title: Gastroduodenal Changes Two Years After Eradication of Helicobacter pylori in a Population-Based Cohort.
abstract: BACKGROUND
  The main cause of chronic gastritis isHelicobacter pylori (H. pylori)infection. Some individuals withH. pylori-related chronic gastritis develop atrophy of the gastric mucosa, a risk factor for gastric neoplasia. WhenH. pylori-associated gastritis is encountered, it is important to be aware of its natural history and reversibility of associated histopathological and hormonal changes.
  
  
  METHODS
  A sample of 501 volunteers from the general population in the municipality of Linkoping, Sweden, was examined with esophago-gastro-duodenoscopy (EGD) with biopsy. Blood samples were collected in the fasting state and the subjects answered a questionnaire concerning lifestyle factors, medications and disease history. At a primary follow-up examination, after 8 years, 314 participants were re-examined and those infected withH. pylorireceived eradication. Two years after successful eradication therapy, 82 participants attended re-examination with EGD and blood sampling, as in the previous examinations.
  
  
  RESULTS
  In this prospective cohort study of a sample of volunteers from the general population, all of the 82 participants had chronic gastritis with at least one positiveH. pyloritest before eradication therapy. During follow-up, non-steroid-inflammatory-drug (NSAID) use had decreased significantly (P = 0.007, McNemar). TheH. pyloriserology was still positive in 79/82 subjects (P = 0.007, McNemar). The basal gastrin and cholecystokinin (CCK) concentrations both had decreased (P < 0.001 for both, Wilcoxon), whereas the P-somatostatin had increased (P < 0.001, Wilcoxon). Symptoms included in the self-administered symptom questionnaire concerned the last 3 months showed no big difference at all. The inflammation had decreased in both antrum (before 2/38/42/0 and after 60/22/0/0, P < 0.0001) and corpus (before 3/54/22/3 and after 58/23/1/0, P < 0.0001). Changes in the inflammatory activity had decreased significantly in both the antrum (P < 0.001) and the corpus (P < 0.001). Intestinal metaplasia was without changes. Regarding the duodenal bulb, the inflammation decreased.
  
  
  CONCLUSIONS
  Being aware of the natural history of chronic gastritis, even beyond eradication ofH. pylori, is important because of the associations to gastric neoplasia and ulcer disease. The blood mirror of gastroduodenal parameters showed decreased values, except for somatostatin that increased and a symptomatology with no significant changes although, morphologically determined, both inflammation and atrophy had decreased.
authors: Department of Surgery and Department of Clinical and Experimental Medicine, Linkoping University, 58185 Linkoping, Sweden.
authors: Stefan
authors: S
authors: Redeen
authors: Department of Pathology, National University Health System, 119074 Singapore, Singapore.
authors: Fredrik
authors: F
authors: Petersson
authors: Department of Surgery and Department of Clinical and Experimental Medicine, Linkoping University, 58185 Linkoping, Sweden.
authors: Stergios
authors: S
authors: Kechagias
authors: Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Denmark.
authors: Jens
authors: J
authors: Rehfeld
authors: Department of Surgery and Department of Clinical and Experimental Medicine, Linkoping University, 58185 Linkoping, Sweden.
authors: Kurt
authors: K
authors: Borch
keywords: Duodenitis; Follow-up; Gastrin; Gastritis; Helicobacter pylori; Metaplasia; Somatostatin; Symptoms