Changing patterns of Helicobacter pylori gastritis in long-standing acid suppression.
BACKGROUND
Helicobacter pylori colonization and associated inflammation are influenced by local acid output. Infected subjects with acid-related diseases, such as gastroesophageal reflux disease (GERD) are likely to have an antral-predominant gastritis. We hypothesized that long-term acid suppression would result in relatively greater bacterial colonization in the corpus leading to diffuse or corpus-predominant gastritis and that this would be prevented by prior H. pylori eradication.


METHODS
To investigate this, we conducted a prospective, double-blind trial of the effect on gastric histology of 12-month maintenance treatment with omeprazole in H. pylori-positive GERD patients randomly assigned to either an eradication or omeprazole-alone regime. A control group of 20 H. pylori-negative GERD patients also received omeprazole throughout the study period. Biopsies taken at baseline and at 12 months were graded "blind" by a single observer according to the updated Sydney System. The 41 H. pylori-positive subjects with grade B or C esophagitis were randomly assigned (20 to omeprazole alone, 21 to eradication) and 33 subjects completed the 12-month study.


RESULTS
There was a significant decline in antral chronic inflammation in initially positive patients between baseline and end in both the eradication group (p =.035) and the omeprazole-alone group (p =.008). However, corpus chronic inflammation increased in the omeprazole-alone group (p =.0156) but decreased in the eradication group. The change toward corpus predominance between baseline and end for the omeprazole-alone group is highly significant (p =.0078). Furthermore, 5 of 11 in the omeprazole-alone group developed mild corpus atrophy, compared to 0 of 8 who had undergone H. pylori eradication. The change in frequency of corpus atrophy between the two groups is significant (p =.02).


CONCLUSIONS
In H. pylori-positive subjects with GERD, long-term acid suppression leads to a shift from antral- to corpus-predominant gastritis that can be prevented by prior eradication. The shift is accompanied by an increase in corpus atrophy. H. pylori infection should be eradicated prior to long-term acid suppression with proton pump inhibitors.
Moayyedi
P
P
Centre for Digestive Diseases, General Infirmary at Leeds, Leeds, UK.
Wason
C
C
Peacock
R
R
Walan
A
A
Bardhan
K
K
Axon
A T
AT
Dixon
M F
MF
D000293:Adolescent; D000328:Adult; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000627:therapeutic use*; D017291:Clarithromycin / Q000627:therapeutic use; D004311:Double-Blind Method; D004359:Drug Therapy, Combination; D005260:Female; D005753:Gastric Mucosa / Q000382:microbiology* / Q000473:pathology; D005756:Gastritis / Q000188:drug therapy* / Q000382:microbiology / Q000473:pathology; D005764:Gastroesophageal Reflux / Q000188:drug therapy; D016481:Helicobacter Infections / Q000188:drug therapy / Q000382:microbiology; D016480:Helicobacter pylori / Q000254:growth & development*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D008875:Middle Aged; D009853:Omeprazole / Q000627:therapeutic use*; D011446:Prospective Studies; D014011:Tinidazole / Q000627:therapeutic use
D000900:Anti-Bacterial Agents; D000897:Anti-Ulcer Agents; D014011:Tinidazole; D017291:Clarithromycin; D009853:Omeprazole