Evaluation of a Standardized Protocol Using Lepirudin or Argatroban for Heparin-Induced Thrombocytopenia

Kennedy, Kenneth; Steinke, Doug; King, Shawn; Poe, Kevin; Reeves, Jordan; Short, Marintha

doi:10.2174/187152511798120886

Cited by 2 publications

(1 citation statement)

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“…In a small study, s.c. lowdose desirudin has been compared with argatroban in patients suspected to have HIT. While the number of patients is too small to draw any conclusions on efficacy, no increase in major bleeding complications was observed [Kennedy et al 2011].…”

Section: Lepirudin and Desirudinmentioning

confidence: 89%

Recent advances in the diagnosis and treatment of heparin-induced thrombocytopenia

Bakchoul

Greinacher

2012

Therapeutic Advances in Hematology

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Heparin-induced thrombocytopenia (HIT) is a drug-mediated, prothrombotic disorder caused by immunization against platelet factor 4 (PF4) after complex formation with heparin or other polyanions. After their binding to PF4/heparin complexes on the platelet surface, HIT antibodies are capable of intravascular platelet activation by cross-linking Fcγ receptor IIA leading to a platelet count decrease and/or thrombosis. Diagnosis of HIT is often difficult. This, and the low specificity of the commercially available immunoassays, leads currently to substantial overdiagnosis of HIT. Timing of onset, the moderate nature of thrombocytopenia, and the common concurrence of thrombosis are very important factors, which help to differentiate HIT from other potential causes of thrombocytopenia. A combination of a clinical pretest scoring system and laboratory investigation is usually necessary to diagnose HIT. Although HIT is considered to be a rare complication of heparin treatment, the very high number of hospital inpatients, and increasingly also hospital outpatients receiving heparin, still result in a considerable number of patients developing HIT. If HIT occurs, potentially devastating complications such as life-threatening thrombosis make it one of the most serious adverse drug reactions. If HIT is strongly suspected, all heparin must be stopped and an alternative nonheparin anticoagulant started at a therapeutic dose to prevent thromboembolic complications. However, the nonheparin alternative anticoagulants bear a considerable bleeding risk, especially if given to patients with thrombocytopenia due to other reasons than HIT. While established drugs for HIT are disappearing from the market (lepirudin, danaparoid), bivalirudin, fondaparinux and potentially the new anticoagulants such as dabigatran, rivaroxaban and apixaban provide new treatment options.

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Section: Lepirudin and Desirudinmentioning

confidence: 89%