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John G. Kelton - One of the best experts on this subject based on the ideXlab platform.
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a platelet viability assay pva for the diagnosis of Heparin Induced Thrombocytopenia
Platelets, 2019Co-Authors: Nikola Ivetic, Angela Huynh, John G. Kelton, Donald M Arnold, James W. Smith, Ishac NazyAbstract:AbstractDiagnosing Heparin-Induced Thrombocytopenia (HIT) requires functional assays measuring platelet activation as they are highly specific and sensitive. A useful functional test for diagnosing...
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nonHeparin anticoagulants for Heparin Induced Thrombocytopenia
The New England Journal of Medicine, 2013Co-Authors: John G. Kelton, Donald M Arnold, Shannon M BatesAbstract:A 57-year-old man remains in the hospital after experiencing complications from knee-replacement surgery 7 days ago. Low-molecular-weight Heparin prophylaxis is initiated on the first postoperative day. Compression ultrasonography performed for left leg swelling noted on day 7 shows a proximal deep-vein thrombosis. A complete blood count reveals that his platelet count has decreased from 300×10 9 per liter to 125×10 9 per liter, and an enzyme immunoassay for Heparin-Induced Thrombocytopenia shows a high titer of antibodies against platelet factor 4 (PF4)–Heparin complexes. The patient has normal renal function. The physician in the intensive care unit wonders about the best treatment.
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A spontaneous prothrombotic disorder resembling Heparin-Induced Thrombocytopenia.
The American journal of medicine, 2008Co-Authors: Michael Makris, Richard M. Jay, John G. KeltonAbstract:Abstract Background Antibodies against the "self" protein, platelet factor 4 (PF4), bound to Heparin—the cause of immune Heparin-Induced Thrombocytopenia—are believed invariably to be triggered by preceding Heparin therapy. We describe a novel syndrome, spontaneous Heparin-Induced Thrombocytopenia , in which clinical and serologic features characteristic of this adverse drug reaction develop in patients despite the absence of preceding Heparin therapy. Methods Three patients met the study criteria (clinical and serologic features of Heparin-Induced Thrombocytopenia without preceding Heparin exposure), of whom 2 patients were identified among 225 patients (0.89%, 95% confidence interval, 0.11%-3.17%) with serologically confirmed Heparin-Induced Thrombocytopenia recognized during an 18-year period at 1 hospital. The platelet serotonin-release assay was used to detect Heparin-dependent immunoglobulin G-Induced platelet activation, and 2 enzyme immunoassays were used to detect antibodies against PF4/Heparin. Results Two patients presented with Thrombocytopenia and multiple arterial thrombosis, and 1 patient presented with anaphylactoid reactions after 2 subcutaneous injections of low-molecular-weight Heparin. All 3 patients had high levels of platelet-activating anti-PF4/Heparin antibodies of immunoglobulin G class at presentation despite the absence of previous Heparin exposure. However, each patient did have a preceding infectious or inflammatory event; 1 patient had concomitant antiphospholipid antibodies. Conclusion Circumstances other than Heparin use can trigger a spontaneous disorder that closely mimics Heparin-Induced Thrombocytopenia, further supporting the autoimmune nature of this adverse drug reaction.
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treatment of Heparin Induced Thrombocytopenia a critical review
JAMA Internal Medicine, 2004Co-Authors: Jack Hirsh, Nancy M Heddle, John G. KeltonAbstract:Heparin-Induced Thrombocytopenia (HIT) is a serious complication of Heparin therapy that has a high rate of morbidity (thrombosis and amputation) and mortality. In the past, a number of different anticoagulants have been used to treat HIT in an attempt to prevent these complications. More recently, direct thrombin inhibitors have become popular. This systematic review summarizes the risk for thrombosis in HIT patients when Heparin therapy is stopped; evidence of the efficacy of thrombin inhibitors in patients with HIT with and without thrombosis; evidence supporting the use of thrombin inhibitors in patients with a history of HIT who require a coronary intervention procedure; and the risk for bleeding when antithrombotic agents are used.
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delayed onset Heparin Induced Thrombocytopenia and thrombosis
Annals of Internal Medicine, 2001Co-Authors: John G. KeltonAbstract:Delayed-onset Heparin-Induced Thrombocytopenia should be suspected when patients present with Thrombocytopenia and thrombosis up to 3 weeks after exposure to Heparin. This syndrome could be caused ...
