Heparin-induced thrombocytopenia in solid organ transplant recipients: The current scientific knowledge

Abstract

Exposure to heparin is associated with a high incidence of immunization against platelet factor 4 (PF4)/heparin complexes. A subgroup of immunized patients is at risk of developing heparin-induced thrombocytopenia (HIT), an immune mediated prothrombotic adverse drug effect. Transplant recipients are frequently exposed to heparin either due to the underlying end-stage disease, which leads to listing and transplantation or during the transplant procedure and the perioperative period. To review the current scientific knowledge on anti-heparin/PF4 antibodies and HIT in transplant recipients a systematic PubMed literature search on articles in English language was performed. The definition of HIT is inconsistent amongst the publications. Overall, six studies and 15 case reports have been published on HIT before or after heart, liver, kidney, and lung transplantation, respectively. The frequency of seroconversion for anti-PF4/heparin antibodies ranged between 1.9% and 57.9%. However, different methods to detect anti-PF4/heparin antibodies were applied. In none of the studies HIT-associated thromboembolic events or fatalities were observed. More importantly, in patients with a history of HIT, reexposure to heparin during transplantation was not associated with thrombotic complications. Taken together, the overall incidence of HIT after solid organ transplantation seems to be very low. However, according to the current knowledge, cardiac transplant recipients may have the highest risk to develop HIT. Different alternative suggestions for heparin-free anticoagulation have been reported for recipients with suspected HIT albeit no official recommendations on management have been published for this special collective so far.

Keywords: Heparin; Heparin-induced thrombocytopenia; Organ; Transplantation.

Figure 1

The frequency of antibody seroconversion, activating heparin-induced thrombocytopenia antibodies (serotonin release assay/heparin induced platelet activation assay), thrombocytopenia, and clinically manifest heparin-induced thrombocytopenia thrombotic syndrome are illustrated as an “iceberg”[4,9,10]. The waterline indicates the threshold between positive laboratory findings and clinical appearance of HIT. HIT: Heparin-induced thrombocytopenia.

Figure 2

Modified iceberg model of the assumed frequency of antibody seroconversion, activating heparin-induced thrombocytopenia antibodies (serotonin release assay/heparin induced platelet activation assay), thrombocytopenia, and clinically manifest heparin-induced thrombocytopenia thrombotic syndrome according to the current knowledge on heparin-induced thrombocytopenia in solid organ transplant recipients. HIT: Heparin-induced thrombocytopenia.