Short communication| Volume 12, ISSUE 3, P247-252, September 1986

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Immunogenetic markers in chlorpromazine-induced tardive dyskinesia

  • Rosa T. Canoso
    Address reprint request to: Dr. R.T. Canoso, Hematology Section, VA Medical Center, Brockton, MA 02401, U.S.A.
    Hematology Section, Medical Service and Neurology Service, VA Medical Center,Brockton /West Roxbury, USA

    Harvard Medical School, Boston, MA U.S.A.
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  • Jorge A. Romero
    Hematology Section, Medical Service and Neurology Service, VA Medical Center,Brockton /West Roxbury, USA

    Harvard Medical School, Boston, MA U.S.A.
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  • Edmond J. Yunis
    Division of Immunogenetics, Dana Farber Cancer Institute, USA

    Harvard Medical School, Boston, MA U.S.A.
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      The presence and severity of tardive dyskinesia were determined in 66 patients with chronic psychiatric disorders treated with chlorpromazine. The patients were classified according to the presence of antinuclear antibodies, the lupus anticoagulant, and the HLA antigen Bw44. The severity of orofacial dyskinesia was estimated using the Rockland Research Institute Scale. Patients with autoantibodies and the Bw44 antigen had higher tardive dyskinesia scores than those with AAB without the Bw44 antigen and also patients without autoantibodies regardless of their HLA phenotype (P < 0.01). These studies suggest that the presence of autoantibodies in association with the HLA Bw44 antigen is related to, and can be a predictor of, neurological complications of long-term chlorpromazine therapy.

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