Theodore E. Warkentin - One of the best experts on this subject based on the ideXlab platform.
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Heparin Induced Thrombocytopenia in critically ill patients
Seminars in Thrombosis and Hemostasis, 2015Co-Authors: Theodore E. WarkentinAbstract:Many critically ill patients receive Heparin, either before intensive care unit (ICU) admission (e.g., postcardiac surgery), for prophylaxis/treatment of thrombosis, for hemodialysis/filtration, or even incidentally (e.g., flushing of intravascular catheters), and are therefore at risk for developing immune Heparin-Induced Thrombocytopenia (HIT), a prothrombotic drug reaction caused by platelet-activating antiplatelet factor 4 (PF4)/Heparin antibodies. However, HIT explains at most 1 in 100 thrombocytopenic ICU patients (HIT frequency 0.3–0.5% vs. 30–50% background frequency of ICU-associated Thrombocytopenia), and most patients who form anti-PF4/Heparin antibodies do not develop HIT; hence, HIT overdiagnosis often occurs. This review discusses HIT-related issues relevant to ICU patients, including how to (1) distinguish HIT both clinically and serologically from non-HIT–related Thrombocytopenia; (2) recognize HIT-mimicking disorders, such as the acute disseminated intravascular coagulation (DIC)/liver necrosis-limb necrosis syndrome; (3) prevent HIT in the ICU through use of low-molecular-weight Heparin; and (4) treat HIT, including awareness of “PTT confounding” when anticoagulating patients with DIC.
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Heparin-Induced Thrombocytopenia.
Current opinion in critical care, 2015Co-Authors: Theodore E. WarkentinAbstract:Purpose of reviewThrombocytopenia and Heparin exposure are common in critically ill patients, yet immune Heparin-Induced Thrombocytopenia (HIT), a prothrombotic adverse effect of Heparin, rarely accounts for Thrombocytopenia in this patient population. The review discusses the clinical and laborator
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Heparin Induced Thrombocytopenia in critically ill patients
Critical Care Clinics, 2011Co-Authors: Theodore E. WarkentinAbstract:Critically ill patients commonly evince Thrombocytopenia, either evident on admission to the intensive care unit (ICU) or that develops during their stay. Heparin-Induced Thrombocytopenia (HIT) explains Thrombocytopenia in only approximately 1/100 critically ill patients; also, only 1 or 2 in 10 ICU patients with a positive PF4-dependent enzyme immunoassay has “true” HIT. Thus, there is major potential for overdiagnosis of HIT in the ICU. A recent study showing that dalteparin is associated with a reduced frequency of HIT indicates that critically ill patients too can benefit from the HIT-reducing potential of this low molecular weight Heparin preparation.
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Heparin Induced Thrombocytopenia
Hematology-oncology Clinics of North America, 2007Co-Authors: Theodore E. WarkentinAbstract:Heparin-Induced Thrombocytopenia (HIT) is an immune-mediated adverse drug effect that is characterized by platelet activation, hypercoagulability, and a resulting increased risk for thrombosis, both venous and arterial. This disorder is autoimmune-like, because the target antigen is a multimolecular complex of the "self" protein, platelet factor 4, and Heparin. HIT usually begins 5 to 10 days after starting Heparin, especially when administered intra- or perioperatively, although a rapid onset of Thrombocytopenia can occur if Heparin is given to a patient with circulating HIT antibodies that resulted from a recent Heparin exposure. The clinical diagnosis is supported if Heparin-dependent, platelet-activating antibodies are detectable. Treatment includes cessation of Heparin and use of an alternative non-Heparin anticoagulant, such as danaparoid, lepirudin, or argatroban. Warfarin must be avoided or postponed, as the acute phase of HIT poses a high risk for coumarin necrosis, particularly limb loss due to venous limb gangrene.
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Heparin Induced Thrombocytopenia
Dm Disease-a-month, 2005Co-Authors: Theodore E. WarkentinAbstract:Heparin-Induced Thrombocytopenia (HIT) is an adverse prothrombotic disorder caused by an immune response to complexes of platelet factor 4 and polyanions. The clinical relevance of HIT results from the wide use of Heparin, which is the reason that the absolute number of patients affected by HIT is high. HIT is currently the most frequent immune-mediated adverse drug reaction affecting blood cells.
