Page 121 - Helicobacter pylori and Gastric Cancer: From Tumor microenvironment to Immunotherapy

Helicobacter Pylori
Helicobacter pylori
approach is not common in daily practice, because of patient discomfort, cost, logistic and time restrictions. Hence, many physicians rely to an important extent on endoscopic evaluation for the detection of AG. To which extent this is a problem is not well understood. A Swedish study found a sensitivity and specificity for moderate to severe atrophic gastritis in the gastric corpus of 67 % and 85 %, respectively[25] and concluded that macroscopic features as observed during gastroscopy are of very limited value in the evaluation of whether or not gastritis or H. pylori infection are present. A Korean study, however, reported that endoscopic and histological atrophic gastritis show relatively good correlations[16, 25]Hence further studies, investigating presentation in different geographical contexts are necessary to clarify to which extent endoscopic observation alone can accurately assess AG. The present study was initiated to fill this void.
Our results show that the efficacy of endoscopy to detect AG is moderate and shows substantial regional variation, possibly caused by different presentation and incidence of AG at different locations around the globe. Generally speaking the performance of endoscopic screening is not good enough to rely on it alone and histological confirmation of the endoscopic diagnosis remains necessary. In conjunction with geographical variations in the performance of endoscopic observation to detect AG, it is fair to say that local validation remains essential. The agreement rate for atrophy was significantly higher for patients in the Nigerian than for those in Iran. Much more patients, however, in the Iranian cohort displayed extended atrophy, which is more easily misdiagnosed. The two populations also had different concordance between endoscopic diagnosis and microscopic diagnosis in the multivariate analysis, suggesting that this difference may be associated with differences in the background of the two populations. Indeed, the two populations differed in host genetic factors, diet, and bacterial virulence. For example, there are ethnic and.or geographical differences in the H. pylori cytotoxin associated gene A (CagA), one of the most important virulence factors for gastric mucosal injury and atrophy. The CagA gene is polymorphic and is primarily classified into East Asian and Western types based on sequences in its 3′ coding region[10]. Previous studies have clarified the differences in gastritis and atrophy among patients infected with East Asian CagA-positive, Western CagA-positive, and CagA-negative H. pylori[26]], with differences in virulence ppotentially provoking differences in agreement rates. In Iran the cagA gene genotype was found to predominate in gastric adenocarcinoma patients[27]. But obviously further studies, linking such variations
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