Introduction: A clearer understanding of the factors affecting the cure rate of Helicobacter pylori infection might lead to the development of novel prevention strategies and therapeutic targets.
Areas Covered: This review covers two important issues that affect the eradication of H. pylori: bacterial and host factors. Several virulence factors have been shown to be predictors for gastroduodenal diseases. Successful treatment of H. pylori infection also depends on host genetic factors such as CYP2C19 and IL-1B. The latest evidence on host genetic factors is discussed.
Expert Opinion: The authors identify three main targets for achieving effective eradication therapy. The first therapeutic target is to identify counter measures for antibiotic-resistant H. pylori strains. Thus, antibiotic susceptibility should be checked in all patients, ideally, before the start of eradication treatment. The second therapeutic target is the inhibition of acid suppression. Maintaining a high intragastric pH for 24 h increases the effectiveness of some antibiotics and the eradication effects for H. pylori. The third therapeutic target is to identify high-risk groups; the CYP2C19 and IL-1B polymorphisms are candidates for significant risk factors. A personalized medical approach will likely increase the cure rate of H. pylori infection.
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http://dx.doi.org/10.1517/14728222.2015.1073261 | DOI Listing |
Parasitol Int
January 2025
Department of Health Sciences, Unit of Clinical Microbiology, "Magna Græcia" University of Catanzaro "Mater Domini" Teaching Hospital, Catanzaro, Italy; Department of Health Sciences, Unit of Clinical Microbiology, "Magna Græcia" University of Catanzaro "Mater Domini" Teaching Hospital, Catanzaro, Italy. Electronic address:
Background: Ascaris lumbricoides is a nematode that parasitizes the human gastrointestinal tract, and it is the cause of the most common helminthic infections worldwide. It predominates in areas of poor sanitation. Early diagnosis of this intestinal infection is pivotal to avoid its severe and lethal complications such as gut obstruction, volvulus, and perforation.
View Article and Find Full Text PDFBMJ Open Gastroenterol
December 2024
Division of Gastroenterology & Hepatology, Weill Cornell Medicine, New York, New York, USA
Objective: Globally, over 50% of the population is affected by , yet research on its prevalence and impact in patients with obesity undergoing laparoscopic sleeve gastrectomy (LSG) is inconclusive. This study aimed to assess the prevalence of infection in individuals with obesity undergoing LSG, evaluate the percentage of postoperative staple-line leaks, and explore the potential link between infection and staple-line leaks.
Methods: This retrospective analysis assessed adult patients with class III obesity who underwent LSG between 2015 and 2020 at a tertiary care hospital in Riyadh, Saudi Arabia.
J Clin Med
December 2024
Department of Oncological, Transplant and General Surgery, Faculty of Medicine, Medical University of Gdansk, 80-214 Gdansk, Poland.
: (HP) is under investigation for its potential role in postoperative complications. While some studies indicate no impact, they often cite short or incomplete follow-up. This study aims to compare 1-year outcomes in groups with and without active HP infection after bariatric surgery, also assessing HP prevalence in postoperative specimens of sleeve gastrectomy (SG) patients.
View Article and Find Full Text PDFCancers (Basel)
January 2025
Faculty of Medicine, University of Ljubljana, Vrazov trg 2, 1000 Ljubljana, Slovenia.
Background/objectives: Gastric intestinal metaplasia (GIM) is considered an irreversible preneoplastic precursor for gastric adenocarcinoma in adults. However, its significance in children and the long-term outcome remain poorly understood.
Methods: All children diagnosed with GIM between 2000 and 2020 were identified at a large tertiary referral centre.
Cancers (Basel)
December 2024
Division of Hematology and Oncology, School of Medicine, University of Alabama at Birmingham, Birmingham, AL 35233, USA.
Dysbiosis in the gut microbiota plays a significant role in GI cancer development by influencing immune function and disrupting metabolic functions. Dysbiosis can drive carcinogenesis through pathways like immune dysregulation and the release of carcinogenic metabolites, and altered metabolism, genetic instability, and pro-inflammatory signalling, contributing to GI cancer initiation and progression. infection and genotoxins released from dysbiosis, lifestyle and dietary habits are other factors that contribute to GI cancer development.
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