Andreas Greinacher - One of the best experts on this subject based on the ideXlab platform.
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autoimmune Heparin Induced Thrombocytopenia
Journal of Thrombosis and Haemostasis, 2017Co-Authors: Andreas Greinacher, Kathleen SellengAbstract:Summary Autoimmune Heparin-Induced Thrombocytopenia (aHIT) indicates patients with anti-PF4/polyanion antibodies that are able to activate platelets strongly even in the absence of Heparin (Heparin-independent platelet activation). Nevertheless, as seen with serum obtained from patients with otherwise typical HIT, serum-Induced platelet activation is inhibited at high Heparin concentrations (10-100 IU/mL Heparin). Further, upon serial dilution, aHIT serum will usually exhibit Heparin-dependent platelet activation. Clinical syndromes associated with aHIT include: delayed-onset HIT, persisting HIT, spontaneous HIT, fondaparinux-associated HIT, Heparin “flush”-Induced HIT, and severe HIT (platelet count <20×109/L) with associated disseminated intravascular coagulation (DIC). Recent studies implicate anti-PF4 antibodies that are able to bridge two PF4 tetramers even in the absence of Heparin, likely facilitated by non-Heparin platelet-associated polyanions (chondroitin sulfate, polyphosphates); nascent PF4-aHIT-IgG complexes recruit additional Heparin-dependent HIT antibodies, leading to formation of large multimolecular immune complexes and marked platelet activation. aHIT can persist for several weeks, and serial fibrin d-dimers and fibrinogen levels, rather than the platelet count, may be helpful to monitor treatment response. Although standard anticoagulant therapy for HIT ought to be effective, published experience indicates frequent failure of partial thromplastin time (PTT)-adjusted anticoagulants (argatroban, bivalirudin), probably due to underdosing in the setting of HIT-associated DIC, known as “PTT confounding.” Thus, non-PTT-adjusted therapies such as danaparoid and fondaparinux or even direct oral anticoagulants, such as rivaroxaban or apixaban, are suggested therapies, especially for long-term management of persisting HIT. In addition, emerging data indicate that high-dose intravenous gammaglobulin can interrupt HIT antibody-Induced platelet activation, leading to rapid platelet count recovery. This article is protected by copyright. All rights reserved.
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CORRECTION REVIEW Heparin-Induced Thrombocytopenia and Cardiac Surgery
2016Co-Authors: Andreas GreinacherAbstract:Unfractionated Heparin given during cardiopulmonary bypass is remarkably immunogenic, as 25 % to 50 % of postcardiac surgery patients develop Heparin-dependent antibodies during the next 5 to 10 days. Sometimes, these antibodies strongly activate platelets and coagulation, thereby causing the prothrombotic disorder, Heparin-Induced Thrombocytopenia. The risk of Heparin-Induced Thrombocytopenia is 1 % to 3 % if unfractionated Heparin is continued beyond the first postoperative week. When cardiac surgery is urgently needed for a patient with acute or subacute Heparin-Induced Thrombocytopenia, options include an alternative anticoagulant (bivalirudin, lepirudin, or danaparoid) or combining unfractionated Heparin with a platelet antagonist (epoprostenol or tiro-fiban). As Heparin-Induced Thrombocytopenia antibodies are transient, unfractionated Heparin alone is appropriate in a patient with previous Heparin-Induced thrombocy-topenia whose antibodies have disappeared
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Review Heparin-Induced Thrombocytopenia
2015Co-Authors: Krystin Krauel, Karina Althaus, Sixten Selleng, Andreas GreinacherAbstract:Summary Heparin-Induced Thrombocytopenia (HIT), typically occurring in the second week of he-parin therapy, is an antibody-mediated ad-verse drug reaction associated with increased thrombotic risk. The most important antigens are located on platelet factor 4 (PF4)/Heparin complexes. HIT is always caused by platelet-activating antibodies, but not all PF4/Heparin-reactive antibodies cause HIT. Thus, tests have a high negative, but only a moderate, positive predictive value. Clinical suspicion of HIT requires cessation of Heparin and substitution with an alternative anticoagulant. As these drugs have an increased bleeding risk, they should be used in therapeutic doses only if HIT is considered very likely. Avoiding/postponing coumarin is crucial in minimizing microthrom-botic complications. Recent studies of HIT im-munobiology suggest that HIT mimics immun-ity against repetitive antigens, as are relevant in microbial defense. Thus, understanding HIT may help unravel why host defenses can trigger autoimmunity. Correspondence to
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Heparin Induced Thrombocytopenia
