Background/aims: This study was undertaken to evaluate the effect of eradication therapy on the symptoms of Helicobacter pylori positive non-ulcer dyspepsia patients.
Methods: Twenty-four patients participated in the study and the symptoms of daytime epigastric pain, night or hunger pain, nausea, vomiting, regurgitation, bloating, belching, early satiety and anorexia were scored at the beginning, the 15th day after starting eradication therapy (amoxicillin 2 gr bid, clarithromycin 2 gr bid and omeprazole 40 mg daily for two weeks) and during the third and sixth months. Gastric emptying of radiolabelled solid meal was determined at baseline and during the third month.
Results: The Helicobacter pylori eradication rate was 79% and symptom scores significantly decreased during the follow-up period in both of the groups, irrespective of Helicobacter pylori status. The mean symptom scores of the 24 patients at baseline, day 15 and and months three and six were as follows: 1.275, 0.274, 0.496 and 0.238 respectively. Symptom scores for the 19 patients with Helicobacter pylori eradication were 1.084, 0.263, 0.347 and 0.215 respectively while in the five patients in whom Helicobacter pylori eradication therapy failed it was 2.0, 0.314, 1.06 and 0.32 respectively. Of the 16.6% Helicobacter pylori positive non-ulcer dyspepsia patients who had delayed gastric emptying of solids, there was no change after eradication therapy. Nine patients, including all of those in whom eradication therapy failed, required further medication (antacids/prokinetics) for continuing symptoms one month after completion of treatment.
Conclusions: The results of this study suggest that Helicobacter pylori is a causal factor in symptoms of non-ulcer dyspepsia and that eradication therapy improves symptoms and endoscopic findings but has no effect on gastric emptying.
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Int J Biol Macromol
January 2025
Supplementary General Sciences Department, Faculty of Oral and Dental Medicine, Future University in Egypt, Cairo 11835, Egypt.
Helicobacter pylori (H. pylori) is an extremely prevalent human pathogen globally that leads to severe illnesses. Sadly, the worldwide issue of H.
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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