title: Abnormal gastroesophageal flap valve is highly associated with endoscopic reflux esophagitis after Helicobacter pylori eradication.
abstract: BACKGROUND
  Whether or not eradicating Helicobacter pylori worsens reflux esophagitis remains controversial. We investigated the relationship between gastroesophageal flap valve grading and endoscopic reflux esophagitis (in patients with peptic ulcer and gastritis) before and after H. pylori eradication in a case controlled study. Whether endoscopic assessment of the gastroesophageal flap valve allows prediction of endoscopic reflux esophagitis development or exacerbation was also assessed.
  
  
  METHODS
  A total of 220 patients with peptic ulcer or chronic gastritis, who received H. pylori eradication therapy, were followed for at least 6 months (range, 6-34 months) for endoscopic changes. Another 88 age- and disease-matched H. pylori-positive controls, without eradication therapy, were also enrolled. Gastroesophageal flap valve grade (I-IV) was assessed using the Hill classification.
  
  
  RESULTS
  Endoscopic reflux esophagitis incidence was significantly (p < .01) higher in abnormal gastroesophageal flap valve (grades III and IV) than in normal gastroesophageal flap valve (grades I and II) cases in both H. pylori eradication and control groups. The rate of new endoscopic reflux esophagitis after eradication was significantly (p < .01) higher in the abnormal than in the normal gastroesophageal flap valve group (54.5% vs. 9.1%). By contrast, the endoscopic reflux esophagitis exacerbation rate in patients with endoscopic reflux esophagitis before eradication was low (4.5%) and endoscopic reflux esophagitis improvement was observed in 40.9% of these patients.
  
  
  CONCLUSIONS
  These results suggest gastroesophageal flap valve grading by endoscopy to be useful for predicting the risk of newly developing endoscopic reflux esophagitis after H. pylori eradication, in addition to predicting the presence of endoscopic reflux esophagitis.
authors.affiliation: 3rd Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
authors.forename: Rie
authors.initials: R
authors.lastname: Takeuchi
authors.forename: Kimitoshi
authors.initials: K
authors.lastname: Kato
authors.forename: Shigeaki
authors.initials: S
authors.lastname: Mizuno
authors.forename: Yo
authors.initials: Y
authors.lastname: Kawamura
authors.forename: Fumio
authors.initials: F
authors.lastname: Kawamura
authors.forename: Ariyoshi
authors.initials: A
authors.lastname: Iwasaki
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Arakawa
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D004942:Esophagitis, Peptic / Q000209:etiology*; D004943:Esophagogastric Junction / Q000473:pathology*; D004945:Esophagoscopy; D004947:Esophagus / Q000473:pathology*; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology*; D005756:Gastritis / Q000150:complications; D005773:Gastroscopy; D016481:Helicobacter Infections / Q000150:complications / Q000188:drug therapy*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010437:Peptic Ulcer / Q000150:complications; D012307:Risk Factors