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Hypercoagulable states

R L Nachman¹, R Silverstein

¹Department of Medicine, New York Hospital-Cornell Medical Center, NY 10021.

Annals of Internal Medicine

|October 15, 1993

Summary

This summary is machine-generated.

Hypercoagulable states, both inherited and acquired, increase thromboembolism risk. Deficiencies in endothelial anticoagulant functions cause primary hypercoagulability, while activated surfaces drive secondary forms.

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Area of Science:

Hematology
Vascular Biology
Thrombosis Research

Background:

Hypercoagulable states are characterized by an elevated risk of thromboembolism.
These states can be inherited or acquired, stemming from complex pathophysiologic mechanisms.

Purpose of the Study:

To elucidate the pathophysiologic mechanisms of inherited and secondary hypercoagulable states.
To evaluate the frequency, natural history, diagnosis, and management of related clinical disorders.

Main Methods:

Literature review of hematology textbooks and computerized indexes.
Formulation of a hypothesis based on existing literature and experimental studies.

Main Results:

Inherited hypercoagulable states involve disordered endothelial thromboregulation (e.g., deficiencies in antithrombin III, protein C, protein S).

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Acquired hypercoagulable states arise from endothelial activation, leading to a prothrombotic phenotype (e.g., antiphospholipid syndrome, cancer).

Conclusions:

Normal thromboregulation is primarily a function of the vessel wall.
Deficiencies in endothelial anticoagulant activities define primary hypercoagulable states.
Activated endothelial cells contribute to secondary or acquired hypercoagulability.