scholarly journals Platelet Aggregometry Curve Type

2020 ◽  
Author(s):  



1985 ◽  
Vol 53 (03) ◽  
pp. 360-365 ◽  
Author(s):  
Gerhard K M Endresen ◽  
Øystein Førre

SummarySeveral antibody fractions and sera from patients with rheumatoid arthritis, systemic lupus erythematosus and chronic idiopathic thrombocytopenic purpura were examined for their ability to bind to normal platelets using immunofluorescent staining techniques. Platelet aggregometry was used to study the activating capacity of the samples.Both C1q, C1s, C1 inactivator, fibrinogen, factor VIII-related antigen, alpha1-acid glycoprotein, alpha1-antitrypsin, beta2-micro- globulin and isoantigens A and B, as well as fibronectin and plasminogen were found on the platelet surface. Only antibodies to C1q, C1s and beta2-microglobulin were able to induce platelet aggregation. Sera containing immune complexes or platelet autoantibodies revealed positive surface staining for IgG, or for IgG and IgM. These sera also induced aggregation of platelets. Sera not containing immune complexes or autoantibodies gave negative staining and aggregation results. Thus, only some of the ligand receptor interactions were able to induce platelet aggregation.



1985 ◽  
Vol 53 (02) ◽  
pp. 219-220 ◽  
Author(s):  
M V Vickers ◽  
S G Thompson

SummaryAn experiment designed to assess the components of variability of a number of measures of platelet aggregability showed that the ADP ED50 (the estimated dose of adenosine diphosphate at which primary aggregation occurs at half its maximum velocity) had the least method error of any of the parameters measured, but that none had a very high between-person component of variability. A simultaneous comparison of a syringe technique and a free-flowing technique for venepuncture revealed no differential effects on the aggregation parameters measured. An enforced increase in the stirring speed in the aggregometer led to an experiment which showed that such a change did not apparently affect the ED50s.



Author(s):  
Mrinalini Kotru ◽  
Deepti Mutereja ◽  
Abhishek Purohit ◽  
Seema Tyagi ◽  
Manoranjan Mahapatra ◽  
...  

Abstract. Background: Bleeding is a common clinical presentation. Even patients with mild bleeding disorders are extensively investigated for ascertaining the cause. The present study was conducted in order to evaluate the extent of the possibility of diagnosis in mild bleeding disorders.Material and Methods: This was a prospective study of patients referred for work up of mild bleeding for a period of 13 months. A complete blood count, peripheral smear examination, Prothrombin time, Partial Thromboplastin time and Thrombin Time, Platelet Aggregometry test, tests for von Willebrand’s disease and Platelet function 3 availability were measured. Results: 164 patients presented with mild bleeding, in 114 of the  patients a single site of bleeding was present. Epistaxis was the most common presentation (39%). Cutaneous bleeding (petechiae and purpura) was the next common site. History of a major bleeding tendency in the family was present only in 11 patients. The investigations showed that VWD (17/164), followed by clotting disorders (CD) mainly mild hemophilia (15/164) were the most common diagnosable cause. There were also 4 cases of hypofibrinogenemia. The disorders of platelets (Platelet function defects/PFD) were the least common (9/164). Rest 123 (75%) patients could not be diagnosed on the basis of these investigations and were labeled as  Bleeding disorders – Unclassified (BDC). Conclusion: n our study, 75% of the patients with mild bleeding remained undiagnosed even after extensive laboratory workup, thus raising a very pertinent question that is it necessary that all mild bleeders submit to a broad battery of investigations, as the diagnosis continues to be elusive despite extensive workup.



2012 ◽  
Vol 130 (4) ◽  
pp. 616-621 ◽  
Author(s):  
Kaneo Satoh ◽  
Isao Fukasawa ◽  
Kazuya Kanemaru ◽  
Shigemi Yoda ◽  
Yukio Kimura ◽  
...  


