scholarly journals Pruebas de función plaquetaria por el sistema PFA-200

2020 ◽  
Vol 24 (2) ◽  
pp. 162-164 ◽  
Author(s):  
Laura Rivillas-Rigol ◽  
Jennifer C. Vizcaíno-Carruyo ◽  
Verónica J. Tangarife- Castaño ◽  
Germán Campuzano-Zuluaga ◽  
Ana Isabel Toro-Montoya

Las pruebas de función plaquetaria realizadas con el analizador PFA-200 (del inglés, Platelet Function Analyzer) han venido reemplazando el tiempo de sangría, una prueba ya obsoleta, de acuerdo con el College of American Pathologists (CAP) y la American Society for Clinical Pathology (ASCP). Este analizador, mediante un sistema que utiliza cartuchos, posee la capacidad de simular in vitro las condiciones hemodinámicas del paciente para el tamizaje rápido, sencillo y automatizado de la disfunción plaquetaria. Las pruebas son de utilidad para evaluar la función plaquetaria en pacientes con alteraciones como enfermedad de von Willebrand y otras trombocitopatías congénitas o adquiridas, y evalúa la disfunción plaquetaria causada por inhibidores de la agregación plaquetaria, como la aspirina. Además, son de gran utilidad para el tamizaje prequirúrgico y en los embarazos de alto riego. Este sistema ofrece con su más reciente prueba, la INNOVANCE® PFA-200 P2Y, la posibilidad de evaluar la respuesta de pacientes que están siendo tratados con antagonistas del receptor plaquetario P2Y12, como son clopidogrel, prasugrel y ticagrelor, determinando el porcentaje de adhesión y agregación plaquetaria, logrando discriminar entre un paciente antiagregado y un paciente resistente al tratamiento.

1995 ◽  
Vol 21 (S 02) ◽  
pp. 106-112 ◽  
Author(s):  
Sourav Kundu ◽  
Eric Heilmann ◽  
Reynaldo Sio ◽  
Carmen Garcia ◽  
Rosa Davidson ◽  
...  

A new in vitro system for the detection of platelet dysfunction, PFA-100™* has been developed. It provides a quantitative measure of platelet function in anticoagulated whole blood. The system comprises a microprocessor-controlled instrument and a disposable test cartridge containing a biologically active membrane. The instrument aspirates a blood sample under constant vacuum from the sample reservoir through a capillary and a microscopic aperture cut into the membrane. The membrane is coated with collagen and epinephrine or adenosine 5’-diphosphate. The presence of these biochemical stimuli, and the high shear rates generated under the standardized flow conditions, result in platelet attachment, activation, and aggregation, slowly building a stable platelet plug at the aperture. The time required to obtain full occlusion of the aperture is reported as the m“closure time.” We have found that impairment of von Willebrand factor, or inhibition of platelet receptors glycoprotein Ib or IIblIIIa with monoclonal antibodies or peptides, resulted in abnormal closure times. An antifibrinogen antibody, in contrast, failed to show any effect. The test appears to be sensitive to platelet adherence and aggregation abnormalities. The PFA-100™ system has potential applications in routine evaluation of platelet function in the clinical setting because of its accuracy, ease of operation, and rapid turnaround of results. * Under evaluation


1996 ◽  
Vol 2 (4) ◽  
pp. 241-249 ◽  
Author(s):  
Sourav K. Kundu ◽  
Eric J. Heilmann ◽  
Reynaldo Sio ◽  
Carmen Garcia ◽  
Roy A. Ostgaard

A new in vitro system for the evaluation of platelet function, PFA-100 (currently under evaluation) is characterized. The system monitors platelet aggrega tion on a collagen-epinephrine-coated membrane as whole blood sample is aspirated under controlled flow conditions through a microscopic aperture cut into the membrane. The time required for the platelet plug to oc clude the aperture (closure time) is indicative of the plate let function in the sample. Incubation of normal blood samples with antibodies to glycoprotein (GP) Ib, GPIIb- IIIa, von Willebrand factor, or with the peptide Arg-Gly- Asp-Ser, resulted in a concentration-dependent prolonga tion in closure time. An anti-fibrinogen antibody did not impact the closure time. Closure time was also prolonged when the hematocrit or the platelet count was lowered to pathological values. The study indicates that PFA-100 could detect defects in platelet adhesion or aggregation. The simplicity of the test makes PFA-100 unique for rapid screening of a variety of platelet dysfunction.


