28 research outputs found

    Higher number of Helicobacter pylori CagA EPIYA C phosphorylation sites increases the risk of gastric cancer, but not duodenal ulcer

    Get PDF
    <p>Abstract</p> <p>Background</p> <p><it>Helicobacter pylori </it>infection is one of the most common infections worldwide and is associated with gastric cancer and peptic ulcer. Bacterial virulence factors such as CagA have been shown to increase the risk of both diseases. Studies have suggested a causal role for CagA EPIYA polymorphisms in gastric carcinogenesis, and it has been shown to be geographically diverse. We studied associations between <it>H. pylori </it>CagA EPIYA patterns and gastric cancer and duodenal ulcer, in an ethnically admixed Western population from Brazil. CagA EPIYA was determined by PCR and confirmed by sequencing. A total of 436 patients were included, being 188 with gastric cancer, 112 with duodenal ulcer and 136 with gastritis.</p> <p>Results</p> <p>The number of EPIYA C segments was significantly associated with the increased risk of gastric carcinoma (OR = 3.08, 95% CI = 1.74 to 5.45, p < 10<sup>-3</sup>) even after adjustment for age and gender. Higher number of EPIYA C segments was also associated with gastric atrophy (p = 0.04) and intestinal metaplasia (p = 0.007). Furthermore, patients infected by <it>cag</it>A strains possessing more than one EPIYA C segment showed decreased serum levels of pepsinogen I in comparison with those infected by strains containing one or less EPIYA C repeat. Otherwise, the number of EPIYA C segments did not associate with duodenal ulcer.</p> <p>Conclusions</p> <p>Our results demonstrate that infection with <it>H. pylori </it>strains harbouring more than one CagA EPIYA C motif was clearly associated with gastric cancer, but not with duodenal ulcer.</p> <p>Higher number of EPIYA C segments was also associated with gastric precancerous lesions as demonstrated by histological gastric atrophic and metaplastic changes and decreased serum levels of pepsinogen I.</p

    Úlcera pĂ©ptica gastroduodenal e infecção pelo Helicobacter pylori na criança e adolescente Gastroduodenal peptic ulcer and Helicobacter pylori infection in children and adolescents

    No full text
    OBJETIVO: Apresentar aspectos relevantes relativos Ă  Ășlcera pĂ©ptica gastroduodenal e Ă  infecção pelo Helicobacter pylori na criança e adolescente. FONTES DOS DADOS : Livros tĂ©cnicos e bases de dados MEDLINE e LILACS de 1966 a 2006. SÍNTESE DOS DADOS : A Ășlcera pĂ©ptica na criança e adolescente pode ser primĂĄria, associada Ă  infecção pelo H. pylori, ou secundĂĄria, na qual os mecanismos etiopatogĂȘnicos dependem da doença de base. A infecção Ă© adquirida predominantemente na infĂąncia, com taxas de prevalĂȘncia que variam de 56,8 a 83,1% nas crianças que vivem nas regiĂ”es mais pobres do Brasil e de aproximadamente 10% nas crianças abaixo de 10 anos de idade nos paĂ­ses desenvolvidos. A infecção pode ser diagnosticada por mĂ©todos invasivos, que investigam a presença da bactĂ©ria, ou de DNA, RNA ou produtos bacterianos em fragmentos de biĂłpsia da mucosa gĂĄstrica obtida Ă  endoscopia; tambĂ©m pode ser diagnosticada atravĂ©s de mĂ©todos nĂŁo-invasivos, que compreendem a pesquisa de anticorpos anti-H. pylori em amostras de soro, urina ou saliva, a pesquisa de antĂ­genos da bactĂ©ria nas fezes e o teste respiratĂłrio com urĂ©ia marcada com carbono-13. O mĂ©todo de escolha para o diagnĂłstico da Ășlcera pĂ©ptica Ă© a endoscopia digestiva alta, com a vantagem adicional de, durante o procedimento, permitir a obtenção de fragmentos de mucosa gĂĄstrica para o diagnĂłstico da infecção e estudo histopatolĂłgico. CONCLUSÕES: A infecção por H. pylori Ă© a principal causa de Ășlcera pĂ©ptica na infĂąncia. A erradicação da bactĂ©ria com antimicrobiano Ă© acompanhada de cura da doença, sendo, portanto, indicada em todas as crianças H. pylori-positivas com Ășlcera pĂ©ptica em atividade, recorrente, cicatrizada ou complicada.<br>OBJECTIVE: To show important aspects of gastroduodenal peptic ulcer and of Helicobacter pylori infection in children and adolescents. SOURCES: Technical textbooks and MEDLINE and LILACS databases including publications between 1966 and 2006. SUMMARY OF THE FINDINGS : The etiology of peptic ulcer in children and adolescents may be primary, associated with H. pylori infection, or secondary, in which etiopathogenic mechanisms rely upon the underlying disease. The infection is acquired predominantly in childhood, with prevalence rates between 56.8 and 83.1% in children who live in the poorest Brazilian regions, amounting to nearly 10% in children aged less than 10 years in industrialized countries. The infection can be diagnosed by invasive methods, which investigate the presence of the bacterium, or of DNA, RNA or bacterial products in biopsy fragments of the gastric mucosa obtained at endoscopic examination; it can also be diagnosed through noninvasive methods, which include the detection of anti-H. pylori antibodies in serum, urine or saliva samples, detection of bacterial antigens in stool samples, and the carbon 13-labeled urea breath test. However, upper gastrointestinal endoscopy is the method of choice for the diagnosis of peptic ulcer, as it allows collecting fragments from the gastric mucosa during the procedure for the diagnosis of infection and for histopathological analysis. CONCLUSIONS: H. pylori infection is the major cause of peptic ulcer among children. Eradication of the bacterium with antimicrobial therapy results in the cure of the disease, and is therefore indicated for all children with H. pylori infection with an active, recurrent, healed, or complicated peptic ulcer

    Immunoblotting for the serodiagnosis of Helicobacter pylori  infection in Brazilian patients with and without gastric carcinoma

    No full text
    We evaluated the performance of a commercial immunoblotting in the serodiagnosis of Helicobacter pylori infection in Brazilian patients. The presence of anti-H. pylori antibodies was also investigated in a group of 20 duodenal ulcer patients after successful treatment. One hundred and ninety one patients were studied. Among the 164 infected patients, 46 had gastric carcinoma. The duodenal ulcer patients were treated with antimicrobial drugs and the eradication of the microorganism was confirmed in all of them one month after the end of the treatment by the 13C-urea breath test. Sera were assayed for H. pylori antibodies using the Helicoblot 2.0 (Genelabs Diagnostics, Singapore). The sensitivity, specificity, positive, and negative predictive values of the test were 93.9%, 92.6%, 98.7%, and 71.4%, respectively. The sensitivity of the test was similar in patients with (93.5%) and without (95.7%) gastric carcinoma. Twenty-four months after the end of the treatment, the band of 116 kDa was still detected in one of the patients. In conclusion, the Helicoblot 2.0 is an accurate test to diagnose H. pylori infection and although it can not be employed to monitor the bacterium eradication, it may be useful for diagnosing past infection, especially in gastric carcinoma patients
    corecore