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Analytical Cellular Pathology
Volume 2015, Article ID 164840, 7 pages
http://dx.doi.org/10.1155/2015/164840
Research Article

Epstein-Barr Virus Association with Peptic Ulcer Disease

1Unidad de Investigación Médica en Enfermedades Infecciosas y Parasitarias (UIMEIP), Hospital de Pediatría, CMN Siglo-XXI, Instituto Mexicano del Seguro Social (IMSS), Avenida Cuauhtémoc 330, Colonia Doctores, Delegación Cuauhtémoc, 06720 Ciudad de México, DF, Mexico
2Centro de Investigación en Salud Poblacional, Instituto Nacional de Salud Pública, Avenida Universidad 655, Colonia Santa María Ahuacatitlán, 62100 Cuernavaca, MOR, Mexico
3Unidad de Investigación en Virología y Cáncer, Hospital Infantil de México Federico Gómez, Dr. Márquez 162, Colonia Doctores, Delegación Cuauhtémoc, 06720 Ciudad de México, DF, Mexico

Received 30 April 2015; Accepted 15 June 2015

Academic Editor: Francisco Aguayo Gonzalez

Copyright © 2015 María G. Cárdenas-Mondragón et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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 of HP infection 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 the HP virulence 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.