Platelet function analysis (aggregometry)

"Live platelets are concentrated by slow centrifugation to generate platelet rich plasma (PRP). Sub-samples of PRP are subjected to a panel of agonists that promote platelet aggregometry via different mechanisms to delineate functional abnormalities. Our laboratories employ an extended agonist panel, as below:

● ADP activates the the P2Y1 & P2Y12 surface receptors to trigger an enzyme cascade for calcium mobilisation
● Arachidonic acid is converted by the enzyme cyclo-oxygenase to thromboxane A2 which activates other platelets
● Collagen activates surface receptors to ensure adhesion and release of granule contents
● Ristocetin promotes VWF/GpIb interaction
● Epinephrine interacts with surface receptors and enhances other agonists
● Thrombin receptor agonist peptide (TRAP) activates the primary surface receptor for thrombin to ensure adhesion and release of granule contents
● A23187 is a calcium ionophore enabling investigation of calcium flux over the platelet membrane
● U46619 is a thromboxane mimetic

The agonists activate intra-platelet enzyme cascades that mobilise the GpIIbIIIa surface receptor which binds fibrinogen to promote aggregation.

Release of intra-platelet ADP is also assessed using whole blood aggregometry

Platelet function analysis is reported with interpretive comments"
Clinical details: 
"Platelets are anucleate fragments of the cytoplasm of their parent cell, the megakaryocyte. They circulate predominantly at the margins of blood vessels in a dormant, resting state, but are capable of a rapid and dramatic response to various stimuli arising from vessel trauma. They have a complex structure that facilitates their specialised functions, of which the main ones are listed below:

● Interaction with collagen-captured VWF to form the initial barrier to blood loss
● Propagate the clot via platelet aggregation
● Provide the platform for secondary haemostasis
● Localisation mechanisms
● Maintain endothelial junction integrity

Exposure of sub-endothelial collagen after vessel trauma promotes binding of VWF which tethers platelets via their GpIb receptor. Blood flow rolls the platelet over where it forms stable associations via separate collagen binding receptors which also serves to activate the platelet. Activated platelets change their shape to promote effective physical interaction and release of the contents of cytoplasmic granules which activate more platelets and promote platelet-to-platelet aggregation via fibrinogen bridging of receptors on adjacent platelets. Biochemical pathways are also activated to promote aggregation, and the phospholipid membrane re-organises to promote localisation of secondary haemostasis to stabilise the platelet plug.

Reduced platelet numbers, receptor deficiency/dysfunction, granule deficiency or granule content deficiency, biochemical abnormalilties and drug interactions can lead to bleeding disorders. Platelet aggregometry involves stimulating live platelets with a panel of agonists that promote platelet aggregometry via different mechanisms."
Reference range: 

Interpretive reporting

Sample type and Volume required: 
Contact laboratory.
Turnaround time: 
Analysed immediately, report within 7 - 10 days
Special sample instructions: 

30 ml of blood is taken into citrate anticoagulant and delivered directly to the laboratory for immediate analysis on live platelets. Analysis must be complete within 4 hours of venepuncture.

Diagnostic Haemostasis and Thrombosis Department
020 7188 2797
St Thomas' Hospital
North Wing - 4th and 5th Floors
Westminster Bridge Road
London SE1 7EH

Laboratory opening times
For clinical advice or interpretation of results, please contact the laboratory in the first instance.

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Last updated: 07/08/2015