Normally aggregation of platelets is mediated through GpIIb-IIIa receptors on platelets which get attached to multivalent Von willebrand factor (vWF) or divalent fibrin molecules. The aggregation inducers for such type of aggregation (mediated by GpIIb-IIa) are ADP , Collagen and Thrombin (Factor IIa).
Another type of receptors on platelets, GpIb-IX-V are involved in platelet “adhesion” to sub-endothelial matrix or Collagen.
Ristocetin is an antibiotic which seems to have ability to attach itself to these GpIb-IX-V receptors and cause platelet “aggregation”.
Now since these GpIb-IX-V receptors are absent in Bernard–Soulier syndrome, Ristocetin is unable to aggregate platelets in this condition. However aggregation by ADP, collagen and thrombin is normal since it is mediated through GpIIb-IIIa receptors.
In Glanzmann's thrombasthenia due to absence of GpIIb-IIIa receptors aggregation by ADP, Collagen & thrombin is abnormal, but aggregation by Ristocetin is normal since GpIb-IX-V receptors are available.
Hope this clarifies your doubts.
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