Erythrocyte Lewis antigen phenotypes of dyspeptic patients in Taiwan--correlattion of host factor with Helicobacter pylori infection.
Because of the molecular mimicry between Helicobacter pylori lipopolysaccharide and host Lewis blood-group antigens, Lewis antigen may mediate specific H. pylori binding to surface epithelial cells in gastric mucosa. We, therefore, tested whether different Lewis antigen phenotypes have different prevalence rates of H. pylori infection, and determined the specific H. pylori-related disease entities or histologic features. A total of 342 dyspeptic patients without previous anti-H. pylori therapy were enrolled after endoscopy. The Lewis phenotypes, defined as Le(a-b-), Le(a-b+), Le(a+b-), and Le(a+b+) subtypes, were determined from the expression or absence of Lewis antigens (Le(a) and Le(b)) on erythrocytes in each patient using monoclonal antibodies. The H. pylori-specific gastric histology was evaluated using the updated Sydney's system. Of 342 patients, 233 (68.1%) had H. pylori infection. The H. pylori infection rates were significantly higher in patients with Lewis phenotypes Le(a+b-) and Le(a+b+) (p < 0.05). Patients expressing the Le(a) antigen had a higher H. pylori infection rate than those without the Le(a) antigen (80.8 vs 64%, p < 0.005). In H. pylori-infected patients, patients expressing Le(b) antigen had a lower rate of gastroduodenal ulcers than those without Le(b) antigen (46.9 vs 61.4%, p < 0.05). H. pylori-positive patients who expressed the Le(b) antigen had higher bacterial density and inflammation severity in the gastric cardia than those who did not. Patients who expressed the Le(a) antigen had lower bacterial density, less chronic inflammation severity, and lower frequency of lymphoid follicles in the gastric cardia than those who did not (p < 0.05). The erythrocyte Lewis phenotype can be a significant host factor related to susceptibility, different histologic patterns, and clinical outcomes of H. pylori infection in Taiwan.