title: Helicobacter pylori associated gastric diseases and lymphoid tissue hyperplasia in gastric antral mucosa.
abstract: OBJECTIVE
  To investigate the relation between Helicobacter pylori associated gastroduodenal diseases and lymphoid tissue hyperplasia in the antral mucosa and to pursue its evolution after eradication of H pylori.
  
  
  METHODS
  Gastric antral biopsy specimens were obtained from 438 patients with H pylori positive gastroduodenal diseases (185 chronic gastritis, 69 gastric ulcer, and 184 duodenal ulcer) and 50 H pylori negative healthy controls. Lymphoid follicles and aggregates were counted and other pathological features were scored according to the updated Sydney system for classification of chronic gastritis. After a course of anti-H pylori treatment, biopsy specimens were obtained at four to six weeks, 12 months, and 24 months in the chronic gastritis patient group.
  
  
  RESULTS
  The total prevalence of lymphoid follicles and aggregates in the biopsies was 79.9% (350 of 438; 95% confidence intervals (CI), 0.76 to 0.84). The prevalence and density of lymphoid follicles and aggregates were significantly different in the various gastroduodenal diseases. The highest prevalence (89.9%; 95% CI, 0.83 to 0.97) and density (0.82) of lymphoid follicles and aggregates occurred in patients with gastric ulcers. The lowest prevalence of lymphoid follicles and aggregates was found in patients with chronic gastritis (74.6%; 95% CI, 0.68 to 0.81), and the lowest density of lymphoid follicles and aggregates (0.56) was seen in patients with duodenal ulcers. The prevalence and density of lymphoid follicles and aggregates correlated strongly with the activity and severity of gastric antral mucosal inflammation. The eradication of H pylori resulted in a decrease in the prevalence and density of lymphoid follicles and aggregates.
  
  
  CONCLUSIONS
  The prevalence and density of lymphoid follicles and aggregates in gastric antral mucosal biopsies correlated closely with H pylori infection.
authors.affiliation: Department of Pathology, Renji Hospital, Shanghai Second Medical University, Shanghai Institute of Digestive Disease, Shanghai 200001, China. xiaoyu64@public7.sta.ne.cn
authors.forename: X Y
authors.initials: XY
authors.lastname: Chen
authors.forename: W Z
authors.initials: WZ
authors.lastname: Liu
authors.forename: Y
authors.initials: Y
authors.lastname: Shi
authors.forename: D Z
authors.initials: DZ
authors.lastname: Zhang
authors.forename: S D
authors.initials: SD
authors.lastname: Xiao
authors.forename: G N J
authors.initials: GN
authors.lastname: Tytgat
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D002908:Chronic Disease; D004381:Duodenal Ulcer / Q000382:microbiology / Q000473:pathology; D005260:Female; D005500:Follow-Up Studies; D005753:Gastric Mucosa / Q000473:pathology; D005756:Gastritis / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000150:complications* / Q000188:drug therapy; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008875:Middle Aged; D019310:Pseudolymphoma / Q000382:microbiology* / Q000473:pathology; D013272:Stomach Diseases / Q000382:microbiology* / Q000473:pathology; D013276:Stomach Ulcer / Q000382:microbiology / Q000473:pathology