Summary
Antiphospholipid antibodies, namely lupus anticoagulant (LA), anticardiolipin (aCL)
type A and type B antibodies, are frequently associated with immune-mediated thrombocytopenia.
Antiphospholipid antibodies have been suggested to bind to the phospholipids of the
platelet membrane, thus participating to the process of platelet destruction, which
leads to thrombocytopenia. However, a clear antiphospholipid (aPL) demonstration of
such a role has never been given for antibodies. Conversely, autoantibodies directed
against membrane-associated glycoproteins (GP) have been shown to be pathogenet- ically
linked to the development of thrombocytopenia in patients with idiopathic thrombocytopenic
purpura. For this reason, we have measured anti-GPIb/IX and GPlIb/IIIa IgG in the
plasma of 68 patients with aPL antibodies by ELISA. The monoclonal antibody-specific
immobilization of platelet antigen (MAIPA) assay was used.
Twenty-seven out of 68 patients with antiphospholipid antibodies (40%) had increased
plasma levels of anti-GP antibodies. In particular, 7 of them had elevated anti-GPIIb/IIIa
levels only, 6 had anti-GPIb/IX antibodies only, whereas in the remaining 14 cases
both types of autoantibodies were found elevated. The level of anti-GP antibodies
in plasma did not correlate with age, sex, clinical associated conditions, history
of thrombosis, IgG aCL titer or the presence of a phospholipid- dependent inhibitor
of coagulation. In contrast, a statistically significant association between thrombocytopenia
and high anti-GP antibody titer was observed (p = 0.0458).
To establish whether there was cross-reactivity between antiphospholipid and anti-GP
antibodies, adsorption experiments were performed using eardiolipin-containing liposomes
or washed, normal, resting platelets. When patients’ plasma was mixed with resting
washed platelets, only anti-GP antibodies were adsorbed on platelet membrane and subsequently
eluted from platelets. Conversely, binding to cardio- lipin-containing liposomes but
not to platelet surface was demonstrated for antiphospholipid antibodies.
In conclusion, our data indicate that high levels of anti-platelet glycoprotein antibodies
are more frequently found in patients with antiphospholipid antibodies and thrombocytopenia
and that they might be responsible, more than LA and/or aCL antibodies, for the development
of thrombocytopenia.
