Background/Aims: It has been known that genetic factors, for example, blood group, non-secretor and HLA system, are associated with duodenal ulcer and that Helicobacter pylori infection is the major cause of peptic ulcer. However, Helicobacter pylori is also found in non-ulcer dyspepsia and asyrnptomatic patients without ulcer formation. But, it is still not known regarding what kind of genetic factors have an effect on ulcer formation at the time of Helicobacter pylori infection. This study was performed to make clear wbich genetic factors are re1ated with duodenal ulcers among Koreans, and what kind of genetic factors could influence on the ulcer formation in the patients with Helicobacter pylori infection according to ABO blood groups and HLA antigen.'.. Methods: The duodenal ulcer patients (36), non-ulcer dyspepsia (19) and norraal healthy controls (103) were included in this study. Helicobacter pylori infection was detected with phenol red spray method in vivo which was confirmed with Warthin-Starry silver stain. HLA antigen expression (HLA-A,B) of peripheral blood T lymphocytes was studied with microlymphocytotoxicity teclmique. Results: Tbe frequency of HLA-A 33 was higher in duodenal ulcer patients (l4/36, 38.9%) compared with the control group (21/103, 20.4%). On the contrary, no difference in HLA-B has been shown between duodenal ulcer patients and controls. Among patients with Helicobacter pylori infection, blood group 0 was significant1y more frequent in patients with duodenal ulcers (21/36, 58.3%) than in non-ulcer dyspepsia (5/19, 26.3%). In patients with HLA-A 33, blood group 0 was significantly more frequent in duodenal ulcer patients (7/)4, 50%) than in non-ulcer dyspepsia patients (0/7, 0%). Conclusions: In Helicobacter pylori-infected patients, HLA-A 33 is related with duodenal ulcers and the patients with both blood group 0 and HI.A-A 33 are more likely to have duodeual ulcers than those with HLA-A 33 and without blood groop O. (Korean J Gastrnenterol 1996; 28:623 - 631)