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Coagulation Theory, Principles, and Concepts
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
The primary coagulation activities of platelets are what have been referred to as platelet factor 3 and platelet factor 4 activities. Platelet factor 3 refers to the “lipid” surface that is required for the assembly of coagulation factors. Platelet factor 4 is a platelet component that is released when platelets are activated. It neutralizes the anticoagulant activity of heparin or heparans. For several years there has also been the suggestion that platelets providing a binding site for factor XI, but this remains a debatable issue (110–113).
Miscellaneous: Dextran, Dermatan Sulfate, Low Molecular Weight Heparinoids (Org 10172), Pentosan Polysulfate (Sp54), Defibrinating Agents (Ancrod And Reptilase)
Published in Hau C. Kwaan, Meyer M. Samama, Clinical Thrombosis, 2019
M. M. Samama, P. C. Desnoyers, H. C. Kwaan
Heparin, heparan sulfate, and dermatan sulfate (DS) are the only glycosaminoglycans which possess the iduronate residue.15 DS has anticoagulant activity similar to other compounds already discussed, but this specific activity is low. DS has a molecular weight of about 25 kDa. In vitro, on a gravimetric basis, 70 times more DS is needed than heparin to give similar anticoagulant activity as tested by the activated partial thromboplastin time. When Factor Xa is added to normal plasma, thrombin generation is inhibited by DS, by the same conditions as its amidolytic activity. Factor IIa (thrombin), but not Factor Xa, is also inhibited.16,17 The antithrombin activity of DS is dependent on the presence of heparin cofactor II, but not antithrombin III. Heparin cofactor II forms a stable equimolar complex with thrombin. The speed of the formation of this complex is 1000 times greater when DS is present. Platelet factor 4 can inhibit the function of DS activity. In contrast, histidinerich glycoprotein can inhibit antithrombin activity of heparin in the presence of DS.18,21
Platelet Disorders Douglas Triplett
Published in Genesio Murano, Rodger L. Bick, Basic Concepts of Hemostasis and Thrombosis, 2019
Caen and Legrand have described a disorder in which there is an apparent abnormality of collagen, rather than the platelet.84 They found that in their group of patients, the platelet counts were essentially normal, as were platelet factor 3, platelet factor 4, and platelet acid phosphotase content. However, the bleeding times were strikingly prolonged. Platelet aggregation studies performed with adenosine diphosphate (ADP) and collagen were essentially normal, as were platelet retention studies. Electron microscopy of collagen taken from the connective tissue of these patients was abnormal. Acid-extractable skin collagen taken from skin biopsies in these cases was unable to induce aggregation in platelet-rich plasma from normal controls. Clinically, these patients suffered from easy bruising, spontaneous hemorrhages, and abnormal wound healing.
Aortic thrombosis and acute limb ischemia after ChAdOx1 nCov-19 (Oxford-AstraZeneca) vaccination: a case of vaccine-induced thrombocytopenia and thrombosis (VITT)
Published in Acta Chirurgica Belgica, 2023
Maaike Vierstraete, Toon Sabbe
An ELISA (enzyme-linked immunosorbent assay) assay (Hyphen Biomed) was performed and detected anti-PF4 antibodies (platelet factor 4) in the patient’s serum (Optical Density (OD) of 3.66). An additional functional platelet activation assay (serotonin release assay (SRA)) was positive, strongly suggesting the diagnosis of VITT. Noteworthy, the blood sample for analysis was taken before the administration of heparin per operatively. The patient stayed in the intensive care unit for 2 days. Because of a tickling cough, a pulmonary CT angiography was performed on postoperative day 2. Pulmonary embolism was excluded. The platelet count rose steadily, and on postoperative day 5 his platelet count was 60 × 103/µL which allowed us to increase his therapeutic anticoagulation to Fondaparinux (7.5 mg/d) based on his body weight (Figure 2). No transfusions of red blood cells or platelets were administered, no plasma exchange was performed.
SARS-CoV-2 Infection Dysregulates Host Iron (Fe)-Redox Homeostasis (Fe-R-H): Role of Fe-Redox Regulators, Ferroptosis Inhibitors, Anticoagulants, and Iron-Chelators in COVID-19 Control
Published in Journal of Dietary Supplements, 2023
Sreus A.G. Naidu, Roger A. Clemens, A. Satyanarayan Naidu
Heparin as a therapeutic anticoagulant is linked to a 10 − 15% risk of significant bleeding (305). Factors that may increase bleeding risk include old age, recent trauma or surgery, cardiopulmonary resuscitation, longer hospital stay, and decreased white blood cell/platelet counts (306). These risk factors are common among patients with COVID-19. Heparin-induced thrombocytopenia (HIT), a rare complication of heparin therapy, is estimated to occur in 0.2–3% of patients (307). The adverse HIT reaction results from the development of antibodies against platelet factor 4, which triggers thrombocytopenia. Repurposing of heparin and its derivatives as first-line therapeutics against SARS-CoV-2 is promising; however, this clinical approach needs an in-depth evaluation (308).
Immunopathology of COVID-19 and its implications in the development of rhino-orbital-cerebral mucormycosis: a major review
Published in Orbit, 2022
Tarjani Vivek Dave, Akshay Gopinathan Nair, Joveeta Joseph, Suzanne K Freitag
Platelets are one of the key cells in the innate immune response. While their primary role is in hemostasis, another important role is in the immune response against pathogens, by inhibiting their dissemination through the circulation, which could increase the severity of infection.46 Platelets help in fighting microbes by producing antimicrobial peptides such as platelet factor 4.47 Typical hematologic features of COVID-19 include thrombocytopenia, lymphopenia, and neutrophilia.48 NK cells modulate the immune response that is mounted when a pathogen is encountered. There is a reduction in the number of NK cells and blunting of the effector functions of NK cells in COVID-19.46 This results in a decrease in the clearance of infected and activated cells and also results in an unabated elevation of toxic inflammatory markers.46 Previous literature has clearly shown that SARS-CoV can cause infection of the dendritic cells (DC). This can lead to an upregulation of inflammatory chemokines following a very poor antiviral cytokine expression.49,50 Dendritic cells play a prime role in specific T-cell responses, cytokine production, and antigen presentation.49 In patients with COVID-19, a loss of DC function could lead to delayed response of the immune system.