Please use this identifier to cite or link to this item: http://www.repositorio.ufc.br/handle/riufc/9559
Title in Portuguese: Occurrence of Helicobacter pylori and Epstein-Barr virus infection in endoscopic and gastric cancer patients from Northern Brazil
Author: Souza, Carolina Rosal Teixeira de
Oliveira, Kátia Soares de
Ferraz, Jefferson José Sodré
Leal, Mariana Ferreira
Calcagno, Danielle Queiroz
Seabra, Aline Damasceno
Khayat, André Salim
Montenegro, Raquel Carvalho
Alves, Ana Paula Negreiros Nunes
Assumpção, Paulo Pimentel
Smith, Marília Cardoso
Burbano, Rommel Rodríguez
Keywords: Neoplasias Gástricas
Helicobacter pylori
Gastrite
Issue Date: Oct-2014
Publisher: BMC Gastroenterology
Citation: SOUZA, C. R. T. de et al. Occurrence of Helicobacter pylori and Epstein-Barr virus infection in endoscopic and gastric cancer patients from Northern Brazil. BMC gastroenterology, v. 14, n. 1, p. 1-9, out., 2014.
Abstract: Background: Helicobacter pylori (HP) and Epstein-Barr virus (EBV) have been associated with cancer development. We evaluated the prevalence of HP, HP CagA+ and EBV infection in gastric cancer (GC) samples from adults and in gastric tissues from patients who underwent upper endoscopy (UE). Methods: Samples from UE and GC were collected to investigate the presence of HP infection and the HP virulence factor CagA by a urease test and PCR. The presence of EBV was detected by Eber-1 in situ hybridization. Results: In UE, 85.5% of juvenile patients showed some degree of gastritis (45.3% of patients with mild gastritis and 54.7% with moderate/severe gastritis) and patients with mild gastritis were younger than patients with moderate/ severe gastritis. Among adults, 48.7% presented mild gastritis and 51.3% moderate/severe gastritis. HP infection was detected in 0% of normal mucosa, 58.5% of juvenile gastritis patients, 69.2% of adult gastritis patients and 88% of GC patients. In these same groups, HP CagA+ was detected in 0%, 37.7%, 61.5% and 67.2% of tissue samples, respectively. In juvenile patients, HP infection was more common in those with gastritis than in normal samples (p = 0.004). The patients with either HP or HP CagA+ were older than patients without these pathogens (p < 0.05). In juvenile patients, HP infection was more frequent in cases of moderate/severe gastritis than in cases of mild gastritis (p = 0.026). Moreover, in patients with GC, HP infection was more frequent in males than in females (p = 0.023). GC patients with HP CagA+ were older than patients with HP CagA- (p = 0.027). HP CagA+ was more common in intestinal-type than diffuse-type GC (p = 0.012). HP CagA+ was also associated with lymph-node (p = 0.024) and distal (p = 0.005) metastasis. No association between EBV infection and HP infection or any clinicopathological variable was detected. Conclusions: Our results suggest that HP is involved in the pathophysiology of severe gastric lesions and in the development of GC, particularly when CagA+ is present. EBV was not the primary pathogenic factor in our samples.
URI: http://www.repositorio.ufc.br/handle/riufc/9559
metadata.dc.type: Artigo de Periódico
ISSN: 1471-230X
Appears in Collections:DFIFA - Artigos publicados em revista científica

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