scholarly journals The Differences Levels of RANTES and PF4 Based on the Storage of Platelet Concentrate

2021 ◽  
Vol 27 (3) ◽  
pp. 301
Author(s):  
Ni Made Rindra Hermawathi ◽  
Betty Agustina Tambunan ◽  
Arifoel Hajat
Keyword(s):  
Platelet Rich Plasma ◽  
Critical Role ◽  
Platelet Concentrate ◽  
Blood Component ◽  
Severe Thrombocytopenia ◽  
Allergic Reactions ◽  
Primary Therapy ◽  
Storage Duration ◽  
Pathology Laboratory ◽  
Platelet Factor

Blood component transfusion is often used as the primary therapy as it is still considered safe. Platelet Concentrate (PC) transfusion plays a critical role in preventing bleeding in patients with severe thrombocytopenia. Allergic reactions are the most frequent transfusion reactions after PC administration. Regulated on Activation Normal T-Cell Expressed and Secreted (RANTES) and Platelet Factor 4 (PF4) cytokines released by platelets during PC storage are responsible for allergic reactions after transfusion. The purpose of this study was to analyze changes in RANTES and PF4 levels during PC storage. This study was an observational analytical research with a time series design carried out at the Clinical Pathology Laboratory and Blood Bank of the Dr. Soetomo Hospital, Surabaya, from June to July 2019. RANTES and PF4 levels in 27 bags derived from Platelet Rich Plasma (PRP) on storage for day 1, day 3, and day five were measured using the ELISA sandwich method. Subject same variant test or Friedman test was used for statistical analysis. The results showed no significant differences in RANTES and PF4 levels based on the storage duration of PCs on days 1, 3, and 5, with p=0.717, and p=0.614, respectively. There was no difference in the storage of PCs from day 1 to day five, and there was no effect on allergic reactions after PC transfusion.

The Effect of Lysed Platelets on Neutralization of Heparin In Vitro with Protamine as Measured by the Activated Coagulation Time (ACT)

1991 ◽  
Vol 66 (02) ◽  
pp. 213-217 ◽  
Author(s):  
Arthur P Bode ◽  
William J Castellani ◽  
Edna D Hodges ◽  
Susan Yelverton
Keyword(s):  
Platelet Rich Plasma ◽  
Coagulation Time ◽  
Platelet Factor ◽  
Platelet Suspension ◽  
Antiheparin Activity ◽  
Unit Increase ◽  
Heparin Anticoagulation ◽  
Heparin Activity ◽  
Activated Coagulation Time

SummaryThe effect of lysed platelets on the activated coagulation time (ACT) was studied in heparinized whole blood during titration with protamine. Frozen-thawed washed platelet suspension, or a chromatography fraction thereof, or autologous frozen-thawed platelet-rich plasma was added in various dilutions to freshly drawn blood anticoagulated with 3,000 USP units/1 heparin. After a 10 min incubation, the amount of protamine needed to restore the ACT to baseline ("protamine titration dose") was determined. We found that the protamine titration dose decreased in proportion to the amount of lysed platelet material added; expressed as a percentage of the total number of platelets present, each unit increase in lysed platelets produced a 1.7% ±0.8 (SD) reduction in the protamine dose needed to normalize the ACT. A heparin activity assay showed that this effect was not due to antiheparin activity of lysed platelets such as platelet factor 4 (PF4). Our data indicate that the procoagulant activity of platelet membranes reduced the sensitivity of the ACT to heparin. These findings suggest that membranous platelet microparticles may cause an inaccurate calculation, based on the ACT, of a protamine dose to reverse heparin anticoagulation in cardiopulmonary bypass procedures.

Antiheparin Activity of Human Serum and Platelet Factor 4

1973 ◽  
Vol 30 (01) ◽  
pp. 093-105 ◽  
Author(s):  
C.H.J Sear ◽  
L Poller ◽  
F.R.C Path
Keyword(s):  
Molecular Weight ◽  
Ionic Strength ◽  
Blood Serum ◽  
Whole Blood ◽  
Platelet Rich Plasma ◽  
Gel Filtration ◽  
Normal Serum ◽  
Platelet Factor ◽  
Mean Values ◽  
Antiheparin Activity

SummaryThe antiheparin activity of normal serum has been studied by comparing the antiheparin activities of sera obtained from normal whole blood, platelet-rich plasma and platelet-’free’ plasma with a purified platelet extract during differential isoelectric precipitation and by gel filtration chromatography.The mean values for the activity of PRP-serum and PFP-serum were 106% (S.D. 11) and 10% (S.D. 3) of untreated whole blood respectively. The activity of whole blood serum, PRP serum and whole blood serum plus platelet extract precipitated under identical physical conditions, i.e. pH 7.0, I =0.008, indicating that the activities of the three samples are probably associated with PF4. PF4 precipitated from human platelet extract at pH 4.0, but this is probably due to the difference in the two biochemical environments investigated, i.e. serum and platelet extract.The gel filtration experiments revealed striking similarities between the major antiheparin activities of serum and platelet extract. At physiological pH and ionic strength both activities were associated with high molecular weight material, but at physiological pH and elevated ionic strength both activities behaved as much smaller entities of molecular weight between 25,000 and 30,000 daltons and it seems very likely that both activities are associated with the same molecule, i.e. PF4.

