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Optimising the management of HIT

Instrumentation Laboratory
8 August, 2012  
HIT is a severe, adverse reaction to heparin, paradoxically resulting in venous and/or arterial thrombosis.  It is one of the most common of all adverse drug effects, due to the sheer volume of patients receiving heparin therapy.(1) Approximately 0.2–2% of patients treated with heparin (over 12 million patients/year in the US, alone) develop HIT.  If HIT is untreated, risk for serious sequelae, including pulmonary embolism, stroke, or death, increases significantly.(2) Positive outcomes depend on early and accurate diagnosis and prompt initiation of alternative anticoagulants.(3)
When should HIT be suspected?
Diagnosis of HIT is based on clinical and laboratory criteria.  The clinical likelihood of HIT can be evaluated using the ‘4Ts’ scoring system.4 Typical features of HIT include a platelet count fall of  >50% versus baseline (typically within 5–14 days after heparin administration), venous and/or arterial thromboses, skin necrosis, and anaphylactic reactions.  The ‘4Ts’ scoring system assigns a low, intermediate or high probability, based on the presentation of the following: thrombocytopenia; timing of platelet count fall; thrombosis or other sequelae; and the possibility of other causes for thrombocytopenia.  Assessing for HIT at first clinical suspicion is critical to prompt diagnosis and optimising patient outcomes.
Why test for HIT?
Clinical symptoms of HIT are also common to other conditions, making diagnosis based on clinical criteria alone insufficient. Traditional laboratory testing methods require specialised technicians and lengthy wait-times.  This combination can result in the assumption of HIT without consultation of laboratory results, leading to unnecessary therapeutic changes. Administration of alternative anticoagulants potentially can increase bleeding risk, drug cost, and length of hospital stay,(5) and make the transition to warfarin challenging.  Excluding HIT can prevent unnecessary and labour-intensive changes in anticoagulant therapy, in the majority of HIT-suspected cases. Immunologic assays that detect antibodies commonly associated with HIT (platelet-factor 4 heparin (PF4-H) antibodies)(6) with precision and accuracy have the ability to accomplish this efficiently.
Fully automated HIT antibody detection
Rapid, on-demand detection of HIT antibodies optimises therapeutic decisions.  Instrumentation Laboratory (IL) is at the forefront of HIT testing solutions, offering the only suite of assays that are fully automated on haemostasis analysers. HemosIL® HIT-Ab(PF4-H) is available on the ACL TOP® Family of Hemostasis Testing Systems; while HemosIL AcuStar HIT-Ab(PF4-H) and HemosIL AcuStar HIT-IgG(PF4-H) for the ACL AcuStar® Hemostasis Testing System provide additional isotype-specific formats using highly sensitive, chemiluminescent technology.  
Unlike existing manual processes, HemosIL assays are ready-to-use, produce results in minutes — on-demand, 24/7 — allowing clinicians to make timely, well-informed therapeutic decisions. Designed exclusively for automated haemostasis testing systems, HemosIL HIT assays ensure ultimate simplicity and efficiency throughout the testing process — without compromising precision and accuracy. They feature excellent agreement with commercially available ELISA methods(7,8) and offer semi-quantitative results, reducing the potential for technician errors associated with qualitative methods. Additionally, these assays are standardised and validated with cut-off values,(7,8) facilitating results interpretation.  
HemosIL assays for the detection of HIT antibodies present a significant opportunity for automation and standardisation in HIT diagnosis.
Did you know? 
  • HIT should be evaluated in conjunction with a clinical assessment.  
  • Some studies indicate that the HIT antibody titre correlates with HIT likelihood.(9) 
  • Instrumentation Laboratory offers the only HIT antibody assays fully automated on haemostasis systems.
References
  1. Greinacher A et al. Heparin-induced thrombocytopenia. Hämostaseologie 2010;1(Review):17–28. 
  2. Warkentin TE et al. American College of Chest Physicians. Treatment and prevention of heparin-induced thrombocytopenia:  American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 2008 Jun;133(6 Suppl): 340S–380S.
  3. Warkentin TE. Heparin-induced thrombocytopenia. Hematol Oncol Clin North Am 2007;21:589–607.
  4. Lo GK et al. Evaluation of pretest clinical score (4T’s) for the diagnosis of heparin-induced thrombocytopenia in two clinical settings. J Thromb Haemost 2006; 4:759–65.
  5. Smyth MA et al. The financial impact of heparin-induced thrombocytopenia. Chest 2008;134:568–73.
  6. Warkentin TE et al. Sera from patients with heparin-induced thrombocytopenia. Blood 1994; 84: 3691–99.
  7. Davidson SJ, Ortel TL, Smith LJ. Performance of a new, rapid, automated immunoassay for the detection of anti-platelet factor 4/heparin complex antibodies. Blood Coag Fibrinolysis 2011;22(4):340–44.
  8. Legnani C et al. Evaluation of new automated panel of assays for the detection of anti-PF4/heparin antibodies in patients suspected of having heparin-induced thrombocytopenia. Thromb Haemostasis 2010;104.2:402–408.
  9. Warkentin TE et al. Quantitative interpretation of optical density measurements using PF4-dependent enzyme-immunoassays. J Thromb Haemost 2008;6:1304–12.