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

BMC Gastroenterology

Rommel Rodríguez Burbano⁵  Marília Cardoso Smith⁴  Paulo Pimentel Assumpção⁶  Ana Paula Negreiros Nunes Alves¹  Raquel Carvalho Montenegro⁵  André Salim Khayat⁶  Aline Damasceno Seabra⁵  Danielle Queiroz Calcagno⁶  Mariana Ferreira Leal⁴  Jefferson José Sodré Ferraz³  Kátia Soares de Oliveira²  Carolina Rosal Teixeira de Souza⁵ 

[1] Departamento de Patologia Oral, Faculdade de Odontologia, Universidade Federal do Ceará, Fortaleza, CE, Brasil;Instituto de Ciências da Saúde, Universidade Federal do Pará, Belém, PA, Brasil;Centro Universitário do Pará, Belém, PA, Brasil;Disciplina de Genética, Departamento de Morfologia e Genética, Universidade Federal de São Paulo, São Paulo, SP, Brasil;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, Brasil;Núcleo de Pesquisa em Oncologia, Universidade Federal do Pará, Belém, PA, Brasil

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

Others  :  1121782
DOI  :  10.1186/1471-230X-14-179

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

【 摘 要 】

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.

【 授权许可】

   
2014 de Souza et al.; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

Figure 2.

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