Heparin-Induced Thrombocytopenia: A Rapid, Reliable and Practical, Functional Flow-Cytometric Assay

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 1130-1130
Author(s):  
Varda Deutsch ◽  
Michal Cipok ◽  
Sigi Kay ◽  
Yvette Levy ◽  
Shoshana Bar On ◽  
...  
Keyword(s):  
Conflicts Of Interest ◽  
High Sensitivity ◽  
Relative Sensitivity ◽  
Serotonin Release ◽  
Specific Test ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Laboratory Confirmation ◽  
Relative Specificity ◽  
Biological Probe

Abstract Background Heparin-induced thrombocytopenia (HIT) is a serious complication of heparin treatment, associated with morbidity and mortality. HIT is characterized by thrombocytopenia and thrombotic complications secondary to the formation of antibodies (Abs) against heparin-platelet-factor 4 (PF4) complexes. The pathologic mechanism involves the binding of the heparin-immune-complex to the platelet-Fc-receptor, resulting in platelet activation, aggregation, and rapid elimination. The diagnosis of HIT requires laboratory confirmation. Common laboratory testing is based on immune detection of antibodies directed against the PF4/heparin complex (ID-H/PF4-PaGIA or ELISA). However, these assays suffer from methodological limitations, especially low specificity, as compared to the platelet functional assays. The “gold standard” functional test for detecting of platelet-activating antibodies is the radioactive [14C] serotonin-release assay (14C-SRA) (Sheridan D, et al, Blood. 1986;67:27-30, Kelton JG, et al.,Blood.1988;72:925-30). However, the assay includes the use of a radiolabeled biological probe and requires considerable expertise to obtain reliable results. Consequently, its use is limited to research laboratories. Aim To overcome the methodological limitations associated with current assays, we modified a functional flow-cytometry assay (FCA), which exhibits high sensitivity and specificity (Tomer, A. Br J Haematol, 1997;98: 648-656 , Tomer, A., et al, Am J Hematol, 1999;61: 53-61). This assay, similar in concept to the 14C-SRA, determines the capacity of the patient's serum to activate platelets in the presence of heparin, using a fluorescent probe. Methods Consecutive samples from 254 patients clinically suspected for HIT were tested. The FCA assay was compared with the standard ID-H/PF4-PaGIA antigenic assay (DiaMed, Switzerland) with two dilutions to assess specificity (Nellen, V., et al.,Haematologica, 2012;97: 89-97). Results Of the total 254 samples tested, 48 (19%) were positive by PaGIA, compared to 13 (5.1%) positive by the functional FCA (Table 1). The number of PaGIA positive samples was reduced to 24 (9.4%) by 1:16 dilution, and to 14 (5.5%) by 1:32 dilution. All FCA positive samples were positive at all PaGIA dilutions (relative sensitivity 93%). Thirty PaGIA negative samples were all negative by the FCA (relative specificity 100%). Conclusion The results suggest that the functional FCA is a practical, sensitive, and highly specific test for the reliable diagnosis of HIT. Disclosures: No relevant conflicts of interest to declare.

Heparin-Induced Thrombocytopenia: Comparison Between the Standard Gel-Particle Assay (PaGIA) and the Functional Flow Cytometric Assay.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 5060-5060
Author(s):  
Aaron Tomer
Keyword(s):  
Conflicts Of Interest ◽  
Multiorgan Failure ◽  
Relative Sensitivity ◽  
Serotonin Release ◽  
Detection Methods ◽  
Antibody Detection ◽  
Flow Cytometric Assay ◽  
Heparin Induced Thrombocytopenia ◽  
Flow Cytometric ◽  
Relative Specificity

