Background: Several studies have shown that acid-suppressing treatment leads to aggravation of Helicobacter pylori gastritis in the corpus. It remains unclear whether this augmentation of the inflammation reverts to baseline after termination of treatment.
Methods: In 114 H. pylori-infected duodenal ulcer patients we investigated the gastritis parameters in antral and corpus mucosa before treatment, after 6 and 12 months of therapy, and 6 months after termination of treatment with 15 mg lansoprazole or 150 mg ranitidine/day.
Results: Lansoprazole and ranitidine led to a significant aggravation of gastritis in the corpus after 6 and 12 months of treatment. However, while there was no change in gastritis in the antrum with ranitidine, treatment with lansoprazole led to partial elimination of H. pylori with improvement of the inflammation in this part of the stomach. Following termination of therapy, the observed changes reverted to baseline. No increase in intestinal metaplasia and/or atrophy in the antrum or corpus was observed.
Conclusion: Both substances are associated with an aggravation of H. pylori gastritis in the corpus. However, only lansoprazole leads to a partial elimination of H. pylori with improvement of the inflammation in the antrum. The changes provoked by acid-suppressing treatment revert to baseline after termination of therapy.
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http://dx.doi.org/10.1046/j.1365-2036.1998.00370.x | DOI Listing |
Oxf Med Case Reports
January 2025
Department of Pathology, Okayama Saiseikai General Hospital, 1-17-18 Ifuku-Cho, Kita-Ku, Okayama-shi, Okayama 700-8551, Japan.
Autoimmune gastritis (AIG) is a chronic condition in which the body's immune system mistakenly attacks the stomach lining, specifically targeting parietal cells that produce stomach acid and intrinsic factors. After the infection was eradicated, AIG developed in an elderly woman with symptoms of the disease. 1.
View Article and Find Full Text PDFTherap Adv Gastroenterol
January 2025
Digestive Disease Unit, Department of Medical-Surgical Sciences and Translational Medicine, Sant'Andrea Teaching Hospital, Sapienza University of Rome, via di Grottarossa 1035, Rome 00189, Italy.
Background: Efficacy of eradication regimens in (Hp) infection is commonly reported with proton pump inhibitors (PPIs). In patients with corpus atrophic gastritis, characterized by impaired acid secretion, PPI treatment is questionable.
Objectives: The current study aimed to assess in clinical practice the tolerability and eradication rate of modified eradication regimens without PPI as first-line treatment in patients with histologically Hp-positive corpus atrophic gastritis.
Prz Gastroenterol
December 2024
Department of Pathology, Detagen Pathology Laboratory, Kayseri, Turkey.
Introduction: Gastroesophageal reflux disease (GERD) is a common disease that negatively affects the quality of life, and its pathophysiology is multifactorial.
Aim: Our study aims to investigate the relationship between histological and topographic characteristics of () gastritis and the symptoms, presence, and severity of oesophagitis in patients with reflux symptoms.
Material And Methods: The symptoms, demographic data, and physical examination results of the patients admitted with gastrointestinal complaints were recorded and oesophagogastroduodenoscopies were performed.
Nutrients
December 2024
Oncological Gastroenterology, Centro di Riferimento Oncologico di Aviano (CRO), National Cancer Institute, IRCCS, 33081 Aviano, Italy.
Background/objectives: Gastric cancer (GC) incidence remains high worldwide, and the survival rate is poor. GC develops from atrophic gastritis (AG), associated with () infection, passing through intestinal metaplasia and dysplasia steps. Since eradication does not exclude GC development, further investigations are needed.
View Article and Find Full Text PDFBMJ Open Gastroenterol
January 2025
Gastroenterology, Homerton University Hospital, London, UK.
Objective: Gastric adenocarcinoma (GAC) is the 17th most common cancer in the UK with a 5-year survival rate of 22%. GastroPanel (Biohit Oyj; Helsinki, Finland) is an ELISA kit that measures pepsinogen I (PGI); pepsinogen II (PGII); gastrin-17 (G-17); and Helicobacter pylori IgG antibodies (Hp IgG). PGI and the PGI/PGII ratio correlate inversely with the severity of chronic atrophic gastritis (AG).
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