title: Clinical significance of HLA-DRB1*0410 in Japanese patients with idiopathic thrombocytopenic purpura.
abstract: We performed HLA-A, -B, and -C antigen and -DR DNA typing in 111 Japanese patients with idiopathic thrombocytopenic purpura (ITP). DRB1*0410 was significantly increased in ITP patients compared with healthy controls (relative risk = 9.52, P < .05), but the other DRB1*04 alleles showed no significant differences. On HLA-DR serotyping, patients with Vogt-Koyanagi-Harada disease (VKH) had a high frequency of DR4, so we compared the frequencies of DRB1*04 suballeles between ITP and VKH. The high frequency of DRB1*04 was dependent on DRB1*0405 in VKH, but on DRB1*0410 in ITP. Plasma autoantibodies were studied in 111 patients using a microtiter well assay. Thirty-six patients had anti-GPIIb/IIIa autoantibodies, and antibody positivity was associated with HLA-DR4 (29 of 36, 80.6% v 28 of 75, 37.3%) but not with DRB1*0410. When HLA-DR4 and DRB1*0410 were compared between patients with a good or poor response to prednisolone, HLA-DR4 was decreased and DRB1*0410 was significantly decreased (chi2 = 11.455, P < .01) in patients with a good response. In conclusion, this study showed that genetically determined factors influence the course of ITP. However, our findings should be considered preliminary because of possible racial differences in HLA status between Japanese and other ITP patients.
authors.affiliation: First Department of Internal Medicine and the Department of Blood Transfusion, Kansai Medical University, Osaka, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Nomura
authors.forename: T
authors.initials: T
authors.lastname: Matsuzaki
authors.forename: Y
authors.initials: Y
authors.lastname: Ozaki
authors.forename: M
authors.initials: M
authors.lastname: Yamaoka
authors.forename: C
authors.initials: C
authors.lastname: Yoshimura
authors.forename: K
authors.initials: K
authors.lastname: Katsura
authors.forename: G L
authors.initials: GL
authors.lastname: Xie
authors.forename: H
authors.initials: H
authors.lastname: Kagawa
authors.forename: T
authors.initials: T
authors.lastname: Ishida
authors.forename: S
authors.initials: S
authors.lastname: Fukuhara
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D044466:Asian People / Q000235:genetics; D001323:Autoantibodies / Q000276:immunology; D001327:Autoimmune Diseases / Q000188:drug therapy / Q000453:epidemiology / Q000208:ethnology / Q000235:genetics* / Q000276:immunology; D004198:Disease Susceptibility; D005260:Female; D005838:Genotype; D006684:HLA-DR Antigens / Q000235:genetics*; D015804:HLA-DR4 Antigen / Q000235:genetics; D059811:HLA-DRB1 Chains; D006650:Histocompatibility Testing; D006801:Humans; D007564:Japan / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000276:immunology; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D011239:Prednisolone / Q000627:therapeutic use; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000188:drug therapy / Q000453:epidemiology / Q000208:ethnology / Q000235:genetics* / Q000276:immunology
chemical_list: D001323:Autoantibodies; D006684:HLA-DR Antigens; D015804:HLA-DR4 Antigen; D059811:HLA-DRB1 Chains; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D011239:Prednisolone