scholarly journals Changes in and significance of platelet function and parameters in Kawasaki disease

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Xiaolan Zheng ◽  
Wenchao Wu ◽  
Yi Zhang ◽  
Gang Wu
Keyword(s):  
Kawasaki Disease ◽  
Platelet Function ◽  
Unknown Etiology ◽  
Distribution Width ◽  
Coronary Artery Abnormality ◽  
Ivig Resistance ◽  
Function Analyzer ◽  
Acquired Heart Disease ◽  
Platelet Function Analyzer ◽  
Inflammatory Vascular Disease

AbstractKawasaki disease (KD) is a systemic febrile, inflammatory vascular disease of unknown etiology. The coronary artery abnormality (CAA) caused by KD has become the most commonly acquired heart disease in children. Initial treatment of intravenous immunoglobulin (IVIG) can reduce the incidence of CAA. Thrombocytosis is common during the course of KD, but changes in and significances of platelet function and parameters are unclear. In this study, we enrolled 120 patients, including 40 patients with KD, 40 febrile controls, and 40 afebrile controls. The platelet function was assessed using the platelet function analyzer (PFA)-200. Platelet parameters, including platelet count (PLT), mean platelet volume (MPV), platelet distribution width (PDW), and platelet hematocrit (PCT) were measured. In the febrile period, the PDW and MPV were lower in KD patients (P < 0.05). The platelet function did not change significantly during the febrile period of KD but weakened in the defervescence phase. No significant differences between the CAA and normal groups, and between IVIG resistance and response groups. The diagnostic cutoff value of the PDW level for predicting KD was 10.85 fL with a sensitivity of 55% and a specificity of 77.5% (area under curve (AUC) = 0.690, 95% confidence interval (CI): 0.574–0.806, P < 0.01). Besides, the MPV level was 9.55 fL with sensitivity of 75% and specificity of 70% (AUC = 0.733, 95%CI: 0.620–0.846, P < 0.001). This is the first longitudinal study of platelet function changes in KD patients using PFA-200. Besides, lower PDW and MPV may be available markers for early diagnosis of KD.

scholarly journals Adequate Platelet Function Inhibition Confirmed by Two Inductive Agents Predicts Lower Recurrence of Ischemic Stroke/Transient Ischemic Attack

2017 ◽  
Vol 2017 ◽  
pp. 1-5 ◽  
Author(s):  
Lulu Zhang ◽  
Xiaowei Hu ◽  
Juehua Zhu ◽  
Xiuying Cai ◽  
Yan Kong ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Antiplatelet Therapy ◽  
Platelet Function ◽  
Adenosine Diphosphate ◽  
Aggregation Rate ◽  
Function Analyzer ◽  
Ischemic Attack ◽  
Platelet Function Analyzer ◽  
Platelet Functions

Background. The correlation between platelet function and recurrent ischemic stroke or TIA remains uncertain. Objective. To investigate two inductive agents to detect platelet functions and assess associations with recurrent ischemic stroke/TIA. Method. The study included 738 ischemic stroke/TIA patients. On days 0, 3, and 9 after antiplatelet therapy, platelet function tests were determined by maximum aggregation rate (MAR) using a PL-11 platelet function analyzer and phase matching reagents. Two induction agents were used: arachidonic acid (AA) and adenosine diphosphate (ADP). At 3-month follow-up, recurrence of stroke/TIA was recorded. Result. Cut-off values of adequate platelet function inhibition were MARADP < 35% and MARAA < 35%. Data showed that antiplatelet therapy could reduce the maximum aggregation rate. More importantly, adequate platelet function inhibition of either MARADP or MARAA was not associated with the recurrence of stroke/TIA, but adequate platelet function inhibition of not only MARADP but also MARAA predicts lower recurrence (0/121 (0.00%) versus 18/459 (3.92%), P = 0.0188). Conclusion. The platelet function tested by PL-11 demonstrated that adequate inhibition of both MARADP and MARAA could predict lower risk of ischemic stroke/TIA recurrence.