2005 ◽  
Vol 94 (12) ◽  
pp. 1213-1218 ◽  
Author(s):  
Marco Eugster ◽  
Walter H. Reinhart

SummaryPrimary haemostasis consists of platelet adhesion to subendothelial collagen, their activation and aggregation and finally the formation of a platelet plug. Erythrocytes are involved in this process because they flow in the center of the vessel and push platelets towards the site of action on the vessel wall and enhance shear forces, which activate platelets. In the platelet function analyzer PFA-100® (Dade Behring, Düdingen, Switzerland), the in vivo situation is simulated in vitro with blood being aspirated at high shear rates (5000s-1) through a capillary into a membrane pore with a diameter of 150 μm coated with type I collagen and either epinephrine or adenosine diphosphate. Aggregating platelets plug the pore and stop the flow, which is measured as the closure time. We analysed the influence of erythrocytes on platelet function analyzer measurements by systematic variation of the haematocrit (20,30,40,and 50%) at constant platelet counts of 289±61 ×103/μl plasma, or 152±30 ×103/μl blood, 96±9 ×103/μl blood and 54±5 ×103/μl blood, respectively. An inverse correlation was found between haematocrit and closure time under all circumstances. A decrease of the platelet count by 50 ×103 /μl could be compensated for by a 10% increase in haematocrit. The haematocrit must, therefore, be taken into consideration for the correct interpretation of PFA-100® measurements. Our data also provide a pathophysiological rationale to reduce the risk of bleeding in patients with thrombocytopenia and anaemia by normalizing the haematocrit with erythrocyte transfusions.


2009 ◽  
Vol 101 (01) ◽  
pp. 123-133 ◽  
Author(s):  
Shirley Williams ◽  
Diane Nugent ◽  
Paul Harrison ◽  
Helen Segal ◽  
Anila Syed ◽  
...  

SummaryWe studied the effect of prophylactic aspirin (ASA) ingestion on platelet function in 463 patients with stroke, transient ischemic attack (TIA) or acute coronary disease (ACD), using the Platelet Function Analyzer-100 (PFA-100). We correlated ASA responsiveness with haplotypes of seven candidate genes, selected for their documented role in platelet function, namely, the genes for integrins α2β1and αIIbβ3 (ITGA2, ITGA2B, and ITGB3), platelet glycoproteins Ibα and VI (GPIBA and GP6), the purinergic receptor P2Y1 (P2RY1), and prostaglandin H synthase 1 (PTGS1 = COX1). Non-responsiveness to ASA was defined as the failure of prior ASA ingestion to prolong the PFA-100 closure time (CT) when blood was perfused through cartridges coated with collagen plus epinephrine (CEPI-CT). ASA non-responsiveness was observed in 114 of 463 patients (24.6 %), but was not associated with haplotypes of any of the seven candidate genes. There was also no association between any haplotypes and the CT when blood was perfused through cartridges coated with collagen plus ADP (CADP-CT). The ASA non-responsive cohort had significantly increased whole blood platelet counts (p = 0.03) and plasma von Willebrand Factor antigen levels (p<0.001), which likely contributes to resistance to the inhibitory effects of ASA in the PFA-100.


2001 ◽  
Vol 95 (5) ◽  
pp. 1220-1225 ◽  
Author(s):  
Nicola A. Horn ◽  
Lothar de Rossi ◽  
Tilo Robitzsch ◽  
Klaus E. Hecker ◽  
Gabriele Hutschenreuter ◽  
...  

