scholarly journals Use of Edoxaban for the Treatment of Heparin-Induced Thrombocytopenia

2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Ryo Kanamoto ◽  
Shinichi Hiromatsu ◽  
Tomoyuki Anegawa ◽  
Kanako Sakurai ◽  
Shohei Yoshida ◽  
...  
Keyword(s):  
Adverse Drug Reaction ◽  
Esophageal Cancer ◽  
Oral Treatment ◽  
Length Of Hospital Stay ◽  
Heparin Therapy ◽  
Vitamin K Antagonist ◽  
Bleeding Complications ◽  
Heparin Induced Thrombocytopenia ◽  
Life Threatening

Heparin-induced thrombocytopenia (HIT) is a life-threatening adverse drug reaction of heparin therapy, which increases a patient’s risk of developing venous and/or arterial thromboembolism. HIT should be treated through discontinuation of heparin and administration of nonheparin anticoagulants such as argatroban. For long-term anticoagulation, parenteral nonheparin anticoagulants are generally converted to oral treatment with a vitamin K antagonist such as warfarin. Although administration of warfarin is recommended to overlap with a nonheparin anticoagulant for a minimum of 5 days, overlapping with argatroban and warfarin presents high risks of bleeding. We describe a case of HIT treated with edoxaban. A 78-year-old man underwent surgery for esophageal cancer and was administered heparin perioperatively. After surgery, he was diagnosed with HIT and venous thromboembolism. We immediately stopped heparin and initiated parenteral argatroban. The patient was subsequently started on edoxaban without any overlap between the two drugs. The treatment was successful. The treatment of edoxaban following argatroban for HIT could reduce bleeding complications and shorten the length of hospital stay. To the best of our knowledge, this is the first report of the use of edoxaban for HIT treatment.

Safety and Efficacy of Argatroban in the Management of Heparin-Induced Thrombocytopenia

2011 ◽  
Vol 4 ◽  
pp. CMBD.S5118 ◽  
Author(s):  
Bernd Saugel ◽  
Roland M. Schmid ◽  
Wolfgang Huber
Keyword(s):  
Arterial Thrombosis ◽  
Pharmacokinetic Profile ◽  
The United States ◽  
Heparin Therapy ◽  
Direct Thrombin Inhibitor ◽  
Thrombin Inhibitor ◽  
Heparin Induced Thrombocytopenia ◽  
Safety And Efficacy ◽  
Increased Risk ◽  
Life Threatening

Heparin-induced thrombocytopenia (HIT) is a life-threatening adverse reaction to heparin therapy that is characterized by thrombocytopenia and an increased risk of venous and arterial thrombosis. According to guidelines, in patients with strongly suspected or confirmed HIT all sources of heparin have to be discontinued and an alternative, nonheparin anticoagulant for HIT treatment must immediately be started. For both the prophylaxis of thrombembolic events in HIT and the treatment of HIT with thrombosis the direct thrombin inhibitor argatroban is approved in the United States. The objective of this review is to describe the mechanism of action and the pharmacokinetic profile of argatroban, to characterize argatroban regarding its safety and therapeutic efficacy and to discuss its place in therapy in HIT.

Diagnosis and treatment of heparin-induced thrombocytopenia

Perfusion ◽  
2003 ◽  
Vol 18 (1) ◽  
pp. 47-53 ◽  
Author(s):  
William J DeBois ◽  
Junli Liu ◽  
Leonard Y Lee ◽  
Leonard N Girardi ◽  
Charles Mack ◽  
...  
Keyword(s):  
New York ◽  
Platelet Inhibition ◽  
Heparin Therapy ◽  
Serotonin Release ◽  
Antibody Detection ◽  
Thrombin Inhibitor ◽  
Heparin Infusion ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Life Threatening

