Anti‐platelet factor 4/heparin antibodies in patients with impaired graft function after liver transplantation. (June 2014)

• Record Type: Journal Article
• Authors: Bakchoul, T.; Assfalg, V.; Zöllner, H.; Evert, M.; Novotny, A.; Matevossian, E.; Friess, H.; Hartmann, D.; Hron, G.; Althaus, K.; Greinacher, A.; Hüser, N.
• Is Part Of: Journal of thrombosis and haemostasis. Volume 12:Number 6(2014:Jun.)
• Page Start: 871
• Page End: 878
• Publication Date: 2014-06
• Subjects: Thrombosis -- Periodicals; Hemostasis -- Periodicals; Blood coagulation disorders -- Periodicals; 616.1
• DOI: 10.1111/jth.12569
• Languages: English
• ISSNs: 1538-7933

Abstract

<abstract abstract-type="main" id="jth12569-abs-0001"> <title>Summary</title> <sec id="jth12569-sec-0001" sec-type="section"> <title>Background</title> <p>Heparin, the standard perioperative anticoagulant for the prevention of graft vessel thrombosis in patients undergoing liver transplantation (LT), binds to the chemokine platelet factor 4 (PF4). Antibodies that are formed against the resulting PF4/heparin complexes can induce heparin‐induced thrombocytopenia. LT is a clinical situation that allows the study of T‐cell dependency of immune responses because T‐cell function is largely suppressed pharmacologically in these patients to prevent graft rejection.</p> </sec> <sec id="jth12569-sec-0002" sec-type="section"> <title>Objectives</title> <p>To investigate the immune response against PF4/heparin complexes in patients undergoing LT.</p> </sec> <sec id="jth12569-sec-0003" sec-type="section"> <title>Patients and Methods</title> <p>In this prospective cohort study, 38 consecutive patients undergoing LT were systematically screened for anti‐PF4/heparin antibodies (enzyme immunoassay and heparin‐induced platelet aggregation assay), platelet count, liver function, and engraftment.</p> </sec> <sec id="jth12569-sec-0004" sec-type="section"> <title>Results</title> <p>At baseline, 5 (13%) of 38 patients tested positive for anti‐PF4/heparin IgG (non‐platelet‐activating) antibodies. By day 20, an additional 5 (15%) of 33 patients seroconverted for immunoglobulin G (two platelet‐activating) antibodies. No patient developed clinical heparin‐induced thrombocytopenia. Two of six patients with graft function failure had anti‐PF4/heparin IgG antibodies at the time of graft function failure. Graft liver biopsy samples from these patients showed thrombotic occlusions of the microcirculation.</p> </sec> <sec id="jth12569-sec-0005" sec-type="section"> <title>Conclusions</title> <p>Anti‐PF4/heparin IgG antibodies are generated despite strong pharmacologic suppression of T cells, indicating that T cells likely have a limited role in the immune response to PF4/heparin complexes in humans.</p> </sec> </abstract>