Patient with recurrent HIT after UFH reexposure for elective heart surgery. Patient 17 in Table 1. (A) First episode of HIT (1998) complicated by symptomatic deep vein thrombosis (DVT) and pulmonary embolism (PE). (B) Second episode of HIT after intraoperative UFH rechallenge (2009). The patient developed HIT on POD7, with associated asymptomatic DVT shown by venous ultrasound (US). (C) Timing of SRA and EIA seroconversion after UFH reexposure. Both the EIA-IgG and SRA became positive on POD6. IgM seroconversion occurred on POD7. Serotonin release at buffer control (ie, at 0 U/mL UFH) was very strong (>90% from POD10 to POD13), which explains why the patient developed HIT despite not receiving postoperative heparin. (D) Assessment of UFH- and fondaparinux-dependent platelet activation in the presence of patient serum at various dilutions. Strong serum-induced platelet activation (>80% serotonin release) was observed at 0 U/mL UFH (ie, buffer control), using neat and 1/8 diluted serum; strong heparin-dependent platelet activation was shown by the increase in serotonin release at 0.3 U/mL UFH compared with buffer control at higher dilutions of serum (1/16, 1/32, 1/64, 1/128). The absence of fondaparinux-dependent platelet activation argues against fondaparinux cross-reactivity as an explanation for the patient’s persisting thrombocytopenia. Fonda, fondaparinux. Reprinted from Warkentin et al¹⁸  with permission.