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Antiphospholipid antibodies directed against a combination of phospholipids
with prothrombin, protein C, or protein S: an explanation for their
pathogenic mechanism? [see comments]
JD Oosting, RH Derksen, IW Bobbink, TM Hackeng, BN Bouma and PG de Groot
Department of Haematology, University Hospital Utrecht, The Netherlands.
Despite many studies on the pathophysiology of antiphospholipid antibodies
(aPL), the mechanism by which aPL causes thrombosis has not been
established. We have tried to elucidate the paradox between the
prolongation of the clotting time of phospholipid-dependent coagulation
tests in vitro and the occurrence of thrombosis in vivo. The effect on
endothelial cell-mediated prothrombinase activity of 30 IgG fractions, of
which 22 prolong the aPTT of normal plasma, was investigated. Only 4 of 22
fractions (18%) inhibited prothrombinase activity when tested on this more
physiologic phospholipid surface, indicating that in most patients with aPL
the prolongation of clotting tests is predominantly as in vitro phenomenon.
It was recently reported that in detection methods for aPL, two plasma
proteins, beta 2-glycoprotein I and prothrombin, enhance the binding of aPL
to phospholipids. We have studied the specificity of the 4 IgG fractions
that inhibit the prothrombinase activity and found that they were directed
against a combination of phospholipids and prothrombin. However, the
involvement of prothrombin in binding of aPL leading to impaired thrombin
generation could still result in both a bleeding and a thrombotic tendency.
Therefore, we proposed a new thrombogenic mechanism for aPL in which aPL
bind to complexes of phospholipids and coagulation proteins, thereby
interfering in different coagulation reactions. We tested this new
hypothesis by investigating the effect of IgG from the same 30 patients on
the activated protein C (APC)-mediated factor Va inactivation in the
absence and presence of protein S. Three IgGs that inhibited APC-mediated
factor Va inactivation independent of protein S and 4 additional IgGs that
inhibited in the presence of protein S were found. Furthermore, we could
specifically adsorb the inhibitory IgG with cardiolipin vesicles to which
APC with or without protein S was bound. In conclusion, these results
suggest that subpopulations of aPL exist that are directed to complexes of
phospholipids and different plasma proteins. The identity of the plasma
proteins involved in the binding of aPL might determine which pathogenic
mechanism causes thrombosis.
Volume 81,
Issue 10,
pp. 2618-2625,
05/15/1993
Copyright © 1993 by The American Society of Hematology
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L. Ziporen, I. Goldberg, M. Arad, M. Hojnik, J. Ordi-Ros, A. Afek, M. Blank, Y. Sandbank, M. Vilardell-Tarres, I. de Torres, et al.
Libman-Sacks endocarditis in the antiphospholipid syndrome: immunopathologic findings in deformed heart valves
Lupus,
June 1, 1996;
5(3):
196 - 205.
[Abstract]
[PDF]
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M. Hojnik, J. George, L. Ziporen, and Y. Shoenfeld
Heart Valve Involvement (Libman-Sacks Endocarditis) in the Antiphospholipid Syndrome
Circulation,
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93(8):
1579 - 1587.
[Abstract]
[Full Text]
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D. Kandiah and S. Krilis
Immunology of antiphospholipid antibodies and their interaction with plasma proteins
Lupus,
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5(2):
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[Abstract]
[PDF]
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H. Salem
Antiphospholipid antibodies and thrombosis: assessment of the potential risk for thrombosis
Lupus,
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[PDF]
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J. Merrill and R. Lahita
The antiphospholipid syndrome and SLE: is there a clue in the link between complement and coagulation?
Lupus,
February 1, 1996;
5(1):
6 - 10.
[Abstract]
[PDF]
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C. Biron, N. Lalloyer, J.L. Tonnelot, D. Larget, J.C. Gris, and J.F. Schved
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Lupus,
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[Abstract]
[PDF]
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S.P. Walton, S.S. Pierangeli, A. Campbell, E. Klein, B. Burchitt, and E.N. Harris
Demonstration of antiphospholipid antibody heterogeneity by phospholipid column chromatography and salt gradient elution techniques
Lupus,
August 1, 1995;
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[Abstract]
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M. Galli and E. M. Bevers
Inhibition of Phospholipid-Dependent Coagulation Reactions by 'Antiphospholipid Antibodies': Possible Modes of Action
Lupus,
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D. C. Hess
Models for Central Nervous System Complications of Antiphospholipid Syndrome
Lupus,
August 1, 1994;
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[Abstract]
[PDF]
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M. D. Lockshin
Antiphospholipid Antibody: Future Developments
Lupus,
August 1, 1994;
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[Abstract]
[PDF]
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P. Comfurius, E. Revers, M. Galli, and R. Zwaal
Regulation of phospholipid asymmetry and induction of antiphospholipid antibodies
Lupus,
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J. Kaburaki, M. Kuwana, M. Yamamoto, S. Kawai, E. Matsuura, and Y. Ikeda
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[Abstract]
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S.D.H. Malnick, Z.M. Sthoeger, A. D'Angelo, L. Crippa, and S. V. D'Angelo
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[Full Text]
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