Article

Factors predicting progression of gastric intestinal metaplasia: Results of a randomised trial on Helicobacter pylori eradication

Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong, 00, Hong Kong
Gut (Impact Factor: 14.66). 10/2004; 53(9):1244-9. DOI: 10.1136/gut.2003.034629
Source: PubMed

ABSTRACT

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.
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.
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.
Eradication of H pylori is protective against progression of premalignant gastric lesions.

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Available from: Enders Ng, Sep 03, 2015
    • "Overall Wong et al, 2004 (7) Fukase et al, 2008 (6) Subtotal Leung et al, 2004 (3) Correa et al, 2000 (1) Subtotal Wong et al, 2012 (9) "
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    ABSTRACT: The effect of Helicobacter pylori (H. pylori) eradication on gastric cancer (GC) prevention is controversial. Intestinal metaplasia (IM) seems to be a "point of no return" in the precancerous cascade. We performed a meta-analysis of randomized controlled trials (RCTs) to illustrate this issue. The MEDLINE, EMBASE, Cochrane Library were searched for relevant RCTs that were published in any language up to March 2014. By dividing participants into subgroups based on their baseline diagnoses as group <IM (normal, non-atrophic gastritis, atrophic gastritis) and group ≥IM(intestinal metaplasia, dysplasia), the relative risk (RR) of GC in each study compared treatment group with control group were pooled using Mantel-Haenszel fixed-effect model and publication bias analyses were performed. Ten studies from eight RCTs were included in this analysis, for a total of 7,955 participants. H. pylori treatment compared with control significantly reduced the risk of GC, with a pooled RR of 0.64 (95 % CI, 0.48-0.85). Subgroup analysis for patients with non-atrophic gastritis, atrophic gastritis (<IM) yielded a similar results (RR = 0.25, 95 % CI, 0.08-0.81). But this difference was not observed in patients with intestinal metaplasia, dysplasia (≥IM) (RR = 0.88; 95 % CI, 0.59-1.31). Our results suggested that patients with Intestinal metaplasia or dysplasia could not benefit from the H. pylori treatment on the risk of GC.
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    • "mucins' profiling) and the IMextent (colonic-type metaplasia prevails significantly in extensive intestinalization), leading to the assumption that the topographical extent of IM per se is a reliable indicator of GC risk (given an appropriate endoscopic biopsy mapping) [20] [21]. Since gastric intestinalization is easy to assess histologically , the IM-extent can be assumed as a (clinically) useful marker of gastric cancer risk [20] [21] [22]. "
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    ABSTRACT: Gastric cancer is the final step in a multi-stage cascade triggered by long-standing inflammatory conditions (particularly Helicobacter pylori infection) resulting in atrophic gastritis and intestinal metaplasia: these lesions represent the cancerization field in which (intestinal-type) gastric cancer develops. Intraepithelial neoplasia is consistently recognized as the phenotypic bridge between atrophic/metaplastic lesions and invasive cancer. This paper addresses the epidemiology, pathology, molecular profiling, and clinical management of advanced precancerous gastric lesions.
    Full-text · Article · Apr 2013 · Best practice & research. Clinical gastroenterology
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    • "Identified risk factors for IM include H. pylori infection, high salt intake, smoking, alcohol consumption, and chronic bile reflux4142434445. It is not clear how metaplastic cells emerge, or what cell they emerge from, but the new cell type is presumably better suited to withstand the altered environment. "

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