María G. Cárdenas-Mondragón
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Javier Torres
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Lourdes Flores-Luna
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Ricardo Carreón-Talavera
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Margarita Camorlinga-Ponce
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Background.Helicobacter pylori(HP) infection and nonsteroidal anti-inflammatory drugs (NSAID) use are considered the main risk to develop peptic ulcer disease (PUD). However, PUD also occurs in the absence ofHPinfection and/or NSAID use. Recently, we have found evidence that Epstein-Barr virus (EBV) reactivation increases the risk to develop premalignant and malignant gastric lesions.Objective. To study a possible association between EBV and PUD.Methods. Antibodies against an EBV reactivation antigen,HP, and theHPvirulence factor CagA were measured in sera from 207 Mexican subjects, controls (healthy individuals,n= 129), and PUD patients (n= 78, 58 duodenal and 20 gastric ulcers). Statistical associations were estimated.Results. Duodenal PUD was significantly associated with high anti-EBV IgG titers (p= 0.022, OR = 2.5), while anti-EBV IgA was positively associated with gastric PUD (p= 0.002, OR = 10.1).Conclusions. Our study suggests that EBV reactivation in gastric and duodenal epithelium increases the risk to develop PUD.