Objective: This study evaluated Helicobacter pylori eradication therapy in terms of symptomatic response in patients with functional dyspepsia. On the other hand, we analyzed the importance of histologic findings as a predictor of treatment response. In particular, we studied whether antral gastritis (which is associated with peptic ulcer) may predict a greater symptomatic response to Helicobacter pylori eradication in functional dyspepsia.
Patients And Methods: This prospective, randomized, single-center trial included 48 patients with functional dyspepsia and Helicobacter pylori infection (27 women and 21 men, mean age 37 +/- 13.5 years). Twenty-seven patients received a 10-day course of rabeprazole, amoxicillin, and clarithromycin (eradication group), followed by 20 mg of rabeprazole for 3 months. Twenty-one patients received 20 mg of rabeprazole for 3 months (control group). Patients were followed up over a 1-year period. All patients completed the Dyspepsia-Related Health Scale Questionnaire, which studies four dimensions: pain intensity, pain disability, non-pain symptoms, and satisfaction with dyspepsia-related health.
Results: There was significant symptomatic improvement (p < 0.002) after 6 and 12 months, which was similar with both treatments. In the multivariate analyses, eradication therapy and less severe symptoms before treatment were the only independent factors. The symptomatic response to Helicobacter pylori eradication after 6 months was significantly greater as compared to control therapy (p = 0.01) in patients with antral gastritis and in the non-pain symptoms dimension of the questionnaire.
Conclusions: Both treatments proved to be clinically beneficial in patients with functional dyspepsia. We observed a tendency to greater symptomatic benefit with Helicobacter pylori eradication therapy when compared to control treatment in patients with functional dyspepsia and in a population with a high prevalence of this infection. There is a tendency to symptomatic benefit with Helicobacter pylori eradication therapy in patients with antral gastritis.
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http://dx.doi.org/10.4321/s1130-01082008000900002 | DOI Listing |
J Cutan Med Surg
January 2025
Division of Dermatology, Jewish General Hospital/Lady Davis Institute for Medical Research, McGill University, Montreal, QC, Canada.
QJM
January 2025
Peking University Traditional Chinese Medicine Clinical Medical School (Xiyuan), Peking University Health Science Center, Beijing, 100091, People's Republic of China.
Gastric cancer (GC) is a significant global health challenge, particularly in high-incidence regions like East Asia. Despite improvements in screening and treatment, the progressive nature of precancerous lesions-such as atrophic gastritis, intestinal metaplasia, and dysplasia-necessitates effective prevention strategies. This review evaluates the role of chemoprevention in GC, focusing on agents designed to target these precancerous lesions.
View Article and Find Full Text PDFEur J Clin Invest
January 2025
Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, Connecticut, USA.
Background: Several studies have investigated the association between Helicobacter pylori colonization and gastrointestinal malignancies. However, inconsistent results have been found, leaving no clear consensus.
Materials And Methods: Umbrella review of meta-analyses of observational studies aiming to understand the association between Helicobacter pylori colonization and gastrointestinal cancers in humans.
World J Gastroenterol
January 2025
Department of Therapy, North Caucasus State Academy, Cherkessk 369000, Russia.
() infection has a protective effect on gastroesophageal reflux disease (GERD). Both of these diseases have a very high incidence and prevalence. As a result, GERD often recurs after anti- therapy.
View Article and Find Full Text PDFTrends Mol Med
January 2025
Institute of Experimental Internal Medicine, Otto von Guericke University Magdeburg, 39120 Magdeburg, Germany. Electronic address:
Ubiquitinylation of proteins regulates manifold processes and is reversed by deubiquitinylating enzymes (DUBs), which are therefore implicated in a plethora of cellular processes. DUBs are frequently upregulated in many diseases, while in a few cases downregulation of DUBs is associated with disease progression. This review focuses on the involvement of DUBs in the development and progression of gastrointestinal diseases with a particular emphasis on hepatic steatosis and hepatocellular, cholangio-, esophageal, gastric, colorectal, and pancreatic ductal carcinomas.
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