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| http://dx.doi.org/10.3324/haematol.2021.280366 | DOI Listing |
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Complement activation as a biomarker for platelet activating antibodies in heparin-induced thrombocytopenia (HIT).
J Thromb Haemost
December 2024
Division of Hematology, Duke University Medical Center, Durham, NC. Electronic address:
Background: IgG antibodies (Abs) to platelet factor 4 complexed to heparin (PF4/H) commonly occur after heparin exposure but cause life-threatening complications of heparin-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).
Objectives: Recent studies indicate that complement activation is an important serologic property of HIT Abs and is essential for FcγRIIA-mediated cellular activation.
Combination of 2 Quantitative Immunoassays and Clinical Score Algorithm to Reduce False-Negative Results in Heparin-Induced Thrombocytopenia: Prevalence Study of Mauriziano Hospital in Turin, Italy.
J Appl Lab Med
September 2024
SC Laboratorio Analisi, Azienda Ospedaliera Ordine Mauriziano, Turin, Italy.
Article Synopsis
- Heparin-induced thrombocytopenia (HIT) is a serious condition caused by antibodies that activate platelets and accurate diagnosis is crucial but difficult; this study aimed to assess a new diagnostic laboratory algorithm for suspected HIT using specific immunoassays.
- The study analyzed 163 patients, utilizing a two-step approach with Chemiluminescence (CliA) followed by ELISA testing to rule out or confirm HIT; the algorithm successfully excluded HIT in 88% of cases and made predictions about platelet aggregation in a subset of patients.
- The findings showed a HIT prevalence of 3.1%, consistent with existing literature, and indicated that the combined approach could quickly rule out HIT in a majority of patients, although individual
Challenges in the Monitoring of Therapeutic Plasma Exchange during Acute Heparin-Induced Thrombocytopenia in Adults under ECMO.
TH Open
January 2024
Université de Paris, INSERM U1148, LVTS, F-75018, Paris, France.
Therapeutic plasma exchange (TPE) has been proposed to remove heparin-induced thrombocytopenia (HIT) antibodies before planned thoracic surgery in patients with acute HIT and to allow brief re-exposure to heparin during surgery. In patients on extracorporeal membrane oxygenation (ECMO), simultaneous administration of TPE and alternative nonheparin anticoagulant therapies is challenging. We report 2 patients on ECMO with acute HIT who underwent repeated TPE to enable cardiothoracic surgery with the use of heparin.
View Article and Find Full Text PDFMolecular architecture and platelet-activating properties of small immune complexes assembled on heparin and platelet factor 4.
Commun Biol
March 2024
Department of Chemistry, University of Massachusetts-Amherst, Amherst, MA, USA.
Heparin-induced thrombocytopenia (HIT) is an adverse reaction to heparin leading to a reduction in circulating platelets with an increased risk of thrombosis. It is precipitated by polymerized immune complexes consisting of pathogenic antibodies that recognize a small chemokine platelet factor 4 (PF4) bound to heparin. Characterization of these immune complexes is extremely challenging due to the enormous structural heterogeneity of such macromolecular assemblies and their constituents.
View Article and Find Full Text PDFA career in solving clinical-pathological conundrums: Heyde syndrome, anti-platelet factor 4 disorders, and microvascular limb ischemic necrosis.
Int J Lab Hematol
May 2024
Department of Pathology and Molecular Medicine, and Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
Hematology is a clinical specialty with strong roots in the laboratory; accordingly, the lab can help solve perplexing clinical problems. This review highlights clinical-pathological conundrums addressed during my 35-year hematology career at McMaster University. Heyde syndrome is the association between aortic stenosis and bleeding gastrointestinal (GI) angiodysplasia where the bleeding is usually cured by aortic valve replacement; the chance reading of a neonatal study showing reversible deficiency of high-molecular-weight (HMW) multimers of von Willebrand factor (vWF) following surgical correction of congenital heart disease provided the key insight that a subtle deficiency of HMW multimers of vWF explains Heyde syndrome.
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