title: Reversal of fundic atrophy after eradication of Helicobacter pylori.
abstract: OBJECTIVE
  We sought to evaluate the effect of Helicobacter pylori eradication in patients with fundic atrophic gastritis.
  
  
  METHODS
  Acid secretion, gastric emptying, and histology were evaluated in 20 patients with fundic atrophic gastritis and H. pylori infection. After investigation, 10 patients (Group 1) received an eradicating treatment and 10 (Group 2) did not receive any treatment. One year later, the baseline investigations were repeated. Subsequently, patients in Group 2 received the same treatment given to patients in Group 1 and were reevaluated 12 months later. A further follow-up was performed in both groups 36 months after the treatment.
  
  
  RESULTS
  At 1-yr follow-up, all the patients in Group 1 were H. pylori negative whereas all the patients in Group 2 were still infected. In Group 1, there was a significant improvement of both fundic atrophy and acid secretion, compared with baseline (p < 0.01). In Group 2, no substantial modification of either histological or functional parameters was observed at the first follow-up; conversely, a significant (p < 0.01) improvement of fundic atrophy and acid secretion was detected in these patients 12 months after eradication of the bacterium. Histological pattern remained unchanged at 36 months of follow-up in both groups. Gastric emptying remained, on the average, unaffected by the treatment; however, three patients with delayed gastric emptying at entry had normal gastric emptying after eradication of H. pylori.
  
  
  CONCLUSIONS
  Our data suggest that mucosal atrophy can be reduced or even reversed by the eradication of H. pylori, and this is associated with a recovery of gastric function.
authors.affiliation: Institute of Medical Clinic & Gastroenterology, Department of Pathology, Hospital S. Orsola-Malpighi, University of Bologna, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Tucci
authors.forename: L
authors.initials: L
authors.lastname: Poli
authors.forename: C
authors.initials: C
authors.lastname: Tosetti
authors.forename: G
authors.initials: G
authors.lastname: Biasco
authors.forename: W
authors.initials: W
authors.lastname: Grigioni
authors.forename: O
authors.initials: O
authors.lastname: Varoli
authors.forename: C
authors.initials: C
authors.lastname: Mazzoni
authors.forename: G F
authors.initials: GF
authors.lastname: Paparo
authors.forename: V
authors.initials: V
authors.lastname: Stanghellini
authors.forename: G
authors.initials: G
authors.lastname: Caletti
mesh_terms: D000658:Amoxicillin / Q000627:therapeutic use; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000627:therapeutic use; D001284:Atrophy / Q000188:drug therapy / Q000473:pathology; D005260:Female; D005500:Follow-Up Studies; D005744:Gastric Acid / Q000378:metabolism; D005746:Gastric Emptying; D005748:Gastric Fundus / Q000473:pathology; D005756:Gastritis / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology*; D016481:Helicobacter Infections / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008795:Metronidazole / Q000627:therapeutic use; D008875:Middle Aged; D009942:Organometallic Compounds / Q000627:therapeutic use
chemical_list: D000900:Anti-Bacterial Agents; D000897:Anti-Ulcer Agents; D009942:Organometallic Compounds; D008795:Metronidazole; D000658:Amoxicillin; C002791:bismuth tripotassium dicitrate