TY - JOUR
T1 - Anti-neuronal antibodies in antiphospholipid syndrome with central nervous system involvement
T2 - The difference from systemic lupus erythematosus
AU - Tishler, M.
AU - Alosachie, I.
AU - Chapman, Y.
AU - Korcyn, A.
AU - Lorber, M.
AU - Mevorach, D.
AU - Tane, D.
AU - Barka, N.
AU - Lin, H. C.
AU - Alarcon-Segovia, D.
AU - Youinou, P.
AU - Peter, J. B.
AU - Shoenfeld, Y.
PY - 1995
Y1 - 1995
N2 - The presence of antineuronal antibodies was compared in 43 patients with primary aPLS and 57 patients with neuropsychiatric SLE. Fifty-eight patients with Guillain-Barre 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.
AB - The presence of antineuronal antibodies was compared in 43 patients with primary aPLS and 57 patients with neuropsychiatric SLE. Fifty-eight patients with Guillain-Barre 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.
KW - Antineuronal antibodies
KW - Antiphospholipid syndrome
KW - Autoimmunity
KW - CNS
UR - http://www.scopus.com/inward/record.url?scp=0028929554&partnerID=8YFLogxK
U2 - 10.1177/096120339500400212
DO - 10.1177/096120339500400212
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C2 - 7795619
AN - SCOPUS:0028929554
SN - 0961-2033
VL - 4
SP - 145
EP - 147
JO - Lupus
JF - Lupus
IS - 2
ER -