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Anti-neuronal antibodies in antiphospholipid syndrome with central nervous system involvement: the difference from systemic lupus erythematosus

Research Unit of Autoimmune Diseases, Department of Medicine 'B', Sheba Medical Center, Tel Hashomer and The Department of Rheumatology, Tel Aviv Medical Center, Ichilov Hospital, Tel Aviv University Sackler School of Medicine

Iyad Alosachie

Specialty Laboratories, Santa Monica, CA, USA

Yoav Chapman

Department of Neurology, Tel Aviv Medical Center

Amos Korcyn

Department of Neurology, Tel Aviv Medical Center

Margalit Lorber

Department of Immunology, Rambam Hospital, Haifa

Dror Mevorach

Department of Medicine, Hadassah Hospital, Mount Scopus, Jerusalem

David Tane

Research Unit of Autoimmune Diseases, Department of Medicine 'B', Sheba Medical Center, Tel Hashomer and The Department of Rheumatology, Tel Aviv Medical Center, Ichilov Hospital, Tel Aviv University Sackler School of Medicine

Noori Barka

Specialty Laboratories, Santa Monica, CA, USA

Hun-Chi Lin

Specialty Laboratories, Santa Monica, CA, USA

Donato Alarcon-Segovia

Department of Immunology and Rheumatology, Instituto Nacional de la Nutricion 'Salvador Zubiran', Mexico City, Mexico

Pierre Youinou

Laboratoire d'Immunologie, Centre Hospitalier Regional and Universitaire, Brest, France

James B Peter

Specialty Laboratories, Santa Monica, CA, USA

Yehuda Shoenfeld

Research Unit of Autoimmune Diseases, Department of Medicine 'B', Sheba Medical Center, Tel Hashomer and The Department of Rheumatology, Tel Aviv Medical Center, Ichilov Hospital, Tel Aviv University Sackler School of Medicine

The presence of antineuronal antibodies was compared in 43 patients with primary aPLS and 57 patients with neuropsychiatric SLE. Fifty-eight patients with Guillain-Barré syndrome and 72 normal healthy donors served as control groups. Seventeen patients in the study group had aPLS associated with CNS involvement. Antineuronal antibodies were studied in the sera employing a novel flow cytometric assay. The frequency of antineuronal antibodies in patients with aPLS and CNS involvement was not significantly different from that of patients with aPLS without CNS disease or from that found in the control groups (12%, 19% and 7%, respectively). However, it was significantly different from that found in SLE patients with CNS involvement (60%) (P < 0.001). Our results provide further evidence that unlike CNS-SLE, the major mechanism of CNS involvement in patients with primary aPLS might not be autoantibody (antineuronal) mediated, but rather 'thrombotic' in origin, or due to yet unknown factors.

Key Words: antiphospholipid syndrome • autoimmunity • CNS • antineuronal antibodies

Lupus, Vol. 4, No. 2, 145-147 (1995)
DOI: 10.1177/096120339500400212


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