BABA2 AS A RISK FACTOR FOR DUODENAL ULCER IN CHILDHOOD

Gifone Aguiar Rocha (F. Medicina/UFMG); Sergio de Assis Batista (ICB-UFMG); Juliana Pinto Silva (ICB-UFMG); Andreia Maria Camargos Rocha (F. Medicina/UFMG); Paulo Bittencourt (HC-UFMG); Mônica Maria Demas Álvares Cabral (F. Medicina/UFMG); Dulciene Maria de Magalhães Queiroz (F. Medicina/UFMG)

Helicobacter pylori infection is acquired predominantly in childhood and persists lifelong. The infection may progress to different clinical outcomes as different as duodenal ulcer and gastric carcinoma. Although the factors that determine the outcome of the infection are not well understood, bacterial virulence factors have been suggested to play important roles. One of the major viulence factors of H. pylori is the cytotoxin vaculating cytotoxin (VacA), which causes cytoplasmic vacuolation in gastric epithelial cells. Another well characterized virulence factor is the cytotoxin-associatyed antigen (CagA), which is encoded by a one of the genes located in the cag pathogenicity island. The blood group antigen binding adhesin BabA encoded by the babA2 gene, mediates the adherence of H. pylori to human Lewis B blood group antigen on gastric epithelial cells. The attachment may facilitate H. pylori colonization and efficient delivery of virulence factors such as VacA and CagA to the host cells, resulting in severe gastric inflammation. In Western populations, the babA2 gene has been associated with peptic ulcer and gastric carcinoma. However, there are no studies evaluating babA2 virulent marker in children with duodenal ulcer. Therefore, we investigated the presence of babA2, by PCR, using the primer set described by Gerhard et al, in 137 children (37 with duodenal ucler, 64 boys, mean age 10.28 ± 3.75 yr; range 1-18 yr). Since the results were ambiguous, we sequenced a DNA fragment containing the primer annealing sites and the signal sequence of the gene of all strains. cagA status was evaluated by PCR using two sets of primers. Gastritis was classified according to the revised Sydney system. Data were analyzed by logistic models, adjusting for confounding factors. babA2 was present in all H. pylori strains, but nucleotide deletions (121 - 88.3%) and a nucleotide substitution C→T 114 (83.2%) were observed in the upstream region near to the gene signal sequence. The nucleotide substitution was associated with the nucleotide deletions (p<10^-3). The nucleotide substitution was negatively associated with the degree of polymorphonuclear neutrophil cells (p=0.04), the presence of lymphoid follicles (p = 0.05) and erosion (p = 0.001) in the corpus mucosa, suggesting a functional mutation. In the multivariate analyses, cagA status (OR = 4.4, 95%C I= 1.6 - 12.2), male gender (OR = 4.1, 95%CI = 1.6 - 10.2) and age (OR=1.2, 95%CI=1.1-1.4) were independently associated with duodenal ulcer, but the babA2 variations were not. Grants/ FAPEMIG/CNPq.