Causes of platelet aggregation disorders

Determination of platelet aggregation with various aggregation inducers plays a key role in the differential diagnosis of thrombocytopathy.

Disorders of platelet aggregation in various diseases

Type of thrombocytopathy	Aggregation stimulator and aggregation disruptor
	ADP		Collagen	Adrenalin	Ristocetin
	Primary wave	Secondary wave
Thrombasthenia	Pathology	Pathology	Pathology	Pathology	Norm
Essential athrombia	Pathology	Pathology	Pathology	Pathology	Norm
Aspirin-like defect	Norm	Pathology	Pathology	Pathology	Norm
Bernard-Soulier syndrome	Norm	Norm	(+,-)	(+,-)	Norm
Wiskott-Aldrich syndrome	Pathology	Pathology	Pathology	Pathology	Norm
Von Willebrand disease	Norm	Norm	Norm	Norm	Reduced (pathological)

(+,-) - has no diagnostic value.

Depending on the functional and morphological characteristics of platelets, the following groups of thrombocytopathies are distinguished.

• Hereditary disaggregating thrombocytopathies without a defect in the release reaction (secondary wave). This group includes:
  • Glanzmann's thrombasthenia, which is characterized by a disorder of ADP-dependent aggregation, with normal ristocetin aggregation;
  • essential athrombia - when exposed to small amounts of ADP, aggregation is not induced, but when the amount of ADP doubles, it approaches normal;
  • May-Hegglin anomaly - collagen-dependent aggregation is disrupted, the release reaction upon stimulation with ADP and ristocetin is preserved.
• Partial disaggregation thrombocytopathy. This group includes diseases with a congenital defect of aggregation with one or another aggregant, or inhibition of the release reaction.
• Disturbance of the release reaction. This group of diseases is characterized by the absence of the second wave of aggregation upon stimulation with a small amount of ADP and adrenaline. In severe cases, ADP- and adrenaline-dependent aggregation is absent. Collagen-dependent aggregation is not detected.
• Diseases and syndromes with insufficient accumulation and storage pool of aggregation mediators. This group includes diseases characterized by impaired ability of platelets to accumulate and release serotonin, adrenaline, ADP and other factors of blood platelets. In the laboratory, this group is characterized by a decrease in all types of aggregation and the absence of a second wave of aggregation.

A decrease in platelet aggregation in response to ADP administration is observed in pernicious anemia, acute and chronic leukemia, and myeloma. In patients with uremia, aggregation is reduced when stimulated by collagen, adrenaline, and ADP. Hypothyroidism is characterized by a decrease in platelet aggregation when stimulated by ADP. Acetylsalicylic acid, penicillin, indomethacin, chloroquine, and diuretics (in particular, furosemide when used in high doses) contribute to a decrease in platelet aggregation, which should be taken into account when treating with these drugs.

In surgical operations complicated by bleeding, disturbances in the vascular-platelet hemostasis system in most cases are caused not by a disturbance in the aggregation and other functional properties of platelets, but by the presence of thrombocytopenia of varying degrees.

[ 1 ], [ 2 ], [ 3 ], [ 4 ], [ 5 ], [ 6 ], [ 7 ], [ 8 ]