprazole (OME), 0.2 g/L metronidazole (MTZ)/0.1 g/L clarithromycin (CLR) in drinking water. Oxidative stress analysis, bacterial load analysis, qPCR, gastric histopathology examinations were performed in our study. Ethanol-induced acute gastric ulcer was restored by OCT alone at doses of 2.5 mg/kg, or combined with OME as indicated by markedly reducing Gastrin, Il-6 and Il1b expression through induction of Muc5ac and Occludin, significantly improving hyperacidity and gastric bleeding. As well, OCT combined with MTZ/CLR restored the integrity of gastric mucosa damaged by H. pylori via elevating the expression of Muc5ac and somatostatin receptor 2, decreasing inflammation and increasing the number of chorionic or glands. Besides, OCT is more suitable for long-term medication in the treatment of chronic gastritis than OME. In conclusion, our results proved that the newly developed oral OCT-based therapies were more effective to reverse gastric mucosa damage and inflammation in ethanol and H. pylori infection-induced gastric injury, it is of great significance for supplementing new clinical regimens for the treatment of acute and chronic gastritis.