Monitoring Acetylsalicylic Acid Effects with the Platelet Function Analyzer PFA-100

2005 ◽  
Vol 31 (04) ◽  
pp. 411-415 ◽  
Author(s):  
Martin Feuring ◽  
Armin Schultz ◽  
Ralf Losel ◽  
Martin Wehling
Keyword(s):  
Acetylsalicylic Acid ◽  
Platelet Function ◽  
Function Analyzer ◽  
Platelet Function Analyzer

scholarly journals Variables influencing Platelet Function Analyzer-100TM closure times in healthy individuals

2005 ◽  
Vol 130 (5) ◽  
pp. 759-767 ◽  
Author(s):  
Hannelore Haubelt ◽  
Christof Anders ◽  
Anette Vogt ◽  
Petra Hoerdt ◽  
Ulrich Theo Seyfert ◽  
...  
Keyword(s):  
Platelet Function ◽  
Healthy Individuals ◽  
Function Analyzer ◽  
Platelet Function Analyzer

scholarly journals The Role of Platelet Function Analyzer Testing in Cardiac Surgery Transfusion Management

2017 ◽  
Vol 44 (2) ◽  
pp. 106-113 ◽  
Author(s):  
Dejana Bogdanic ◽  
Nenad Karanovic ◽  
Jela Mratinovic-Mikulandra ◽  
Branka Paukovic-Sekulic ◽  
Dijana Brnic ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Platelet Function ◽  
Function Analyzer ◽  
Platelet Function Analyzer

The influence of the haematocrit on primary haemostasis in vitro

2005 ◽  
Vol 94 (12) ◽  
pp. 1213-1218 ◽  
Author(s):  
Marco Eugster ◽  
Walter H. Reinhart
Keyword(s):  
Platelet Function ◽  
Type I Collagen ◽  
Inverse Correlation ◽  
Type I ◽  
Membrane Pore ◽  
Closure Time ◽  
Function Analyzer ◽  
Platelet Function Analyzer

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.

Description of an In Vitro Platelet Function Analyzer-PFA-100™

1995 ◽  
Vol 21 (S 02) ◽  
pp. 106-112 ◽  
Author(s):  
Sourav Kundu ◽  
Eric Heilmann ◽  
Reynaldo Sio ◽  
Carmen Garcia ◽  
Rosa Davidson ◽  
...  
Keyword(s):  
Platelet Function ◽  
Quantitative Measure ◽  
Biologically Active ◽  
High Shear Rates ◽  
Function Analyzer ◽  
Potential Applications ◽  
Time Required ◽  
Platelet Function Analyzer ◽  
Von Willebrand

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

scholarly journals Functional benefits of corticosteroid and IVIG combination therapy in a coronary artery endothelial cell model of Kawasaki disease

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Takashi Inoue ◽  
Shokei Murakami ◽  
Kenji Matsumoto ◽  
Akio Matsuda
Keyword(s):  
Coronary Artery ◽  
Kawasaki Disease ◽  
Combination Therapy ◽  
Molecular Mechanisms ◽  
Ivig Therapy ◽  
Unknown Etiology ◽  
High Dose ◽  
Ivig Resistance ◽  
Tnf Α ◽  
Clinical Benefits

Abstract Background Kawasaki disease (KD) is the most common pediatric systemic vasculitides of unknown etiology. Recent clinical studies led to reappraisal of the usefulness of initial combination therapy of intravenous immunoglobulin (IVIG) plus a corticosteroid for patients with severe KD. However, the molecular mechanisms underlying the clinical benefits of that combination therapy remain unclear. Here, we used cultured human coronary artery endothelial cells (HCAECs), as a mimic of KD, to study the possible mechanisms responsible for the clinical benefits of adding a corticosteroid to standard IVIG therapy for patients with severe KD. Methods HCAECs were stimulated with TNF-α, IL-1α or IL-1β in the presence and absence of high-dose IgG and/or dexamethasone (DEX). The mRNA and protein concentrations for high-mobility group box-1 (HMGB1), IL-1α, IL-6 and granulocyte-colony stimulating factor (G-CSF) in the culture supernatants were measured by quantitative PCR (qPCR) and ELISA, respectively. Apoptosis was evaluated by the caspase 3/7 activities. Results DEX, but not IgG, significantly inhibited apoptosis caused by inflammatory stimuli, resulting in effective reduction of HMGB1 and IL-1α protein release by HCAECs. As previously reported, DEX or IgG alone significantly suppressed TNF-α-induced production of IL-6 and G-CSF and mRNA expression, but induction of those cytokines by IL-1 s (IL-1α and IL-1β) was resistant to high-dose IgG. Conclusions A corticosteroid can effectively inhibit the release of HMGB1 and IL-1α, which may be involved in IVIG resistance in KD. Since high-dose IgG does not have such beneficial anti-cytotoxic effects, adding a corticosteroid to standard IVIG therapy may help prevent the progression of IVIG resistance in KD.

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