title: Genetic analysis of HLA- and HPA-typing in idiopathic (autoimmune) thrombocytopenic purpura patients treated with cepharanthin.
abstract: We performed genetic analysis of human leukocyte antigen (HLA) and human platelet antigen (HPA) in 45 patients with cepharanthin-treated idiopathic thrombocytopenic purpura. HLA-typing was performed by the polymerase chain reaction-restriction fragment length polymorphism method, and HPA-typing by a polymerase chain reaction-sequence-specific primer method. There were 14 responders and 31 nonresponders. Responders included many patients who had already been treated with prednisolone. HLA-DRB1*0901 was significantly more common in responders than in nonresponders. In contrast, HLA-DRB1*0410 and DQB1*0401 were significantly more common in nonresponders. The a/b genotype of HPA-2a/2a (Ko(b)/Ko(b)) was significantly increased in responders. In contrast, HPA-2a/2b (Ko(b)/Ko(a)) and HPA-3a/3b (Bak(a)/Bak(b)) were significantly more common in nonresponders. These findings suggest that genetic studies of HLA and HPA can predict the response of idiopathic thrombocytopenic purpura to cepharanthin.
authors.affiliation: The First Department of Internal Medicine, Kansai Medical University, Moriguchi, Osaka, Japan. fwkg4681@mb.infoweb.ne.jp
authors.forename: S
authors.initials: S
authors.lastname: Nomura
authors.forename: T
authors.initials: T
authors.lastname: Matsuzaki
authors.forename: M
authors.initials: M
authors.lastname: Yamaoka
authors.forename: Y
authors.initials: Y
authors.lastname: Ozaki
authors.forename: M
authors.initials: M
authors.lastname: Nagahama
authors.forename: C
authors.initials: C
authors.lastname: Yoshimura
authors.forename: H
authors.initials: H
authors.lastname: Kagawa
authors.forename: S
authors.initials: S
authors.lastname: Nakayama
authors.forename: S
authors.initials: S
authors.lastname: Fukuhara
mesh_terms: D000328:Adult; D000368:Aged; D000470:Alkaloids / Q000494:pharmacology / Q000627:therapeutic use*; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology / Q000627:therapeutic use*; D016824:Antigens, Human Platelet / Q000032:analysis* / Q000235:genetics; D001324:Autoantigens / Q000235:genetics* / Q000276:immunology; D001327:Autoimmune Diseases / Q000188:drug therapy / Q000235:genetics* / Q000276:immunology / Q000628:therapy; D044182:Benzylisoquinolines; D001792:Blood Platelets / Q000276:immunology; D003131:Combined Modality Therapy; D004351:Drug Resistance / Q000235:genetics; D004705:Endocytosis / Q000187:drug effects; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006680:HLA Antigens / Q000032:analysis* / Q000235:genetics; D006683:HLA-DQ Antigens / Q000032:analysis / Q000235:genetics; D059866:HLA-DQ beta-Chains; D006684:HLA-DR Antigens / Q000032:analysis / Q000235:genetics; D059811:HLA-DRB1 Chains; D006801:Humans; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D018807:Polymorphism, Single-Stranded Conformational; D011239:Prednisolone / Q000627:therapeutic use; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000188:drug therapy / Q000235:genetics* / Q000276:immunology / Q000628:therapy; D013156:Splenectomy; D016896:Treatment Outcome; D052117:Benzodioxoles
chemical_list: D000470:Alkaloids; D000893:Anti-Inflammatory Agents; D000894:Anti-Inflammatory Agents, Non-Steroidal; D016824:Antigens, Human Platelet; D001324:Autoantigens; D044182:Benzylisoquinolines; D006680:HLA Antigens; D006683:HLA-DQ Antigens; D059866:HLA-DQ beta-Chains; D006684:HLA-DR Antigens; D059811:HLA-DRB1 Chains; D011239:Prednisolone; C115212:2a alloantigen, human; C044561:3a alloantigen, human; C069051:HLA-DQB1 antigen; C006947:cepharanthine; D052117:Benzodioxoles