Risultati per: Helicobacter Pylori: algoritmo terapeutico di eradicazione

This randomized clinical trial evaluates the effects of Helicobacter pylori stool antigen assessment plus fecal immunochemical testing (FIT), vs FIT alone, on gastric cancer incidence and mortality among adults in Taiwan.

Gastric cancer is a leading cause of cancer death globally. Although endoscopy-based screening has led to a decrease in gastric cancer mortality in Eastern Asian countries with populations at high risk, lack of risk stratification and the cost of health care infrastructure and trained personnel limit its use in most of the world. Availability of noninvasive biomarkers for the identification of high-risk individuals could optimize endoscopy-based screening programs for a more general application, including in regions where gastric cancer rates in the general population are low.

Introduction
Helicobacter pylori is a type of Gram-negative microaerobic bacteria that inhabits the gastric mucosal epithelium. It can cause various gastrointestinal diseases including gastritis, peptic ulcer and gastric cancer. White blood cells (WBC) are common immune cells, the increase in whose countoften indicates the presence of an infection. Currently, the relationship between H. pylori and WBC count remains full of controversy. This study aims to further elucidate the effects of H. pylori on WBC count in a population undergoing physical examination.

Methods and analysis
A total of 864 participants who underwent physical examination and 14C urea breath test (UBT) were retrospectively enrolled in this study from January to June 2021. The overall population was divided into H. pylori-negative (Hp–) and H. pylori-positive (Hp+) groups based on the disintegration per minute (DPM) value detected by UBT. Spearman’s correlation analysis was used to assess the correlation between DPM and WBC count. General linear regression models were applied to assess the potential factors contributing to the increase in WBC count. Generalised additive model (GAM) was performed to identify the non-linear relationship between DPM and WBC count. Additionally, a piecewise linear regression was used to examine the threshold effect of the DPM on WBC count.

Results
403 subjects were diagnosed with H. pylori infection. The WBC and platelet (PLT) counts in the Hp+ group were significantly higher than those in the Hp– group. Additionally, the prevalence of H. pylori infection gradually increased with the WBC count quartiles (38.89% and 54.67% in quartile 1 and quartile 4, respectively). Spearman’s correlation analysis showed that the DPM value significantly correlated with WBC count (r=0.089, p=0.009) and PLT count (r=0.082, p=0.017). The linear model revealed a positive independent association of H. pylori infection and DPM with WBC count (βHp+=0.398 (95% CI 0.170, 0.625), p

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We thank Bornschein et al for their interest in the British Society of Gastroenterology guidelines on the management of functional dyspepsia (FD).1 2 They raise issues regarding the role of repeated Helicobacter pylori testing and eradication in patients with uninvestigated dyspepsia, as part of a ‘test and treat’ approach, which is the most effective strategy for managing the condition.3 However, they extrapolate this to cover FD, although most patients with uninvestigated dyspepsia will have FD as the cause of symptoms.4 We agree that H. pylori leads to severe complications including peptic ulcer or gastric cancer. There is unequivocal evidence that eradicating the bacterium in patients with peptic ulcer leads to a highly significant reduction in the risk of ulcer recurrence, with a number needed to treat of two or three.5 There is also evidence that treating infected patients after…

Among other changes, the 2024 version of these guidelines suggests that clinicians use clarithromycin and levofloxacin to treat H. pylori only if susceptibility is proven.

Gastric metaplasia may arise as a consequence of chronic inflammation and is associated with an increased risk of gastric cancer development. While Helicobacter pylori (Hp) infection and autoimmune gastritis (AIG) both induce gastric metaplasia, possible distinctions in resulting metaplastic cells and their respective cancer risks requires further investigation.

