Heparin-induced thrombocytopenia: a practical review
Review published in Reviews in Cardiovascular Medicine (2010)
Abstract
Heparin-induced thrombocytopenia (HIT) remains under-recognized despite its potentially devastating outcomes. It begins when heparin exposure stimulates the formation of heparin-platelet factor 4 antibodies, which in turn triggers the release of procoagulant platelet particles. Thrombosis and thrombocytopenia that follow comprise the 2 hallmark traits of HIT, with the former largely responsible for significant vascular complications. The prevalence of HIT varies among several subgroups, with greater incidence in surgical as compared with medical populations. HIT must be acknowledged for its intense predilection for thrombosis and suspected whenever thrombosis occurs after heparin exposure. Early recognition that incorporates the clinical and serologic clues is paramount to timely institution of treatment, as its delay may result in catastrophic outcomes. The treatment of HIT mandates an immediate cessation of all heparin exposure and the institution of an antithrombotic therapy, most commonly using a direct thrombin inhibitor. Current "diagnostic" tests, which primarily include functional and antigenic assays, have more of a confirmatory than diagnostic role in the management of HIT. Special attention must be paid to cardiac patients who are often exposed to heparin multiple times during their course of treatment. Direct thrombin inhibitors are appropriate, evidence-based alternatives to heparin in patients with a history of HIT, who need to undergo percutaneous coronary intervention. As heparin remains one of the most frequently used medications today with potential for HIT with every heparin exposure, a close vigilance of platelet counts must be practiced whenever heparin is initiated.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Zusammenfassung
Practical clinical review of HIT pathogenesis, diagnostic tests (functional and antigenic assays), and treatment with direct thrombin inhibitors (including lepirudin and bivalirudin) — emphasizes cardiology-context use during PCI.
Warum dies für die Hirudotherapie relevant ist
This review summarizes heparin-induced thrombocytopenia (HIT), covering its pathophysiology, diagnosis, and management, with attention to cardiac patients who face repeated heparin exposure. The abstract states that treatment mandates cessation of all heparin and institution of alternative antithrombotic therapy, most commonly a direct thrombin inhibitor. The abstract does not mention hirudin, leeches, leech therapy, or the leech secretome, and no direct connection to hirudotherapy is made. Any relevance to ASH's domain is therefore absent or at most indirect, since the review discusses anticoagulation management generically without reference to leech-derived substances. The article is a review and does not provide primary data.
Zitation
Heparin-induced thrombocytopenia: a practical review.
Hong MS, Amanullah AM · Reviews in Cardiovascular Medicine, 2010
Verwandter klinischer Kontext
Erfahren Sie, wie diese Forschung mit der klinischen Praxis verknüpft ist
Zur ASH-Bibliothek hinzugefügt: May 27, 2026 · Letzte Aktualisierung der Website: June 18, 2026