Effect of Congo Red on Blood Platelets and Leucocytes of Rabbits and Cats

1971 ◽  
Vol 26 (03) ◽  
pp. 488-492 ◽  
Author(s):  
Th B. Tschopp ◽  
H.-R Baumgartner ◽  
A Studer
Keyword(s):  
Fatty Acids ◽  
Congo Red ◽  
Platelet Rich Plasma ◽  
Blood Platelets ◽  
Severe Thrombocytopenia ◽  
Ultrastructural Alterations ◽  
Indirect Mechanism

SummaryIn rabbits and cats Congo red administered intravenously causes severe thrombocytopenia and ultrastructural alterations of platelets and leucocytes, similar to those produced by some fatty acids and endotoxin. Transient leucopenia is followed by leucocytosis. In contrast, incubation of Congo red in citrated blood or platelet rich plasma has no effect. Therefore, an indirect mechanism is postulated to explain the in vivo effect of Congo red.

The Effect of Collagen Mediated Platelet Release on Plasma Prekallikrein Activation

1984 ◽  
Vol 51 (01) ◽  
pp. 037-041 ◽  
Author(s):  
K M Weerasinghe ◽  
M F Scully ◽  
V V Kakkar
Keyword(s):  
Platelet Aggregation ◽  
Healthy Volunteers ◽  
Platelet Rich Plasma ◽  
Age Groups ◽  
Inhibitory Effect ◽  
Age Group ◽  
Platelet Factor ◽  
Activated Platelets ◽  
Platelet Release ◽  
Collagen Treatment

SummaryCollagen mediated platelet aggregation caused -5.6 ± 6.7% inhibition and +39.1 ± 15.2% potentiation of prekallikrein activation in plasma from normal healthy volunteers between 20–40 and 50–65 years of age, respectively (n = 15, p <0.01). The amouns of platelet factor-four (PF4) released in the two groups were not significantly different. Collagen treatment in the presence of indomethacin caused +11.5 ± 3.6% and +59.6 ± 19.5% potentiation in the 20–40 and 50–65 age groups respectively (p <0.02). Adrenaline mediated platelet aggregation caused -55.2 ± 7.1% and -35.2 ± 8.3% inhibition in the 20–40 and 50–65 age groups, respectively. Collagen treatment of platelet-deficient-plasma and platelet-rich-plasma in EDTA also caused potentiation of prekallikrein activation.The results indicate that the observed degree of prekallikrein activation after platelet aggregation is a net result of the inhibitory effect of PF4 and the potentiatory effect of activated platelets. The potentiatory effect was greater after collagen treatment as compared to adrenaline treatment, and in the 50–65 age group as compared to the 20–40 age group.

An investigation of the inflammatory cytokine and chemokine network in systemic sclerosis

2011 ◽  
Vol 70 (6) ◽  
pp. 1115-1121 ◽  
Author(s):  
Veronica Codullo ◽  
Helen M Baldwin ◽  
Mark D Singh ◽  
Alasdair R Fraser ◽  
Catherine Wilson ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Mononuclear Cells ◽  
Platelet Rich Plasma ◽  
Critical Role ◽  
Serum Levels ◽  
Pcr Analysis ◽  
Peripheral Blood Mononuclear ◽  
Matrix Deposition ◽  
Disease Subtype ◽  
Inflammatory Chemokines

ObjectivesSystemic sclerosis (SSc) is characterised by vasculopathy, an aberrantly activated immune system and excessive extracellular matrix deposition. Inflammatory chemokines control migration of cells to sites of tissue damage; their removal from inflamed sites is essential for resolution of the inflammatory response. The atypical chemokine receptor D6 has a critical role in this physiological balance. To explore potential deregulation of this system in SSc, inflammatory chemokine and D6 expression were compared with that in healthy controls (HC).MethodsSerum levels of inflammatory mediators were assessed by luminex analysis. Peripheral blood mononuclear cells (PBMCs) were used in molecular and immunocytochemical analysis. Platelet-rich plasma was collected and assessed by western blotting for D6 expression levels. Sex-matched HC were used for comparison.Results72 patients with SSc and 30 HC were enrolled in the study. The chemokines MCP-1/CCL2, MIP-1α/CCL3, MIP-1β/CCL4 and IL-8/CXCL8 were significantly increased in patients with SSc, regardless of disease subtype and phase. Quantitative PCR analysis revealed a significant 10-fold upregulation of D6 transcripts in patients with SSc compared with controls, and this was paralleled by increased D6 protein expression in the PBMCs of patients with SSc. Platelet lysates also showed strong D6 expression in patients with SSc but not in controls. Importantly, high levels of D6 expression correlated with reduced levels of its ligands in serum.ConclusionsInflammatory chemokines and the regulatory receptor D6 are significantly upregulated in SSc and high D6 levels are associated with lower systemic chemokine levels, indicating that some patients control systemic chemokine levels using D6. These results suggest that chemokines may represent a therapeutic target in SSc.

