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  • Title: Histological and functional recovery in patients with multifocal atrophic gastritis after eradication of Helicobacter pylori infection.
    Author: Savarino V, Mela GS, Zentilin P, Lapertosa G, Bisso G, Mele MR, Pivari M, Mansi C, Vigneri S, Celle G.
    Journal: Ital J Gastroenterol Hepatol; 1999; 31(1):4-8. PubMed ID: 10091096.
    Abstract:
    BACKGROUND/AIMS: To assess the effect of Helicobacter pylori eradication on gastric histology and physiology in patients with multifocal atrophic gastritis over 1-year period. PATIENTS: Fourteen consecutive patients with histological evidence of chronic gastritis and Helicobacter pylori infection diagnosed by histology and serology entered this study. Patients with pernicious anaemia, gastric ulcer or carcinoma, duodenal ulcer, reflux oesophagitis and regular intake of nonsteroidal anti-inflammatory drugs were excluded. METHODS: Patients underwent triple anti-Helicobacter treatment for one week, which resulted successful in all subjects on the basis of negative CLO test and histology as well as 50% decrease in IgG antibodies after 4 weeks and 6 months of treatment, respectively. Histological and functional investigations were performed at baseline, 6 and 12 months after Helicobacter pylori eradication. Histological assessment of inflammatory cell infiltrates was performed on multiple biopsy specimens of the corpus and fundus. Functional tests were 24-hour continuous gastric pH-metry, fasting serum gastrin assay and pepsinogen I levels. RESULTS: There was a progressive significant improvement (p < 0.01-0.001) in acute and chronic inflammatory cell infiltrates in the gastric mucosa throughout the 12-month period. Functional recovery with increase in gastric acidity (p < 0.01) and decrease in gastrin and pepsinogen I levels (p < 0.001) was more evident at the 6-month than at the 12-month checkpoint after Helicobacter pylori eradication (p = NS for gastric pH and p < 0.02 for the other two variables) between 6 and 12 months. CONCLUSIONS: Eradication of Helicobacter pylori infection significantly improves the inflammatory status of oxyntic mucosa and this promotes an almost complete functional recovery. However, the non-parallel behaviour of gastric acidity, which was maximal at 6-month checkpoint, and histological parameters which continued to improve throughout the entire 12-month observation period, seems to indicate that removal of acid-inhibitory substances induced by Helicobacter pylori infection was also responsible for the more rapid recovery of gastric secretory function.
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