title: Idiopathic thrombocytopenic purpura: better therapeutic responses of patients with B- or T-cell clonality than patients without clonality.
abstract: Results of recent studies of the pathogenesis of idiopathic thrombocytopenic purpura (ITP) have suggested activated helper T-cells drive B-lymphocytes to produce antibodies. Twenty-eight children and 85 adults with ITP entered this study. We performed polymerase chain reaction (PCR) using framework III variable region (V(H) FRIII)- and joining region (J(H))-specific primers to analyze immunoglobulin heavy-chain gene rearrangement (IgH GR) for B-cell clonality. We used multiplex PCR to analyze T-cell receptor (TCR) gamma-chain gene rearrangement (TCRgamma GR) for T-cell clonality. We diagnosed 10 cases as acute ITP and 97 cases as chronic ITP. The IgH GR result was positive in 77.8% of the acute-form cases and in 58.8% of the chronic-form cases. The TCRgamma GR result was positive in 11.1% of the acute cases and in 10.6% of the chronic cases. There was no difference in frequency of clonality between the acute and chronic forms. After treatment the platelet count normalized in 81.8% (36/44) of the chronic ITP cases with B-cell clonality and in 88.9% (8/9) of the chronic ITP cases with T-cell clonality, compared with a normalized platelet count in 46.2% (12/26) of the chronic ITP cases without clonality. The patients with T- or B-cell clonality appeared to have better therapeutic responses than patients without clonality. In conclusion, T- and B-cell clonality may play a positive role in determining therapeutic response.
authors.affiliation: Department of Laboratory Medicine, Asan Medical Center and University of Ulsan College of Medicine, Seoul, Korea.
authors.forename: J
authors.initials: J
authors.lastname: Kim
authors.forename: C J
authors.initials: CJ
authors.lastname: Park
authors.forename: H S
authors.initials: HS
authors.lastname: Chi
authors.forename: M J
authors.initials: MJ
authors.lastname: Kim
authors.forename: J J
authors.initials: JJ
authors.lastname: Seo
authors.forename: H N
authors.initials: HN
authors.lastname: Moon
authors.forename: T T
authors.initials: TT
authors.lastname: Ghim
authors.forename: S W
authors.initials: SW
authors.lastname: Kim
authors.forename: J H
authors.initials: JH
authors.lastname: Lee
authors.forename: G H
authors.initials: GH
authors.lastname: Lee
authors.forename: J S
authors.initials: JS
authors.lastname: Lee
mesh_terms: D000293:Adolescent; D000328:Adult; D001327:Autoimmune Diseases / Q000276:immunology / Q000473:pathology / Q000628:therapy*; D016175:B-Lymphocyte Subsets / Q000473:pathology; D002648:Child; D002675:Child, Preschool; D002999:Clone Cells / Q000473:pathology; D003131:Combined Modality Therapy; D005260:Female; D015326:Gene Rearrangement, B-Lymphocyte, Heavy Chain; D015334:Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007223:Infant; D008297:Male; D010976:Platelet Count; D016133:Polymerase Chain Reaction; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000276:immunology / Q000473:pathology / Q000628:therapy*; D013156:Splenectomy; D016176:T-Lymphocyte Subsets / Q000473:pathology; D016896:Treatment Outcome
chemical_list: D007166:Immunosuppressive Agents