Helicobacter Pylori
Copyright ©2008 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Nov 14, 2008; 14(42): 6481-6487
Published online Nov 14, 2008. doi: 10.3748/wjg.14.6481
Relation of atrophic gastritis with Helicobacter pylori-CagA+ and interleukin-1 gene polymorphisms
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
Rafaela Sierra, Clas Une, Vanessa Ramírez, Warner Alpízar-Alpízar, Patricia Cuenca, Institute of Health Research, University of Costa Rica, San José 2060, Costa Rica
María I González, Department of Statistics, University of Costa Rica, San José 2060, Costa Rica
José A Ramírez, Department of Pathology, Calderón Guardia Hospital, Costa Rica, San José 2060, Costa Rica
Antoine de Mascarel, Francis Mégraud, University Victor Segalen Bordeaux 2, 146, rue Leo-Saignat, Case 76, Bordeaux Cedex 33076, France
Guillermo Pérez-Pérez, Departments of Medicine and Microbiology, New York University School of Medicine, NYU. Langone Medical Center, 550 First Avenue, New York 10016, United States
Author contributions: Sierra R designed the research; Une C, Ramírez V, Alpízar-Alpízar W, Ramírez JA and De Mascarel A performed the research; Cuenca P contributed materials; Pérez-Pérez G and Mégraud F contributed analytic tools; Sierra R, Une C and González MI analyzed the data; Sierra R and Une C wrote the paper.
Supported by The Centre Culturel et de Cooperation Scientifique de l'Ambassade de France au Costa Rica and the University of Costa Rica, No. 742-99-340
Correspondence to: Dr. Clas Une, Institute of Health Research, University of Costa Rica, San José 2060, Costa Rica. allan.une@ucr.ac.cr
Telephone: +506-2-2073290 Fax: +506-2-2075130
Received: May 14, 2008
Revised: September 16, 2008
Accepted: September 23, 2008
Published online: November 14, 2008
Abstract

AIM: 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.

Keywords: Atrophic gastritis; Pepsinogen; Peptic ulcers; Helicobacter pylori-CagA; Interleukins