Heparin-induced thrombocytopenia. Pathogenesis, frequency, avoidance and management.

Heparin-induced thrombocytopenia (HIT) is an immunoglobulin-mediated adverse drug reaction associated with a high risk of thrombotic complications. The pathogenic antibody, usually immunoglobulin (Ig) G (HIT-IgG), recognises a multimolecular complex of heparin and platelet factor 4, resulting in platelet activation via platelet Fc receptors. In addition to in vivo platelet activation, it is now recognised that there is a concomitant activation of coagulation, as shown by marked elevations in thrombin-antithrombin complex levels. It is possible that this increased thrombin generation predisposes HIT patients to a newly recognised complication: warfarin-induced venous limb gangrene. This syndrome is characterised clinically by necrosis complicating deep venous thrombosis in the absence of large-vessel arterial occlusion, and appears to result from acquired protein C deficiency during warfarin therapy for deep vein thrombosis and HIT. The recommended treatment for HIT is an agent that reduces thrombin generation, either indirectly via factor Xa inhibition [e.g. danaparoid sodium (a mixture of anticoagulant glycosaminoglycans)] or directly using a specific thrombin inhibitor (e.g. recombinant hirudin; argatroban). HIT is potentially preventable: there is a lower frequency of HIT, associated thrombosis and HIT-IgG seroconversion in patients treated with low-molecular-weight heparins, compared with unfractionated heparin.

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

Heparin-induced thrombocytopenia (HIT) is an immunoglobulin-mediated adverse drug reaction associated with a high risk of thrombotic complications. The pathogenic antibody, usually immunoglobulin (Ig) G (HIT-IgG), recognises a multimolecular complex of heparin and platelet factor 4, resulting in...

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

Explore how this research connects to clinical practice

More peer-reviewed studies in Drug Development.

• Novel Leech Antimicrobial Peptides — Hirunipins — Kumar et al. (2025)
• Medicinal Leech Genome Assembly — Anticoagulant Gene Catalog — Kvist et al. (2020)
• Effects of hirudotherapy on liver functions, lipid profile, and insulin sensitivity in rats with metabolic syndrome — Bilden A et al. (2026)
• Hirudotherapy in Medicine and Dentistry — Jha K et al. (2015)
• Medicinal leech therapy (hirudotherapy): a brief overview — Singh A (2010)
• HIRUDOTHERAPY IN PRESBYACUZIS PRAECOX IN CLEAN-UP WORKERS AFTER THE CHORNOBYL ACCIDENT DURING THE POST-CATASTROPHE YEARS — Zabolotnyi D, Mishchanchuk N (2019)
• Investigation of oxidant-antioxidant status in patients treated with hirudotherapy: an experimental study — Sarikan I, Savas H (2024)
• Leech therapeutic applications — Abdualkader A et al. (2013)
• Non-Occlusive Mesenteric Ischemia Due to Hirudotherapy: A Case Report — Akalın Ç, Ekmen N (2020)
• Leech therapy: a history — Hyson J (2005)

Browse all ASH-analysed research →