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limitations of warfarin and heparin therapy

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limitations of warfarin and heparin therapy
Discuss problems and limitations of warfarin and heparin therapy, and show how these might be overcome by the new generation of direct oral anticoagulants.
Anticoagulant drugs are used to prevent thrombosis in patients at long-term risk, in non-thrombotic patients when a high risk situation occurs and to treat established thromboembolism. The main anticoagulant drugs currently in use in the UK are warfarin, heparin and various analogues of heparin. These drugs are effective in the treatment and prevention of thromboembolism, and have been used as complementary anticoagulants for almost 70 years ((Harbrecht 2011)). However, they have well documented draw backs and necessitate routine coagulation monitoring. These drawbacks alongside an increased understanding of the coagulation pathway have pushed the research and development of new anticoagulant agents. Rivaroxaban and Dabigatran are direct inhibitors of factor IIa (thrombin) and factor Xa (FXa) respectively. These drugs are under intense investigation in clinical trials and appear very promising.

Heparin
Unfractionated heparin (UFH) is a polysaccharide composed of between 10 and 100 saccharide units ((Hoffbrand 2004)). It inhibits all serine proteases to various extents but its main effect is inhibition of thrombin (IIa) and factor Xa (FXa) for which it requires antithrombin (AT) as a cofactor. It binds to the enzyme inhibitor AT inducing a conformational change causing activation of the enzyme. AT inactivates thrombin and FXa and upon heparin binding, its activity is increased by up to 1000-fold. Once bound to heparin, AT under goes a conformational change allowing it to be cleaved by FXa, hence irreversibly inhibiting FXa from its procoagulant activity. For thrombin inhibition, heparin must bind to AT and thrombin, forming a ternary complex. The heparin polysaccharide must be at least 18 saccharide units long to be able to bind thrombin. By inactivating thrombin and preventing its formation,



References: FAVALORO, E. J. and LIPPI, G. (2011). Laboratory testing and/or monitoring of the new oral anticoagulants/antithrombotics: For and against? Clinical chemistry and laboratory medicine : CCLM / FESCC, 49 (5), 755-757. HARBRECHT, U. (2011). Old and new anticoagulants. Hamostaseologie, 31 (1), 21-27. HIRSH, J., et al. (2008). Parenteral anticoagulants: American college of chest physicians evidence-based clinical practice guidelines (8th edition). Chest, 133 (6 Suppl), 141S-159S. HOFFBRAND, A. V. (2004). Postgraduate haematology edited by A.V. hoffbrand. 5th ed., Oxford, Blackwell. LEVINE, M. N., et al. (1994). A randomized trial comparing activated thromboplastin time with heparin assay in patients with acute venous thromboembolism requiring large daily doses of heparin. Archives of internal medicine, 154 (1), 49-56. SAMAMA, M. M. and GUINET, C. (2011). Laboratory assessment of new anticoagulants. Clinical chemistry and laboratory medicine : CCLM / FESCC, 49 (5), 761-772.

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