Antiphospholipid Antibodies (aPL) as Prognostic Markers

While antiphospholipid antibodies (aPL) are traditionally used diagnostically in the context of antiphospholipid syndrome (APS) or lupus erythematosus (SLE), a 10-year cohort study published in The American Journal of Medicine (2026) now demonstrates their prognostic significance. The study shows that aPL positivity—independent of APS or SLE—is a strong predictor of long-term mortality and hospital readmission.

Conducted at Sheba Medical Center (Israel), these findings have critical implications for healthcare systems, where aPL testing is increasingly recognized as a key tool for risk assessment in autoimmune and thrombotic disorders¹. They investigated almost 5,000 patients without APS or SLE using classical aPL ELISAs as recommended by the classification criteria.

📌 Key Findings

Anti-cardiolipin IgG and Lupus anticoagulant (LA) showed the strongest associations with mortality, independent of APS or SLE diagnosis, thrombotic history, or other comorbidities.
Low-titer IgM aPL (anti-β2GPI, anti-cardiolipin) were also linked to increased mortality, challenging traditional classification criteria that often underweight IgM antibodies²³.
Thrombotic events did not explain the risk, suggesting non-thrombotic mechanisms (e.g., endothelial dysfunction, inflammation).

Patients (no APS or SLE)	aPL-Positive (n=1,485)	aPL-Negative (n=3,316)	Hazard Ratio (HR)
10-Year Mortality	21.8%	12%	1.40
1-Year Readmission	40.9%	32.8%	1.25

🏥 Clinical Implications and conclusion

This study highlights the prognostic significance of anti-phospholipid antibodies (aPL) positivity in hospitalized patients, independent of traditional risk factors. The findings underscore the importance of including aPL testing in risk stratification frameworks to identify high-risk individuals early.

The prognostic value of anti-cardiolipin IgG, which can act in a cofactor-independent manner⁴, further emphasizes the need for comprehensive aPL testing beyond β2GPI-dependent antibodies. Recent studies also demonstrate that some aPLs bind directly to cell-surface targets such as the EPCR/LBPA complex—where LBPA is a phospholipid structurally similar to phosphatidylglycerol and cardiolipin—and that statins may inhibit this binding⁵. This supports the pathogenic role of cofactor-independent aPLs and highlights the importance of detecting all relevant aPL subtypes.

Read more on the value of aPL in severe pregnancy complications due to obstetric anti-phospholipid syndrome, here 👈.

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