Recognition and Management of Heparin-Induced Thrombocytopenia (HIT) and Thrombosis

Alving, Barbara M.; Krishnamurti, Chitra

doi:10.1055/s-2007-996138

Cited by 19 publications

(8 citation statements)

References 34 publications

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“…Nevertheless, in each case the clinicians caring for these patients not only considered the diagnosis of HIT but, in three of the four cases the patients were also tested for the heparin-associated antiplatelet antibody. We as others [4] wrestled with the implication of the differential diagnosis. We chose to continue heparin therapy because of the strong indication for effective anticoagulation therapy in these cases.…”

Section: Discussionmentioning

confidence: 99%

“…Despite excellent recent reviews regarding HIT [1][2][3], the differential diagnosis of HIT often receives little attention. Most clinicians have encountered the unpleasant dilemma characterized by possible severe complications of heparin on the one hand but strong indications for anticoagulant therapy on the other with relatively few therapeutic alternatives in between [4].…”

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confidence: 99%

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Thrombocytopenia due to acute venous thromboembolism and its role in expanding the differential diagnosis of heparin‐induced thrombocytopenia

Kitchens

2004

American J Hematol

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Thrombocytopenia is an uncommon but serious consequence of heparin administration. Occasionally patients with massive acute venous thromboembolism (VTE) will develop thrombocytopenia. As heparin or some thrombin inhibitor is strongly indicated in acute VTE, it is important to distinguish this event from heparin-induced thrombocytopenia (HIT). Four patients are presented who developed thrombocytopenia so early in their course of VTE and/or therapy with heparin that HIT was considered unlikely. The mean nadir platelet count for these four patients was 60,000/ml occurring at a mean time of 18 hr after the initiation of heparin therapy. Because of strong indications to continue heparin for their acute VTE in the face of a very low likelihood that they did have HIT, heparin was continued with excellent results and resolution of the thrombocytopenia. The literature of this subject is reviewed. Thrombocytopenia following VTE is actually rather common, but it is usually milder than in these four cases. In some cases such as these four, the thrombocytopenia can be sudden and rather severe causing diagnostic confusion with HIT. Am.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Thrombocytopenia due to acute venous thromboembolism and its role in expanding the differential diagnosis of heparin‐induced thrombocytopenia

Kitchens

2004

American J Hematol

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“…While most often asymptomatic, thrombocytopenia may be associated with a prothrombotic state, contributing to venous or arterial thrombosis through development of antibodies to a complex of heparin with platelet factor 4. 40 The incidence of thrombocytopenia is reduced in patients treated with LMWH as opposed to IVUH. 22 An additional, underappreciated advantage of transitional LMWH among stroke patients is the release from constraint it imposes on rehabilitation therapy.…”

Section: Discussionmentioning

confidence: 99%

Safety and Cost of Low-Molecular-Weight Heparin as Bridging Anticoagulant Therapy in Subacute Cerebral Ischemia

Kalafut

Gandhi

Kidwell

et al. 2000

Stroke

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Background and Purpose-Anticoagulation with intravenous unfractionated heparin (IVUH) while awaiting therapeutic oral anticoagulant levels is a common practice in patients with acute and subacute cerebral ischemia. A promising alternative strategy is to use bridging subcutaneous low-molecular-weight heparin (LMWH), which may have a favorable risk-benefit profile compared with IVUH and may permit earlier discharge with completion of transition to warfarin therapy as an outpatient. Methods-A LMWH, enoxaparin 1 mg/kg BID, was used as bridging anticoagulation therapy in 24 consecutive patients admitted to a university stroke center in whom the treatment plan included transition from acute to chronic anticoagulation. The LMWH group was contrasted with the preceding 24 patients transitioned to warfarin with IVUH at the same center. Results-Fewer patients in the LMWH bridging therapy group experienced neurological worsening than in the IVUH bridging therapy group (2/24 versus 8/24; Pϭ0.033). Fewer total adverse events were noted in the LMWH group than in the IVUH cohort (3 versus 20; Pϭ0.002). Fifteen of the 24 LMWH patients (62.5%) were discharged while still receiving LMWH and completed transition to warfarin as outpatients, receiving an average of 3.6 days of outpatient transitional therapy. In these 15 patients, use of LMWH was associated with a net savings of $2197 per patient. Conclusions-In this pilot cohort with subacute cerebral ischemia, bridging LMWH appeared to be safer than bridging IVUH and was associated with reduced hospital stay and reduced total cost of care.

