Infecção por Helicobacter pylori e lesões precursoras de câncer gástrico: prevalência e fatores associados em um laboratório de referência no Sudeste do Brasil / Helicobacter pylori infection and gastric cancer precursor lesions: prevalence and associated factors in a reference laboratory in southeastern brazil

ABSTRACT BACKGROUND: Helicobacter pylori infection is the most important risk factor for gastric atrophy and intestinal metaplasia, both considered gastric cancer precursor lesions. Therefore, the investigation of the occurrence of H. pylori infection, precursor lesions and associated factors guides the adoption of specific strategies for the control this type of cancer. OBJECTIVE: To evaluate the prevalence of H. pylori infection in patients undergoing upper digestive endoscopy, as well as the prevalence of intestinal metaplasia, atrophy and chronic inflammation and their association with H. pylori infection. METHODS: A retrospective study was performed based on reports of gastric endoscopic biopsies performed in a private laboratory affiliated to the Brazilian Public Health System (SUS). Patients were evaluated for age, gender and type of health service. The samples were evaluated for the presence of H. pylori, and also of chronic inflammation, intestinal metaplasia and glandular atrophy. RESULTS: Of a total of 4,604 patients (mean age 51±16.6), 63.9% were female and 63.1% coming from private health care service. The prevalence of H. pylori infection was 31.7% (n=1,459), and the percentage of infection was significantly higher in patients from public health service (42.0%) in relation to patients from private health service (25.6%). Among H. pylori (+) patients, a higher percentage of intestinal metaplasia (17.7% vs 13.3%) and glandular atrophy (17.6% vs 6.9%) were observed when compared to those H. pylori (-) (P<0.01). From the patients H. pylori (+) with at least one type of precursor lesion (n=418), 161 (38.5%) had metaplasia and chronic inflammation, 160 (38.3%) had atrophy and chronic inflammation and finally 97 (23.2%) presented metaplasia, atrophy and chronic inflammation simultaneously. CONCLUSION: The present study reinforces the association of H. pylori infection with gastric cancer precursor lesions in a Brazilian population, emphasizing the importance of infection prevention measures, as well as the treatment of infected patients, especially in regions with lower socioeconomic levels that show a higher prevalence of infection by H. pylori.

RESUMO CONTEXTO: A infecção por Helicobacter pylori é o fator de risco mais importante para atrofia gástrica e metaplasia intestinal, ambas consideradas lesões precursoras do câncer gástrico. Portanto, a investigação da ocorrência de infecção por H. pylori, das lesões precursoras e dos fatores associados orienta a adoção de estratégias específicas para o controle deste tipo de câncer. OBJETIVO: Avaliar a prevalência de infecção por H. pylori em pacientes submetidos à endoscopia digestiva alta, bem como a prevalência de metaplasia intestinal, atrofia e inflamação crônica e a associação destas com a infecção por H. pylori. MÉTODOS: Foi realizado um estudo retrospectivo com base em laudos de biópsias endoscópicas gástricas realizadas em laboratório privado afiliado ao Sistema Único de Saúde (SUS). Os pacientes foram avaliados quanto à idade, sexo e tipo de serviço de saúde. As amostras foram avaliadas quanto à presença de H. pylori e também de inflamação crônica, metaplasia intestinal e atrofia glandular. RESULTADOS: Do total de 4.604 pacientes (idade média de 51±16,6), 63,9% eram do sexo feminino e 63,1% provenientes de serviços de saúde privado. A prevalência de infecção por H. pylori foi de 31,7% (n=1.459) e o percentual de infecção foi significativamente maior nos pacientes do serviço público de saúde (42,0%) em relação aos pacientes do serviço privado de saúde (25,6%). Entre os pacientes com H. pylori (+), foi observado maior percentual de metaplasia intestinal (17,7% vs 13,3%) e atrofia glandular (17,6% vs 6,9%) quando comparados aos H. pylori (-) (P<0,01). Dos pacientes H. pylori (+) com pelo menos um tipo de lesão precursora (n=418), 161 (38,5%) apresentaram metaplasia e inflamação crônica, 160 (38,3%) apresentaram atrofia e inflamação crônica e, finalmente, 97 (23,2%) apresentaram metaplasia, atrofia e inflamação crônica simultaneamente. CONCLUSÃO: O presente estudo reforça a associação da infecção por H. pylori com lesões precursoras de câncer gástrico em uma população brasileira, enfatizando a importância de medidas de prevenção de infecção, bem como o tratamento de pacientes infectados, principalmente em regiões com níveis socioeconômicos mais baixos que apresentam maior prevalência de infecção por H. pylori.

Chronic prostatitis alters the prostatic microenvironment and accelerates preneoplastic lesions in C57BL/6 mice

BACKGROUND: Chronic prostatitis has been supposed to be associated with preneoplastic lesions and cancer development. The objective of this study was to examine how chronic inflammation results in a prostatic microenvironment and gene mutation in C57BL/6 mice. METHODS: Immune and bacterial prostatitis mouse models were created through abdominal subcutaneous injection of rat prostate extract protein immunization (EAP group) or transurethral instillation of uropathogenic E. coli 1677 (E. coli group). Prostate histology, serum cytokine level, and genome-wide exome (GWE) sequences were examined 1, 3, and 6 months after immunization or injection. RESULT: In the EAP and E. coli groups, immune cell infiltrations were observed in the first and last months of the entire experiment. After 3 months, obvious proliferative inflammatory atrophy (PIA) and prostatic intraepithelial neoplasia (PIN) were observed accompanied with fibrosis hyperplasia in stroma. The decrease in basal cells (Cytokeratin (CK) 5+/p63+) and the accumulation of luminal epithelial cells (CK8+) in the PIA or PIN area indicated that the basal cells were damaged or transformed into different luminal cells. Hic1, Zfp148, and Mfge8 gene mutations were detected in chronic prostatitis somatic cells. CONCLUSION: Chronic prostatitis induced by prostate extract protein immunization or E. coli infection caused a reactive prostatic inflammation microenvironment and resulted in tissue damage, aberrant atrophy, hyperplasia, and somatic genome mutation.