Heparin-induced Platelet Antibody (HIPA)

Serum, frozen

1 mL

0.5 mL

Red-top tube or gel-barrier tube

Assist in the diagnosis of heparin-induced thrombocytopenia

HIPA results should not be the sole basis for establishing the diagnosis of heparin-induced thrombocytopenia. Some patients with HIPA will not develop symptoms of heparin-induced thrombocytopenia (HIT). Microbial contamination, lipemia, icterus, or hemolysis may interfere with this test and immune complexes or immunoglobulin aggregates in the patient sample can produce false-positive results. Heparin in the sample (>1 unit/mL) can produce false-negative results.

HIPA is measured by enzyme immunoassay (EIA) using platelet factor 4 complexed polyvinyl sulfonate (PVS) that is coated to the wells of a microtiter plate. The PVS acts like heparin, exposing antigenic sites for HIPA binding.

0.0−0.4 OD units

HIT, also referred to as heparin-associated thrombocytopenia (HAT), occurs in 1% to 5% of patients treated with standard unfractionated heparin.^1-3 The most common form of HIT presents as a mild thrombocytopenia one to five days after initiation of heparin therapy. Type I HIT is not thought to be immune in etiology and may be mediated by a direct interaction between heparin and circulating platelets, causing platelet clumping or sequestration. This type of heparin-associated thrombocytopenia often occurs in patients on their first exposure to heparin.¹ In this condition, platelet counts typically normalize within a few days, regardless of whether or not heparin therapy is continued.

Type II HIT is a much more clinically-significant, immune-mediated response to heparin that is frequently associated with the production of HIPA. Type II HIT can be associated with severe thrombosis, with the platelet count decreasing typically by 50%. The thrombocytopenia typically begins later than that of type I HIT, usually occurring some 5 to 10 days after the initiation of heparin therapy in patients who had never been previously exposed to heparin. Patients with prior exposure to heparin can develop thrombocytopenia more quickly on re-exposure due to earlier sensitization. In type II HIT, heparin is thought to bind to platelet factor 4, be found on platelets and endothelial cells, and to produce a conformational change, exposing antigenic sites for antibody formation.² These antibodies bind to the heparin-PF4 complex and can activate platelets, resulting in the formation of microparticles and thrombin generation, with subsequent production of potentially severe venous or arterial thrombosis. Heparin treatment should be stopped and alternative anticoagulation considered in patients who develop type II HIT.^1,2

Like other serologic (EIA based) assays, this assay has a high negative predictive value and only a moderate positive predictive value for HIT.⁴ Recent studies have shown that the magnitude (optical density, OD) of the result relative to the cutoff of 0.4 OD can provide useful information regarding the probability of developing HIT.^4-8 The likelihood of developing HIT is significantly higher when the OD is >2.0 than when the OD is closer to the cutoff.^4-8 One recent study revealed that patients with negative results just below the cutoff of 0.4 OD have a high probability of having positive results on repeat testing a few days later.⁹