Abstract 5060 Background Heparin-induced thrombocytopenia and thrombosis (HIT) is an immune-mediated complication that may develop in patients sensitized to heparin. Approximately 5% of patients treated with full dose heparin develop clinical HIT, with about half develop thrombosis that may be associated with severe morbidity and death. However, antibodies may be detected in up to 30% of patients. Thus, current antibody-detection methods carry certain limitations, which pose a serious clinical dilemma in the diagnosis and treatment of HIT. Objectives To compare the gel-particle immuno-assay (PaGIA) for the detection of antibodies against heparin-PF4 complex, with the functional flow cytometric assay (FCA) which determines the capacity of the patient's serum to activate platelets in the presence of heparin, similar in concept to the gold-standard, the radioactive Serotonin-release assay. Methods Sequential samples from patients clinically suspected for HIT were tested by both PaGIA and the FCA (Tomer 1997, 1999). Results 118 samples were tested. Positive: 9 (7.6%) patients tested positive by PaGIA, compared to 19 (16.1%) by the FCA. 7,out of the 9 (77.8%) PaGIA -positive samples were also positive by the FCA (relative sensitivity). Negative: 97 out of 109 gel-negative samples (89.0%) were also negative by the FCA (relative specificity). Thrombosis occurred in 3 of the 9 PaGIA-positive (33%) patients, and in 7 of the 19 FCA-positive (36.8%) patients. Of the 12 PaGIA -negative but FCA-positive patients, 4 (33%) had thrombosis. Death rate was also higher among FCA-positive (n=3) compared to PaGIA-positive (n=1) patients. Of the two PaGIA -positive but FCA-negative patients, one had APLA syndrome (APS) with chronic thrombocytopenia, and one had sepsis with cardiogenic shock and multiorgan failure. ROC-Plot: Overall, the FCA showed significantly higher correlation with the clinical presentation of HIT (4Ts score), compared to the PaGIA (AUC 0.86 vs. 0.62, p<0.001) Conclusion The functional FCA demonstrates superior sensitivity and specificity compared to the antibody- detection PaGIA gel-particle assay. The feasible functional FCA (results in 1.5 hr) might be useful for initial diagnosis of HIT, and particularly for confirmation of HIT in patients with confounding presentation, including negative antibody-detection assay. Disclosures No relevant conflicts of interest to declare.

Intricacies Of Treating Heparin Induced Thrombocytopenia With Preexisting Antiphospholipid Syndrome and Renal Insufficiency

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4819-4819 ◽  
Author(s):  
Pouyan Gohari ◽  
Philip Rubin
Keyword(s):  
Renal Insufficiency ◽  
Antiphospholipid Syndrome ◽  
Conflicts Of Interest ◽  
Current Treatment ◽  
Serotonin Release ◽  
Fixed Dose ◽  
Thrombin Inhibitor ◽  
Cerebral Vein ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia

Treatment of heparin induced thrombocytopenia (HIT) requires the use of alternatives anticoagulants, such as a direct thrombin inhibitor – argatroban. Use of argatroban relies on frequent laboratory monitoring of the activated partial thromboplastin time (aPTT) to maintain an adequate level of anticoagulation. This requirement poses a challenge in patients with prolonged baseline aPTT, such as in antiphospholipid syndrome. While other assays are being explored they require an extended turn around time because of their limited availability. We present a case of a 63 year old male with a history of antiphospholipid syndrome, end stage renal disease on hemodialysis, hepatitis C, and on long term anticoagulation with warfarin for cerebral vein thrombosis. His hospital course required transition to unfractionated heparin and subsequently developed thrombocytopenia. A heparin-platelet factor 4 ELISA antibody assay was performed for an intermediate clinical likelihood of HIT and returned positive. Although not confirmed with the gold standard serotonin release assay (SRA), clinical suspicion for HIT obligated treatment with an alternative anticoagulant. Conventional dosing and administration of argatroban however could not be performed because of the patient’s prolonged baseline aPTT. Other agents such as fondaparinux were also not possible in the setting of renal insufficiency. Short of other treatment techniques accepted in this unique set of circumstances we practiced a fixed dose argatroban (0.5 mcg/kg/min for Child’s class B cirrhosis). The patient tolerated the empiric dosing well until discontinued because of a negative SRA. This case demonstrates the limitations of current treatment recommendations of HIT and need for further investigation in similar patients. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Comparison of Two Different ELISA Methods for Heparin-Induced Thrombocytopenia (HIT) Screening on an Automated ELISA Platform

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 4935-4935
Author(s):  
Tatsiana Mardovina ◽  
John G Chromczak ◽  
Paul W Riley
Keyword(s):  
Predictive Value ◽  
False Negative ◽  
High Sensitivity ◽  
Clinical Findings ◽  
Serotonin Release ◽  
Laboratory Evaluation ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Negative Results ◽  
4T Score