Hamostaseologie, 2010Co-Authors: Andreas Greinacher, Karina Althaus, Krystin Krauel, Sixten SellengAbstract:Heparin-Induced Thrombocytopenia (HIT), typically occurring in the second week of Heparin therapy, is an antibody-mediated adverse drug reaction associated with increased thrombotic risk. The most important antigens are located on platelet factor 4 (PF4)/Heparin complexes. HIT is always caused by platelet-activating antibodies, but not all PF4/Heparin-reactive antibodies cause HIT. Thus, tests have a high negative, but only a moderate, positive predictive value. Clinical suspicion of HIT requires cessation of Heparin and substitution with an alternative anticoagulant. As these drugs have an increased bleeding risk, they should be used in therapeutic doses only if HIT is considered very likely. Avoiding/postponing coumarin is crucial in minimizing microthrombotic complications. Recent studies of HIT immunobiology suggest that HIT mimics immunity against repetitive antigens, as are relevant in microbial defense. Thus, understanding HIT may help unravel why host defenses can trigger autoimmunity.
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comprar Heparin Induced Thrombocytopenia fourth edition andreas greinacher 9781420045086 informa healthcare
2007Co-Authors: Andreas GreinacherAbstract:Tienda online donde Comprar Heparin-Induced Thrombocytopenia, Fourth Edition al precio 153,43 € de Andreas Greinacher | Theodore E. Warkentin, tienda de Libros de Medicina, Libros de Medicina Interna - Cardiologia general
Deepa Rj Arachchillage - One of the best experts on this subject based on the ideXlab platform.
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frequency of Thrombocytopenia and Heparin Induced Thrombocytopenia in patients receiving extracorporeal membrane oxygenation compared with cardiopulmonary bypass and the limited sensitivity of pretest probability score
Critical Care Medicine, 2020Co-Authors: Deepa Rj Arachchillage, Michael Laffan, Sanjay Khanna, Christophe Vandenbriele, Farah Kamani, Maurizio Passariello, Alexander F Rosenberg, Winston BanyaAbstract:OBJECTIVES To ascertain: 1) the frequency of Thrombocytopenia and Heparin-Induced Thrombocytopenia; 2) positive predictive value of the Pretest Probability Score in identifying Heparin-Induced Thrombocytopenia; and 3) clinical outcome of Heparin-Induced Thrombocytopenia in adult patients receiving venovenous- or venoarterial-extracorporeal membrane oxygenation, compared with cardiopulmonary bypass. DESIGN A single-center, retrospective, observational cohort study from January 2016 to April 2018. SETTING Tertiary referral center for cardiac and respiratory failure. PATIENTS Patients who received extracorporeal membrane oxygenation for more than 48 hours or had cardiopulmonary bypass during specified period. INTERVENTIONS None. MEASUREMENTS AND MAIN RESULTS Clinical and laboratory data were collected retrospectively. Pretest Probability Score and Heparin-Induced Thrombocytopenia testing results were collected prospectively. Mean age (± SD) of the extracorporeal membrane oxygenation and cardiopulmonary bypass cohorts was 45.4 (± 15.6) and 64.9 (± 13), respectively (p < 0.00001). Median duration of cardiopulmonary bypass was 4.6 hours (2-16.5 hr) compared with 170.4 hours (70-1,008 hr) on extracorporeal membrane oxygenation. Moderate and severe Thrombocytopenia were more common in extracorporeal membrane oxygenation compared with cardiopulmonary bypass throughout (p < 0.0001). Thrombocytopenia increased in cardiopulmonary bypass patients on day 2 but was normal in 83% compared with 42.3% of extracorporeal membrane oxygenation patients at day 10. Patients on extracorporeal membrane oxygenation also followed a similar pattern of platelet recovery following cessation of extracorporeal membrane oxygenation. The frequency of Heparin-Induced Thrombocytopenia in extracorporeal membrane oxygenation and cardiopulmonary bypass were 6.4% (19/298) and 0.6% (18/2,998), respectively (p < 0.0001). There was no difference in prevalence of Heparin-Induced Thrombocytopenia in patients on venovenous-extracorporeal membrane oxygenation (8/156, 5.1%) versus venoarterial-extracorporeal membrane oxygenation (11/142, 7.7%) (p = 0.47). The positive predictive value of the Pretest Probability Score in identifying Heparin-Induced Thrombocytopenia in patients post cardiopulmonary bypass and on extracorporeal membrane oxygenation was 56.25% (18/32) and 25% (15/60), respectively. Mortality was not different with (6/19, 31.6%) or without (89/279, 32.2%) Heparin-Induced Thrombocytopenia in patients on extracorporeal membrane oxygenation (p = 0.79). CONCLUSIONS Thrombocytopenia is already common at extracorporeal membrane oxygenation initiation. Heparin-Induced Thrombocytopenia is more frequent in both venovenous- and venoarterial-extracorporeal membrane oxygenation compared with cardiopulmonary bypass. Positive predictive value of Pretest Probability Score in identifying Heparin-Induced Thrombocytopenia was lower in extracorporeal membrane oxygenation patients. Heparin-Induced Thrombocytopenia had no effect on mortality.
