title: Relationship between fundic endocrine cells and gastric acid secretion in hypersecretory duodenal ulcer diseases.
abstract: BACKGROUND
  Acid hypersecretion is associated with duodenal ulcer disease in the following conditions: Zollinger-Ellison syndrome (ZES) and antral gastrin cell hyperfunction (AGCH) due to hypergastrinaemia, or hypersecretory duodenal ulcer (HDU) without hypergastrinaemia.
  
  
  OBJECTIVE
  To evaluate whether quantitative changes in fundic ECL and D cells may be involved in acid hypersecretion.
  
  
  METHODS
  Seven ZES, six AGCH and six HDU Helicobacter pylori-positive patients were compared. Basal (BAO) and pentagastrin-stimulated gastric acid secretions (PAO), and morphometry of fundic ECL and D cells were performed. The six AGCH and six HDU patients were investigated again using the same tests 1 year after H. pylori eradication.
  
  
  RESULTS
  Median PAO values were no different in all the hypersecretory conditions studied. The median volume density of ECL cells in ZES was significantly higher than in controls (2.75, range 1.74-5.8 vs. 0.73, 0.52-1.11: P < 0.05), whereas it was in the control range in AGCH and HDU patients (0.77, range 0.20-1.39 and 0.99, range 0.42-1.51; respectively). The count of fundic D cells was significantly lower in AGCH patients than in all other investigated groups (median 0.16, range 0.1-0.52; P < 0.05). Cure of infection in AGCH and HDU patients did not modify the ECL cell volume density, whereas a significant increase in the count of fundic D cells was observed in AGCH patients. Thus, the ECL/D cell index was significantly affected in AGCH patients (P < 0.05), being higher during H. pylori infection (median 6, range 0.7-9.25) than after the cure (median 2.12, range 1.10-3.5). BAO and PAO were not affected by H. pylori eradication in either group.
  
  
  CONCLUSIONS
  The study provides evidence, for the first time, that quantitative alterations in the fundic endocrine cells are not involved in acid hypersecretion of patients with hypersecretory states, and that eradication of H. pylori does not restore normal acid secretion values.
authors.affiliation: IV Surgical Department, University La Sapienza, Rome, Italy.
authors.forename: B
authors.initials: B
authors.lastname: Annibale
authors.forename: M R
authors.initials: MR
authors.lastname: Aprile
authors.forename: G
authors.initials: G
authors.lastname: Ferraro
authors.forename: M
authors.initials: M
authors.lastname: Marignani
authors.forename: S
authors.initials: S
authors.lastname: Angeletti
authors.forename: G
authors.initials: G
authors.lastname: D'Ambra
authors.forename: P
authors.initials: P
authors.lastname: Caruana
authors.forename: C
authors.initials: C
authors.lastname: Bordi
authors.forename: G
authors.initials: G
authors.lastname: Delle Fave
mesh_terms: D000328:Adult; D004381:Duodenal Ulcer / Q000382:microbiology / Q000503:physiopathology*; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005748:Gastric Fundus / Q000166:cytology / Q000502:physiology*; D019863:Gastrin-Secreting Cells / Q000502:physiology; D016481:Helicobacter Infections / Q000188:drug therapy / Q000503:physiopathology; D016480:Helicobacter pylori / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010418:Pentagastrin / Q000494:pharmacology; D015043:Zollinger-Ellison Syndrome / Q000503:physiopathology*
chemical_list: D010418:Pentagastrin