A Successful Venous Thromboprophylaxis in a Patient with Vaccine-induced Immune Thrombotic Thrombocytopenia (VITT): a case report of the first reported case in Thailand

2021 ◽  
Author(s):  
Archrob Khuhapinant ◽  
Tarinee Rungjirajittranon ◽  
Bundarika Suwanawiboon ◽  
Yingyong Chinthammitr ◽  
Theera Ruchutrakool
Keyword(s):  
Asian Population ◽  
High Dose ◽  
Severe Thrombocytopenia ◽  
Imaging Studies ◽  
Fatal Complication ◽  
Platelet Factor ◽  
High Dose Dexamethasone ◽  
Prophylactic Dose ◽  
Spontaneous Platelet Aggregation ◽  
Very High

Abstract BackgroundVaccine-induced immune thrombotic thrombocytopenia (VITT) is a rare but fatal complication of Coronavirus Disease 2019 vaccine. Many reports of VITT have mostly been in the Caucasian population. Here, we present first reported case from an oriental population.Case presentationA 26-year-old female who had severe headache and severe thrombocytopenia 8 days after administration of the ChAdOx1 nCoV-19 vaccine developed by AstraZeneca. Although no thrombosis was demonstrated by imaging studies, she had very highly elevated d-dimer level during hospitalization. Serology for antibody against platelet factor 4 was positive on several days with very high optical density readings. Furthermore, we found the antibody could induce spontaneous platelet aggregation without the presence of heparin. We decided to treat her with intravenous immunoglobulin, high-dose dexamethasone, and a prophylactic dose of apixaban. She improved rapidly and was discharged from the hospital 6 days after admission. Neither thrombocytopenia nor thrombosis was subsequently detected at three weeks follow-up.ConclusionsDespite lower rate of thrombosis, VITT can present in Asian population. Early detection and prompt treatment of VITT can improve patients’ clinical outcome. Thromboprophylaxis of non-heparin anticoagulants also results in prevention of clot formation.

scholarly journals Fibronectin modulates formation of PF4/heparin complexes and is a potential factor for reducing risk of developing HIT

Blood ◽  
2019 ◽  
Vol 133 (9) ◽  
pp. 978-989 ◽  
Author(s):  
Krystin Krauel ◽  
Patricia Preuße ◽  
Theodore E. Warkentin ◽  
Catja Trabhardt ◽  
Sven Brandt ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Platelet Rich Plasma ◽  
Enzyme Linked Immunosorbent Assay ◽  
Heparin Binding ◽  
Plasma Fibronectin ◽  
Platelet Factor ◽  
Washed Platelet ◽  
Plasma Factor ◽  
Heparin Complexes ◽  
Patient Groups

Abstract Heparin-induced thrombocytopenia (HIT) is caused by platelet-activating anti–platelet factor 4 (PF4)/heparin antibodies. Platelet activation assays that use “washed” platelets are more sensitive for detecting HIT antibodies than platelet-rich plasma (PRP)–based assays. Moreover, heparin-exposed patients vary considerably with respect to the risk of PF4/heparin immunization and, among antibody-positive patients, the risk of subsequent “breakthrough” of clinical HIT with manifestation of thrombocytopenia. We used washed platelets and PRP, standard laboratory HIT tests, and physicochemical methods to identify a plasma factor interfering with PF4/heparin complexes and anti-PF4/heparin antibody–platelet interaction, thus explaining differences in functional assays. To investigate a modulating risk for PF4/heparin immunization and breakthrough of HIT, we also tested 89 plasmas from 2 serosurveillance trials. Fibronectin levels were measured in 4 patient groups exhibiting different degrees of heparin-dependent immunization and expression of HIT. The heat-labile plasma protein, fibronectin, inhibited PF4 binding to platelets in a dose-dependent fashion, particularly in washed (vs PRP) systems. Fibronectin also inhibited PF4/heparin binding to platelets, anti-PF4/heparin antibody binding to PF4/heparin complexes, and anti-PF4/heparin antibody–induced platelet activation as a result of PF4/heparin complex disruption. In addition, plasma fibronectin levels increased progressively among the following 4 patient groups: enzyme-linked immunosorbent assay (ELISA)+/serotonin-release assay (SRA)+/HIT+ &lt; ELISA+/SRA+/HIT− ∼ ELISA+/SRA−/HIT− &lt; ELISA−/SRA−/HIT−. Altogether, these findings suggest that fibronectin interferes with PF4/heparin complex formation and anti-PF4/heparin antibody–induced platelet activation. Reduced fibronectin levels in washed platelet assays help to explain the greater sensitivity of washed platelet (vs PRP) assays for HIT. More importantly, lower plasma fibronectin levels could represent a risk factor for PF4/heparin immunization and clinical breakthrough of HIT.

