UFH reexposure for cardiac surgery in a patient with history of HIT who is now SRA negative but EIA-IgG positive. Patient 22 in Table 1. (A) Clinical summary. The patient had HIT in May 2015. UFH reexposure to permit mitral valve repair was performed in November 2015. The patient received postoperative anticoagulation with danaparoid sodium. The postoperative course was unremarkable except for atrial fibrillation (POD14), which was treated with subcutaneous danaparoid followed by oral apixaban (continued at discharge). (B) Serological summary (including seroconversion after reexposure). The patient tested strongly positive for HIT antibodies at HIT diagnosis, including EIA-IgG/IgA/IgM >4.00 OD units (PF4 Enhanced, Immucor GTI Diagnostics, Waukesha, WI), EIA-IgG (McMaster Platelet Immunology Laboratory) 2.67 OD units (90% inhibition by high heparin), and a positive SRA (peak serotonin release, 92% at 0.1 U/mL UFH, with 34% serotonin release at buffer control). At 24-week follow-up (day −29), the SRA tested negative (<10% serotonin release), but the EIA-IgG remained positive at 0.85 OD units (68% inhibition by high heparin). After reexposure to UFH, the patient developed repeat strongly positive seroconversion by SRA and EIA-IgG and weakly positive seroconversion by EIA-IgA. The buffer control reactivity in the SRA remained negative throughout the postoperative period. Later testing for danaparoid cross-reactivity (POD12 blood sample) showed a peak of 79% serotonin release in the presence of danaparoid (panel C). (C) Positive testing for danaparoid cross-reactivity. POD12 serum was later tested for danaparoid cross-reactivity; patient serum-induced serotonin-release at buffer control (ie, at 0 U/mL UFH) was weakly positive (21% release), which increased to a peak of 79% serotonin release at 0.3 anti-factor Xa U/mL (final) danaparoid, thus confirming in vitro cross-reactivity.