title: Aplastic anemia successfully treated with rituximab: the possible role of aplastic anemia-associated autoantibodies as a marker for response.
abstract: A 1-yr-old Japanese male infant developed hepatitis-associated aplastic anemia (AA), and anti-thymocyte globulin (ATG) plus cyclosporine A (CsA) was administered without any appreciable effects. Laboratory examination of the patient's serum obtained before therapy revealed various autoantibodies, such as PA-IgG, anti-platelets, anti-single-stranded DNA (ssDNA), and anti-double-stranded DNA (dsDNA) antibodies (Abs) in addition to anti-DRS-1 Abs and anti-moesin Abs, both of which are known to be detectable in approximately 40% of all patients presenting with AA. He was therefore treated with 17.5 mg/kg/d rituximab 5.5 months after ATG/CsA therapy. The same rituximab therapy was repeated three times once a month thereafter. His neutrophil counts started to increase 50 d after the first rituximab therapy and he achieved a complete remission at 16 months after the last rituximab administration. All of the autoantibodies including anti-ssDNA, dsDNA, DRS-1, and moesin became undetectable when he attained the remission. Anti-CD20 monoclonal antibody therapy may be effective in a subset of patients with AA characterized by the presence of autoantibodies.
authors.affiliation: Department of Hematology, School of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Ishikawa, Japan. takamaz@med3.m.kanazawa-u.ac.jp
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Takamatsu
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Yagasaki
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Takahashi
authors.forename: Asahito
authors.initials: A
authors.lastname: Hama
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Saikawa
authors.forename: Akihiro
authors.initials: A
authors.lastname: Yachie
authors.forename: Shoichi
authors.initials: S
authors.lastname: Koizumi
authors.forename: Seiji
authors.initials: S
authors.lastname: Kojima
authors.forename: Shinji
authors.initials: S
authors.lastname: Nakao
mesh_terms: D000741:Anemia, Aplastic / Q000276:immunology* / Q000473:pathology / Q000628:therapy*; D000974:Antibodies, Antinuclear / Q000097:blood; D058846:Antibodies, Monoclonal, Murine-Derived / Q000627:therapeutic use*; D000961:Antilymphocyte Serum / Q000627:therapeutic use; D001323:Autoantibodies / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D001853:Bone Marrow / Q000473:pathology; D019748:Carbon-Carbon Double Bond Isomerases / Q000276:immunology; D016572:Cyclosporine / Q000627:therapeutic use; D064006:Dodecenoyl-CoA Isomerase; D006801:Humans; D007223:Infant; D008297:Male; D008840:Microfilament Proteins / Q000276:immunology; D012074:Remission Induction; D000069283:Rituximab; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D000974:Antibodies, Antinuclear; D058846:Antibodies, Monoclonal, Murine-Derived; D000961:Antilymphocyte Serum; D001323:Autoantibodies; D015415:Biomarkers; D008840:Microfilament Proteins; C071058:moesin; D000069283:Rituximab; D016572:Cyclosporine; D019748:Carbon-Carbon Double Bond Isomerases; D064006:Dodecenoyl-CoA Isomerase; C119738:ECI2 protein, human