The Role of Factor XI in a Dilute Thromboplastin Assay of Extrinsic Coagulation Pathway

2001 ◽  
Vol 85 (06) ◽  
pp. 1055-1059 ◽  
Author(s):  
Shilong Xiong ◽  
Xiaofan He ◽  
Fayi Liu ◽  
Jianzhong Han ◽  
Juncheng Li ◽  
...  
Keyword(s):  
Blood Coagulation ◽  
Platelet Rich Plasma ◽  
Critical Role ◽  
Extrinsic Pathway ◽  
Thrombin Inhibition ◽  
Normal Plasma ◽  
Low Concentrations ◽  
Plasma Depletion ◽  
Coagulation Pathway

SummaryBlood coagulation has been thought to be composed of both intrinsic and extrinsic pathways. Recent evidence strongly supports the critical role of the extrinsic pathway in the initiation of blood coagulation. This investigation established an assay that examines the role of FXI in the thromboplastin-initiated (extrinsic) coagulation based on this new concept. Plasma clotting times were measured at different concentrations of thromboplastin with activated FXII inhibited (FXIIa-inhibited Diluted Thromboplastin Time, FXIIaiDTT). Only at low concentrations of thromboplastin was FXIIaiDTT of FXI-deficient plasma significantly prolonged than that of normal plasma. Depletion of FXI from normal plasma prolonged its FXIIaiDTT and replenishment of FXI shortened it. FXIIaiDTTs of both FVIII-deficient and FIX-deficient plasma were remarkably prolonged, and addition of normal plasma dose-dependently shortened it. Furthermore, earlier α-thrombin inhibition was directly correlated with decreasing FXa generation. The amount of FXa production was: platelet-rich plasma > platelet-poor plasma > FXI-deficient plasma. Therefore, our findings from the FXIIaiDTT assays not only support the critical role of extrinsic pathway in blood coagulation initiation, but also demonstrate the importance of FXI as an amplifier of thrombin generation in thromboplastin-initiated coagulation.

Heparin-induced thrombocytopenia: when a low platelet count is a mandate for anticoagulation

Hematology ◽  
2009 ◽  
Vol 2009 (1) ◽  
pp. 225-232 ◽  
Author(s):  
Thomas L. Ortel
Keyword(s):  
Platelet Count ◽  
Heparin Therapy ◽  
Severe Thrombocytopenia ◽  
Drug Induced ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Immune Mediated ◽  
Number Of Patients ◽  
Increased Risk ◽  
Antibody Levels

Abstract Heparin-induced thrombocytopenia (HIT) is an immune-mediated disorder caused by the development of antibodies to platelet factor 4 (PF4) and heparin. The thrombocytopenia is typically moderate, with a median platelet count nadir of ~50 to 60 × 109 platelets/L. Severe thrombocytopenia has been described in patients with HIT, and in these patients antibody levels are high and severe clinical outcomes have been reported (eg, disseminated intravascular coagulation with microvascular thrombosis). The timing of the thrombocytopenia in relation to the initiation of heparin therapy is critically important, with the platelet count beginning to drop within 5 to 10 days of starting heparin. A more rapid drop in the platelet count can occur in patients who have been recently exposed to heparin (within the preceding 3 months), due to preformed anti-heparin/PF4 antibodies. A delayed form of HIT has also been described that develops within days or weeks after the heparin has been discontinued. In contrast to other drug-induced thrombocytopenias, HIT is characterized by an increased risk for thromboembolic complications, primarily venous thromboembolism. Heparin and all heparin-containing products should be discontinued and an alternative, non-heparin anticoagulant initiated. Alternative agents that have been used effectively in patients with HIT include lepirudin, argatroban, bivalirudin, and danaparoid, although the last agent is not available in North America. Fondaparinux has been used in a small number of patients with HIT and generally appears to be safe. Warfarin therapy should not be initiated until the platelet count has recovered and the patient is systemically anticoagulated, and vitamin K should be administered to patients receiving warfarin at the time of diagnosis of HIT.

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