[Antiphospholipid antibody syndrome in systemic lupus erythematosus]

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This article reviews antiphosphospholipid antibody syndrome in systemic lupus erythematosus, detailing the pathophysiology of beta 2-glycoprotein binding and outlining treatment strategies including steroids, cyclophosphamide, plasmapheresis, and Danazol.

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Abstract

Various hemostatic abnormalities that can be met in the course of apparently unrelated diseases are caused by antiphospholipid antibodies (APA). Nearly on half of the population with antibodies detectable in serum suffer from systemic lupus erythematosus (SLE) or the disease will be diagnosed in the future. The supposition considering that APA do not bind phospholipids directly becomes popular recently. They bind serum beta 2-Glycoprotein. The APA-beta 2 GIP complexes speed up prothrombin activation and make beta 2 GIP less available for serum C- and S-protein transformation. APA are a heterogenous population of antibodies. Postinfectious APA differ from those found in autoimmune diseases. Thrombotic events caused by APA are treated according to general principles. Steroid therapy is essential in treatment programme of SLE with APA. In severe cases it is supplemented by intravenous cyclophosphamide. Plasmapheresis and intravenous immunoglobulins are of limited usefulness. In severe resistant thrombocytopenia one can try to introduce Danazol carefully.

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MeSH descriptors

Antiphospholipid Syndrome Lupus Erythematosus, Systemic Antibodies, Antiphospholipid Antibodies, Antiphospholipid Antiphospholipid Syndrome Antiphospholipid Syndrome Antiphospholipid Syndrome Cyclophosphamide Cyclophosphamide Danazol Danazol Humans Immunoglobulins, Intravenous Immunoglobulins, Intravenous Lupus Erythematosus, Systemic Plasmapheresis Steroids Steroids Thrombocytopenia Thrombocytopenia

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openalex
last seen: 2026-05-10T10:40:25.691325+00:00
pubmed
last seen: 2026-10-08T22:00:22.376048+00:00
License: CC0 · commercial use OK