Effects of Argatroban Therapy, Demographic Variables, and Platelet Count on Thrombotic Risks in Heparin-Induced Thrombocytopenia

Lewis, Bruce E.; Wallis, Diane E.; Hursting, Marcie J.; Levine, Robert L.; Leya, Fred

doi:10.1378/chest.129.6.1407

Cited by 123 publications

(96 citation statements)

References 21 publications

(44 reference statements)

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“…stopped and replaced with an alternative anticoagulant, which may be associated with a higher risk of bleeding and may be difficult to monitor [21,[25][26][27][28][29]. Our data showed that 20.9% of all samples referred for HIT investigation to a reference laboratory were positive in the EIA but negative in the SRA (presumed false-positive HIT test).…”

Section: Discussionmentioning

confidence: 79%

Pitfalls in the diagnosis of heparin‐Induced thrombocytopenia: A 6‐year experience from a reference laboratory

et al. 2015

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Heparin-induced thrombocytopenia (HIT) is caused by platelet-activating antibodies against complexes of platelet factor 4 (PF4) and heparin. The diagnosis of HIT is contingent on accurate and timely laboratory testing. Recently, alternative anticoagulants for the treatment of HIT have been introduced along with algorithms for better HIT diagnosis. However, the increased reliance on immunoassays for the diagnosis of HIT may have harmful consequences due to the high rate of false positive results. To compare trends and implications of current HIT testing approaches, we analyzed results over a six-year period from the McMaster University Platelet Immunology Reference Laboratory. From 2008 to 2013, 8,546 samples were investigated for HIT using both an in-house IgG-specific anti-PF4/heparin enzyme immunoassay (EIA) and the serotoninrelease assay (SRA). Of 8,546 samples tested, 13.4% were true-positives (positive in both assays); 65.6% were true-negatives (negative in both assays); 20.9% were presumed false positive for HIT (EIA-positive/SRAnegative); and 0.2% were EIA-negative/SRA-positive. The frequency of EIA-positive/SRA-negative results increased over time (from 12.9% in 2008 to 22.9% in 2013). We found that the number of SRA-negative samples was reduced from referring centers that used an immunoassay as an initial screen; however, 41% of those samples tested negative in the immunoassay and in the SRA at the reference laboratory. The suspicion of HIT continues at a high rate and the agreement between the EIA and SRA test results remains problematic.

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Section: Discussionmentioning

confidence: 79%

Pitfalls in the diagnosis of heparin‐Induced thrombocytopenia: A 6‐year experience from a reference laboratory

et al. 2015

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“…Arterial thrombosis occurs more commonly in the lower limbs, followed by cerebral arteries and lastly the coronary arteries, the reversal order of atherothrombosis. Several retrospective cohort studies [115][116][117][118] indicate that among patients who develop isolated HIT, 25-50% will develop clinically evident thrombosis after stopping heparin, with or without substitution by coumadin, usually within the first week [119,120]. The risk of fatal thrombosis is 5% [115].…”

Section: Clinical Presentationmentioning

confidence: 99%

Thrombocytopenic conditions—autoimmunity and hypercoagulability: Commonalities and differences in ITP, TTP, HIT, and APS

Kravitz

Shoenfeld

2005

American J Hematol

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Immune thrombocytopenia purpura (ITP), thrombotic thrombocytopenia purpura (TTP), heparin‐induced thrombocytopenia (HIT), and antiphospholipid syndrome (APS) are clinical conditions associated with significant morbidity and mortality. These well‐defined clinical syndromes have in common several properties: (1) their pathogenesis is immune mediated, specifically by autoantibodies; (2) thrombocytopenia is a hallmark in these four conditions; (3) except for the case of ITP, platelet and endothelial cell activation occurs in TTP, HIT, and APS, resulting in a prothrombotic state and an increased risk of thrombosis. Although these four immune‐mediated syndromes are well‐defined diseases, several case reports and studies have documented the association of two diseases in the same patient, illustrating the concept of the kaleidoscope of autoimmunity. Am. J. Hematol. 80:232–242, 2005. © 2005 Wiley‐Liss, Inc.

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“…The incidence of major bleeding in previous studies involving argatroban and UFH used in heparin-induced thrombocytopenia (HIT; 6.9 vs. 6.7%) (23), in HIT with thrombosis syndrome (5.7 vs. 7.0%) (34), in percutaneous coronary intervention (0% vs. 3.0%) (35), and in acute myocardial infarction (19% vs. 20%) (36) do not reveal apparent differences in major bleeding; however, in accordance with various studies, argatroban improves the clinical outcome (23,34,35,36).…”

Section: Discussionmentioning

confidence: 99%

Early initiation of argatroban therapy in the management of acute superior mesenteric venous thrombosis

Zeng

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Acute superior mesenteric venous thrombosis (ASMVT) is an intractable disease with poor prognosis. Argatroban, a direct thrombin inhibitor, may be a novel anticoagulant method in the therapy of ASMVT. The aim of the present study was to assess the efficacy and safety of early argatroban therapy in ASMVT patients. The current retrospective study reviewed a consecutive series of ASMVT patients receiving early argatroban therapy during hospitalization between March 2013 and April 2014, with 18 ASMVT patients included in the study. Of these, 16 patients without hepatic dysfunction underwent anticoagulant therapy with argatroban with a mean dose of 1.57±0.34 µg/kg/min and a mean duration of 12.2±3.7 days, while their activated partial thromboplastin time (aPTT) was elevated to 1.95±0.26 times the baseline value. In addition, 2 hepatic dysfunction patients received therapy with a dose of 0.41 µg/kg/min and 0.46 µg/kg/min, and with aPTT of 1.68 and 1.62 times the baseline value, respectively. Overall, 94% (n=17) of the patients presented clinical improvement, while 88% (n=16) of patients presented partially or completely dissolved thrombus in contrast-enhanced computed tomography images. The incidence of surgery and bowel resection was 6% (excluding 1 case with intestinal necrosis detected on admission). Furthermore, 11% (n=2) of patients experienced a bleeding episode, however no major bleeding or mortality occurred during hospitalization. During the follow-up, the mortality and the recurrence rate were 6% and 11%, respectively. In conclusion, early initiation of argatroban treatment may be an effective and safe therapy in ASMVT, manifesting efficient resolution of the thrombus, rapid improvement of symptoms, low incidence of bowel resection and bleeding complication, and low mortality rate.

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Effects of Argatroban Therapy, Demographic Variables, and Platelet Count on Thrombotic Risks in Heparin-Induced Thrombocytopenia

Cited by 123 publications

References 21 publications

Pitfalls in the diagnosis of heparin‐Induced thrombocytopenia: A 6‐year experience from a reference laboratory

Pitfalls in the diagnosis of heparin‐Induced thrombocytopenia: A 6‐year experience from a reference laboratory

Thrombocytopenic conditions—autoimmunity and hypercoagulability: Commonalities and differences in ITP, TTP, HIT, and APS

Early initiation of argatroban therapy in the management of acute superior mesenteric venous thrombosis

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