Invited Lecture(JGES)
Thu. November 2nd   14:00 - 14:30   Room 4: Portopia Hotel South Wing Portopia Hall
Invited Lecture4
The point of no return in the pathogenesis of H. pylori-associated gastric cancer
David Y. Graham
Baylor College of Medicine
Clinical programs designed to reduce deaths from gastric cancer are designed to screen populations at high risk to detect and ablate/remove mucosal lesions before they reach the stage when depth of invasion has breached the muscularis mucosa or metastasis has occurred. Advances in endoscopy and endoscopic therapy have evolved to the point that programs involving regular endoscopic surveillance and targeted therapy are able to achieve these goals. However, Hp prevalence, rates of histologic progression, and thus cancer risk have rapidly changed such that in many populations most screening is done primarily in those with low cancer risk. The current guidelines are generally not been regularly reconsidered in order to not continue to offer screening who are unlikely to benefit. Progression of risk is halted by Hp eradication such that point of no return (or risk of development of gastric cancer is locked and does not increase following eradication). It follows that gastric cancer screening should only be offered to those who have achieved Hp eradication or are currently incurable. The costs and benefits of gastric cancer screening depends on the gastric cancer risk of the individuals enrolled. In most countries, screening should be limited to those with post Hp eradication and high risk gastric atrophy scores (e.g., OLGA or OLGIM 3/4 or Kimura Takemoto scores of O-1 or greater) or ABC pepsinogen scores of C or D. The rapid decline in the prevalence of Hp and of the decline in the rate of increase in atrophic scores has resulted in patient's age no longer being a valid basis for screening. The population should be divided into categories such as no risk (never infected or eradication before development of significant atrophy), low risk (e.g., OLGA stage 1 or 2 or K-T less than O-1), after eradication, high risk (e.g., OLGA 3/4 or K-T O-1) and very high risk (post resection of early-stage cancer). For practical and clinical purposes and for risk stratifying populations for intervention the point of no return would be defined based on the etiology combined with the extent and severity of atrophy. The rapid and ongoing change in Hp infection and in the age-related extent of damage has reduced the efficacy of age-related screening to prevent gastric deaths. In the future I predict that screening programs will focus on Hp eradication with subsequent screening limited to those in higher risk categories.
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