Brief Reports
Copyright ©The Author(s) 2005. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Aug 21, 2005; 11(31): 4891-4894
Published online Aug 21, 2005. doi: 10.3748/wjg.v11.i31.4891
Lewis blood genotypes of peptic ulcer and gastric cancer patients in Taiwan
Chi-Jung Yei, Jan-Gowth Chang, Mu-Chin Shih, Sheng-Fung Lin, Chao-Sung Chang, Fu-Tsong Ko, Kuang-Yang Lin, Ta-Chih Liu
Chi-Jung Yei, Blood Bank, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan, China
Jan-Gowth Chang, Mu-Chin Shih, Department of Laboratory Medicine, China Medical University and Hospital, Taichung, Taiwan, China
Sheng-Fung Lin, Chao-Sung Chang, Ta-Chih Liu, Division of Hematology/Oncology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan, China
Fu-Tsong Ko, Kuang-Yang Lin, Department of Internal Medicine, Taipei Municipal Jen-Ai Hospital, Taipei, Taiwan, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Ta-Chih Liu, MD, Division of Hematology/Oncology, Department of Internal Medicine, Kaohsiung Medical University Hospital, 100 Shih-Chuan 1st Road, Kaohsiung, Taiwan, China. d730093@cc.kmu.edu.tw
Telephone: +886-7-3121101-6113 Fax: +886-7-3162429
Received: January 4, 2005
Revised: January 23, 2005
Accepted: January 26, 2005
Published online: August 21, 2005
Abstract

AIM: The Lewis b (Leb) antigen has been implicated as a possible binding site for attachment of Helicobacter pylori (H pylori) to gastric mucosa. However, studies both supporting and denying this association have been reported in the literature. Differences in secretor (Se) genotype have been suggested as a possible reason for previous discrepancies. Therefore, we investigated the relationship between Le and Se genotypes and H pylori infection rates in people with peptic ulcer or gastric cancer.

METHODS: Peripheral blood samples were obtained from 347 patients with endoscopic evidence of peptic ulcer disease (235 cases of duodenal ulcer, 62 of gastric ulcer, and 50 of combined duodenal ulcer/ gastric ulcer) and 51 patients with gastric cancer on endoscopy. Peripheral blood specimens from 101 unrelated normal volunteers were used as controls. Lewis phenotype was determined using an antibody method, whereas Le and Se genotypes were determined by DNA amplification and restriction enzyme analysis. Gastric or duodenal biopsies taken from patients with endoscopic evidence of peptic ulcer or gastric cancer were cultured for H pylori. Isolates were identified as H pylori by morphology and production of urease and catalase. The H pylori infection status was also evaluated by rapid urease test (CLO test), and urea breath test (13C-UBT). Results of studies were analyzed by chi-square test (taken as significant).

RESULTS: H pylori was isolated from 83.7% (303/347) of patients with peptic ulcer disease. Statistical analysis did not show any significant difference in Lewis phenotype or genotype between patients with and without H pylori infection. No significant association was found between Lewis genotype and peptic ulcer or gastric cancer.

CONCLUSION: Lewis blood genotype or phenotype may not play a role in the pathogenesis of H pylori infection. However, bacterial strain differences and the presence of more than one attachment mechanism may limit the value of epidemiological studies in elucidating this matter.

Keywords: Lewis histoblood group; Helicobacter pylori; Peptic ulcer; Gastric cancer