Causes of impaired platelet aggregation

The determination of platelet aggregation with various aggregation inducers plays a crucial role in the differential diagnosis of thrombocytopathies.

Disorders of platelet aggregation in various diseases

Type of thrombocytopathy	Stimulant aggregation and aggregation violations
	ADP		Collagen	Adrenalin	Ristocetin
	Primary wave	Secondary wave
Thrombosis	Pathology	Pathology	Pathology	Pathology	Norm
Essential thrombosis	Pathology	Pathology	Pathology	Pathology	Norm
Aspirin-like defect	Norm	Pathology	Pathology	Pathology	Norm
Bernard-Soulier Syndrome	Norm	Norm	(+, -)	(+, -)	Norm
Viscota-Aldrich syndrome	Pathology	Pathology	Pathology	Pathology	Norm
Von Willebrand's Disease	Norm	Norm	Norm	Norm	Reduced (pathological)

(+, -) - has no diagnostic value.

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

• Hereditary disaggregational thrombocytopathies without disturbance of the release reaction (secondary wave). This group includes:
  • Glącmann's thrombastia, which is characterized by a violation of ADP-dependent aggregation, with normal ristocetin-aggregation;
  • essential atrombia - under the influence of small amounts of ADP, aggregation is not induced, and when the amount of ADP doubles, it approaches normal;
  • the May-Heglin anomaly - collagen-dependent aggregation is disrupted, the release reaction with stimulation of ADP and ristocetin is preserved.
• Partial disaggregation thrombocytopathy. This group includes diseases with a congenital defect aggregation with one or another aggregate, or inhibition of the release reaction.
• Disruption of the release reaction. For this group of diseases, there is a lack of a second aggregation wave when stimulated with a small amount of ADP and epinephrine. In severe cases, there is no ADP and adrenaline-dependent aggregation. Collagen-dependent aggregation is not detected.
• Diseases and syndromes with an insufficient pool of accumulation and storage of mediators aggregation. This group includes diseases characterized by a violation of the ability of platelets to accumulate and release serotonin, adrenaline, ADP and other factors of the blood platelets. Laboratory for this group is characterized by a decrease in all types of aggregation and the absence of a second wave of aggregation.

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

In surgical operations complicated by bleeding, violations in the system of vascular-platelet hemostasis in most cases are caused not by a violation of aggregation and other functional properties of platelets, but by the presence of thrombocytopenia of one degree or another.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12]