Effects of high dose vitamin C treatment on Helicobacter pylori infection
and total vitamin C concentration in gastric juice.
Jarosz M; Dzieniszewski J; Dabrowska-Ufniarz E; Wartanowicz M; Ziemlanski
S; Reed PI
European Journal of Cancer Prevention 1998 Dec;7(6):449-54
gastric juice total vitamin C concentration in the presence of Helicobacter
pylori (H. pylori) infection probably plays a role in gastric carcinogenesis.
In vitro vitamin C has been shown to inhibit the growth of H. pylori.
The aims of this study were to determine the effect of high dose vitamin
C administration on H. pylori infection and on gastric juice total vitamin
C concentration in patients with H. pylori related chronic gastritis.
Sixty patients with dyspeptic symptoms and proven chronic gastritis and
H. pylori infection, who were undergoing routine endoscopy, entered the
study after giving informed consent. They were randomly coded into two
treatment groups. Group 1 (controls, n = 28) were treated with antacids
for 4 weeks and Group 2 (n = 32) received vitamin C 5g daily also for
4 weeks. Nine patients did not complete the study and were excluded. Plasma
and gastric juice total vitamin C levels were measured at baseline, at
the end of 4 weeks treatment and again 4 weeks after treatment cessation.
In the control group H. pylori infection remained unchanged in all 24
patients throughout as did the mean gastric juice total vitamin C concentration.
However, in the vitamin C treated group eight of 27 patients (30%) who
completed the treatment course the H. pylori infection was eradicated
(P = 0.01). In these patients the mean gastric juice total vitamin C concentration
rose significantly from 7.2 +/- 1.6 micrograms/ml after 4 weeks treatment
(P < M 0.001) and 19.8 micrograms/ml 4 weeks after treatment was discontinued
(P < 0.001). In the remaining 19 patients with persistent H. pylori
infection, the mean gastric juice total vitamin C concentration rose less
than in those with successful H. pylori eradication; 6.3 +/- 1.7 micrograms/ml
before treatment, 10.8 +/- 1.5 micrograms/ml after 4 weeks treatment (P
< 0.05) and a return to pre-treatment levels (7.1 +/- 2.7 micrograms/ml)
4 weeks after vitamin C intake stopped. There were no side effects of
vitamin C treatment. This study has shown that 4 weeks daily high
dose vitamin C treatment in H. pylori infected patients with chronic gastritis
resulted in apparent H. pylori eradication in 30% of those treated. In
those patients there was also a highly significant rise in gastric juice
total vitamin C concentration which persisted for at least 4 weeks after
the treatment ceased. A significant, though less marked, gastric juice
total vitamin C concentration increase was observed during vitamin C treatment
even in subjects with persistent H. pylori infection, though this was
not maintained after treatment ended. The mechanism whereby vitamin C
treatment appeared to result in H. pylori eradication is unclear.