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British Journal of Anaesthesia, 2002, Vol. 88, No. 4 467-469
© 2002 The Board of Management and Trustees of the British Journal of Anaesthesia

Editorial

Editorial I

Heparin resistance

J. A. M. Anderson1 and E. L. Saenko2

1Northern Ireland Haemophilia and Thrombosis Centre, Department of Haematology, Belfast City Hospital, Lisburn Road, Belfast, Northern Ireland, UK. 2Department of Biochemistry, Holland Laboratory, American Red Cross, 15601 Crabbs Branch Way, Rockville, MD 20855, USA.

Heparin was discovered at the beginning of the twentieth century by McLean (1916).1 Twenty years later (1936) its chemical structure was accredited to the Swedish chemist Jorpes.2 Sixty-five years on it is the most widely used anticoagulant, but are all its actions fully understood? How does it achieve pain relief when administered intravenously for the treatment of overt deep venous thrombosis? Why do some recipients develop heparin-associated thrombocytopenia, and what is the relevance of the occurrence of heparin resistance?

Heparin is a negatively charged, sulphated glycosaminoglycan, composed of alternating uronic and glucuronic acid residues. Commercial preparations are isolated from porcine intestinal mucosa or bovine lung, and are heterogeneous mixtures of polysaccharide chains ranging in molecular weight from 3000 to 30 000, with a mean molecular weight of 15 000.3 Heparin principally exerts its anticoagulant effect by activating antithrombin (AT); the heparin-antithrombin (H-AT) complex then inactivates thrombin, activated factor X (fXa) . . . [Full Text of this Article]

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