title: Evolution of gastritis in patients with gastric erosions.
abstract: OBJECTIVE
  Gastric erosions are mainly associated with Helicobacter pylori infection and non-steroidal anti-inflammatory drugs (NSAIDs), but there has been no information available on the long-term evolution of gastritis in subjects with erosions.
  
  
  METHODS
  A series of 117 patients with gastric erosions without peptic ulcer disease and matched controls without erosions or ulcers were studied. Available subjects underwent endoscopy and biopsy 17 years later. Parietal cell antibodies were analysed at the first visit.
  
  
  RESULTS
  Fifty-two patients and 67 controls were available for follow-up. Since H. pylori was a major determinant of gastritis, only subjects with unchanged H. pylori status were included in the evaluation of gastritis progression. At the follow-up visit, gastric erosions were present in 38% (16/42) of the patients and 11% (5/46) of the controls (p=0.005). In H. pylori-negative subjects, no evolution of histological changes was seen. In H. pylori-positive subjects, body gastritis was initially less active in the erosion group. With time, antral gastritis worsened only in the erosion group. Parietal cell antibodies were more common in the control group (23%; erosion patients 0%; p=0.01), which also showed worsening of gastritis (p=0.003) and aggravation of atrophy (p=0.002) in the body mucosa.
  
  
  CONCLUSIONS
  Gastritis in H. pylori-positive subjects with gastric erosions shows evolution of antral predominance, body predominance including development of atrophic changes being rare. Accordingly, patients with erosions share the characteristics of gastritis of the duodenal ulcer phenotype. These findings support the importance of H. pylori and acid in the pathogenesis of gastric erosions in H. pylori-positive patients.
authors.affiliation: Department of Internal Medicine, Division of Gastroenterology, University of Oulu, Finland. kari.toljamo@tyks.fi
authors.forename: Kari T
authors.initials: KT
authors.lastname: Toljamo
authors.forename: Seppo E
authors.initials: SE
authors.lastname: Niemelä
authors.forename: Anna-Liisa
authors.initials: AL
authors.lastname: Karvonen
authors.forename: Tuomo J
authors.initials: TJ
authors.lastname: Karttunen
mesh_terms: D001707:Biopsy, Needle; D016022:Case-Control Studies; D015331:Cohort Studies; D018450:Disease Progression; D004381:Duodenal Ulcer / Q000473:pathology / Q000503:physiopathology; D005260:Female; D005387:Finland / Q000453:epidemiology; D005500:Follow-Up Studies; D005753:Gastric Mucosa / Q000382:microbiology / Q000473:pathology*; D005756:Gastritis / Q000453:epidemiology / Q000473:pathology*; D005773:Gastroscopy / Q000379:methods; D016481:Helicobacter Infections / Q000175:diagnosis / Q000453:epidemiology / Q000473:pathology*; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D010437:Peptic Ulcer / Q000473:pathology / Q000503:physiopathology; D012016:Reference Values; D018570:Risk Assessment; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric