In APS, the prolonged aPTT is caused by lupus anticoagulant (LA), an immunoglobulin that binds to phospholipid-protein complexes in vitro. When patient plasma is mixed with normal plasma:
In contrast, factor deficiencies (e.g., Factor VIII deficiency) will show correction on mixing because the normal plasma supplies the missing factor.
| Criterion | Details |
|---|---|
| Clinical | Thrombosis (arterial/venous) OR pregnancy morbidity (≥3 consecutive losses <10 weeks OR ≥1 unexplained fetal death ≥10 weeks) |
| Laboratory | Lupus anticoagulant (LA) OR Anticardiolipin (aCL) IgG/IgM ≥40 GPL/MPL units OR Anti-β2-glycoprotein-I IgG/IgM ≥40 units |
| Timing | Lab abnormality must be present on ≥2 occasions ≥12 weeks apart |
APS is a paradoxical thrombophilia: despite prolonged aPTT (which would suggest bleeding), patients have increased thrombotic risk. This is because the anticoagulant effect is in vitro only; in vivo, the antibodies promote thrombosis via:
The statement "Prolonged aPTT that corrects on mixing with normal plasma" is NOT a feature of APS. This is the key distinction. Correction on mixing indicates a factor deficiency, not LA. The presence of non-correcting prolonged aPTT is what makes APS unique and diagnostically important.
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