Differential effects of Helicobacter pylori eradication on oxidative DNA damage at the gastroesophageal junction and at the gastric antrum.
OBJECTIVE
Helicobacter pylori-associated gastritis causes accumulation of reactive oxygen species in the mucosal compartment. This prospective study evaluates DNA oxidative damage in biopsy samples obtained from both the antrum and the gastroesophageal junction (GEJ) before and after H. pylori eradication.


METHODS
Thirty-two consecutive H. pylori-positive patients underwent endoscopy with multiple biopsy sampling (i.e., antrum, incisura angularis, fundus, and cardia at the GEJ). After H. pylori eradication, 32 patients underwent a checkup endoscopy (mean interval, 5.7 months); in a subgroup of 13 subjects, a third endoscopy procedure was also performed (mean interval, 18 months). Additional biopsy samples (two from the antrum and two from the GEJ) were used to assess 8-hydroxydeoxyguanosine (8OHdG) levels using both high-pressure liquid chromatography with electrochemical detector and ELISA.


RESULTS
In the antral compartment, no significant modifications of 8OHdG levels were assessed after H. pylori eradication. Conversely, following eradication, 8OHdG levels significantly increased (high-pressure liquid chromatography with electrochemical detector, P = 0.04; ELISA method, P = 0.05) in biopsy samples taken from the GEJ, and a further increase was documented in the subgroup of patients who underwent a third endoscopy (P = 0.01). The increasing trend was more relevant in patients in whom H. pylori-cagA-positive strains were eradicated and in those affected by hiatal hernia.


CONCLUSIONS
The levels of DNA adducts in the antral mucosa are not modified by H. pylori eradication; conversely, H. pylori eradication significantly increases the oxidative adducts at the GEJ. The clinical and biological importance of this situation and whether and how it relates to a higher risk of precancerous lesions is open to debate.
Farinati
Fabio
F
Dipartimento di Scienze Chirurgiche e Gastroenterologiche, Sezione di Gastroenterologia, Policlinico Universitario, Via Giustiniani 2, 35128 Padova, Italy. fabio.farinati@unipd.it
Cardin
Romilda
R
Russo
Valentina M
VM
Busatto
Graziella
G
Franco
Monica
M
Falda
Alessandra
A
Mescoli
Claudia
C
Rugge
Massimo
M
D000897:Anti-Ulcer Agents / Q000627:therapeutic use*; D018736:DNA Adducts / Q000187:drug effects / Q000302:isolation & purification; D004249:DNA Damage; D004935:Esophageal Diseases / Q000188:drug therapy* / Q000382:microbiology / Q000473:pathology; D004943:Esophagogastric Junction / Q000382:microbiology*; D005260:Female; D005756:Gastritis / Q000188:drug therapy* / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008875:Middle Aged; D009853:Omeprazole / Q000627:therapeutic use*; D011446:Prospective Studies; D011706:Pyloric Antrum / Q000382:microbiology*
D000897:Anti-Ulcer Agents; D018736:DNA Adducts; D009853:Omeprazole