BACKGROUND: Heparin-induced thrombocytopenia (HIT) is an adverse complication of unfractionated and low molecular weight heparin caused by antibodies recognizing platelet factor 4-heparin (PF4/hep) complexes leading to platelet activation. The diagnosis of HIT is based on the combination of the clinical picture, using the 4T score along with screening and confirmatory methods to detect platelet activating anti‐PF4/H antibodies. OBJECTIVES: Performance was evaluated for two enzyme linked immunosorbent assays (ELISAs), 1) Asserachrom HPIA , Diagnostica Stago Inc., Parsippany, NJ, USA and 2) LIFECODES PF4 Enhanced, Immucor, Inc., Norcross, GA, USA for screening-based detection of PF4/hep antibodies. METHODS: ELISA assays were run per manufacturer recommendations and adapted for automation on a Dynex DS2 automated ELISA platform. Performance characteristics of the two immunoassays were assessed, including sensitivity, specificity, concordance with serotonin release assay (SRA), positive predictive value (PPV) and negative predictive value (NPV). 21 samples were used in the study. Results: Both assays, Asserachrom HPIA and LIFECODES PF4 Enhanced demonstrated 100% sensitivity and NPV, confirming both assays' reliability to detect and rule out HIT (see table). The diagnostic specificity was significantly higher for Asserachrom HPIA vs. LIFECODES PF4 Enhanced (77.8% vs 31.6%). Asserachrom HPIA showed fewer false positive results, with PPV of 42.9% for Asserachrom HPIA vs. 13.3% for LIFECODES PF4 Enhanced. No false negative results were found for either assay. Asserachrom HPIA demonstrated 81.0% concordance with SRA, vs. 38.1% for LIFECODES PF4 Enhanced. CONCLUSIONS: HIT is a life-threatening disorder, with diagnosis depending on clinical findings using the 4T score along with laboratory evaluation. Combining the 4T score with PF4/hep antibody screening increases the accuracy of excluding HIT. Our observations indicate Asserachrom HPIA provides results with high sensitivity and specificity, minimizing false positivess, allowing use of alternative anticoagulants more selectively in at risk patients, to potentially improve patient management while minimizing costs. Disclosures Mardovina: Diagnostica Stago, Inc.: Employment. Chromczak:Diagnostica Stago, Inc.: Employment. Riley:Diagnostica Stago, Inc.: Employment.

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.

Pathophysiology of Heparin-Induced Thrombocytopenia

2000 ◽  
Vol 124 (11) ◽  
pp. 1657-1666 ◽  
Author(s):  
Fabrizio Fabris ◽  
Sarfraz Ahmad ◽  
Giuseppe Cella ◽  
Walter P. Jeske ◽  
Jeanine M. Walenga ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Serotonin Release ◽  
Platelet Factor 4 ◽  
Thrombin Inhibitors ◽  
Platelet Factor ◽  
Cellular Activation ◽  
Heparin Induced Thrombocytopenia ◽  
New Information ◽  
Study Selection ◽  
Release Assay

Abstract Objective.—This review of heparin-induced thrombocytopenia (HIT), the most frequent and dangerous side effect of heparin exposure, covers the epidemiology, pathophysiology, clinical presentation, diagnosis, and treatment of this disease syndrome. Data Sources and Study Selection.—Current consensus of opinion is given based on literature reports, as well as new information where available. A comprehensive analysis of the reasons for discrepancies in incidence numbers is given. The currently known mechanism is that HIT is mediated by an antibody to the complex of heparin–platelet factor 4, which binds to the Fc receptor on platelets. New evidence suggests a functional heterogeneity in the anti-heparin-platelet factor 4 antibodies generated to heparin, and a “superactive” heparin-platelet factor 4 antibody that does not require the presence of heparin to promote platelet activation or aggregation has been identified. Up-regulation of cell adhesion molecules and inflammatory markers, as well as preactivation of platelets/endothelial cells/leukocytes, are also considered to be related to the pathophysiology of HIT. Issues related to the specificity of currently available and new laboratory assays that support a clinical diagnosis are addressed in relation to the serotonin-release assay. Past experience with various anticoagulant treatments is reviewed with a focus on the recent successes of thrombin inhibitors and platelet GPIIb/IIIa inhibitors to combat the platelet activation and severe thrombotic episodes associated with HIT. Conclusions.—The pathophysiology of HIT is multifactorial. However, the primary factor in the mediation of the cellular activation is due to the generation of an antibody to the heparin-platelet factor 4 complex. This review is written as a reference for HIT research.

