Clinical features of heparin-induced thrombocytopenia including risk factors for thrombosis

2005 ◽  
Vol 94 (07) ◽  
pp. 132-135 ◽  
Author(s):  
Beate Farner ◽  
Hartmut Kroll ◽  
Thomas Kohlmann ◽  
Theodore E. Warkentin ◽  
Petra Eichler ◽  
...  

SummaryImmune mediated heparin induced thrombocytopenia (HIT) is a prothrombotic adverse effect of heparin. However, only a subgroup of patients with HIT develops thromboembolic complications. We aimed to identify risk factors for developing HITassociated thrombosis. We analyzed a registry of patients with clinical suspicion of HIT who tested positive using a sensitive functional assay. Patient information was obtained by a standardized questionnaire. By multivariate analysis the association of age, gender, type of patient population, and magnitude of the platelet count decline with the frequency, type (venous or arterial), and temporal pattern of thrombotic events was assessed. In 408 HIT patients we observed predominance of venous thrombosis (2.4:1), with 40% of patients developing a pulmonary embolism. However, in the subgroup of post-cardiovascular surgery patients there was predominance of arterial thrombosis (1:8.5). The type of arterial thrombosis (limb artery thrombosis > thrombotic stroke > myocardial infarction) was the converse of that observed with typical atherothrombotic clots in non-HIT populations. In 59.8% of patients HIT-related thrombosis manifested either on the same day a platelet count decrease >50% was documented (26.3%) or before the decrease in platelet counts (33.5%).The most important risk factors for thrombosis were orthopedic/trauma surgery and the magnitude of platelet count decrease. HIT-associated thrombosis occurs in a considerable proportion of patients before platelet counts decrease by more than 50%.

2017 ◽  
Vol 117 (10) ◽  
pp. 1868-1874 ◽  
Author(s):  
Jo-Ann Sheppard ◽  
Theodore Warkentin ◽  
Andrew Shih

SummaryOne of the standard distinctions between type 1 (non-immune) and type 2 (immune-mediated) heparin-induced thrombocytopenia (HIT) is the transience of thrombocytopenia: type 1 HIT is viewed as early-onset and transient thrombocytopenia, with platelet count recovery despite continuing heparin administration. In contrast, type 2 HIT is viewed as later-onset (i. e., 5 days or later) thrombocytopenia in which it is generally believed that platelet count recovery will not occur unless heparin is discontinued. However, older reports of type 2 HIT sometimes did include the unexpected observation that platelet counts could recover despite continued heparin administration, although without information provided regarding changes in HIT antibody levels in association with platelet count recovery. In recent years, some reports of type 2 HIT have confirmed the observation that platelet count recovery can occur despite continuing heparin administration, with serological evidence of waning levels of HIT antibodies (“seroreversion”). We now report two additional patient cases of type 2 HIT with platelet count recovery despite ongoing therapeutic-dose (1 case) or prophylactic-dose (1 case) heparin administration, in which we demonstrate concomitant waning of HIT antibody levels. We further review the literature describing this phenomenon of HIT antibody seroreversion and platelet count recovery despite continuing heparin administration. Our observations add to the concept that HIT represents a remarkably transient immune response, including sometimes even when heparin is continued.


Hematology ◽  
2009 ◽  
Vol 2009 (1) ◽  
pp. 225-232 ◽  
Author(s):  
Thomas L. Ortel

Abstract Heparin-induced thrombocytopenia (HIT) is an immune-mediated disorder caused by the development of antibodies to platelet factor 4 (PF4) and heparin. The thrombocytopenia is typically moderate, with a median platelet count nadir of ~50 to 60 × 109 platelets/L. Severe thrombocytopenia has been described in patients with HIT, and in these patients antibody levels are high and severe clinical outcomes have been reported (eg, disseminated intravascular coagulation with microvascular thrombosis). The timing of the thrombocytopenia in relation to the initiation of heparin therapy is critically important, with the platelet count beginning to drop within 5 to 10 days of starting heparin. A more rapid drop in the platelet count can occur in patients who have been recently exposed to heparin (within the preceding 3 months), due to preformed anti-heparin/PF4 antibodies. A delayed form of HIT has also been described that develops within days or weeks after the heparin has been discontinued. In contrast to other drug-induced thrombocytopenias, HIT is characterized by an increased risk for thromboembolic complications, primarily venous thromboembolism. Heparin and all heparin-containing products should be discontinued and an alternative, non-heparin anticoagulant initiated. Alternative agents that have been used effectively in patients with HIT include lepirudin, argatroban, bivalirudin, and danaparoid, although the last agent is not available in North America. Fondaparinux has been used in a small number of patients with HIT and generally appears to be safe. Warfarin therapy should not be initiated until the platelet count has recovered and the patient is systemically anticoagulated, and vitamin K should be administered to patients receiving warfarin at the time of diagnosis of HIT.


Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3972-3972
Author(s):  
Joseph E. Spahr ◽  
Neeraj Agarwal ◽  
George M. Rodgers

Abstract Introduction: In January 2000, two patients with severe Immune-Mediated Thrombocytopenia (ITP) at our institution were successfully treated with prolonged infusions of IVIg and platelets. The dose of IVIg was 1 g/kg given by continuous infusion over 24 hours with concurrent platelets (1 pheresis unit every 8 hours). Based on these preliminary results, we evaluated this protocol in a larger series of 40 ITP patients. Methods: We performed an IRB-approved retrospective review of adult hospitalized patients with ITP treated with this regimen from January 2000 - December 2005. Patients with clinically significant thrombocytopenia and either active bleeding, need for anticoagulation, or requirement for a surgical procedure received the combined treatment. The subjects received IVIg and platelets as described above. Additional treatments, such as steroids, immunosupressives, or rituximab, as well as splenectomy were utilized at the discretion of the hematologist overseeing their care. Results: The average age of patients treated was 52 years. The majority of patients ranged from 20–80 years old, but 12.5% were older than 80 years. The average pretreatment platelet count was 10,000/μl, with an increase to 55,000/μl after 24 hours, and 69,000/μl after 48 hours. By 72 hours, the average platelet count had begun to decline, although the platelet count remained at an acceptable level (58,200/μl). After 24 hours, 62.7% of patients had a platelet count > 50,000/μl. Bleeding was controlled initially in all patients, and those requiring a procedure experienced no bleeding complications. Over half of the patients (52.5%) required additional treatments for recurrent or refractory ITP, and 32.5% of the patients underwent splenectomy. Six of the 21 patients requiring later retreatment (29%) received IVIg and platelets again in a similar fashion. The average retreatment platelet counts after 24 and 48 hours were 53,000/μl and 49,000/μl respectively, with clinical improvement in bleeding in all patients. No side effects of the combined treatment were noted. The response rates for the 3 IVIg products used were similar. Discussion: For ITP, IVIg and platelets are considered to be first line treatment for patients with very low platelet counts, active bleeding, or those requiring urgent procedures. There is limited literature on the optimal dose and schedule for administration of IVIg and platelets. Our approach for administration of IVIg and platelets concurrently was associated with minimal side effects, resolution of bleeding, ability to safely undergo procedures, and rapid restoration of adequate platelet counts. Additionally, elderly patients had equivalent benefit with no increased side effects, indicating that this regimen is appropriate and safe for patients of all age groups.


Hematology ◽  
2010 ◽  
Vol 2010 (1) ◽  
pp. 135-143 ◽  
Author(s):  
Andreas Greinacher ◽  
Kathleen Selleng

Abstract The many comorbidities in the severely ill patient also make thrombocytopenia very common (∼ 40%) in intensive care unit patients. The risk of bleeding is high with severe thrombocytopenia and is enhanced in intensive care patients with mild or moderately low platelet counts when additional factors are present that interfere with normal hemostatic mechanisms (eg, platelet function defects, hyperfibrinolysis, invasive procedures, or catheters). Even if not associated with bleeding, low platelet counts often influence patient management and may prompt physicians to withhold or delay necessary invasive interventions, reduce the intensity of anticoagulation, order prophylactic platelet transfusion, or change anticoagulants due to fear of heparin-induced thrombocytopenia. One approach to identify potential causes of thrombocytopenia that require specific interventions is to consider the dynamics of platelet count changes. The relative decrease in platelet counts within the first 3 to 4 days after major surgery is informative about the magnitude of the trauma or blood loss, whereas the dynamic of the platelet count course thereafter shows whether or not the physiologic compensatory mechanisms are working. A slow and gradual fall in platelet counts developing over 5 to 7 days is more likely to be caused by consumptive coagulopathy or bone marrow failure, whereas any abrupt decrease (within 1–2 days) in platelet counts manifesting after an initial increase in platelet counts approximately 1 to 2 weeks after surgery strongly suggests immunologic causes, including heparin-induced thrombocytopenia, other drug-induced immune thrombocytopenia, and posttransfusion purpura.


Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 756-756
Author(s):  
Jori E. May ◽  
Kimberly D. Martin ◽  
Laura J. Taylor ◽  
Eric L. Wallace ◽  
Marisa B. Marques

Abstract Background: Heparin-induced thrombocytopenia (HIT) is a rare disorder with potential to cause significant morbidity and mortality. Early identification and initiation of non-heparin anticoagulation can prevent devastating thrombotic events. However, over-testing is common and can lead to result misinterpretation, unnecessary heparin avoidance, and increased cost. When there is concern for HIT, guidelines from the American Society of Hematology recommend calculation of the 4Ts score to determine the need for laboratory testing. The Choosing Wisely® initiative recommends against laboratory testing in patients with a low probability score of ≤3. In patients with an intermediate or high probability score (≥4), screening with enzyme-linked immunosorbent assay (ELISA) is performed first. If positive, the diagnosis of HIT is confirmed with a functional assay, commonly the serotonin release assay (SRA). Methods: In an effort to increase recognition of HIT, providers at a large academic medical center received a non-interruptive alert in the electronic medical record (EMR) on all patients in whom the platelet count declined by ≥50% starting in Aug 2017. We performed a retrospective evaluation of 1) the number of alerts and 2) all ELISA results obtained with or without an alert, over a 90-day period (Dec 2019 to March 2020). A 4Ts score was calculated by chart review by the first author in real-time as the alert was sent (blinded to ELISA and SRA results). Among those patients with multiple alerts or test orders, the first instance was used for analysis. Demographic and clinical characteristics were reported using frequencies and percentages, means (standard deviation, SD), and medians (interquartile range, IQR). Patients with alerts and ELISA testing ordered were compared with 2 groups: 1) patients with alerts but no ELISA ordered; 2) patients with no alerts but ELISA ordered. Comparisons were performed using chi squared tests, Fisher's exact tests, t-tests and Wilcoxon rank-sum tests as appropriate. Results: In the 90-day observation period, 302 alerts were fired in 270 patients (Figure 1). Thirty alerts (28 patients, 10%) were generated for patients admitted for organ donation or post-stem cell transplantation, for whom platelet count decline was expected. Excluding these patients, there were 272 alerts in 242 patients (approximately 3 alerts per day in a 1,157-bed hospital). Of patients with alerts, 22 (8%) had a platelet count inaccuracy (i.e. platelets clump or another reason) and 18 (7%) did not receive heparin prior to platelet decline, for a cumulative total of 40 (15%) inappropriate alerts. In patients with an alert, the ELISA was ordered more frequently for those with a lower platelet nadir (77x10 9/L vs. 115x10 9/L, p<0.0001) or in those with a thrombotic event (11 patients (17%) vs. 6 patients (4%), p=0.0021) (Table 1). Those without an ELISA ordered were more likely to have a low 4Ts score (23 patients (36%) vs. 81 patients (58%), p<0.0001). In addition to 71 patients with an alert, an ELISA was also ordered for 67 patients without an alert (n=138) (Figure 1). Close to half of ELISA-tested patients had a low 4Ts score (n=51, 46%) (Figure 2). In patients with an alert and ELISA not ordered, 18 (27%) had an intermediate or high 4Ts score. Seven patients were diagnosed with HIT based on a positive SRA, 6 with an alert and 1 without. The alert demonstrated a sensitivity of 86% (95% CI, 59.8-100%) and specificity of 50% (95% CI, 41.8-58.9%) with a positive predictive value of 0.0845 (95% CI, 0.0198-0.1492) and negative predictive value of 0.9851 (95% CI, 0.9560-1.0000). Conclusion: An EMR alert based on platelet count decline had multiple shortcomings including frequent inappropriate firings and a lack of guidance on appropriate indications for testing. This evaluation of institutional testing practices indicates frequent use and misinterpretation of ELISA discordant with evidence-based guidelines. Although prompt diagnosis of HIT is important, alternative strategies for identification of at-risk patients and communication of recommended actions to providers should be considered. Because the 4Ts score includes variables difficult to automate in the EMR, our institution is exploring electronic consultation and real-time expert provider access to overcome these limitations. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.


Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 719-719
Author(s):  
Kathleen Pao Lynn Cheok ◽  
Rakchha Chhetri ◽  
Li Yan A Wee ◽  
Arabelle Salvi ◽  
Simon McRae ◽  
...  

Aim: Although 40-65% of myelodysplastic syndromes (MDS) patients are thrombocytopenic and require platelet transfusions, there is limited literature on the risk factors predictive of bleeding and the burden of immune mediated platelet refractoriness (PLT-R). Objectives: To evaluate the prevalence of thrombocytopenia, incidence of bleeding events, platelet transfusion dependency (PLT-TD) and immune-mediated platelet refractoriness (PLT-R) in MDS patients. Methods: A retrospective analysis of 754 MDS patients enrolled in the South Australian MDS (SA-MDS) registry was performed. Platelet counts <100, <50 and <20 (x109/L) were used to define mild, moderate and severe thrombocytopenia respectively. The severity of bleeding events was classified according to the International Society of Thrombosis and Haemostasis (ISTH) classification. PLT-TD was defined as transfusion of at least one unit of platelets each month for four consecutive months. All other patients were classified as transfusion independent (PLT-TI). Immune mediated PLT-R was defined if a patient had HLA-class I or HPA antibodies, poor platelet increments and required HLA-matched platelets. Medication history with regards to anticoagulation and/or antiplatelet therapy was also collected. Results: At diagnosis, 332 (45%) patients had thrombocytopenia and 106 (14%) patients had moderate to severe thrombocytopenia. During the study period, 249 bleeding events were recorded in 162 (21%) patients with a cumulative incidence of 33% (Fig 1A). Of the 249 bleeding events, 85 (34%) were major and 164 (66%) were clinically relevant minor bleeding. Notably, 16, 90 and 5 bleeding events were intracranial, gastrointestinal, intraocular respectively. While 41% (96/235) bleeding events occurred in the setting of moderate to severe thrombocytopenia, 21% and 38% (Fig 1B) of bleeding events occurred at platelet counts of >50-100 and >100x109/L respectively. Twenty-eight percent (69/249) bleeding events were associated with concomitant anticoagulation and/or antiplatelet therapy and importantly, platelets counts were >50x109/L and >100 x109/L in 57 (83%) and 46 (67%) at the time of bleeding events, respectively. During the disease course, 393 (52%) patients required at least one unit of platelet transfusion. 106 (14%) patients were PLT-TD and had significantly poor overall survival (OS) compared to PLT-TI (26 vs 42 months, p<0.0001). In total, 30/393 (7%) required HLA-matched platelet transfusions. 20/30 (66%) of PLT-R patients were female receiving disease modifying therapy (DMT). This was substantiated by cox regression analysis, demonstrating that females (HR=5.32, p=0.0006), older age (HR=0.97, p=0.028) and haemoglobin (Hb) at diagnosis (HR=1.03, p=0.009) were independent risk factors for PLT-R. Importantly, 20/76 (25%) female patients receiving platelets and DMT developed immune mediated PLT-R requiring HLA matched platelets. Conclusions: In our cohort of MDS patients, cumulative incidence of bleeding is 33% and 59% of the bleeding events occurred at platelet counts >50X109/L. For all bleeding events that occurred while on anticoagulation and/or antiplatelet therapy, 83% events occurred with platelet counts >50 x 109/L. Therefore, guidelines for anticoagulation and/or antiplatelet therapy are required for MDS patients. We also showed that development of PLT-TD is associated with poor OS. Importantly, 1 in 4 female MDS patients receiving platelets and DMT required HLA-matched platelets. Platelet transfusions practices should be optimised for these high-risk groups. Disclosures No relevant conflicts of interest to declare.


Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 1141-1141 ◽  
Author(s):  
Shuoyan Ning ◽  
Brent Kerbel ◽  
Jeannie Callum ◽  
Yulia Lin

Abstract Introduction: Lumbar puncture (LP) is a frequently performed diagnostic and therapeutic intervention in adult oncology patients. While thrombocytopenia is common in this patient population, the minimum "safe" platelet count required for LPs is unknown. Recent guidelines from the AABB (American Association of Blood Banks) recommend a pre-procedure platelet count of 50 x 109/L. However this recommendation is largely based on expert opinion, and there remains a paucity of studies in the adult oncology literature to address this important question. Methods: We retrospectively reviewed all oncology patients ≥18 years who underwent 1 or more LPs over a 2 year period at a single tertiary care institution to determine 1) the range of platelet counts at which LPs are performed; 2) the rate of traumatic taps; and 3) the rate of hemorrhagic complications. Laboratory, clinical, and transfusion information were extracted through the Laboratory Information System, chart review, and blood bank database, respectively. Thrombocytopenia was defined as a platelet count of < 150 x 109/L. Pre-LP platelet counts were those collected ≤24 hours from, and closest to the time of the LP. The following bleeding risk factors were documented: end stage renal disease; platelet dysfunction; von Willebrand disease; hemophilia. Anticoagulation, anti-platelet, and non-steroidal inflammatory use was also recorded, with accuracy limited by the study's retrospective nature. All patients with coagulopathy were excluded (INR ≥ 1.5, aPTT ≥ 40, fibrinogen ≤ 1.0). Traumatic tap was defined as 500 or more red blood cells per high-power field in the cerebrospinal fluid. A follow up of 1 week after LP was used to capture any hemorrhagic complications. Results: From January 2013 to December 2014, 135 oncology patients underwent 369 LPs; 64 (47.4%) patients were female, and the mean age was 59 years (range 20-87). 119 (88.1%) patients had a primary hematological diagnosis. 113 (30.6%) LPs were performed in thrombocytopenic patients. 28 (7.6%) procedures had a pre-procedure platelet count of ≤ 50 x 109/L, with 18 receiving a single platelet transfusion on the day of the LP. Of these 18 transfusions, only 1 had a post-transfusion platelet count available prior to LP with no improvement in platelet count (33 x 109/L). 15 transfusions had post-LP platelet counts within 24 hours of the transfusion (8 below 50 x 109/L with lowest 14 x 109/L), 1 had post-LP platelet count within 24-48 hours (54 x 109/L) and 1 did not have a post-transfusion platelet count. Traumatic taps occurred in 17 (15.0%) LPs in patient with thrombocytopenia, compared to 26 (11.0%) LPs in patients with a normal platelet count (fisher's exact test P=0.39). There was 1 traumatic tap in a patient with a pre-LP platelet count of ≤ 50 x 109/L; however, this patient received a pre-LP platelet transfusion for a platelet count of 42 x 109/L and had a post-LP platelet count of 66 x 109/L. Presence of bleeding risk factors did not increase the risk of a traumatic tap (present in 48.8% of traumatic taps vs. 88.3% of non-traumatic taps). There were no hemorrhagic complications. Conclusion: Among this cohort of adult oncology patients undergoing diagnostic and therapeutic LPs, there were no hemorrhagic complications. There was no significant increase in traumatic taps in patients with thrombocytopenia or bleeding risk factors. While platelet transfusions were frequently administered for patients with a platelet count of ≤ 50 x 109/L, post-transfusion platelet counts were infrequently assessed prior to the procedure. Our findings question whether a platelet transfusion threshold of 50 x 109/L is necessary for lumbar puncture.Table 1.Platelet Count Pre-LP(x109/L)Number of LPsNumber of Traumatic TapsNumber of Hemorrhagic Complications0-90N/AN/A10-2030021-5070051-1003380101-1495270> 150242270Unknown1400< 50 x 109/L and received platelet transfusion on day of LP181*0Total369430*There was one traumatic tap in a patient with a platelet count of 42 x 109/L who received a platelet transfusion pre-LP. The post transfusion platelet count was 66 x 109/L. Disclosures No relevant conflicts of interest to declare.


2020 ◽  
Vol 10 (3) ◽  
pp. 32256-32256
Author(s):  
Haleh Talaie ◽  
◽  
Sayed Masoud Hosseini ◽  
Maryam Nazari ◽  
Mehdi Salavati Esfahani ◽  
...  