Colorectal cancer (CRC) has low survival rates and can be influenced by various factors, including genetics, lifestyle and an altered microbiome.1 Recent studies indicate that Helicobacter pylori infection may also play a role in CRC development.2 This is of significant concern as over half of the world’s population carries H. pylori, which can cause gastric inflammation and potentially lead to cancer.3 In a recent study,4 we demonstrated that H. pylori infection in Apc-mutant mice could accelerate tumour development by causing immune and epithelial changes that are linked to tumorigenesis. We observed similar changes in H. pylori-infected patients.4 In addition, we found that treating the infection with antibiotics such as clarithromycin, metronidazole and omeprazole, at an early stage of infection can eradicate H. pylori4 and reduce the tumour occurrence to a normal level.4 These findings revealed…

Background and aims
This study aimed to evaluate the efficacy and safety of vonoprazan and tetracycline (VT) dual therapy as first-line treatment for Helicobacter pylori infection in patients with penicillin allergy.

Methods
In this randomised controlled trial, treatment-naïve adults with H. pylori infection and penicillin allergy were randomised 1:1 to receive either open-label VT dual therapy (vonoprazan 20 mg two times per day+tetracycline 500 mg three times a day) or bismuth quadruple therapy (BQT; lansoprazole 30 mg two times per day+colloidal bismuth 150 mg three times a day+tetracycline 500 mg three times a day+metronidazole 400 mg three times a day) for 14 days. The primary outcome was non-inferiority in eradication rates in the VT dual group compared with the BQT group. Secondary outcomes included assessing adverse effects.

Results
300 patients were randomised. The eradication rates in the VT group and the BQT group were: 92.0% (138/150, 95% CI 86.1% to 95.6%) and 89.3% (134/150, 95% CI 83.0% to 93.6%) in intention-to-treat analysis (difference 2.7%; 95% CI –4.6% to 10.0%; non-inferiority p=0.000); 94.5% (138/146, 95% CI 89.1% to 97.4%) and 93.1% (134/144, 95% CI 87.3% to 96.4%) in modified intention-to-treat analysis (difference 1.5%; 95% CI –4.9% to 8.0%; non-inferiority p=0.001); 95.1% (135/142, 95% CI 89.7% to 97.8%) and 97.7% (128/131, 95% CI 92.9% to 99.4%) in per-protocol analysis (difference 2.6%; 95% CI –2.9% to 8.3%; non-inferiority p=0.000). The treatment-emergent adverse events (TEAEs) were significantly lower in the VT group (14.0% vs 48.0%, p=0.000), with fewer treatment discontinuations due to TEAEs (2.0% vs 8.7%, p=0.010).

Conclusions
VT dual therapy demonstrated efficacy and safety as a first-line treatment for H. pylori infection in the penicillin-allergic population, with comparable efficacy and a lower incidence of TEAEs compared with traditional BQT.

Trial registration number
ChiCTR2300074693.

Objectives
To assess the utility of Helicobacter pylori antibody testing, we evaluated the correlation between the H. pylori antibody titre and H. pylori-associated pathogenicity and the changes in antibody titre after H. pylori eradication therapy.

Design
A retrospective observational cohort study.

Setting and participants
From 2004 to 2016, medical check-ups were performed in different regions of Japan. In total, 324 subjects infected with H. pylori who received H. pylori eradication therapy were enrolled; H. pylori was eradicated in 266 of these subjects. We examined the associations between H. pylori antibody titre with pepsinogen and the presence or absence of H. pylori-associated pathogenic proteins, such as cytotoxin-associated gene A and vacuolating cytotoxin gene A, at baseline and after H. pylori eradication therapy.

Results
The H.pylori antibody titre showed a positive correlation with pepsinogen II and a negative correlation with the pepsinogen I/II ratio. Moreover, the H.pylori antibody titre significantly correlated with the positive rates of H. pylori-associated pathogenic protein before eradication therapy. Antibody titres decreased after eradication, the pepsinogen I/II ratio increased and the H. pylori-associated pathogenic protein-positive rate decreased in patients with successful eradication. The determination of eradication using the decline in antibody titre 6 months after eradication therapy was useful (area under the receiver operating characteristic curve: 0.98).

Conclusions
Our data indicate that the H. pylori antibody titre may represent the degree of pathogenicity. The H. pylori antibody titre was associated with attenuation of pathogenicity in patients with H. pylori eradication, indicating the clinical utility of H. pylori antibody testing.