Background Previous studies have reported conflicting results about the effect of sevoflurane on platelet aggregation. To clarify this point, we investigated the effects of sevoflurane on platelet antigen expression and function in vitro. Methods Human whole blood was incubated for 1 h with 0.5 and 1 minimum alveolar concentration sevoflurane, 21% O(2), and 5% CO(2). A control sample was kept at the same conditions without sevoflurane. After stimulation with adenosine diphosphate or thrombin receptor agonist peptide 6, samples were stained with fluorochrome conjugated antibodies, and the expression of platelet glycoproteins GPIIb/IIIa, GPIb, and P-selectin, as well as activated GPIIb/IIIa, were measured with two-color flow cytometry. In addition, platelet function was assessed by means of thromboelastography and using the platelet function analyzer 100. Results Already in subanesthetic concentrations, sevoflurane inhibits unstimulated and agonist-induced GPIIb/IIIa surface expression and activated GPIIb/IIIa expression on platelets in whole blood. The agonist-induced redistribution of GPIb into the open canalicular system was also impaired by sevoflurane, whereas no effect on P-selectin expression in activated platelets could be found. Sevoflurane significantly reduced the maximum thromboelastographic amplitude. Furthermore, platelet function analyzer 100 closure times were significantly prolonged. Conclusion The results show that sevoflurane significantly impairs platelet antigen expression in vitro. It is especially the inhibition of GPIIb/IIIa expression and activation that impairs bleeding time as reflected in thromboelastographic measurements and platelet function analyzer 100 closure times. The exact inhibitory mechanism remains unclear.


2013 ◽  
Vol 60 (7) ◽  
pp. 1184-1187 ◽  
Author(s):  
Swati Naik ◽  
Jun Teruya ◽  
Jennifer E. Dietrich ◽  
Purvi Jariwala ◽  
Esther Soundar ◽  
...  

2020 ◽  
Vol 22 (12) ◽  
pp. 1214-1218
Author(s):  
Elizabeth C Hiebert ◽  
David L Panciera ◽  
Katie M Boes ◽  
Lara Bartl

Objectives Cats with hyperthyroidism have been reported to develop thromboembolism, with and without echocardiographic abnormalities consistent with hyperthyroidism. The objective of this study was to compare platelet function in cats with hyperthyroidism with euthyroid age-matched cats. We hypothesized that cats with hyperthyroidism have shortened collagen and adenosine diphosphate (C-ADP) closure times as measured with the platelet function analyzer (PFA-100) in comparison with healthy, age-matched controls. Methods Sixteen hyperthyroid and nine euthyroid healthy cats >7 years of age were recruited from the hospital population. Platelet function, measured using the C-ADP closure times by the PFA-100, and platelet count were measured in healthy euthyroid cats and cats with hyperthyroidism. Results Mean ± SD closure times were not significantly different between control (66.3 ± 9.6 s) and hyperthyroid cats (65.9 ± 11.5 s; P = 0.75). The mean ± SD closure times of hyperthyroid cats that either were untreated or received methimazole for ⩽3 weeks (n = 6; mean 68.5 ± 15.4 s) was not different than that of cats treated for >3 weeks (n = 10; mean 64.3 ± 8.9 s; P = 0.57). The mean automated platelet count was higher in the hyperthyroid group than in the control group ( P = 0.023). Conclusions and relevance Platelet function, as measured by closure time under high shear conditions using C-ADP as an agonist, was not affected by hyperthyroidism in this group of cats. Further research is needed to determine if a hypercoagulable state exists in hyperthyroid cats and the potential roles platelets and von Willebrand factor may have.


2004 ◽  
Vol 191 (2) ◽  
pp. 449-455 ◽  
Author(s):  
Andra H. James ◽  
Andrea S. Lukes ◽  
Leo R. Brancazio ◽  
Elizabeth Thames ◽  
Thomas L. Ortel

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