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Platelet-mediated thrombosis is a primary
underlying mechanism leading to cardiovascular life-threatening
clinical events. Control of excessive platelet responses
is an essential aspect of antithrombotic therapy. Antiplatelet
agents have proven to be effective in the prevention
of myocardial infarction, ischemic stroke and subsequent
complications. Platelets are inhibited by many drugs:
aspirin, ticlopidine, clopidogrel, Reopro (TM) and many
others. However, clinicians feel that more effective
and safer drugs are required. New compounds and therapeutic
targets are currently under research taking advantage
of genomics and proteomics technologies.
Bleeding disorders can result from defects in the blood
vessels or from abnormalities in blood clotting factors
or in platelets. Deficiencies of platelets that lead
to hemorrhagic episodes can be quanti- or qualitative.
Among the latter, both congenital and acquired syndromes
such as von Willebrand disease, Bernard-Soulier syndrome,
Glanzmann thrombasthenia, other membrane receptor defects,
storage pool disease, aspirin-like defects, myeloproliferative
disorders, liver disease, and uremia have been defined.
Many hemorrhagic episodes can be prevented or controlled
with platelet transfusions. The increasing demand of
platelet transfusions generates occasional shortness
of supply at Blood Bank Centers. Therefore, the possibility
of developing platelet preparations or synthetic substitutes
which could be stored for longer periods while maintaining
low risk of biological contamination is highly desirable. |
