Scientific Calendar June 2026

Heparin-induced thrombocytopenia

Heparin is a naturally occurring glycosaminoglycan isolated from animal tissues (for example, cattle) which serves as an effective and inexpensive anticoagulant in clinical practice. Heparins are also used to prevent clotting in external devices exposed to blood, such as ECMO circuits for extracorporeal life support, haemodialysis and haemofiltration.

Heparin-induced thrombocytopenia (HIT) is a severe complication that can occur in patients exposed to heparins, including unfractionated heparin (UFH) and low-molecular-weight heparin (LMWH). Patients with HIT may develop thromboembolic complications associated with significant morbidity and mortality.

Unlike the benign HIT type I, HIT type II is a life-threatening, immune-mediated reaction in which transient heparin-dependent autoantibodies activate platelets and cause thrombocytopenia. (1)

Current guidelines (2,3) recommend that, as a first step in patients suspected of HIT type II, a pre-test probability assessment using the 4Ts score should be performed; the score is available online. Based on guideline recommendations and expert opinion, no further testing is indicated if a low probability has been assessed (score ≤ 3). (1–3) A 4Ts score of 4–8 not only prompts testing for HIT-specific IgG antibodies but also requires immediate cessation of heparin therapy and substitution with an alternative anticoagulant appropriate for the patient’s original indication for anticoagulation.

Laboratory diagnosis requires detection of heparin–PF4-specific antibodies using modern chemiluminescence immunoassays, such as the automated Sysmex HISCL™ HIT IgG Assay Kit on the CN-3500 and CN-6500 analysers. These assays employ a heparin–PF4 complex to capture HIT IgG antibodies, followed by enzyme-conjugated secondary antibodies to detect the captured antibodies. However, detection of HIT IgG antibodies does not confirm clinical HIT type II. For a definitive diagnosis, functional assays that detect antibodies capable of binding and cross-linking the platelet Fc gamma RIIA receptor and triggering platelet activation – such as the heparin‐induced platelet activation (HIPA) assay or the serotonin‐release assay (SRA) – are crucial. (2–4)