Heparin, a drug responsible for a majority of drug deaths in patients who are reasonably healthy,1 still eludes precise definition as to its structural composition.2 Derived from mast cells of bovine lung and porcine gut, heparin preparations may vary in purity and antigenic effects. The in vivo effect of heparin is made more difficult to predict or standardize because the activity of heparin is dependent on an interaction with plasma and platelet antithrombins, substances whose levels are determined in part by their consumption in normal or abnormal clot formation. The optimal therapeutic level of heparinization is empirical, monitored by in vitro assays of the whole blood clotting or partial thromboplastin times, both gauging the anticoagulant but not necessarily the antithrombotic effects of the drug. It is not surprising that many iatrogenic problems are created with the use of heparin because of this interplay of many variables and unknowns
Duffy TP. Heparin-Induced Thrombocytopenia. JAMA. 1979;241(22):2424. doi:10.1001/jama.1979.03290480058029
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