Predictive value of scoring tools in determining heparin-induced thrombocytopenia in patients on extracorporeal membrane oxygenation

Perfusion ◽  
2019 ◽  
Vol 35 (5) ◽  
pp. 378-383 ◽  
Author(s):  
Jaclyn Sullivan ◽  
Erica Bak ◽  
Mary Jane Sullivan ◽  
Payal K. Gurnani
Keyword(s):  
Extracorporeal Membrane Oxygenation ◽  
Predictive Value ◽  
Medical Center ◽  
High Sensitivity ◽  
Serotonin Release ◽  
Heparin Induced Thrombocytopenia ◽  
Membrane Oxygenation ◽  
Observational Cohort ◽  
Post Cardiopulmonary Bypass ◽  
Scoring Tools

There are currently no scoring tools validated for use in predicting heparin-induced thrombocytopenia in patients receiving extracorporeal membrane oxygenation. This study aims to determine the predictive value of the Warkentin 4T score, Lilo-Le Louet score, and the heparin-induced thrombocytopenia expert probability score in detecting heparin-induced thrombocytopenia in patients on extracorporeal membrane oxygenation. This was a single center, retrospective, observational cohort study of patients at Rush University Medical Center. Heparin-induced thrombocytopenia–positive patients were defined as those with an optical density greater than or equal to 0.4, consistent with a positive anti-platelet 4 heparin antibody. Out of 39 patients on extracorporeal membrane oxygenation with suspected heparin-induced thrombocytopenia, six (15.4%) were found to be anti-platelet 4–positive. A heparin-induced thrombocytopenia diagnosis was confirmed by serotonin-release assay in two patients (5.1%). The 4T, heparin-induced thrombocytopenia expert probability, and Lilo-Le Louet scoring tools all demonstrated a low positive predictive value (21.4%, 16.7%, and 6.7%, respectively), with the 4T and heparin-induced thrombocytopenia expert probability scores demonstrating the highest specificity (66.7% and 84.8%, respectively) and lowest sensitivity (50% and 16.7%, respectively). The Lilo-Le Louet score had high sensitivity (100%) and low specificity (12.5%) in post-cardiopulmonary bypass patients. Based on the findings of this study, all three scoring tools have limited utility for predicting heparin-induced thrombocytopenia in patients on extracorporeal membrane oxygenation.

Serologic Results in >1000 Patients With Suspected Heparin-Induced Thrombocytopenia

2007 ◽  
Vol 14 (4) ◽  
pp. 410-414 ◽  
Author(s):  
Suresh G. Shelat ◽  
Anne Tomaski ◽  
Eleanor S. Pollak
Keyword(s):  
Laboratory Diagnosis ◽  
Serotonin Release ◽  
Enzyme Linked Immunosorbent Assay ◽  
Functional Assay ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Life Threatening ◽  
Release Assay ◽  
Pathogenic Antibodies

Heparin-induced thrombocytopenia (HIT) can lead to life-threatening and limb-threatening thrombosis. HIT is thought to be initiated by the interaction of pathogenic antibodies toward a complex platelet factor 4 (PF4) and heparin (PF4:H), which can activate platelets and predispose to thrombosis. As such, the laboratory diagnosis of HIT includes antigenic and functional assays to detect antibodies directed at PF4:H complexes. We performed a retrospective analysis of 1017 consecutive samples tested by serotonin-release assay and by enzyme-linked immunosorbent assay (ELISA). Most samples showed no serologic evidence of HIT, whereas 4% to 5% of samples demonstrated both antigenic and functional serological evidence for HIT. Approximately 12% to 18% of samples showed immunologic evidence of anti-PF4:H antibodies but without functional evidence of serotonin release in vitro. Interestingly, a small minority of samples (0.7%) caused serotonin release but were negative in the ELISA. The results are presented using cutoff values established at our hospital and for the ELISA manufacturer. This study provides a pretest probability of the serologic results from an antigenic assay (ELISA) and a functional assay (serotonin-release assay) in patients clinically suspected of having HIT.

