Heparin-induced thrombocytopenia.

Heparin-induced thrombocytopenia (HIT) is an immune-mediated adverse drug effect that is characterized by platelet activation, hypercoagulability, and a resulting increased risk for thrombosis, both venous and arterial. This disorder is autoimmune-like, because the target antigen is a multimolecular complex of the "self" protein, platelet factor 4, and heparin. HIT usually begins 5 to 10 days after starting heparin, especially when administered intra- or perioperatively, although a rapid onset of thrombocytopenia can occur if heparin is given to a patient with circulating HIT antibodies that resulted from a recent heparin exposure. The clinical diagnosis is supported if heparin-dependent, platelet-activating antibodies are detectable. Treatment includes cessation of heparin and use of an alternative non-heparin anticoagulant, such as danaparoid, lepirudin, or argatroban. Warfarin must be avoided or postponed, as the acute phase of HIT poses a high risk for coumarin necrosis, particularly limb loss due to venous limb gangrene.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Heparin-induced thrombocytopenia.

Leech-derived molecules this paper discusses, each with a full profile in the ASH compound registry:

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