2011 ◽  
Vol 100 (10) ◽  
pp. 907-914 ◽  
Author(s):  
Tobias Behr ◽  
Bernhard Kuch ◽  
Werner Behr ◽  
Wolfgang von Scheidt


2006 ◽  
Vol 96 (12) ◽  
pp. 781-788 ◽  
Author(s):  
Andreas Calatzis ◽  
Sandra Penz ◽  
Hajna Losonczy ◽  
Wolfgang Siess ◽  
Orsolya Tóth

SummarySeveral methods are used to analyse platelet function in whole blood. A new device to measure whole blood platelet aggregation has been developed, called multiple electrode platelet aggregometry (MEA). Our aim was to evaluate MEA in comparison with the single platelet counting (SPC) method for the measurement of platelet aggregation and platelet inhibition by aspirin or apyrase in diluted whole blood. Platelet aggregation induced by different concentrations of ADP, collagen and TRAP-6 and platelet inhibition by apyrase or aspirin were determined in citrateor hirudin-anticoagulated blood by MEA and SPC. MEA indicated that spontaneous platelet aggregation was lower, and stimulated platelet aggregation was higher in hirudin- than citrate-anticoagulated blood. In hirudin-anticoagulated, but not citrate-anticoagulated blood, spontaneous platelet aggregation measured by MEA was inhibited by apyrase. For MEA compared with SPC the dose response-curves of agonist-induced platelet aggregation in citrate- and hirudin-blood showed similar EC50 values for TRAP, and higher EC50 values for ADP (non-significant) and collagen (p<0.05). MEA and the SPC method gave similar results concerning platelet-inhibition by apyrase and aspirin. MEA was more sensitive than SPC to the inhibitory effect of aspirin in collagen-induced aggregation. In conclusion, MEA is an easy, reproducible and sensitive method for measuring spontaneous and stimulated platelet aggregation, and evaluating antiplatelet drugs in diluted whole blood. The use of hirudin as an anticoagulant is preferable to the use of citrate. MEA is a promising technique for experimental and clinical applications.



Neurosurgery ◽  
2016 ◽  
Vol 63 ◽  
pp. 187 ◽  
Author(s):  
Babu Guai Welch ◽  
Salah G. Aoun ◽  
G. Lee Pride ◽  
Kim L. Rickert ◽  
Jonathan A. White ◽  
...  


Blood ◽  
2009 ◽  
Vol 114 (2) ◽  
pp. 261-263 ◽  
Author(s):  
Alfonso Quintás-Cardama ◽  
Xin Han ◽  
Hagop Kantarjian ◽  
Jorge Cortes

Abstract Dasatinib is associated with increased risk of bleeding among patients with chronic myeloid leukemia, even in the absence of thrombocytopenia, suggesting the presence of a hemostatic defect. We tested platelet aggregation in 91 patients with chronic myeloid leukemia in chronic phase either off-therapy (n = 4) or receiving dasatinib (n = 27), bosutinib (n = 32), imatinib (n = 19), or nilotinib (n = 9). All but 3 patients simultaneously receiving imatinib and warfarin had normal coagulation studies. All 4 patients off therapy had normal platelet aggregation. Impaired platelet aggregation on stimulation with arachidonic acid, epinephrine, or both was observed in 70%, 85%, and 59% of patients on dasatinib, respectively. Eighty-five percent of patients on bosutinib, 100% on nilotinib, and 33% on imatinib had normal platelet aggregation. Dasatinib 400 nM induced rapid and marked prolongation of closure time to collagen/epinephrine in normal whole blood on the PFA-100 system. In conclusion, dasatinib and, to some extent, imatinib produce abnormalities in platelet aggregometry testing.



1996 ◽  
Vol 26 (2) ◽  
pp. 98-106 ◽  
Author(s):  
A.C. Matzdorff ◽  
B. Kemkes-Matthes ◽  
R. Voss ◽  
H. Pralle


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