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Frequency of Thrombocytopenia and Heparin-Induced Thrombocytopenia in Patients Receiving Extracorporeal Membrane Oxygenation Compared With Cardiopulmonary Bypass and the Limited Sensitivity of Pretest Probability Score
'Ovid Technologies (Wolters Kluwer Health)', 2020Co-Authors: Deepa Rj Arachchillage, Laffan Mike, Khanna Sanjay, Vandenbriele Christophe, Kamani Farah, Passariello Maurizio, Rosenberg Alex, Banya Winston, Ledot StephaneAbstract:OBJECTIVES: To ascertain: 1) the frequency of Thrombocytopenia and Heparin-Induced Thrombocytopenia; 2) positive predictive value of the Pretest Probability Score in identifying Heparin-Induced Thrombocytopenia; and 3) clinical outcome of Heparin-Induced Thrombocytopenia in adult patients receiving venovenous- or venoarterial-extracorporeal membrane oxygenation, compared with cardiopulmonary bypass. DESIGN: A single-center, retrospective, observational cohort study from January 2016 to April 2018. SETTING: Tertiary referral center for cardiac and respiratory failure. PATIENTS: Patients who received extracorporeal membrane oxygenation for more than 48 hours or had cardiopulmonary bypass during specified period. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Clinical and laboratory data were collected retrospectively. Pretest Probability Score and Heparin-Induced Thrombocytopenia testing results were collected prospectively. Mean age (± SD) of the extracorporeal membrane oxygenation and cardiopulmonary bypass cohorts was 45.4 (± 15.6) and 64.9 (± 13), respectively (p < 0.00001). Median duration of cardiopulmonary bypass was 4.6 hours (2-16.5 hr) compared with 170.4 hours (70-1,008 hr) on extracorporeal membrane oxygenation. Moderate and severe Thrombocytopenia were more common in extracorporeal membrane oxygenation compared with cardiopulmonary bypass throughout (p < 0.0001). Thrombocytopenia increased in cardiopulmonary bypass patients on day 2 but was normal in 83% compared with 42.3% of extracorporeal membrane oxygenation patients at day 10. Patients on extracorporeal membrane oxygenation also followed a similar pattern of platelet recovery following cessation of extracorporeal membrane oxygenation. The frequency of Heparin-Induced Thrombocytopenia in extracorporeal membrane oxygenation and cardiopulmonary bypass were 6.4% (19/298) and 0.6% (18/2,998), respectively (p < 0.0001). There was no difference in prevalence of Heparin-Induced Thrombocytopenia in patients on venovenous-extracorporeal membrane oxygenation (8/156, 5.1%) versus venoarterial-extracorporeal membrane oxygenation (11/142, 7.7%) (p = 0.47). The positive predictive value of the Pretest Probability Score in identifying Heparin-Induced Thrombocytopenia in patients post cardiopulmonary bypass and on extracorporeal membrane oxygenation was 56.25% (18/32) and 25% (15/60), respectively. Mortality was not different with (6/19, 31.6%) or without (89/279, 32.2%) Heparin-Induced Thrombocytopenia in patients on extracorporeal membrane oxygenation (p = 0.79). CONCLUSIONS: Thrombocytopenia is already common at extracorporeal membrane oxygenation initiation. Heparin-Induced Thrombocytopenia is more frequent in both venovenous- and venoarterial-extracorporeal membrane oxygenation compared with cardiopulmonary bypass. Positive predictive value of Pretest Probability Score in identifying Heparin-Induced Thrombocytopenia was lower in extracorporeal membrane oxygenation patients. Heparin-Induced Thrombocytopenia had no effect on mortality.status: publishe
Winston Banya - One of the best experts on this subject based on the ideXlab platform.
