Monika Laszkowska, James F O'Mahony, Daniela S Gutiérrez-Torres, John D Murphy, Omonefe Omofuma, Benjamin Blake, Margaret J Zhou, Duco T Mülder, M Constanza Camargo, Anne I Hahn, Robert J Huang, Chin Hur, Uri Ladabaum, Ann G Zauber, Reinier Meester, Iris Lansdorp-Vogelaar, Jennifer M Yeh
Journal: Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association 2024;22(8):1605-1617.e46
PMID: 38438000
BACKGROUND & AIMS
The prevalence of precursor lesions for gastric cancer (GC) and the differential burden between countries of varying GC risk is not well-understood. We conducted a systematic review and meta-analysis to estimate the global prevalence of precursor lesions.
METHODS
We estimated the prevalence of atrophic gastritis (AG), gastric intestinal metaplasia (IM), and dysplasia in regions with low, medium, and high GC incidence. Because IM is an advanced manifestation of AG, we assessed the prevalence of less advanced precursors, regardless of the presence of more advanced lesions. Prevalence was sub-stratified by Helicobacter pylori infection, symptomatology, and period (<2000, 2000-2010, and >2010).
RESULTS
Among the 582 articles that underwent full-text review, 166 studies met inclusion criteria. The global prevalence estimates of AG, IM, and dysplasia were 25.4%, 16.2%, and 2.0%, respectively, on the basis of 126 studies that reported the prevalence of less advanced precursors, regardless of the presence of more advanced lesions. The prevalence of all precursor lesions was higher in high and medium compared with low GC incidence countries (P < .01). Prevalence of AG and IM was significantly higher among H pylori-infected individuals (P < .01) but not statistically different between symptomatic and asymptomatic individuals (P > .17). All precursors demonstrated a secular decrease in prevalence over time.
CONCLUSIONS
Gastric precursor lesions have differences in prevalence in regions with differential GC incidence and are associated with H pylori infection. Because of the substantial prevalence of precursor lesions in both symptomatic and asymptomatic individuals, symptomatic evaluation may not be sufficient to identify individuals at risk. These estimates provide important insights for tailoring GC prevention strategies.
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