Occurrence of Helicobacter pyloriand Epstein-Barr virus infection in endoscopic and gastric cancer patients from Northern Brazil

BMC Gastroenterology

Research Article

Jefferson José Sodré Ferraz¹  Mariana Ferreira Leal²  Ana Paula Negreiros Nunes Alves³  Marília Cardoso Smith⁴  Kátia Soares de Oliveira⁵  Aline Damasceno Seabra⁶  Raquel Carvalho Montenegro⁶  Carolina Rosal Teixeira de Souza⁶  Rommel Rodríguez Burbano⁶  Danielle Queiroz Calcagno⁷  André Salim Khayat⁷  Paulo Pimentel Assumpção⁷ 

[1] Centro Universitário do Pará, Belém, PA, Brazil;Departamento de Ortopedia e Traumatologia, Universidade Federal de São Paulo, São Paulo, SP, Brazil;Disciplina de Genética, Departamento de Morfologia e Genética, Universidade Federal de São Paulo, São Paulo, SP, Brazil;Departamento de Patologia Oral, Faculdade de Odontologia, Universidade Federal do Ceará, Fortaleza, CE, Brazil;Disciplina de Genética, Departamento de Morfologia e Genética, Universidade Federal de São Paulo, São Paulo, SP, Brazil;Instituto de Ciências da Saúde, Universidade Federal do Pará, Belém, PA, Brazil;Laboratório de Citogenética Humana, Instituto de Ciências Biológicas, Universidade Federal do Pará, Rua Augusto Corrêa, 01 – Guamá. CEP 66075-110. Caixa postal 479, Belém, PA, Brazil;Núcleo de Pesquisa em Oncologia, Universidade Federal do Pará, Belém, PA, Brazil;

关键词: Helicobacter pylori;    Epstein-Barr virus;    Gastritis;    Gastric cancer;   

DOI  :  10.1186/1471-230X-14-179

 received in 2014-01-23, accepted in 2014-10-01,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundHelicobacter 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).MethodsSamples 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.ResultsIn 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.ConclusionsOur 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.

【 授权许可】

CC BY   
© de Souza et al.; licensee BioMed Central Ltd. 2014