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See 1 citation in 2007 by KORGANOW AS and MARTIN T and PASQUALI JL and POINDRON V:

Presse Med. 2007 Apr;36(4 Pt 2):667-73. Epub 2006 Dec 22.

[Pathogenesis of the antiphospholipid syndrome].

[Article in French]

Author information

1
Service de Médecine Interne et Immunologie Clinique, Hôpitaux Universitaires, Strasbourg. jean-louis.pasquali@chru-strasbourg.fr

Abstract

The antiphospholipid syndrome is characterized by the association of clinical events (thrombosis and/or obstetrical complications) and heterogeneous autoantibodies reacting with complexes of proteins and anionic phospholipids. Most of these recognized proteins can bind to anionic phospholipids and play a role in natural regulation of coagulation. Inhibition by these autoantibodies of the natural regulators of excessive coagulation is probably responsible for the prothrombotic state that characterizes this disease. Animal models have helped explain the mechanisms of obstetrical complications. Human antiphospholipid antibodies passively transferred to pregnant mice directly cause fetal resorption. This effect is mediated by complement fractions and neutrophil activation and is inhibited by heparin. The origin of these autoantibodies is still debated. Physiologically, the cause may be associated with exposure to anionic phospholipids on the surface of apoptotic cells. The affinity maturation process, which leads to the acquisition of somatic mutations, can then generate highly pathogenic antiphospholipid antibodies.

PMID:
17386337
DOI:
10.1016/j.lpm.2006.11.013
[Indexed for MEDLINE]

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