title: Duodenal erosions after eradication of Helicobacter pylori infection.
abstract: BACKGROUND
  There is interest in the development of GERD after Helicobacter pylori eradication. In contrast, the development of duodenal erosions after therapy has received scant attention. Patients were examined after eradication of H pylori infection to determine the frequency of post-therapy duodenal erosions (primary outcome) and whether there was a relation between development of duodenal and esophageal erosions. Additionally, factors were searched for that would identify patients at increased risk for duodenal erosions.
  
  
  METHODS
  A single-center, endoscopist-blinded, observational study was conducted of 196 patients in whom H pylori was eradicated. The presence of esophageal or duodenal erosions was evaluated 4 weeks and 6 months after eradication. Serum gastrin and pepsinogen I (PG I) and II (PG II) levels were also determined for 83 patients entering the study during its final year.
  
  
  RESULTS
  Multiple small duodenal erosions developed in 8.6% of patients after H pylori eradication and were more common in patients with pre-eradication duodenal ulcer (27.8%) compared with those with gastric ulcer (6.7%) or atrophic gastritis (1.4%) (p < 0.05). Duodenal erosions were associated with high levels of PG I before and after eradication. The frequency of duodenal erosions decreased over time (3.1% by 6 months).
  
  
  CONCLUSIONS
  Duodenal erosions occur after H pylori eradication and appear to be related to duodenal ulcer and increased PG I levels, both of which are associated with increased acid secretion. Measurement of PG I may help to identify patients who have duodenal erosions develop after H pylori therapy for studies of the pathogenesis of these lesions.
authors.affiliation: Second Department of Internal Medicine, Wakayama Medical College, 811-1 Kimidera, Wakayama-city, Wakayama, Prefecture 641-0012, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Shiotani
authors.forename: S
authors.initials: S
authors.lastname: Nishioka
authors.forename: M
authors.initials: M
authors.lastname: Iguchi
authors.forename: K
authors.initials: K
authors.lastname: Yanaoka
authors.forename: K
authors.initials: K
authors.lastname: Okada
authors.forename: H
authors.initials: H
authors.lastname: Tamai
authors.forename: Y
authors.initials: Y
authors.lastname: Mantani
authors.forename: H
authors.initials: H
authors.lastname: Itoh
authors.forename: D Y
authors.initials: DY
authors.lastname: Graham
mesh_terms: D004381:Duodenal Ulcer / Q000382:microbiology; D004386:Duodenum / Q000473:pathology*; D016145:Endoscopy, Digestive System; D004947:Esophagus / Q000473:pathology; D005260:Female; D005500:Follow-Up Studies; D005755:Gastrins / Q000097:blood; D005757:Gastritis, Atrophic / Q000382:microbiology; D016481:Helicobacter Infections / Q000188:drug therapy / Q000473:pathology*; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008875:Middle Aged; D020116:Pepsinogen A / Q000097:blood; D020115:Pepsinogen C / Q000097:blood; D011446:Prospective Studies; D013276:Stomach Ulcer / Q000382:microbiology; D013997:Time Factors
chemical_list: D005755:Gastrins; D020115:Pepsinogen C; D020116:Pepsinogen A