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frequency of Thrombocytopenia and Heparin Induced Thrombocytopenia in patients receiving extracorporeal membrane oxygenation compared with cardiopulmonary bypass and the limited sensitivity of pretest probability score
Critical Care Medicine, 2020Co-Authors: Deepa Rj Arachchillage, Michael Laffan, Sanjay Khanna, Christophe Vandenbriele, Farah Kamani, Maurizio Passariello, Alexander F Rosenberg, Winston BanyaAbstract:OBJECTIVES To ascertain: 1) the frequency of Thrombocytopenia and Heparin-Induced Thrombocytopenia; 2) positive predictive value of the Pretest Probability Score in identifying Heparin-Induced Thrombocytopenia; and 3) clinical outcome of Heparin-Induced Thrombocytopenia in adult patients receiving venovenous- or venoarterial-extracorporeal membrane oxygenation, compared with cardiopulmonary bypass. DESIGN A single-center, retrospective, observational cohort study from January 2016 to April 2018. SETTING Tertiary referral center for cardiac and respiratory failure. PATIENTS Patients who received extracorporeal membrane oxygenation for more than 48 hours or had cardiopulmonary bypass during specified period. INTERVENTIONS None. MEASUREMENTS AND MAIN RESULTS Clinical and laboratory data were collected retrospectively. Pretest Probability Score and Heparin-Induced Thrombocytopenia testing results were collected prospectively. Mean age (± SD) of the extracorporeal membrane oxygenation and cardiopulmonary bypass cohorts was 45.4 (± 15.6) and 64.9 (± 13), respectively (p < 0.00001). Median duration of cardiopulmonary bypass was 4.6 hours (2-16.5 hr) compared with 170.4 hours (70-1,008 hr) on extracorporeal membrane oxygenation. Moderate and severe Thrombocytopenia were more common in extracorporeal membrane oxygenation compared with cardiopulmonary bypass throughout (p < 0.0001). Thrombocytopenia increased in cardiopulmonary bypass patients on day 2 but was normal in 83% compared with 42.3% of extracorporeal membrane oxygenation patients at day 10. Patients on extracorporeal membrane oxygenation also followed a similar pattern of platelet recovery following cessation of extracorporeal membrane oxygenation. The frequency of Heparin-Induced Thrombocytopenia in extracorporeal membrane oxygenation and cardiopulmonary bypass were 6.4% (19/298) and 0.6% (18/2,998), respectively (p < 0.0001). There was no difference in prevalence of Heparin-Induced Thrombocytopenia in patients on venovenous-extracorporeal membrane oxygenation (8/156, 5.1%) versus venoarterial-extracorporeal membrane oxygenation (11/142, 7.7%) (p = 0.47). The positive predictive value of the Pretest Probability Score in identifying Heparin-Induced Thrombocytopenia in patients post cardiopulmonary bypass and on extracorporeal membrane oxygenation was 56.25% (18/32) and 25% (15/60), respectively. Mortality was not different with (6/19, 31.6%) or without (89/279, 32.2%) Heparin-Induced Thrombocytopenia in patients on extracorporeal membrane oxygenation (p = 0.79). CONCLUSIONS Thrombocytopenia is already common at extracorporeal membrane oxygenation initiation. Heparin-Induced Thrombocytopenia is more frequent in both venovenous- and venoarterial-extracorporeal membrane oxygenation compared with cardiopulmonary bypass. Positive predictive value of Pretest Probability Score in identifying Heparin-Induced Thrombocytopenia was lower in extracorporeal membrane oxygenation patients. Heparin-Induced Thrombocytopenia had no effect on mortality.