Platelet aggregation test

The normal time it takes to cause clumping is temperature dependent and may vary from laboratory to laboratory. The shape of the vial is also important.

Response to the different "aggregation stimulators" can help to distinguish various platelet defects. In particular, the difference between the response to ristocetin and the other products is important, because ristocetin triggers aggregation through a different mechanism than the other products. The time and pattern of platelet aggregation also varies between stimulators.

Congenital disorders that cause decreased platelet aggregation:

• Glanzmann's thrombasthenia (a rare inherited platelet disorder) -- platelets fail to aggregate in response to normal stimulation but do clump normally in response to ristocetin.
• Bernard-Soulier syndrome (a rare inherited disorder in which platelets are unable to respond to von Willebrand factor) -- platelets aggregate normally in response to most stimulation but do not aggregate in response to ristocetin. The response to collagen is blunted.
• Storage pool disease (a group of disorders characterized by defective stimulation by materials, especially ADP, which trigger platelet aggregation)-- variable abnormalities of platelet aggregation
• Von Willebrand's disease (inherited lack of von Willebrand factor or ristocetin cofactor) -- aggregation with ristocetin is usually abnormal in type I disease and increased in type II.

• use of platelet-inhibiting medications (see special considerations)
• autoimmune disorders that produce antibodies against platelets
• myeloproliferative disorders
• uremia (a result of kidney failure)
• acquired storage pool disorder (platelets are no longer effective because of temporary damage, such as in response to cardiopulmonary bypass or vasculitis)
• fibrin degradation products

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