Heparin-induced thrombocytopenia (HIT) is a major side effect secondary to the administration of heparin. This syndrome is serious and potentially life threatening. This response is the result of antibodies formed against the platelet factor 4 (PF4)/heparin complex. The incidence of this immune-mediated syndrome has been estimated to be 1-3% of all patients receiving heparin therapy. The occurrence of HIT in patients requiring full anticoagulation for cardiopulmonary bypass (CPB), therefore, presents a serious challenge to the cardiac surgery team. The diagnosis of HIT should be based on both clinical and laboratory evidence. While functional assays, platelet aggregation tests, and the serotonin release assay can be used to support the diagnosis, the negative predictive value of these tests is generally less than 50%. In contrast, although non-functional antibody detection assays are more sensitive, they have a low specificity. HIT can be treated in several ways, including cessation of all heparin and giving an alternative thrombin inhibitor, platelet inhibition followed by heparin infusion, and the use of low molecular weight heparins. In this presentation, the pathology and current diagnostic tests, as well as the successful management of patients with HIT undergoing CPB at New York Presbyterian Hospital, are reviewed.

scholarly journals A “Catastrophic” Heparin-Induced Thrombocytopenia

2020 ◽  
Vol 2020 ◽  
pp. 1-3 ◽  
Author(s):  
D. Barcellona ◽  
M. Melis ◽  
G. Floris ◽  
A. Mameli ◽  
A. Muroni ◽  
...  
Keyword(s):  
Antiphospholipid Syndrome ◽  
Bleeding Complications ◽  
Catastrophic Antiphospholipid Syndrome ◽  
Platelet Factor ◽  
Cerebral Vessel ◽  
Heparin Induced Thrombocytopenia ◽  
Unfractioned Heparin ◽  
Platelet Protein ◽  
Pathological Conditions ◽  
Life Threatening

Background. Heparin-induced thrombocytopenia (HIT) is a transient, antibody-mediated thrombocytopenia syndrome that usually follows exposure to unfractioned heparin (UFH) or low-molecular-weight heparin (LMWH). In contrast to other pathological conditions which lead to thrombocytopenia and bleeding complications, HIT results in a paradoxical prothrombotic state. It is caused by antibodies directed to complexes containing UFH or LMWH and a self-platelet protein: the platelet factor 4 (PF4). The heparin-PF4 immune complex leads to activation of platelets, monocytes, and endothelial cells which release procoagulant proteins and tissue factor with subsequent blood coagulation activation. Case Report. We describe the case of a woman undergone to knee replacement and affected by urosepsis who developed a HIT after exposure to enoxaparin. The thrombotic burden was very impressive involving the arterial and venous cerebral vessel and the venous pulmonary, hepatic, and inferior legs vascular beds. The patient was successfully treated with fondaparinux without recurrent thrombosis or bleeding. The clinical scenario could be named “catastrophic HIT” like the catastrophic antiphospholipid syndrome since they have a similar pathogenetic mechanism involving both platelets and monocytes procoagulant activities and a similar clinical manifestation with a life-threatening multiple arterial and/or venous thromboses. Conclusion. Patients presenting with HIT could show a very impressive thrombotic burden resembling to that of the catastrophic antiphospholipid syndrome. A careful differential diagnosis should be made towards other pathological conditions which lead to thrombocytopenia to avoid an unnecessary and potentially harmful platelet transfusion. Although fondaparinux is off-label, its use in patients with HIT is simple and seems to be effective.

Use of Lepirudin in Patients with Heparin-Induced Thrombocytopenia and Renal Failure Requiring Hemodialysis

2001 ◽  
Vol 35 (7-8) ◽  
pp. 885-890 ◽  
Author(s):  
William E Dager ◽  
Richard H White
Keyword(s):  
Renal Failure ◽  
Heparin Therapy ◽  
Activated Partial Thromboplastin Time ◽  
Bleeding Complications ◽  
Renal Elimination ◽  
Intraaortic Balloon Pump ◽  
Heparin Induced Thrombocytopenia ◽  
Acute Thrombosis ◽  
Case Summary ◽  
Intravenous Heparin

