Inhibitory and activating human antiplatelet antibodies

Platelets are essential for the maintenance of haemostasis and, on the othe r hand, play a pivotal role in the formation of a thrombus. It is clear tha t reduced platelet activity will result in a bleeding tendency, whereas sti mulation of platelets can lead to thrombosis. Human antiplatelet antibodies may not only result in thrombocytopenia, but they have also been found either to inhibit or activate platelets, Inhibiti on by antibodies of the function of different receptors on platelets, such as collagen receptors, the glycoprotein (GP) Ib/IX (acquired Bernard-Soulie r syndrome) or the GPIIb/IIIa complex (acquired Glanzmann's thrombasthenia) , results in a haemorrhagic disorder very similar to the situation where th e respective receptors are absent. On the other hand, reports have described a number of antibodies that activ ate platelets. The mechanism by which they do so varies and can involve int eraction with the Fc receptor present on platelets, activation of the compl ement system or direct activation by binding to a signal-transducing antige n. Although the presence of such antibodies is expected to aggravate the probl ems due to the frequently occurring immune thrombocytopenia, treatment of t hese patients essentially relies on classical immunosuppressive therapy. In the case of activating antibodies, antithrombotic measures, such as antico agulants or antiplatelet agents, can be envisaged.