PubMed · 9841335
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R A Marlar, J H Joist, L M Fink. 1998-11-19. Pulmonary embolism.. https://pubmed.ncbi.nlm.nih.gov/9841335/
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The 80th anniversary of the best known glycosaminoglycan, a mixture of mucopolysaccharides, named heparin by Howell and Holt in 1918 is celebrated this year. It was widely used during the last six decades in prevention and treatment of venous thromboembolism causing a significant decrease of death from pulmonary embolism and the morbidity of deep venous thrombosis. Conventional, unfractionated heparin is also administered on many other topics. Some more than ten years ago the fractionated, low-molecular-weight heparins were introduced into clinical practice and it seems increasingly likely that the fractionated preparations of this classic drug will take over the dominating role. The present study intends to summarize the today's possibilities of prevention and treatment of thromboembolism mostly on the venous side of circulation.
Treatment with heparin is associated with two types of thrombocytopenia. One is a mild, transient, nonimmune disorder, generally without adverse clinical consequence. The other, known as heparin-induced thrombocytopenia (HIT), is a potentially serious, immunoglobulin-mediated reaction with a paradoxic high risk of thromboembolic events. Various treatment options for HIT are discussed, with emphasis on pharmacologic approaches that control the increased thrombin generation characteristic of this disorder.
Heparin-induced thrombocytopenia (HIT) is an immunologic complication of drug therapy with potentially serious venous and arterial thrombotic sequelae. Recent studies have provided insight into the molecular and cellular basis of HIT underlying the diagnosis and treatment of this syndrome. Because various approaches to HIT treatment have resulted in mixed success, the use of heparin substitutes, other anticoagulant agents, and adjunctive therapy needs to be clarified. For patients with pre-existing conditions such as deep venous thrombosis or pulmonary embolism, new understanding of the clinicopathologic syndrome of HIT offers the promise of improved antithrombotic therapy. The participation of thrombin in HIT suggests that specific (hirudin and argatroban) thrombin inhibitors may be ideal agents for treating acute HIT.