Risk of lymphoid follicle development in patients with chronic antral gastritis: role of endoscopic features, histopathological parameters, CagA status and interleukin-1 gene polymorphisms.

OBJECTIVE: Helicobacter pylori infection causes gastritis, lymphoid follicle formation and development of MALT lymphoma. We evaluated endoscopic, histological, serological and genetic risk factors associated with lymphoid follicle development in gastritis.
MATERIALS AND METHODS: After upper GI endoscopy, 3 antral biopsies were taken from 120 patients for histological examination. H. pylori was diagnosed using rapid urease test (RUT), modified Giemsa stain and IgG anti-CagA ELISA. Genotyping of IL-1B (-511C/T) and IL-1RN (86 bp VNTR) genes were performed by PCR-RFLP/PCR.
RESULTS: In 120 patients, 45 (37.5%) showed presence of lymphoid follicles in antral gastric mucosa. H. pylori was positive by modified Giemsa stain (26%) RUT (50%) and anti-CagA IgG in 67.5%, The presence of nodularity (p = 0.030), neutrophilic infiltration (p = 0.010), lymphocytic infiltration (p = 0.002), glandular atrophy (p = 0.0001), glandular shortening (p = 0.001), fibrosis (p = 0.0001), plasma cells (p = 0.007), eosinophils (p = 0.012), anti-CagA antibodies (p = 0.003) and H. pylori density (p = 0.020) were associated with risk (odds ratio = 11.5, 3.8, 11.0, 8.4, 3.8, 4.6, 5.8, 16.0, 10.8 and 2.8 respectively) of lymphoid follicle. However, IL-1 gene polymorphisms did not influence lymphoid follicle development
CONCLUSION: The presence of modularity, lymphocytic infiltration, glandular atrophy, glandular shortening, fibrosis, plasma cells, eosinophils and anti-CagA IgG antibodies are risk factors for lymphoid follicle development in patients with gastritis.