Histological and functional recovery in patients with multifocal atrophic gastritis after eradication of Helicobacter pylori infection

Background/Aims. To assess the effect of Helicobacter pylori eradication on gastric histology and physiology in patients with multifocal atrophic gast ritis over 1-year period. Patients. Fourteen consecutive patients with histological evidence of chron ic gastritis and Helicobacter pylori infection diagnosed by by histology an d serology entered this study. Patients with pernicious anaemia, gastric ul cer 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 oil the basis of negative CLO t est and histology as well as 50% decrease in IgG antibodies after 4 weeks a nd 6 months of treatment, respectively Histological and functional investig ations were performed at baseline, 6 and 12 months after Helicobacter pylor i eradication. Histological assessment of inflammatory cell infiltrates was performed on multiple biopsy specimens of the corpus and fundus. Functiona l tests were 24-hour continuous gastric pH-metry, fasting serum gastrin ass ay and pepsinogen 1 levels. Results. There was a progressive significant improvement (p<0.01-0.001) in acute and chronic inflammatory cell infiltrates in the gastric mucosa throu ghout the 12-month period Functional recovery with increase in gastric acid ity (p<0.01) and decrease ill gastrin and pepsinogen I levels (p<0.001) was more evident at the 6-month than at the 12-month checkpoint after Helicoba cter pylori eradication (p=NS for gastric pH and p<0.02 for the other two v ariables) between 6 and 12 months. Conclusions. Eradication of Helicobacter pylori infection significantly imp roves the inflammatory status of oxyntic mucosa and this promotes an almost complete functional recovery However, the non-parallel behaviour of gastri c acidity, which was maximal at 6-month checkpoint, and histological parame ters which continued to improve throughout the entire 12-month observation period, seems to indicate that removal of acid-inhibitory substances induce d by Helicobacter pylori infection was also responsible for the more rapid recovery of gastric secretory function.