Heparin-dependent and -independent anti-platelet factor 4 autoantibodies in patients with systemic lupus erythematosus
Satoh T et al. – Platelet factor 4 (PF4) is an autoimmune target in SLE patients. Heparin–dependent and –independent anti–PF4 autoantibodies may be involved in different aspects of pathophysiology of SLE.Methods
- The authors studied 118 patients with SLE, 78 with primary immune thrombocytopenia (ITP), 27 with primary APS, 2 with HIT (as positive controls) and 47 healthy controls.
- Heparin–dependent and –independent anti–PF4 antibodies were measured with an ELISA.
- Antibody binding was confirmed to be heparin–dependent when inhibited by the presence of a high concentration of heparin.
- Pathogenic anti–PF4 antibody was assessed by serotonin–release assay.
- Heparin–dependent anti–PF4 antibodies were detected in 11 SLE (9%) and 2 primary ITP (3%) patients, but at much lower levels than in HIT patients. In serotonin–release assays, only the HIT sera induced platelet activation in vitro.
- Heparin–independent anti–PF4 antibodies were detected in 17 SLE patients (14%).
- There was no correlation between the levels of heparin–dependent and –independent anti–PF4 antibodies.
- Cross–reactivity between these two antibodies was not detectable by ELISA competitive assay.
- Heparin–dependent anti–PF4 antibodies were associated with thrombocytopenia and IgM aCLs (P = 0.007 for both comparisons), while heparin–independent anti–PF4 antibody levels were correlated with SLE disease activity index (P = 0.0005).
- None of the SLE patients with anti–PF4 antibodies had previous heparin exposure.