Brief Report: Induction of sustained remission in recurrent catastrophic antiphospholipid syndrome via inhibition of terminal complement with eculizumab
Identifieur interne : 001419 ( Main/Exploration ); précédent : 001418; suivant : 001420Brief Report: Induction of sustained remission in recurrent catastrophic antiphospholipid syndrome via inhibition of terminal complement with eculizumab
Auteurs : Iuliana Shapira [États-Unis] ; Danieli Andrade [États-Unis] ; Steven L. Allen [États-Unis] ; Jane E. Salmon [États-Unis]Source :
- Arthritis & Rheumatism [ 0004-3591 ] ; 2012-08.
English descriptors
- Teeft :
- Abdominal pain, Alexion pharmaceuticals, Amputation specimen, Anticardiolipin antibody titers, Anticoagulation, Anticoagulation therapy, Antiphospholipid, Antiphospholipid antibodies, Antiphospholipid syndrome, Arthritis rheum, Catastrophic antiphospholipid syndrome, Clinical evidence, Complement activation, Complement inactivation, Complement inhibition, Consulting fees, Direct thrombin inhibitor, Disease pathogenesis, Eculizumab, Endothelial cell activation, Endothelial cells, Heparin, Histopathologic evidence, Inhibitor, Laboratory confirmation, Maintenance doses, Mouse models, Original magnification, Other week, Pharmacodynamic analyses, Plasma exchange, Plasma therapy, Platelet, Platelet count, Platelet counts, Pulse steroids, Receptor interactions, Recurrent caps, Relapsing caps, Renal transplantation, Right foot, Salmon, Semin thromb hemost, Serum complement activity, Severe chest, Short period, Special surgery, Syndrome, Terminal complement, Terminal complement activation, Therapeutic anticoagulant activity, Thrombocytopenia, Thrombosis, Uremic syndrome.
Abstract
Objective: Catastrophic antiphospholipid syndrome (CAPS) is characterized by histopathologic evidence of small vessel thrombosis, dysfunction of multiple organs occurring over a short period of time, and laboratory confirmation of the presence of antiphospholipid antibodies (aPL). Treatment of CAPS focuses on anticoagulation therapy and on removal of aPL that promote thrombosis by activating endothelial cells, monocytes, and platelets. Studies in animal models support the hypothesis that a more targeted intervention, such as complement inhibition, may be an effective means to prevent aPL‐induced thrombosis. Herein we describe use of an inhibitor of complement activation to treat CAPS that was refractory to conventional therapy. Methods: Our patient was a young man who had recurrent CAPS characterized by multiple arterial thromboses in large and small vessels despite maximal anticoagulation, immunosuppression, and plasma exchange therapy. We treated him with eculizumab, an anti‐C5 monoclonal antibody that blocks activation of terminal complement. Results: Administration of eculizumab, at doses that blocked complement activity, aborted acute progressive thrombotic events, reversed thrombocytopenia, and was associated with no further clinical episodes of thrombosis during >3 years of therapy. Conclusion: This first report of the use and clinical efficacy of eculizumab, an inhibitor of complement activation, in the treatment of CAPS demonstrates both the importance of complement (specifically, terminal complement components) in the pathogenesis of CAPS and the therapeutic benefit of complement inactivation.
Url:
DOI: 10.1002/art.34440
Affiliations:
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Le document en format XML
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<term>Antiphospholipid</term>
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<term>Inhibitor</term>
<term>Laboratory confirmation</term>
<term>Maintenance doses</term>
<term>Mouse models</term>
<term>Original magnification</term>
<term>Other week</term>
<term>Pharmacodynamic analyses</term>
<term>Plasma exchange</term>
<term>Plasma therapy</term>
<term>Platelet</term>
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<term>Platelet counts</term>
<term>Pulse steroids</term>
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<term>Relapsing caps</term>
<term>Renal transplantation</term>
<term>Right foot</term>
<term>Salmon</term>
<term>Semin thromb hemost</term>
<term>Serum complement activity</term>
<term>Severe chest</term>
<term>Short period</term>
<term>Special surgery</term>
<term>Syndrome</term>
<term>Terminal complement</term>
<term>Terminal complement activation</term>
<term>Therapeutic anticoagulant activity</term>
<term>Thrombocytopenia</term>
<term>Thrombosis</term>
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<front><div type="abstract" xml:lang="en">Objective: Catastrophic antiphospholipid syndrome (CAPS) is characterized by histopathologic evidence of small vessel thrombosis, dysfunction of multiple organs occurring over a short period of time, and laboratory confirmation of the presence of antiphospholipid antibodies (aPL). Treatment of CAPS focuses on anticoagulation therapy and on removal of aPL that promote thrombosis by activating endothelial cells, monocytes, and platelets. Studies in animal models support the hypothesis that a more targeted intervention, such as complement inhibition, may be an effective means to prevent aPL‐induced thrombosis. Herein we describe use of an inhibitor of complement activation to treat CAPS that was refractory to conventional therapy. Methods: Our patient was a young man who had recurrent CAPS characterized by multiple arterial thromboses in large and small vessels despite maximal anticoagulation, immunosuppression, and plasma exchange therapy. We treated him with eculizumab, an anti‐C5 monoclonal antibody that blocks activation of terminal complement. Results: Administration of eculizumab, at doses that blocked complement activity, aborted acute progressive thrombotic events, reversed thrombocytopenia, and was associated with no further clinical episodes of thrombosis during >3 years of therapy. Conclusion: This first report of the use and clinical efficacy of eculizumab, an inhibitor of complement activation, in the treatment of CAPS demonstrates both the importance of complement (specifically, terminal complement components) in the pathogenesis of CAPS and the therapeutic benefit of complement inactivation.</div>
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