Abstract

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 Le^a, Le^b, Le^x, and Le^y 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 Le^a in 33.5%, Le^b in 72.9%, Le^x in 86.2%, and Le^y in 97.4% of biopsies from these 188 patients. Patients who expressed Le^b had a higher H pylori density than those who did not express Le^b (p<0.001). Among 139 patients who expressed Le^b, H pylori density increased with a higher Le^b intensity (p<0.05). Gastric atrophy decreased with Le^b intensity and thus resulted in lower H pylori density in the antrum (p<0.05). For the 49 patients without gastric Le^b expression, H pylori density was positively related with Le^x and Le^a expression (p<0.05).

Conclusions: Taiwanese H pylori isolates are 100% babA2 genopositive. Gastric Le^b as well as Le^x intensity may be major determinants of H pylori density. While lacking gastric Le^b expression, Le^x and Le^a were closely related to H pylori colonisation.