Polymorphisms in TNFA and CTLA-4 Genes and the Risk of Heparin Induced Thrombocytopenia.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3414-3414
Author(s):  
Dorothee Leroux ◽  
Claire Pouplard ◽  
Benoit Guillet ◽  
Beatrice Cosne ◽  
Marc Antoine May ◽  
...  
Keyword(s):  
Heart Surgery ◽  
Cytotoxic T Lymphocyte ◽  
Rflp Analysis ◽  
Serotonin Release ◽  
Nucleotide Polymorphisms ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Significant Difference ◽  
Patients At Risk ◽  
High Doses

Abstract Backgroud and objectives: The formation of antibodies (Abs) to heparin platelet factor 4 complexes (H/PF4) associated with heparin-induced thrombocytopenia (HIT) is a T-helper cell dependent event that involves antigen presenting cells (APC) and B-lymphocytes. Polymorphisms of the CTLA-4 (cytotoxic T lymphocyte antigen 4) gene have been described as a risk factor in several autoimmune diseases. In addition, TNFα is a major inflammatory cytokine with potent regulatory functions and polymorphisms in TNFA have also been associated with autoimmune antibody-mediated diseases. We therefore evaluated the possibility that an association between polymorphisms in CTLA-4 (−318 C/T and +49 A/G) or TNFA (−308 G/A) and the development of Abs to H/PF4 and HIT might exist. Methods: Eighty-three patients identified as having developed definite HIT with significant levels of Abs to PVS/PF4 in ELISA (HAT 45, GTI, Brookfield, WI, USA) and positive serotonin release assay were studied (HIT group). Two control groups were studied: the Abneg group consisted of 83 patients who had undergone heart surgery with high doses of unfractionated heparin administered during cardiopulmonary bypass (CPB), and who were tested negative for Abs to PVS/PF4 at the 8th post operative day. The Abpos group consisted of 58 patients who had also undergone CPB but had developed high levels of Abs to PVS/PF4 without significant change in the platelet count post-operatively. Three single nucleotide polymorphisms (SNPs), one in TNFA (−308G/A) and two in CTLA-4 (−318 C/T and +49A/G) were studied by conventional RFLP analysis as described (Astermark et al, Blood 2006 and Astermark et al, Thromb Haemost 2007). Results: The CTLA-4 +49 A/G and −318 C/T genotypes and allele distributions were similar in the 3 groups of patients (Table). In contrast, the frequency of TNFA –308 G/G homozygotes was higher in the HIT group compared to patients without HIT whether they had developed PF4-specific Abs or not (p=0.035). Therefore, the A allele was less frequent in HIT patients (p=0.026, OR 0.49; CI95% 0.26–0.93) but there was no significant difference when comparing patients with and without PF4-dependent antibodies. Genotype Allele frequency Ab neg (n = 82) Ab pos (n = 58) HIT (n = 82) CTLA-4(+49) A/A 31 (38%) 24 (41%) 35 (43%) A/G 40 (49%) 26 (45%) 41 (50%) G/G 11 (13%) 8 (14%) 6 (7%) CTLA-4(−318) C/C 63 (77%) 49 (84%) 67 (82%) C/T 19 (23%) 9 (16%) 17 (21%) T/T 0 0 0 (0%) TNFα(−308) G/G 59 (72%) 41 (71%) 68 (84%) G/A 20 (24%) 15 (26%) 12 (15%) A/A 3 (4%) 2 (3%) 1 (1%) A Allele 0.160 0.160 0.09 G Allele 0.840 0.840 0.910 Conclusion: The TNFA –308 A allele appears to be protective regarding the risk of heparin-induced thrombocytopenia in patients having developed PF4-specific antibodies. A similar effect has been suggested in immune thrombocytopenic purpura (Foster et al, Brit J Haematol 2001) despite individuals with this allele have been identified as high TNFα producers. Therefore, the mechanisms involved for explaining this apparent protective effect of the TNFA −308A allele in patients at risk for HIT have to be identified.

