ArticleJournal of thrombosis and haemostasis : JTH2025
Complement activation as a biomarker for platelet-activating antibodies in heparin-induced thrombocytopenia.
Article in Journal of thrombosis and haemostasis : JTH, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Platelets in infection: intrinsic roles and functional outcomes.Frontiers in immunology · 2025Review
- Advances in our understanding of anti-PF4 related immunothrombosis.Frontiers in immunology · 2025Review
- Article
- BUN and mortality in patients with heparin-induced thrombocytopenia: A retrospective cohort study.Science progressArticle
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Authors and funding
10 authors.
Funding
Abstract
backgroundImmunoglobulin G antibodies (Abs) to platelet factor 4 (PF4) complexed to heparin (PF4/H) commonly occur after H exposure but cause life-threatening complications of H-induced thrombocytopenia (HIT) in only a few patients. Presently, only platelet activation assays reliably distinguish anti-PF4/H Abs that cause disease (HIT Abs) from those likely to be asymptomatic (AAbs).
objectivesRecent studies indicate that complement activation is an important serologic property of HIT Abs and is essential for IgG Fc receptor IIA-mediated cellular activation. As platelet activation by HIT Abs also relies on IgG Fc receptor IIA activation, we correlated the complement- and platelet-activating properties of anti-PF4/H Abs in a clinically annotated patient cohort.
methodsClinical and laboratory features of patients with HIT (n = 8) and AAbs+ (n = 14) were correlated with properties of complement, platelet, and monocyte/neutrophil activation.
resultsExpected clinical and laboratory differences were seen between HIT and AAb+ patients, with HIT patients having lower mean platelet counts, greater percentage drop in platelet counts, higher 4T and HIT expert probability scores, higher anti-PF4 polyclonal and immunoglobulin G Ab levels, and serotonin release assay positivity. Ex vivo assays revealed significant differences in complement activation by HIT vs AAb+ patients, with the extent of complement activation closely correlated with percent serotonin release by anti-PF4/H Abs and matrix metalloproteinase-9 and interleukin-8 release in whole blood.
conclusionThese findings suggest that complement activation strongly correlates with cellular activation endpoints, including platelet and monocyte/neutrophil activation, and if confirmed in a larger prospective study, may serve as a "functional" biomarker for pathogenic HIT Abs.
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