Pharmacotherapy of heparin-induced thrombocytopenia: Therapeutic options and challenges in the clinical practices

Al-Eidan, Fahad A.

doi:10.1016/j.jvn.2014.07.001

Cited by 6 publications

(6 citation statements)

References 78 publications

(64 reference statements)

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“…[14] However, danaparoid is no longer available in the US and manufacturing shortages are common with this agent. [15] Direct oral anticoagulants (DOACs) such as rivaroxaban have an emerging role in the treatment of HIT and are an attractive option due to their oral administration and the limited treatment options for HIT.…”

Section: Unmet Clinical Needs For Heparin-induced Thrombocytopeniamentioning

confidence: 99%

Pharmacogenetics to Prevent Heparin-Induced Thrombocytopenia: what do we know?

Karnes

2018

Pharmacogenomics

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Heparin-induced thrombocytopenia (HIT) is a life-threatening, immune-mediated adverse reaction to heparin anticoagulants. The inability to predict HIT represents a considerable liability associated with heparin administration. Genetic studies of HIT are challenging due to the scarcity of true HIT cases, potential for misclassification, and many environmental risk factors.Genetic studies have not consistently identified risk alleles for HIT, the production of platelet factor 4 (PF4)/heparin antibodies, nor the thromboembolic complications of HIT. Genes implicated in HIT and PF4/heparin antibody levels include FCGR2A, TDAG8, HLA-DR, and others. Compelling evidence also suggests that the FCGR2A H131R polymorphism is associated with HIT-related thrombosis. There is a need for well-powered, multiethnic studies with laboratory confirmation of HIT, detailed patient-and drug-specific data, and inclusion of both serologic and thromboembolic outcomes. Genomic biomarkers identified from such studies offer the possibility of shifting current clinical practice paradigms from early detection and treatment to prevention.

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Section: Unmet Clinical Needs For Heparin-induced Thrombocytopeniamentioning

confidence: 99%

Pharmacogenetics to Prevent Heparin-Induced Thrombocytopenia: what do we know?

Karnes

2018

Pharmacogenomics

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“…Routine clinical and platelet monitoring is required, and patients with new/persistent platelet count reduction and/or new/extended thrombosis should be switched to an alternative anticoagulant [ 13 ]. That being said, the drug is no longer marketed in the US and has suffered manufacturing problems, causing a worldwide shortage in recent years [ 14 ].…”

Section: Current Guidelines For Hitmentioning

confidence: 99%

“…It binds highly selectively without any co-factors and can be used in patients with isolated renal impairment without dose adjustments [ 15 ]. However, its effect requires monitoring and its metabolism is strongly hepatic [ 14 ]. Dose reductions and adjustments for critically ill and cardiac surgery patients, as well as those with impaired liver function, are required for its use.…”

Section: Current Guidelines For Hitmentioning

confidence: 99%

Dabigatran approaching the realm of heparin-induced thrombocytopenia

Siordia

2016

Blood Res

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Heparin-induced thrombocytopenia (HIT) is a serious, immune mediated complication of exposure to unfractionated or low-molecular-weight heparin. Though rare, it is a condition associated with high morbidity and mortality that requires immediate change to alternative anticoagulants for the prevention of life-threatening thrombosis. The direct thrombin inhibitors lepirudin and argatroban are currently licensed for the treatment of HIT. Dabigatran, a novel oral anticoagulant (NOAC) with a similar mechanism of action and effective use in other indications, has recently been proposed as another therapeutic option in cases of HIT. This review serves as an introduction to using dabigatran for this purpose, detailing the clinical aspects of its administration, evidence of its performance compared to other anticoagulants, and the preliminary reports of HIT successfully treated with dabigatran. As the literature on this develops, it will need to include clinical trials that directly evaluate dabigatran against the other NOACs and current treatment options.

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“…LMWH are a group of anticoagulants derived from UFH by chemical or enzymatic depolymerisation methods. They consist of one third the molecular weight of UFH with a mean of 4000 to 5000 Kilo Dalton (KDa) [2,3]. Nowadays, LMWH replace UFH due to a greater inhibitory activity against factor Xa, improved pharmacokinetic properties, longer half-life, and are associated with a significant lower risk of heparin-induced thrombocytopenia [4].…”

Section: Introductionmentioning

confidence: 99%

Hypersensitivity reactions to enoxaparin and unfractionated heparin in a pregnant woman with gestational thrombocytopenia: A case report

Al-Eidan¹,

Al-Qhtani²,

Alsubaie³

et al. 2016

Hematol Med Oncol

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Background: The risk of venous thromboembolism (VTE) and arterial thrombosis (stroke and heart attack) increases in women during pregnancy. Enoxaparin (a low molecular weight heparin) and unfractionated heparin are extensively used in the VTE prophylaxis and therapeutic doses.Aims: We retrospectively describe an apparent relationship between enoxaparin and unfractionated heparin (UFH) in a woman with gestational thrombocytopenia developing a hypersensitivity reactions.Case presentation: we report a clinical scenario of a 43 years old pregnant women (gravida 18, para 12 and living 6) with co-morbid obesity (BMI 47.9) and well known to have a gestational thrombocytopenia during the last two pregnancies. She was administered enoxaparin 0.4ml (40 IU) daily for VTE prophylaxis. After three days, the patient came with hypersensitivity reactions like erythema, pain, swelling, irritation at the site of injection and rash all over the body (lower limbs, abdomen and neck) appeared after the first dose of enoxaparin. Hypersensitivity skin reaction to enoxaparin was suspected and immediately drug was withdrawn. The performed UFH skin test was negative, and then she was prescribed UFH 5000 units subcutaneous every 12 hours. The patient had similar reaction but a severe form and UFH was discontinued. Fondaparinux was the only nonheparin anticoagulant available and was prescribed for this patient.Conclusions: The patient had an allergic drug reaction and provides an evidence of cross-allergenicity between enoxaparin and UFH. Nonheparin anticoagulant improves both rashes and gestational thrombocytopenia.

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Pharmacotherapy of heparin-induced thrombocytopenia: Therapeutic options and challenges in the clinical practices

Cited by 6 publications

References 78 publications

Pharmacogenetics to Prevent Heparin-Induced Thrombocytopenia: what do we know?

Pharmacogenetics to Prevent Heparin-Induced Thrombocytopenia: what do we know?

Dabigatran approaching the realm of heparin-induced thrombocytopenia

Hypersensitivity reactions to enoxaparin and unfractionated heparin in a pregnant woman with gestational thrombocytopenia: A case report

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