platelet factor 4
platelet factor 4
Serum Biomarkers of Allergic Contact Dermatitis: A Pilot Study.
Vilnius, Lithuania. In Int Arch Allergy Immunol, Feb 2016
RESULTS: Serum levels of adiponectin, chemokine (C-C motif) ligand 5 (CCL5), C-reactive protein (CRP), chitinase 3-like 1 (CHI3L1), complement factor D (CFD), endoglin, lipocalin-2, osteopontin, retinol-binding protein 4 (RBP4), and platelet factor 4 (PF4) were significantly higher, whereas levels of trefoil factor 3 (TFF3) were significantly lower, in ACD patients than in healthy controls.
Hamilton, Canada. In Curr Opin Crit Care, Dec 2015
Most patients who form anti-PF4/heparin antibodies do not develop HIT, contributing to HIT overdiagnosis.
The platelet Fc receptor, FcγRIIa.
Melbourne, Australia. In Immunol Rev, Nov 2015
Finally, we present some new data investigating whether levels of the extracellular ligand-binding region of platelet glycoprotein VI which is rapidly shed upon engagement of platelet FcγRIIa by autoantibodies, can report on the presence of pathological anti-heparin/platelet factor 4 immune complexes and thus identify patients with pathological autoantibodies who are at the greatest risk of developing life-threatening thrombosis in the setting of heparin-induced thrombocytopenia.
Pancreatic cancer and thromboembolic disease, 150 years after Trousseau.
Lund, Sweden. In Hepatobiliary Surg Nutr, Oct 2015
The exact pathophysiological mechanisms are still partly understood, but it is known that pancreatic cancer induces a prothrombotic and hypercoagulable state and genetic events involved in neoplastic transformation (e.g., KRAS, c-MET, p53), procoagulant factors [e.g., tissue factor (TF), platelet factor 4 (PF4), plasminogen activator inhibitor type 1 (PAI-1)], mucin production (e.g., through activation of P- and L-selectin) and pro-inflammatory factors [e.g., cytokines, cyclooxygenase-2 (COX-2)] may be implicated.
Dynamic antibody-binding properties in the pathogenesis of HIT.
Philadelphia, United States. In Blood, 2012
Differences in the properties of anti-PF4 antibodies that cause thrombocytopenia not revealed by ELISA that correlate with oligomerization of PF4 and sustained high-avidity interactions that may simulate transient antibody-antigen interactions in vivo.
Temporal aspects of heparin-induced thrombocytopenia.
Hamilton, Canada. In N Engl J Med, 2001
We also investigated the persistence of circulating heparin-dependent antibodies by performing a platelet serotonin-release assay and an assay for antibodies against platelet factor 4. The outcome in seven patients who had previously had an episode of heparin-induced thrombocytopenia and were later treated again with heparin was also examined.