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“…Because of low immunological cross-reactivity with heparin, danaparoid sodium has been used in patients who develop heparin-induced thrombocytopenia. [40] However, it has limitations including a long biological half-life and absence of an effective antidote. Other heparinoids such as dermatan sulfate and heparan sulfate have also shown promising anticoagulant activity in animal models.…”

Section: Danaparoid Sodiummentioning

confidence: 99%

New Targets for Antithrombotic Drugs

Thiagarajan

2002

American Journal of Cardiovascular Drugs

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The normal hemostatic process is initiated by disruption in the vascular continuity and exposure of the subendothelial components. Platelets adhere to subendothelium-bound von Willebrand factor via glycoprotein (GP) Ib complex. This initial interaction per se and the release of platelet agonists transduce signals that lead to the rise in intracellular Ca(2+). The rise in Ca(2+) induces shape change, prostaglandin synthesis, release of granular contents and conformational changes in platelet Gp IIb-IIIa. Gp IIb-IIIa in activated platelets becomes competent to bind fibrinogen and other adhesive proteins and mediates platelet cohesion (primary hemostatic plug). Furthermore, the activated platelet surface provides an efficient catalytic surface for the coagulation reactions, ultimately resulting in the formation of fibrin (secondary hemostasis). Normally the hemostatic process plays a delicate balance between keeping the blood in the fluid state to maintain flow and rapidly forming an occluding plug following vessel injury. Thrombosis occurs because of alteration in this delicate balance. Consequences of thrombosis are a major cause of morbidity and mortality in industrialized countries. Arterial thrombosis occurs in the setting of previous vessel wall injury mostly because of atherosclerosis, while venous thrombosis occurs in areas of stasis. The recent advances in our understanding of the hemostatic process have led to a better elucidation of the mechanism of action of many antithrombotic drugs and identification of new targets for drug development. The molecular target of the well known antiplatelet drug ticlopidine has been identified. Large numbers of IIb-IIIa inhibitors have been developed based on the crystal structure of a potent antagonist echistatin. The mechanism of action of heparin has been defined at the molecular level. As a result a synthetic pentasaccharide, based on antithrombin-binding domain of heparin, has been developed and tested successfully in clinical trials. New generation direct thrombin inhibitors are being developed based on the crystal structure of thrombin. Factor Xa has a critical position at the convergence of intrinsic and extrinsic pathway ways. The clinical tolerability and the efficacy of low molecular weight heparins led to the concept that inhibition of further thrombin generation, by blocking factor Xa alone, can be an effective way of preventing thrombus growth without inactivating thrombin. A large number of specific factor Xa inhibitors are under development. Some of these drugs have already undergone preliminary clinical trials and appear to be promising. Future clinical trials will determine whether these new drugs will provide better risk-benefit ratio in treatment of thrombotic disorders.

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Recognition and Management of Heparin-Induced Thrombocytopenia (HIT) and Thrombosis

Cited by 19 publications

References 34 publications

Thrombocytopenia due to acute venous thromboembolism and its role in expanding the differential diagnosis of heparin‐induced thrombocytopenia

Thrombocytopenia due to acute venous thromboembolism and its role in expanding the differential diagnosis of heparin‐induced thrombocytopenia

Safety and Cost of Low-Molecular-Weight Heparin as Bridging Anticoagulant Therapy in Subacute Cerebral Ischemia

New Targets for Antithrombotic Drugs

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