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dc.creatorSierra Ramos, Rafaela
dc.creatorUne, Clas Allan
dc.creatorRamírez Mayorga, Vanessa
dc.creatorAlpízar Alpízar, Warner
dc.creatorGonzález, María I.
dc.creatorRamírez, José A.
dc.creatorde Mascarel, Antoine
dc.creatorCuenca Berger, Patricia
dc.creatorPérez Pérez, Guillermo Ignacio
dc.creatorMégraud, Francis
dc.date.accessioned2015-05-25T19:49:37Z
dc.date.available2015-05-25T19:49:37Z
dc.date.issued2008-11-14
dc.identifier.citationhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2773333/
dc.identifier.citationhttp://www.wjgnet.com/1007-9327/abstract_en.asp?f=6481&v=14
dc.identifier.issn1007-9327
dc.identifier.urihttps://hdl.handle.net/10669/13318
dc.descriptionArtículo científico -- Universidad de Costa Rica. Instituto de Investigaciones en Salud, 2008es_ES
dc.description.abstractAIM: To determine the association of Helicobacter pylori (H pylori) CagA+ infection and pro-inflammatory polymorphisms of the genes interleukin (IL)-1RN and IL-1B with the risk of gastric atrophy and peptic ulcers in a dyspeptic population in Costa Rica, a country with high incidence and mortality of gastric cancer. METHODS: Seven biopsy specimens, a fasting blood sample and a questionnaire concerning nutritional and sociodemographic factors were obtained from 501 consecutive patients who had undergone endoscopy for dyspeptic symptoms. A histopathological diagnosis was made. Pepsinogen concentrations were analyzed by enzyme linked immunosorbent assay (ELISA). Infection with H pylori CagA+ was determined by serology and polymerase chain reaction (PCR). IL-1B and IL-1RN polymorphisms genotyping was performed by PCR-restriction fragment length polymorphism (PCR-RFLP) and PCR respectively. RESULTS: In this dyspeptic population, 86% were H pylori positive and of these, 67.8% were positive for CagA. Atrophic antral gastritis (AAG) was associated with CagA+ status [odd ratio (OR) = 4.1; P < 0.000] and fruit consumption (OR = 0.3; P < 0.00). Atrophic body gastritis (ABG) was associated with pepsinogen PGI/PGII < 3.4 (OR = 4.9; P < 0.04) and alcohol consumption (OR = 7.3; P < 0.02). Duodenal ulcer was associated with CagA+ (OR = 2.9; P < 0.04) and smoking (OR = 2.4; P < 0.04). PGI < 60 μg/L as well as PGI/PGII < 3.4 were associated with CagA+. CONCLUSION: In a dyspeptic population in Costa Rica, H pylori CagA+ is not associated with ABG, but it is a risk factor for AAG. The pro-inflammatory cytokine polymorphisms IL-1B + 3945 and IL-1RN are not associated with the atrophic lesions of this dyspeptic population.es_ES
dc.description.sponsorshipUniversidad de Costa Rica. Instituto de Investigaciones en Saludes_ES
dc.language.isoen_USes_ES
dc.publisherWorld Journal Gastroenterol 14(42)es_ES
dc.sourceWorld Journal of Gastroenterology, 2008, 14(42): 6481–6487es_ES
dc.subjectAtrophic gastritises_ES
dc.subjectPepsinogenes_ES
dc.subjectPeptic ulcerses_ES
dc.subjectInterleukinses_ES
dc.subjectSalud públicaes_ES
dc.titleRelation of atrophic gastritis with Helicobacter pylori-CagA+ and interleukin-1 polymorphismses_ES
dc.typeartículo original
dc.identifier.doi10.3748/wjg.14.0000
dc.description.procedenceUCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias de la Salud::Instituto de Investigaciones en Salud (INISA)es_ES


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