Risultati per: Helicobacter Pylori: algoritmo terapeutico di eradicazione

Buzzetti su glifozine,semplificazione e riduzione diseguaglianze

Buzzetti su glifozine,semplificazione e riduzione diseguaglianze

H. pylori infection may represent a significant risk factor for the development of colorectal cancer. The effect of anti-H. pylori treatment on colorectal cancer incidence and mortality necessitates further investigation through large-scale, randomized controlled trials with prolonged follow-up durations.

Guglielmino (Siru), ‘necessaria riorganizzazione sistema Rma’

Helicobacter pylori (H. pylori) infection is a major risk factor for gastric cancer (GC); however, whether H. pylori eradication (HPE) benefits the older population remains unclear. We compared GC incidence and mortality between H. pylori-treated individuals and the general population, stratified by age.

George S, Lucero Y, Cabrera C, et al. Protocol for a randomised ‘screen-and-treat’ Helicobacter pylori eradication trial in 14–18-years-old adolescents residing in three regions of Chile: effectiveness and microbiological host implications. BMJ Open 2025;15:e084984. doi:10.1136/bmjopen-2024–0 84 984
This article has been corrected since it was published online. The funding information has been updated from “The funder has no influence on the study’s design, execution, analysis, or publication of results. The funder has no influence on the study’s design, execution, analysis, or publication of results. The funder has no influence on the study’s design, execution, analysis, or publication of results.” to “This trial has received funding from the National Fund for Scientific and Technological Development (Fondecyt 1 220 964 and 1190456). MO received partial funding from the grant ANID PIA AFB 230002. The funder has no influence on the study’s design, execution, analysis, or publication of results.”

To the Editor In a recent trial, there were no differences in gastric cancer incidence or mortality between the 2 treatment groups at a median follow-up of 5.7 years (IQR, 4.9-6.5 years). The progression time from early asymptomatic to symptomatic gastric cancer is unknown and may be longer than the follow-up time of the trial. Presentation of cumulative incidence curves would be helpful to further gauge the effect of the intervention. Furthermore, the study excluded 4 patients with gastric cancer diagnosed on endoscopy after trial entry. While H pylori eradication may not have affected the development of cancer in these patients, excluding them creates bias because the control group was not exposed to gastroscopy with early detection of prevalent cancers. We suggest a recalculation of screening effects including the 4 patients who were excluded. Additionally, we are interested to know if more than 1 H pylori stool test was offered (for example, with subsequent FIT), which would provide information about reinfection and subsequent cancer risk.

In Reply In response to the Letters regarding our recent article, we agree with Dr Shiratori and colleagues that our study requires a longer follow-up period, as was also noted by Drs Kumar and Bretthauer and by Dr Liu and colleagues. In our pragmatic trial, factors such as nonadherence to invitation, difference in participant characteristics, and limited treatment uptake have attenuated the potential benefits observed in earlier trials. To address this, we have provided the cumulative curve as requested and included a future projection based on the observed trends (Figure). In our trial, a nonsignificant 14% risk reduction was observed in 2020. However, with an extended follow-up to 2023, a significant 21% reduction would be expected after projection.

To the Editor Dr Lee and colleagues conducted a randomized, population-based trial in Taiwan to assess whether the addition of the Helicobacter pylori stool antigen (HPSA) test to the standard fecal immunochemical test (FIT) could reduce gastric cancer incidence and mortality. The study reported no significant differences between the 2 groups in gastric cancer incidence (0.032% vs 0.037%; P = .23) or mortality (0.015% vs 0.013%; P = .57). Several points merit further discussion.

To the Editor A recent randomized trial involving residents of Changhua County, Taiwan, offered valuable insights into the effectiveness of HPSA testing combined with FIT for colorectal cancer screening. While the study provides robust data, several key findings warrant further reflection.

To the Editor A recent study shed light on the potential value of FIT combined with HPSA testing in gastric cancer screening, while also indirectly highlighting the potential link between H pylori infection and colorectal carcinogenesis. We would like to discuss aspects of the study that require careful interpretation and further exploration.

Helicobacter pylori infection of the stomach is the main risk factor for gastric non-cardia adenocarcinoma, however less is known on how eradication of Helicobacter pylori influences the risk of this tumor over time, particularly in Western populations. The aim of this study was to delineate how the risk of gastric non-cardia adenocarcinoma develops over time after Helicobacter pylori eradication treatment in a Western population compared with the background population.

We read with great interest the postscript by Arai et al in response to the article by Rugge et al.1 2 The authors did a great job in comparing immunohistochemical staining results of gastric cancer (GC) due to autoimmune gastritis (AIG) and H. pylori infection. They claimed that AIG may be less susceptible to cancer development than H. pylori-related gastritis; however, a few concerns need to be addressed. Firstly, the authors found that the dysplastic transition (TROP2) score of AIG non-cancerous lesions adjacent to cancerous lesions were much lower than H. pylori-related gastritis. They concluded that TROP2-negative metaplasia in AIG cases was less carcinogenic than TROP2-enriched metaplasia in antiparietal cell antibody (APCA)—H. pylori+ cases. However, this could not explain why the cancerous lesions in both groups were diffusely positive for TROP2. If the TROP2-negative metaplasia in AIG cases was less carcinogenic, why did AIG patients…

Introduction
Gastric cancer is a major global health concern, being the final stage of a long-term process, primarily associated with Helicobacter pylori (H. pylori) infection. Early childhood acquisition of H. pylori with low spontaneous eradication rates underscores the need for preventive measures. Our previous pilot treatment study revealed high eradication rates, favourable tolerance profile and a decline in serum biomarkers indicative of gastric damage in asymptomatic school-aged children. The purpose of this study is to determine the potential benefit of a ‘screen-and-treat’ strategy targeting persistently infected, asymptomatic adolescents. Specific aims are to assess eradication efficacy, its clinical and molecular outcomes and potential clinical and microbiological side effects.

Methods and analysis
The screening phase will involve testing 500–1000 asymptomatic adolescents aged 14–18 from three cities in Chile using the urea breath test (UBT) to identify 210 participants with persistent infection. They will proceed to a randomised, non-blinded, controlled trial, receiving either a sequential eradication scheme for H. pylori or no treatment. Follow-up will span up to 24 months post-treatment, involving UBT, gastroenterological assessments and blood and stool sample collections. Concurrently, a subset of 60 uninfected adolescents will undergo matched follow-up. Enzyme-linked immunosorbent assay (ELISA) commercial kits will evaluate gastric damage biomarkers in serum (pepsinogen I and II, gastrin-17, VCAM-1, CXCL13). Stool samples will be employed for Escherichia coli and Enterococcus spp—culture, assessing AMR via the disk diffusion method. H. pylori clarithromycin resistance will be determined by molecular method from stool samples. The gut microbiome will be characterised by amplifying and sequencing the 16S rRNA gene from stool samples, followed by bioinformatics analysis.

Ethics and dissemination
Approved by the Human Research Ethics Committee at the Faculty of Medicine, University of Chile (073–2022). Findings will be disseminated in peer-reviewed journals and scientific meetings to guide future practices.

Trial registration number
NCT05926804.