ACLA are autoantibodies targeting cardiolipin, a phospholipid component of cell membranes. These antibodies are part of the antiphospholipid antibody family and are strongly associated with:
Thrombosis: Venous (e.g., deep vein thrombosis) and arterial (e.g., stroke, myocardial infarction) .
Pregnancy complications: Recurrent miscarriages, fetal growth restriction, and preterm delivery .
Neurological manifestations: Encephalopathy, migraines, and ischemic optic neuropathy .
ACLA testing is performed via immunoassays (IgG/IgM) and is part of the diagnostic criteria for APS when paired with clinical symptoms .
ACLA bind to β2-glycoprotein 1 (β2GP1), a cofactor required for antiphospholipid antibody activity. This interaction disrupts anticoagulant pathways, leading to:
Hypercoagulability: Increased risk of clot formation via platelet activation and endothelial dysfunction .
Placental pathology: Impaired trophoblast invasion and decidual vasculopathy, contributing to pregnancy loss .
Prevalence: Present in 1–5% of the general population; higher in autoimmune diseases like SLE .
APS Subtypes:
Anticoagulation: Lifelong warfarin (target INR 2–3) or heparin for thrombotic APS .
Pregnancy: Low-dose aspirin + prophylactic heparin to reduce miscarriage risk .
Refractory Cases: Rituximab or complement inhibitors under investigation .
ACLA Titers and Thrombosis: Higher titers correlate with recurrent thrombosis and obstetric complications .
Neurological Links: No direct correlation between ACLA levels and encephalopathy, but elevated titers may indicate severe disease .
Infection-Induced ACLA: Transient ACLA positivity occurs in Lyme disease and viral infections, often without clinical APS .