Open AccessThe effect of 5‐year vitamin C supplementation on serum pepsinogen level and Helicobacter pylori infection
Author(s) -
Sasazuki Shizuka,
Sasaki Satoshi,
Tsubono Yoshitaka,
Okubo Shunji,
Hayashi Masato,
Kakizoe Tadao,
Tsugane Shoichiro
Publication year - 2003
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/j.1349-7006.2003.tb01450.x
Subject(s) - medicine , gastroenterology , helicobacter pylori , gastritis , vitamin , pepsin , population , atrophic gastritis , randomized controlled trial , vitamin c , spirillaceae , biology , enzyme , biochemistry , environmental health
We conducted a population‐based, double‐blind, randomized controlled trial to examine the effect of vitamin C supplementation on serum pepsinogen (PG) level, Helicobacter pylori (H. pylori) infection, and cytotoxin‐associated gene A ( Cag A ) status. Subjects aged 40 to 69 years living in one village in Akita prefecture, a high‐risk area for gastric cancer in Japan, were recruited through annual health check‐up programs. Among 635 subjects diagnosed as having chronic gastritis on the basis of serum PG levels, after excluding ineligible cases, 439 subjects were assigned to one of four groups using a 2×2 factorial design (0 or 15 mg/day β‐carotene and 50 or 500 mg/day vitamin C). However, based on the results from two β‐carotene trials in the United States, we discontinued β‐carotene (vitamin C supplementation was continued). Finally, 120 subjects in the low‐dose group (vitamin C 50 mg), and 124 subjects in the high‐dose group (vitamin C 500 mg) completed the 5‐year supplementation. The difference in the change of PGI/II ratio between baseline and after 5‐year follow up was statistically significant between the intervention groups among those who completed the supplementation: ‐0.25 for the low‐dose group and ‐0.13 for the high‐dose group ( P =0.046). To conclude, vitamin C supplementation may protect against progression of gastric mucosal atrophy. (Cancer Sci 2003; 94: 378–382)