OBJECTIVE: To report two cases of successful lepirudin use in two patients with heparin-induced thrombocytopenia (HIT) and renal failure. CASE SUMMARY: Two patients with renal failure requiring hemodialysis developed HIT syndrome during intravenous heparin therapy. Anticoagulation was necessary to prevent recurrent, acute venous thrombosis in one patient and to prevent arterial thrombosis associated with the use of an intraaortic balloon pump in the second. Intravenous lepirudin was initiated at doses of 0.01 mg/kg/h and 0.005 mg/kg/h, respectively, and titrated based on the activated partial thromboplastin time (aPTT). Steady-state doses were 0.015 mg/kg/h to maintain aPTT values of approximately 60 seconds in one patient, and 0.005–0.008 mg/kg/h to achieve an aPTT of approximately 45 seconds in the other patient. DISCUSSION: Lepirudin is one of few anticoagulants that can be safely used in patients with HIT. Because it is eliminated through the kidneys, great care must be taken when administering lepirudin to patients with renal failure; in fact, its use is currently not recommended in patients requiring hemodialysis. Lepirudin effectively prevented acute thrombosis in both of our patients with documented HIT, with no bleeding complications. We describe how we selected the initial doses and report results of aPTT monitoring. CONCLUSIONS: In patients with renal failure who develop HIT, lepirudin is one available alternative to heparin despite its poor renal elimination pattern and subsequently prolonged half-life.

Lepirudin treatment in a boy with suspected HIT II after surgery because of tetralogy of Fallot

2009 ◽  
Vol 29 (02) ◽  
pp. 168-170
Author(s):  
K. Barth ◽  
L. Nakamura ◽  
U. Budde ◽  
R. Arnold ◽  
B. Zieger ◽  
...  
Keyword(s):  
Tetralogy Of Fallot ◽  
Heparin Therapy ◽  
Severe Thrombocytopenia ◽  
Repeated Testing ◽  
Heparin Induced Thrombocytopenia ◽  
Life Threatening ◽  
Therapeutic Measures ◽  
First Time ◽  
Factor Antigen ◽  
Heparin Exposure

SummaryHeparin-induced thrombocytopenia (HIT II) in childhood is rare. Suspected HIT II requires immediate diagnostic and therapeutic measures in order to avoid potentially life threatening complications. Heparin must be stopped immediately.We report on a 6-year old boy who required cardiac surgery due to tetralogy of Fallot. To our knowledge he had been exposed to heparin for the first time during cardiac catheterization on the day before surgery. Preoperatively, platelet count was normal. Postoperatively (3 days after heparin exposure), he developed pulmonary and renal failure and required inotropic cardiac support and dia -lysis. He also developed progressive (severe) thrombocytopenia under heparin therapy on day 2–3 postoperatively. The dialysis filter required daily exchanges due to clotting despite increasing heparin doses. The first ELISA for HIT on postop day 4 was negative. 3 days later a repeated test was positive. Von Wille-brand factor antigen and D-dimers were markedly increased. The patient was immediately switched to lepirudin and subsequently stabilized slowly. No major systemic thrombosis occurred. After lepirudin treatment for 6 weeks the patient was fully recovered and HIT II-testing was negative again. Conclusion: In children with progressive thrombocytopenia in the setting of heparin exposure and signs of major or micro thrombosis HIT II must be ruled out. Even if a first early test turns out negative repeated testing should be performed. Lepirudin anticoagulation is effective and should be monitored correctly. Platelet transfusion should be avoided in HIT II.

scholarly journals Case Report: Concomitant coronary stent and femoral artery thrombosis in the setting of heparin-induced thrombocytopenia

F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 667 ◽  
Author(s):  
Mejdi Ben Messaoud ◽  
Mezri Maatouk ◽  
Mohamed Mehdi Boussaada ◽  
Marouane Mahjoub ◽  
Walid Mnari ◽  
...  
Keyword(s):  
Adverse Drug Reaction ◽  
Femoral Artery ◽  
Unusual Case ◽  
Coronary Stent ◽  
Percutaneous Coronary Interventions ◽  
Heparin Induced Thrombocytopenia ◽  
Artery Thrombosis ◽  
Percutaneous Coronary ◽  
Life Threatening ◽  
Extensive Growth

Heparin induced thrombocytopenia (HIT) is a rare but potentially life threatening  adverse drug reaction. We report an unusual case of concomitant subacute coronary stent and femoral artery thrombosis secondary to HIT. In the current era of extensive growth of heparin use and percutaneous coronary interventions, it’s important for clinicians to remember that such complication might occur and should be prevented.

