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Relation of atrophic gastritis with Helicobacter pylori-CagA^+ and interleukin-1 gene polymorphisms

World Journal of Gastroenterology 2008年第42期14卷 6481-6487页

作者： Rafaela Sierra clas une Vanessa Ramírez Warner Alpízar-Alpízar María I González José A Ramírez Antoine de Mascarel Patricia Cuenca Guillermo Pérez-Pérez Francis Mégraud Institute of Health Research University of Costa Rica San José 2060 Costa Rica Department of Statistics University of Costa Rica San José 2060 Costa Rica Department of Pathology Calderón Guardia Hospital Costa Rica San José 2060 Costa Rica University Victor Segalen Bordeaux 2 146 rue Leo-Saignat Case 76 Bordeaux Cedex 33076 France Departments of Medicine and Microbiology New York University School of Medicine NYU. Langone Medical Center 550 First Avenue New York 10016 United States

AIM： To determine the association of Helicobacter pylori （H pylorl） CagA^＋ infection and pro-inflammatory polymorphisms of the genes interleukin （IL）-IRN 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 PCRrestriction fragment length polymorphism （PCR-RFIP）and PCR respectively. RESULTS： In this dyspeptic population, 86% were Hpylori 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 poly- morphisms IL-1B ＋ 3945 and IL-1RN are not associated with the atrophic lesions of this dyspeptic population.

关键词： Atrophic gastritis Pepsinogen Pepticulcers Helicobacterpylori-CagA Interleukins

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