Journal of Blood Disorders & Transfusion

Autoimmune heparin-induced thrombocytopenia: A case report

5^th World Hematologists Congress

August 18-19, 2016 London, UK

Janine Collins, Greinacher A and MacCallum P

Barts Health NHS Trust, UK
Universitätsmedizin Greifswald, Germany
Queen Mary University of London, UK

Posters & Accepted Abstracts: J Blood Disord Transfus

Abstract:

Thrombocytopenia affects 30-50% critically ill patients. Heparin-induced thrombocytopenia (HIT) is rare (incidence 0.3-0.5%), but crucial to distinguish to treat the paradoxical prothrombotic state. Autoimmune HIT may follow an atypical clinical course. An 86 year old female sustained a tibia/fibula fracture. Enoxaparin 40 mg/day was commenced following intramedullary nailing. On D4 she developed pneumonia, requiring intravenous antibiotics and renal replacement therapy with intravenous unfractionated heparin (UFH) 20000 units per day. The platelet count fell to 25�?109/l (D15) and platelet transfusion was required for vascath insertion. The clinical probability of HIT was intermediate ("4 Ts score" 5/8) and heparin stopped. Rapid particle gel immunoassay (PF4/H-PaGIA) and ELISA (result 1.7 OD; 80% correction with high-dose heparin) were positive for HIT and danaparoid commenced. Subsequently, the "4 Ts" was revised to 3/8 when platelet count nadired (17�?109/l) and vancomycin-induced thrombocytopenia considered. There were no bleeding or thrombotic complications. Thrombocytopenia persisted despite cessation of heparin and vancomycin. On D24 intravenous immunoglobulin (IVIG) was administered with rapid recovery of platelet count. Later, the heparin-induced platelet aggregation (HIPA) functional assay confirmed HIT. The patient serum activated donor platelets with low dose heparin; but also activated platelets in the absence of heparin, indicating autoimmune HIT. In HIT, heparin/PF4/IgG complexes recognize platelet Fc receptors and activate platelets. In autoimmune HIT, PF4/poly anion complexes bind PF4/chondroitin sulfate complexes on platelets with high affinity, clustering PF4 molecules and activating platelets by a heparin-independent mechanism. Therefore, the timing of thrombocytopenia in relation to heparin may be atypical. Other rare cases have responded rapidly to IVIG.

Biography :

Email: janine@cantab.net