[Helicobacter pylori and the progression of gastric cancer: a 10-year cohort study].
OBJECTIVE
To search the role of Helicobacter pylori (H. pylori) in the progression of gastric carcinogenesis.


METHODS
A cohort study was conducted by cluster randomized sampling in Linqu County, a rural area in Shandong Province in northeast China, where the mortality of gastric cancer (GC) is among the highest in the world. In 1989-1990, a gastroscopic examination and serum test was launched among subjects aged 35-64 from 14 randomized villages. Histological diagnosis of gastric mucosa and enzyme-linked immunosorbent assay was used to detect gastric lesions and anti-H. pylori of all participants. A repeated gastroscopic screening was offered to all cohort members in 1994 and 1999 respectively, and all the GC cases, regardless of natural ones or ones by gastroscopy, were registered in the follow-up periods.


RESULTS
Fifty-eight cases of GC were identified in 2469 subjects during the 10-year follow-up, 44 were observed in 1603 H. pylori-positive persons (2.74%) and 14 in 866 H. pylori-negative persons (1.62%). The incidence rate of GC in H. pylori-positive is significantly higher than in H. pylori-negative (OR = 1.871, 95% CI: 1.012 - 3.459). There was no significant difference in the progression of gastric carcinogenesis between H. pylori-positive and H. pylori-negative (P > 0.05) among subjects with normal or superficial gastritis (SG) at baseline. In contrast, the significant difference was found in baseline chronic gastritis (CAG) group (P < 0.01), and the GC incidence rate in H. pylori-positive (7/615) is higher than in H. pylori-negative (0/470, P = 0.019). The difference of gastric lesions between H. pylori-positive and H. pylori-negative in subjects with intestinal metaplasia (IM) and dysplasia (DYS) at baseline was statistically significant after a 10-year follow-up (P < 0.05, P < 0.01, respectively), but the GC incidence rate in H. pylori-positive is similar to the rate in H. pylori-negative at the two groups (17/573 and 7/224 in IM group, P = 0.907; 19/368 and 7/122 in DYS group, P = 0.806).


CONCLUSIONS
H. pylori is a key risk factor that prompts the transition from chronic atrophic gastritis to advanced precancerous lesions and influences the whole progression of precancerous gastric lesions. H. pylori, perhaps can not cause GC directly, increases the risk of GC in company with other carcinogens. H. pylori seemingly has no important effect on the development of GC when gastric mucosa is normal or superficial gastritis, but this conclusion is required to be further confirmed.
Ma
Jun-ling
JL
Department of Epidemiology, School of Oncology, Peking University, Beijing 100034, China.
Zhang
Lian
L
Pan
Kai-feng
KF
Liu
Wei-dong
WD
Feng
Guo-shuang
GS
You
Wei-cheng
WC
D000328:Adult; D015331:Cohort Studies; D005260:Female; D005753:Gastric Mucosa / Q000382:microbiology / Q000473:pathology*; D005773:Gastroscopy; D016481:Helicobacter Infections / Q000382:microbiology*; D016480:Helicobacter pylori / Q000302:isolation & purification* / Q000472:pathogenicity; D006801:Humans; D008297:Male; D008875:Middle Aged; D012494:Sampling Studies; D013274:Stomach Neoplasms / Q000382:microbiology* / Q000473:pathology