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Lupus Anticoagulant Paradox — SCE Rheumatology MCQ

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ModerateAutoimmune SerologyLupus Anticoagulant ParadoxSCE Rheumatology

A 48-year-old woman with systemic lupus erythematosus develops an unprovoked proximal deep-vein thrombosis. Before anticoagulation, her activated partial thromboplastin time is prolonged. The prolongation persists after mixing her plasma 1:1 with normal plasma but shortens substantially when the assay is repeated with excess phospholipid. She has no personal history of abnormal bleeding. Which mechanism best explains these apparently discordant findings?

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Correct answer: B — Antiphospholipid antibodies inhibit phospholipid-dependent coagulation reactions in vitro but promote prothrombotic cellular and inflammatory pathways in vivo

The correct answer is B. Lupus anticoagulant comprises antiphospholipid antibodies that interfere with phospholipid-dependent coagulation reactions in vitro, prolonging an LA-sensitive aPTT or dRVVT. Persistence after mixing supports an inhibitor, while shortening with excess phospholipid demonstrates phospholipid dependence. In vivo, antiphospholipid antibodies promote thrombosis through mechanisms including endothelial, monocyte and platelet activation and complement-mediated inflammation; the prolonged aPTT therefore does not imply protection from thrombosis. An acquired factor VIII inhibitor usually produces bleeding and is not corrected by excess phospholipid. Contact-factor deficiency may markedly prolong aPTT but does not produce this phospholipid-dependent confirmatory pattern. Heparin interference is not specifically reversed by excess phospholipid. Lupus anticoagulant does not generally represent consumption of intrinsic-pathway factors or an inherent bleeding disorder.

Reference: Molhoek JE, de Groot PG, Urbanus RT. The Lupus Anticoagulant Paradox. Seminars in Thrombosis and Hemostasis. 2018;44:445–452. https://pubmed.ncbi.nlm.nih.gov/28898901/