Clinical application of platelet function test

Platelets play an important role in the involvement of thrombosis and atherosclerosis. TXA2, 5HT cause vasoconstriction: PDGF, β-TG, PF4 stimulate smooth muscle cells to cause arteriosclerosis, GPIIb/IIla fibrinogen receptor activation causes platelet aggregation, and fibrin formed by activation of coagulation system constitutes platelet emboli.

Platelet adhesion, aggregation, release products, arachidonic acid metabolism, procoagulant action, and receptor expression are involved in the above process.

In vivo, high shear stress produced by stenotic vessels, products released by various cells, and endothelial damage can all constitute stimuli for activation of platelets. In addition to the above environmental factors, certain characteristics of platelets themselves, such as: genetic polymorphism, the significance of the occurrence of thrombosis is also a new topic that has become more and more important in recent years.

First, the platelet function test project

Bleeding time, adhesion, aggregation, release products, arachidonic acid metabolites, cytosolic free calcium levels, clotting activity, membrane glycoprotein detection, gene polymorphisms, and mutations.

Commonly used methods for detecting function are: platelet aggregation measurement (turbidimetry, impedance method, circulating platelet aggregate, spontaneous platelet aggregation). In recent years, flow cytometry, PFA-100 analysis and laser diffraction have been used to detect minute aggregation. The body also gradually enters the clinical or preclinical stage.

Turbidimetric assay for platelet aggregation is a widely used indicator that can be used as a diagnostic marker for hereditary platelet disease. It can also be used as a thrombotic disease to assess its pathological response, to guide the use of antithrombotic drugs, and as an antiplatelet drug. In the application of turbidimetry, there are several key issues that should be noted: (1) blood collection and separation. (2) Inducer application: type, concentration. (3) Selection of normal values.

Flow cytometry can detect platelet function, metabolism, dusting and receptor expression, and the formation of tiny aggregates as an early sensitive indicator of thrombosis is also being evaluated by laser diffraction, reflecting platelets in the whole blood state. Impedance methods and detection of intraplate calcium levels have shown significance in clinical studies.

Second, the clinical application of platelet function test

1, bleeding disorders

In the two categories of hereditary and acquired, a preliminary diagnosis of hereditary platelet disease can be made using a conventional platelet aggregation test.

2, thrombotic disease

Most thrombotic diseases can detect increased platelet reactivity (this is a certain pathological process for the disease, guiding the treatment of the disease; meaning, the significance of many indicators in the disease is also comparatively studied, some molecular markers reflect platelets High sensitivity in activation). P-selectin is a more sensitive indicator of platelet activation, and platelet aggregation is relatively simple. Recent studies have also shown that platelet activation markers are not meaningful in reflecting platelet activation and are predictive of certain diseases. For example, collagen-induced platelet aggregation increased at 25 weeks of gestation, indicating pre-eclampsia, with high sensitivity and accuracy, and the use of platelet count, MPV and aggregation to predict pre-eclampsia. Using MPV, platelet count, and P-selectin, differences in unstable angina and myocardial infarction were found. This suggests that platelet testing is very useful clinically. In addition to the above-mentioned acquired causes of platelet involvement in functional thrombosis, recent studies have also demonstrated the existence of genetic factors.

Viscous platelet syndrome is autosomal dominant, showing enhanced platelet aggregation response to ADP and/or adrenaline. The intrinsic is divided into three types: type I enhances both ADP and adrenaline aggregation, and type II adrenaline. The aggregation reaction is enhanced, and the type III enhances the aggregation reaction of ADP. In the case of arterial thrombosis of unknown cause, the incidence of intrinsic is 21%. The relationship between platelet membrane glycoprotein gene polymorphism and the risk of arterial thrombosis is under investigation. PLA1 (Leu33)→PL2 (Pro33) of GPIIIa, three polymorphisms on GPba (39bp tandem repeat variation, Thrl45Met, -5T/C), gene polymorphisms and deficiency of collagen receptor GPIa807C/T and Lys505Glu The relationship between blood-borne heart disease, cerebrovascular disease and interventional therapy is mostly between genotype and disease, although the results obtained are preliminary, such as atherosclerosis, heart and brain and peripheral vascular thrombosis, Diseases such as diabetes have led to a new understanding of the relationship between genetic factors and thrombosis.

3. Application in drug monitoring

Anti-platelet drug monitoring usually uses turbidimetric platelet aggregation assay. Of course, PFA-100 is more sensitive. When taking ASA, its platelet inducer is called AA+ADP or collagen. ADP can be used in combination with Bolivia, in the GPIIb/IIIa antagonist therapy leaves, using whole blood platelet aggregation and flow cytometry results - more sensitive than turbidity, heparin treatment caused thrombocytopenia / thrombosis The formation syndrome is also determined by the aggregation method.