Dear Sir, We read with great interest the latest issue of Digestive Diseases and Sciences and, given our particular interests, we would like to briefly comment on three thoughtprovoking papers signed by Genta [1], Uedo [2] and, not last, by Ahn and coworkers [3]. Genta looks at the worldwide epidemiology of gastric cancer (GC) and correlates different socio-economic habits with GC risk. Addressing the etiological co-factors involved in gastric carcinogenesis, Genta notes that, ‘‘The relative influence of ... these factors on the rise and fall of GC is difficult to evaluate; since none is a sufficient cause of cancer, they must have acted synergistically’’ [1]. In this respect, without curbing the ‘‘leading’’ etiological role of H. pylori, we would like to mention that we recently documented a similar prevalence of both H. pylori and Cag-A status coexisting with impressive differences in the incidence of GC in different Siberian populations [4]. Our observation strongly supports the role of factors other than H. pylori in the etiology of ‘‘epidemic’’ GC. As Genta’s editorial suggests, such a constellation of non-Hp, environmental (?) factors should be further and more extensively addressed. Moving on to Uedo’s paper and its conclusive question, ‘‘... from the perspective of a practical endoscopist: do we need to take many biopsy specimens for assessing gastric cancer risk in... routine EGD?’’ [2], the answer is provided by the author a few lines further on: when both ‘‘gastric serology’’ (which is paid too little attention in non-Japanese clinical practice) and clinical examination consistently point to the need for an invasive diagnostic procedure (EGD), there can be no doubt that endoscopy and microscopy combined can identify patients warranting further diagnostic/therapeutic measures. Finally, Ahn and coworkers highlight the increased GC risk associated with the open phenotype of gastritis (i.e., multifocal atrophic gastritis, not restricted to the antrum) [3, 5]. The authors (who do not mention their biopsy sampling protocol) founded their conclusions on an elegant histological/immunohistochemical study, but it is worth noting that distinguishing between complete and incomplete intestinal metaplasia (IM) on the strength of H&E is only partially reliable (mucin histochemistry, i.e., high iron diamine [HID], is more appropriate). The clinical question, however, is whether we should perform (expensive and time-consuming) histochemistry and/or immunohistochemistry stains for a reliable assessment of the risk of GC. As in Ahn’s experience, when intestinalization of the gastric mucosa spreads from the antrum to the oxyntic M. Rugge (&) M. Fassan Department of Medical Diagnostic Sciences and Special Therapies, Surgical Pathology and Cytopathology Unit, University of Padua, Padua, Italy e-mail: massimo.rugge@unipd.it
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