Background and aims: We tested if host gastric Lewis antigens and the babA2 genotype of Helicobacter pylori correlated with clinicohistological outcome. Methods: We enrolled 188 dyspeptic patients (45 with duodenal ulcer, 45 with gastric ulcer, and 98 with chronic gastritis) with H pylori infection, proved by culture and gastric histology, reviewed by the updated Sydney system. Gastric expression of Lewis (Le) antigens Lea, Leb, Lex, and Ley was determined immunochemically to determine intensity (range 0-3). The corresponding 188 H pylori isolates were screened for babA2 genotype by polymerase chain reaction. Results: All H pylori isolates had a positive babA2 genotype. We identified Lea in 33.5%, Leb in 72.9%, Lex in 86.2%, and Ley in 97.4% of biopsies from these 188 patients. Patients who expressed Leb had a higher H pylori density than those who did not express Leb (p<0.001). Among 139 patients who expressed Leb, H pylori density increased with a higher Leb intensity (p<0.05). Gastric atrophy decreased with Leb intensity and thus resulted in lower H pylori density in the antrum (p<0.05). For the 49 patients without gastric Leb expression, H pylori density was positively related with Lex and Lea expression (p<0.05). Conclusions: Taiwanese H pylori isolates are 100% babA2 genopositive. Gastric Leb as well as Lex intensity may be major determinants of H pylori density. While lacking gastric Leb expression, Lex and Lea were closely related to H pylori colonisation.
All Science Journal Classification (ASJC) codes