Relationship of Helicobacter pylori CagA(+) status to gastric juice vitamin C levels.
BACKGROUND
To date it is not known whether gastric juice vitamin C levels are influenced by Helicobacter pylori CagA(+) strains. The aim of the present study, therefore, was to study the impact of H. pylori CagA status on gastric juice vitamin C levels.


METHODS
We studied 30 H. pylori(+) patients, and the results were compared with 10 endoscopically and histologically normal H. pylori(-) subjects (control group) who were similar to the H. pylori(+) group in terms of age and sex. In all patients, gastric juice vitamin C levels were determined and the severity of gastritis was graded on a scale of 0 (absent) to 3 (severe). CagA was determined by immunoblotting the sera from patients against H. pylori antigens.


RESULTS
Among 30 H. pylori(+) patients, 20 were CagA(+) and 10 CagA(-). In the entire group of H. pylori(+) patients, the median gastric juice vitamin C levels (mg L-1) were 16.35 (range 3.5-33.6) and were significantly lower (P < 0.001) than in the control group of H. pylori(-) patients [35.5 (23.1-50.2)]. In addition, in the entire group of H. pylori(+) patients there was a highly significant (P < 0.0001) inverse correlation between the gastritis activity score and the gastric juice vitamin C levels. In the group of H. pylori CagA(+) patients, the median levels of gastric juice vitamin C were 13.8 (3.5-31.2) and were significantly lower than the corresponding levels in both the H. pylori CagA(-) group [24.8 (22-33.6), P < 0.01] and the H. pylori(-) control group [35.5 (23.1-50.2), P < 0.001], the last groups being similar. Furthermore, the gastritis activity median score in the H. pylori CagA(+) group [2 (1-3)] was significantly higher (P < 0.05) than in the H. pylori CagA(-) group [1 (1-2)].


CONCLUSIONS
These data indicate that infection with CagA(+) H. pylori strains significantly lowers the gastric juice vitamin C levels in comparison with CagA(-) H. pylori strains, which might have a significant impact on gastric carcinogenesis.
Rokkas
T
T
Gastroenterology Unit, Army General Hospital, Athens, Greece. sakkor@compulink.gr
Liatsos
C
C
Petridou
E
E
Papatheodorou
G
G
Karameris
A
A
Ladas
S D
SD
Raptis
S A
SA
D000293:Adolescent; D000328:Adult; D000907:Antibodies, Bacterial / Q000097:blood; D000942:Antigens, Bacterial; D001205:Ascorbic Acid / Q000032:analysis*; D001426:Bacterial Proteins / Q000276:immunology / Q000302:isolation & purification*; D015153:Blotting, Western; D002908:Chronic Disease; D005260:Female; D005750:Gastric Juice / Q000737:chemistry*; D005756:Gastritis / Q000209:etiology*; D016481:Helicobacter Infections / Q000276:immunology / Q000382:microbiology*; D016480:Helicobacter pylori / Q000737:chemistry*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies
D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori; D001205:Ascorbic Acid