Background: Platelet count is a readily available biomarker predicting disease severity and risk of mortality in the intensive care units (ICU). This study aims to describe the frequency, to assess the risk factors, and to evaluate the impact of thrombocytopenia on patient outcomes in a Toxicological ICU (TICU).Methods: In this prospective observational Cohort study, we enrolled 184 patients admitted to our TICU from October 1st, 2019, to August 23rd, 2020. Mild/moderate and severe thrombocytopenia were defined as at least one platelet counts less than 150×103/μL and 50×103/μL during the ICU stay, respectively.Results: Of 184 enrolled patients, 45.7% had mild to moderate thrombocytopenia and 5.4% had severe thrombocytopenia. Old age (OR: 1.042, 95%CI: 1.01-1.075, P=0.01), male gender (OR: 4.348, 95%CI: 1.33-14.22, P=0.015), increased international normalized ratio (INR) levels (OR: 3.72, 95%CI: 1.15-112, P=0.028), and administration of some medications including heparin (OR: 3.553, 95%CI: 1.11-11.36, P=0.033), antihypertensive drugs (OR: 2.841, 95%CI: 1.081-7.471, P=0.034), linezolid (OR: 13.46, 95%CI: 4.75-38.13, P<0.001), erythromycin (OR: 19.58, 95%CI: 3.23-118.86, P=0.001), and colistin (OR: 10.29, 95% CI 1.44-73.69, P=0.02) were the risk factors of hospital-acquired thrombocytopenia. The outcomes of patients with normal platelet count were significantly better than those who developed thrombocytopenia (P<0.001).Conclusion: We found that thrombocytopenia could develop in almost 50% of patients admitted to TICU, which is associated with poor prognosis. Additionally, the platelet counts should be closely monitored to administer some medications (heparin, antihypertensive drug, and linezolid), especially in old patients.


2016 ◽  
Vol 116 (11) ◽  
pp. 799-805 ◽  
Author(s):  
Jérôme Rollin ◽  
Claire Pouplard ◽  
Yves Gruel

SummaryFcγ receptors have critical roles in the pathophysiology of heparin-induced thrombocytopenia (HIT), a severe immune-mediated complication of heparin treatment. Activation of platelets, monocytes and neutrophils by platelet-activating anti-PF4/heparin IgG antibodies results in thrombocytopenia, hypercoagulability and thrombosis in susceptible patients, effects that depend on FcγRIIA. In addition, FcγRIIIA receptors probably contribute to clearance of platelets sensitised by HIT immune complexes. FcγRI has also been reported to be involved in monocyte activation by HIT IgG antibodies and synthesis of tissue factor. This review focuses on the role of these FcγRs in HIT pathophysiology, including the potential influence of several gene variations associated with variable risk of HIT and related thrombosis. In particular, the 276P and 326Q alleles of CD148, a protein tyrosine phosphatase that regulates FcγRIIA signalling, are associated with a lower risk of HIT, and platelets from healthy donors expressing these alleles are hyporesponsive to anti-PF4/H antibodies. It was also recently demonstrated that the risk of thrombosis is higher in HIT patients expressing the R isoform of the FcγRIIA H131R polymorphism, with HIT antibodies shown to activate RR platelets more efficiently, mainly explained by an inhibitory effect of normal IgG2, which bound to the FcγRIIA 131H isoform more efficiently. Environmental risk factors probably interact with these gene polymorphisms affecting FcγRs, thereby increasing thrombosis risk in HIT.


Author(s):  
Gowthami M. Arepally ◽  
Anand Padmanabhan

Heparin-induced thrombocytopenia is an immune-mediated disorder caused by antibodies that recognize complexes of platelet factor 4 and heparin. Thrombosis is a central and unpredictable feature of this syndrome. Despite optimal management, disease morbidity and mortality from thrombosis remain high. The hypercoagulable state in heparin-induced thrombocytopenia is biologically distinct from other thrombophilic disorders in that clinical complications are directly attributable to circulating ultra-large immune complexes. In some individuals, ultra-large immune complexes elicit unchecked cellular procoagulant responses that culminate in thrombosis. To date, the clinical and biologic risk factors associated with thrombotic risk in heparin-induced thrombocytopenia remain elusive. This review will summarize our current understanding of thrombosis in heparin-induced thrombocytopenia with attention to its clinical features, cellular mechanisms, and its management.


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