Factors predicting progression of gastric intestinal metaplasia: results of a randomised trial on Helicobacter pylori eradication.
OBJECTIVE
Gastric intestinal metaplasia (IM) is generally considered to be a precancerous lesion in the gastric carcinogenesis cascade. This study identified the risk factors associated with progression of IM in a randomised control study.


METHODS
A total of 587 Helicobacter pylori infected subjects were randomised to receive a one week course of anti-Helicobacter therapy (omeprazole, amoxicillin, and clarithromycin (OAC)) or placebo. Subjects underwent endoscopy with biopsy at baseline and at five years. Severity of IM was graded according to the updated Sydney classification and progression was defined as worsening of IM scores at five years in either the antrum or corpus, or development of neoplasia. Backward stepwise multiple logistic regression was used to identify independent risk factors associated with IM progression.


RESULTS
Of 435 subjects (220 in the OAC and 215 in the placebo group) available for analysis, 10 developed gastric cancer and three had dysplasia. Overall progression of IM was noted in 52.9% of subjects. Univariate analysis showed that persistent H pylori infection, age >45 years, male subjects, alcohol use, and drinking water from a well were significantly associated with IM progression. Duodenal ulcer and OAC treatment were associated with a reduced risk of histological progression. Progression of IM was more frequent in those with more extensive and more severe IM at baseline. With multiple logistic regression, duodenal ulcer (odds ratio (OR) 0.23 (95% confidence interval (CI) 0.09-0.58)) was found to be an independent protective factor against IM progression. Conversely, persistent H pylori infection (OR 2.13 (95% CI 1.41-3.24)), age >45 years (OR 1.92 (95% CI 1.18-3.11)), alcohol use (OR 1.67 (95% CI 1.07-2.62)), and drinking water from a well (OR 1.74 (95% CI 1.13-2.67)) were independent risk factors associated with IM progression.


CONCLUSIONS
Eradication of H pylori is protective against progression of premalignant gastric lesions.
Leung
W K
WK
Department of Medicine and Therapeutics, Prince of Wales Hospital, 30-32 Ngan Shing Street, Shatin, Hong Kong.
Lin
S-R
SR
Ching
J Y L
JY
To
K-F
KF
Ng
E K W
EK
Chan
F K L
FK
Lau
J Y W
JY
Sung
J J Y
JJ
D000368:Aged; D000658:Amoxicillin / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000627:therapeutic use; D017291:Clarithromycin / Q000627:therapeutic use; D018450:Disease Progression; D004359:Drug Therapy, Combination / Q000627:therapeutic use*; D005260:Female; D005756:Gastritis / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000150:complications / Q000188:drug therapy*; D016480:Helicobacter pylori; D006801:Humans; D016015:Logistic Models; D008297:Male; D008679:Metaplasia / Q000382:microbiology / Q000473:pathology; D008875:Middle Aged; D009853:Omeprazole / Q000627:therapeutic use; D011230:Precancerous Conditions / Q000382:microbiology* / Q000473:pathology; D011446:Prospective Studies; D012307:Risk Factors; D013274:Stomach Neoplasms / Q000382:microbiology* / Q000473:pathology / Q000517:prevention & control
D000897:Anti-Ulcer Agents; D000658:Amoxicillin; D017291:Clarithromycin; D009853:Omeprazole