By Theodore E. Warkentin, Andreas Greinacher
Even though first said in 1973, immune heparin-induced thrombocytopenia (HIT) continues to be essentially the most in all probability devastating and widespread adversarial drug reactions encountered by means of physicians. This Fourth version reinforces its status because the top consultant to the exact prognosis and administration of HIT via picking key signs of this ailment and offering transparent intervention options, together with designated info on therapy paradoxes and using substitute anticoagulants to control those serious situations.
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Extra resources for Heparin-Induced Thrombocytopenia, Fourth Edition (Fundamental and Clinical Cardiology)
C. Platelet-Activating Antibodies in the Pathogenesis of HIT Although some limited studies of heparin-dependent platelet aggregation by patient serum were performed in the classic study by Rhodes and colleagues (1973), the next few years saw increasing emphasis on this characteristic feature of HIT antibodies. In 1975, National Institutes of Health investigators Fratantoni et al. described a patient who developed severe thrombocytopenia (4 · 109/L) and pulmonary embolism while receiving therapeutic-dose unfractionated heparin (UFH) to treat deep venous thrombosis.
J Clin Ther Med 2:1645, 1986. Tardy B, Tardy-Poncet B, Fournel P, Venet C, Jospe R, Dacosta A. Lower limb veins should be systematically explored in patients with isolated heparin-induced thrombocytopenia [letter]. Thromb Haemost 82:1199–1200, 1999. Towne JB, Bernhard VM, Hussey C, Garancis JC. White clot syndrome. Peripheral vascular complications of heparin therapy. Arch Surg 114:372–377, 1979. Trowbridge AA, Caraveo J, Green JB III, Amaral B, Stone MJ. Heparin-related immune thrombocytopenia.
The plateletactivating factor was presumed, but not proved, to be caused by an antibody. , 1980). , patient globulin fractions incubated with heparin, platelet-rich plasma, and celiteactivated contact product shortened the clotting time following recalcification). Three patients developed thrombotic complications, and none developed hemorrhage. ” 6 Warkentin A consistent theme was evident from these various reports. Patients developed arterial or venous thrombotic complications, in association with thrombocytopenia that generally began after 5 or more days of heparin treatment.
Heparin-Induced Thrombocytopenia, Fourth Edition (Fundamental and Clinical Cardiology) by Theodore E. Warkentin, Andreas Greinacher