Incidence of Heparin Induced Thrombocytopenia in the Transplant Population: A Large Retrospective Cohort, Single Transplant Centre Experience

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 3320-3320
Author(s):  
Syed Hassan ◽  
Dania Khoulani ◽  
Ami Badami ◽  
Zaid Alirhayim ◽  
Mohamad A. Younes ◽  
...  
Keyword(s):  
Retrospective Cohort ◽  
Conflicts Of Interest ◽  
Organ Transplant ◽  
Serotonin Release ◽  
Confirmatory Test ◽  
Thrombin Inhibitor ◽  
Thromboembolic Events ◽  
Transplant Recipients ◽  
Heparin Induced Thrombocytopenia ◽  
Transplant Patients

Abstract Abstract 3320 Objective: Heparin induced thrombocytopenia (HIT), a prothrombotic complication of heparin therapy, can lead to serious thromboembolic events and cause significant morbidity and mortality. Its occurrence has never been studies in transplant patients, where use of heparin products is very common. We aim to study its prevalence in the transplant population at our institute. Methods: This is a retrospective cohort, single center study which looked into the clinical and laboratory database of all the patients that has undergone any kind of transplant at our institution over a period of 25 years (January 1985 - December 2010). In patients with clinical suspicious of HIT, a pre-test probability was calculated using the 4T scoring system. Results of the laboratory test like the ELISA HIT antibody (HIT ab) test and the functional serotonin release assay test (SRA) along with clinical manifestation of skin necrosis or thromboembolic events were reviewed. Results: Medical records of 2800 patients that has undergone transplant from January 1985- December 2010 were reviewed. HIT antibody assay was performed in 262 patients in which HIT was suspected. Of these, only 48 (18%) patients (mean age 57 ± 11 years, 71% women) had HIT ab positive, 9 were pre transplant recipient and remaining 39 were post transplant recipients. Baseline characteristics of the transplant population are illustrated in Table.1. Confirmatory test, SRA was performed in 8 HIT antibody positive patients, of whom only 4 were positive. The mean 4T score in HIT suspected patients was 3.7 ±1.3, while the score in HIT ab positive patients was 4.2 ± 1.2. Thrombotic complications were seen in 11(0.4%) patients, with the highest incidence rate of 1% in heart transplant recipients. No transplant patient had skin manifestations. Direct Thrombin inhibitor (DTI) was used only in 5 patients who had thrombotic events. No other complication or mortality was reported in any of the HIT ab positive transplant patients. Conclusion: To our knowledge, this is the first study of its kind that has shown very low incidence of HIT in transplant population. In conclusion, transplant patients can safely undergo any type of organ transplant, without having any peri or post operative complications or immediate mortality related to HIT. Disclosures: No relevant conflicts of interest to declare.

Rapid and simple IgG specific test for the exclusion of heparin induced thrombocytopenia (HIT)

2011 ◽  
Vol 49 (12) ◽  
Author(s):  
Hans-Jürgen Kolde ◽  
Ralf Dostatni ◽  
Susanne Mauracher
Keyword(s):  
Anticoagulation Therapy ◽  
Clinical Samples ◽  
Functional Assay ◽  
Specific Test ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Activation Assay ◽  
Specific Igg ◽  
Positive Results ◽  
Specific Igg Antibodies

AbstractThe exclusion of heparin induced thrombocytopenia (HIT) is required for selecting the most appropriate anticoagulation therapy in affected patients. It requires the combination of clinical data with the detection of antibodies directed against platelet factor 4 (PF4) in complex with polyanions (PA) such as heparin.We developed a lateral flow immunoassay (LFIA) for PF4/PA complex specific IgG antibodies based on gold nanoparticles. Unlike most other assays, the initial immune reaction takes place in the liquid phase. The sensitivity of the assay has been adjusted with clinical samples aiming in the reliable detection of sera which are positive in a functional platelet activation assay.Sera from 60 patients with suspected HIT were investigated. LFIA identified correctly all samples (n=20) which were positive in a functional assay (HIPA) and an IgG specific ELISA. It correlated with ELISA, but false positive results were less frequent (7 samples were negative with LFIA and HIPA but positive with ELISA).The LFIA may be a suitable tool for the rapid exclusion of HIT within 10 min.

Sign in / Sign up

Export Citation Format

Share Document