scholarly journals Heparin-induced thrombocytopenia

Blood ◽  
2017 ◽  
Vol 129 (21) ◽  
pp. 2864-2872 ◽  
Author(s):  
Gowthami M. Arepally
Keyword(s):  
Disease Susceptibility ◽  
Clinical Manifestations ◽  
Heparin Therapy ◽  
Laboratory Findings ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Laboratory Features ◽  
Life Threatening ◽  
Pathogenic Antibodies ◽  
Heparin Exposure

Abstract Heparin-induced thrombocytopenia (HIT) is an immune complication of heparin therapy caused by antibodies to complexes of platelet factor 4 (PF4) and heparin. Pathogenic antibodies to PF4/heparin bind and activate cellular FcγRIIA on platelets and monocytes to propagate a hypercoagulable state culminating in life-threatening thrombosis. It is now recognized that anti-PF4/heparin antibodies develop commonly after heparin exposure, but only a subset of sensitized patients progress to life-threatening complications of thrombocytopenia and thrombosis. Recent scientific developments have clarified mechanisms underlying PF4/heparin immunogenicity, disease susceptibility, and clinical manifestations of disease. Insights from clinical and laboratory findings have also been recently harnessed for disease prevention. This review will summarize our current understanding of HIT by reviewing pathogenesis, essential clinical and laboratory features, and management.

Heparin-induced Thrombocytopenia: Pathophysiology, Diagnosis, and Review of Pharmacotherapy

2009 ◽  
Vol 22 (2) ◽  
pp. 149-157 ◽  
Author(s):  
Abir O. Kanaan ◽  
A. Samer Al-Homsi
Keyword(s):  
Myocardial Infarction ◽  
Adverse Drug Reaction ◽  
Randomized Trials ◽  
Clinical Presentation ◽  
Case Reports ◽  
Heparin Therapy ◽  
Thrombin Inhibitors ◽  
Limb Amputation ◽  
Direct Thrombin Inhibitors ◽  
Heparin Induced Thrombocytopenia

Heparin-induced thrombocytopenia is an adverse drug reaction to heparin therapy leading to devastating clinical outcomes including venous thromboembolism, myocardial infarction, stroke, and limb amputation. Heparin cessation alone is not sufficient for the management of heparin-induced thrombocytopenia. Direct thrombin inhibitors, such as argatroban and lepirudin, are considered the mainstay for the management of heparin-induced thrombocytopenia. Case reports support the use of fondaparinux in the management of heparin-induced thrombocytopenia; however, randomized trials are still lacking. This article will review the pathophysiology, clinical presentation, complications, diagnosis, and pharmacotherapy management of heparin-induced thrombocytopenia.

scholarly journals A Case Report of Hematuria in Heparin-Induced Thrombocytopenia: An Unusual Presentation Leading to End Organ Damage

2020 ◽  
pp. 93-96
Author(s):  
Mansoor Abbas Qaiser ◽  
Fateh Sher Chattah ◽  
Samreen Khan ◽  
Zarmina Roop ◽  
Sehreen Jahangir ◽  
...  
Keyword(s):  
Organ Damage ◽  
Renal Vein Thrombosis ◽  
Heparin Therapy ◽  
Rare Presentation ◽  
Immune Disorder ◽  
Heparin Induced Thrombocytopenia ◽  
End Organ Damage ◽  
Vein Thrombosis ◽  
Clinical Scenarios ◽  
Life Threatening

Heparin is commonly used in many clinical scenarios, including venous thromboembolism, acute coronary syndromes, atrial fibrillation, orthopedic surgeries, dialysis, during extracorporeal circulation and peripheral occlusive disease.1 A life-threatening complication following heparin therapy is heparin-induced thrombocytopenia (HIT). Generally, there are two types of HIT. Type 1 HIT is a mild and non-immune disorder that presents early, usually in the first 48 hours after exposure to heparin. It is caused by an interaction between heparin and platelets leading to the formation of platelet aggregates.1,2 Type 2 HIT is an immune-mediated condition which occurs 4-14 days after exposure and sometimes has life-threatening complications.2 HIT has many different manifestations, so it is important to be cautious in a patient who is on heparin for any reason. Here, we are reporting a case of an elderly lady presented with frank hematuria (a rare presentation) later diagnosed as HIT and ultimately had extensive renal vein thrombosis which led to end-organ damage

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