Annexin IV antibody is a calcium-dependent protein widely present in various tissues. It has a high affinity for negatively charged phospholipids in cell membranes and exerts in vitro a potent anticoagulant effect by reducing platelet adhesion and aggregation. It is also a marker of apoptosis and has been associated with the occurrence of thrombotic events in patients with systemic autoimmune diseases, including rheumatoid arthritis (RA), SLE, systemic lupus erythematosus and antiphospholipid antibody syndrome (APLA).1
Apoptosis Annexin IV antibody uncontrolled cell death due to stress or acute trauma that disrupts the inner leaflet of the plasma membrane where phosphatidylserine residues reside. Annexin V binds to PS exposed by such damage and is thus selectively taken up by apoptotic cells and stained with propidium iodide (PI). In contrast, non-apoptotic cells show minimal binding or no staining. Thus, PI/Annexin V is used as a positive control to differentiate apoptosis from necrosis.
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In this bicentric cross-sectional study, a total of 70 patients with SSc were selected and serum anti-annexin V IgG and IgM antibodies were measured at baseline and after 6, 12 and 24 months of follow-up by videocapillaroscopy. There was no correlation between the level of annexin V and age, disease duration or the presence of scleroderma renal crisis, telangiectasias or PAH. However, a positive anti-annexin V result at baseline was associated with a worse quality of life as measured by HAQ-DI.
To our knowledge, this is the first study evaluating anti-annexin V in a large cohort of SSc patients and reporting its relationship with disease severity. Our findings support the hypothesis that a negative interaction between annexin V and anti-phospholipid antibodies contributes to the occurrence of vascular complications in patients with SSc.