Failure of early heparin cessation as treatment for heparin-induced thrombocytopenia

Wallis, Diane E.; Workman, Diane L; Lewis, Bruce E.; Steen, Lowell; Pifarré, Roque; Moran, John F.

doi:10.1016/s0002-9343(99)00124-2

Cited by 333 publications

(239 citation statements)

References 38 publications

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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%

“…The risk of fatal thrombosis is 5% [115]. Early heparin cessation does not reduce the risk of thrombosis in patients with isolated HIT [116], if the response is cessation of heparin rather than substitution with an alternative anticoagulant. Although several assays have been developed for the diagnosis of HIT, these are adjuncts to the development of thrombocytopenia during heparin treatment and the physician's assessment of the clinical probability of HIT.…”

Section: Clinical Presentationmentioning

confidence: 99%

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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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Section: Clinical Presentationmentioning

confidence: 99%

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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“…HIT can lead to severe morbidity including ischemic limb loss and death [3][4][5]. Both clinical and laboratory criteria are required to confirm the diagnosis [6,7] in a timely and reliable manner.…”

Section: Introductionmentioning

confidence: 99%

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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“…The highest risk of thrombosis occurs between the time of diagnosis of HIT and initiation of therapy [24]. In many institutions where the results of HIT assays are not available daily, 14 C-serotonin release assay and HIT antibodies by ELISA testing (platelet factor 4) tests may be only performed weekly. We measured only the time to ordering of diagnostic testing and not time to receipt of results, but waiting for laboratory confirmation of HIT could have delayed therapy by days.…”

Section: Discussionmentioning

confidence: 99%

“…It is important to diagnose and initiate HIT treatment quickly to prevent thrombotic complications. The lower the platelet nadir the more likely the patient will develop a thrombosis [14,15]. Various algorithms and recommendations have been developed to help physicians in diagnosis of HIT; however, the challenge remains detecting a subtle fall in platelet count that remains within 'normal' range [16,17].…”

Section: Introductionmentioning

confidence: 99%

Effectiveness of a clinical decision support system to identify heparin induced thrombocytopenia

Riggio

Cooper

Leiby

et al. 2008

J Thromb Thrombolysis

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Failure of early heparin cessation as treatment for heparin-induced thrombocytopenia

Cited by 333 publications

References 38 publications

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

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

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

Effectiveness of a clinical decision support system to identify heparin induced thrombocytopenia

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