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Presence of autoantibodies to interleukin-8 or neutrophil-activating
peptide-2 in patients with heparin-associated thrombocytopenia
J Amiral, A Marfaing-Koka, M Wolf, MC Alessi, B Tardy, C Boyer-Neumann, AM Vissac, E Fressinaud, M Poncz and D Meyer
Serbio Research Laboratory, Gennevilliers, France.
Eighty-seven patients with heparin-associated thrombocytopenia (HAT) showed
either a positive heparin platelet aggregometry test result and/or the
presence of antibodies to heparin-platelet factor 4 (H-PF4) complexes by
enzyme-linked immunosorbent assay (ELISA). Fifteen of these patients lacked
antibodies to H-PF4, and plasma from these patients was analyzed for the
presence of antibodies to PF4-related chemokines, Neutrophil-activating
peptide-2 (NAP-2) and interleukin-8 (IL-8). Of these 15 patients, 6 showed
antibodies to IL-8 and 3 to the platelet basic protein (PBP)-derived
protein, NAP-2. Antibodies to IL-8 and NAP-2 were not observed in control
patients (n = 38), patients with HAT and H-PF4 autoantibodies (n = 72),
patients with autoimmune diseases (n = 21), or patients with non-HAT
thrombocytopenia (n = 30). Five of these nine patients with anti-IL-8 or
anti-NAP-2 developed thrombosis during heparin treatment, which is not
statistically different from the patients with H-PF4 antibodies. The
existence of autoantibodies to IL-8 and NAP-2 in HAT patients highlights
the significance of chemokines in the pathogenesis of HAT. The contribution
of heparin in vitro was minimal in patients with anti-IL-8 and anti-NAP- 2
antibodies, suggesting a biologic difference from the majority of patients
with HAT and anti-PF4 antibodies. It may be that antibodies to IL-8 and
NAP-2 have weaker affinity for heparin and that the ELISA system may not
reflect in vivo heparin-chemokine complex formation. Alternatively,
antichemokine autoantibodies may predate heparin exposure, and the role of
heparin in initiating HAT may be to mobilize the chemokines and to target
them to platelets, neutrophils, or endothelial cells. Subsequent
chemokine-binding autoantibodies then lead to cell activation resulting in
thrombocytopenia and thrombosis.
Volume 88,
Issue 2,
pp. 410-416,
07/15/1996
Copyright © 1996 by The American Society of Hematology
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