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Aplastic anemia successfully treated with rituximab: the possible role of aplastic anemia‐associated autoantibodies as a marker for response
Author(s) -
Takamatsu Hiroyuki,
Yagasaki Hiroshi,
Takahashi Yoshiyuki,
Hama Asahito,
Saikawa Yutaka,
Yachie Akihiro,
Koizumi Shoichi,
Kojima Seiji,
Nakao Shinji
Publication year - 2011
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.2011.01612.x
Subject(s) - rituximab , medicine , aplastic anemia , autoantibody , immunology , gastroenterology , cd20 , monoclonal , antibody , monoclonal antibody , bone marrow
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.