Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Platelet Function Tests”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed1978

[Results of a new platelet function test in various clinical diseases and in preserved blood].

In healthy persons, patients with thrombocytopenia and patients with arterial disturbances of blood flow with and without administration of Falithrom the pressure recording was carried out after the combined aggregation and adhesion of thrombocytes. The reaction time particularly observed after administration of ADP revealed marked differences in the groups examined, likewise the maximal pressure amplitude in front of the pumped through filter. When Falithrom was administered the thrombocyte functions were clearly impaired. The reduction of the capacity of platelets to obstruct filter pores can impressively be proved even in those thrombocytes stored in ACD-AG-plasma.

Adenosine Diphosphate↗
PubMed1994

Significance of testing platelet functions in vitro.

Platelets respond through discrete receptors to a number of physiological agonists and foreign surfaces with a sequence of measurable responses: shape change, aggregation, secretion and arachidonate liberation. Three secretory responses are distinguished: exocytosis of substances from (1) dense granules, (2) alpha-granules and (3) lysosomes. Free arachidonate, liberated from phospholipids by phospholipase A2, is rapidly converted (by oxygenation) to prostaglandins and thromboxanes which, together with secreted ADP and close cell contact, will cause further platelet activation through 'positive feedback' (autocrine stimulation). Some agonists are classified as 'weak' (ADP, vasopressin, platelet-activating factor [PAF], serotonin) because they depend on autocrine stimulation to promote the full sequence of responses, while others are 'strong' agonists (thrombin, collagen) and activate all responses directly without autocrine stimulation. Adrenaline, long thought to be a platelet agonist per se, most probably acts by amplifying the activation brought about by other, proper, agonists. Such synergistic interaction among agonists is very typical for platelet activation and most likely takes place in vivo. Shape change, aggregation and secretion(s) may be tested by flow cytometry or electron microscopy in vitro under conditions that probably reflect the in vivo situation. However, the aggregation response to weak agonists in vitro is dependent on the extracellular [Ca2+], with biphasic aggregation at the low [Ca2+] present when citrate is used as anticoagulant (or in suspension of washed platelets) but not at the physiological [Ca2+] present in platelet-rich plasma from heparinized blood.

Adenosine Diphosphate↗
PubMedDate not supplied

Extensive coagulation monitoring in patients after implantation of the MicroMed Debakey continuous flow axial pump.

Ventricular assist device (VAD) implantation is associated with impaired primary hemostasis and thromboembolic complications. Recently, a new generation of implantable continuous flow axial pumps was introduced into clinical application. To study the potential thrombogenic properties of this type of pump, we applied extensive platelet monitoring was applied. In our institution, 13 patients received the MicroMed DeBakey VAD as a bridge to transplantation. Routine coagulation tests (platelet count, activated partial thromboplastin time, prothrombin time, antithrombin III activity) and platelet function tests (whole blood aggregometry, thrombelastography, flow cytometry) were performed. No clinically relevant thromboembolic events were detected. No correlation was found between global function tests, platelet aggregation, and thrombelastography. No correlation was detected between platelet activation and hemolysis parameters. Platelet aggregation and coagulation index were significantly suppressed early after operation. A subsequent phase of hyper-aggregability, starting around day 6, suggested the initiation of antiaggregation therapy. Platelet activation markers were upregulated in the postoperative period but were returned to preoperative levels after initiation of aspirin. In contrast to routine coagulation monitoring, platelet function tests reflect in detail the coagulation status of blood pump recipients and the efficiency of antiaggregation therapy. Aspirin and dipyridamole therapy in addition to oral anticoagulation using phenprocoumon may contribute to platelet function and clot mechanics restoration and is, therefore, recommended for patients after VAD implantation.

Adolescent↗
PubMed1997

Haemostatic function in coronary artery disease (CAD).

Tests to evaluate haemostatic function bleeding time (BT), prothrombin time (PT) partial thromboplastin time with kaolin (PTTK), thrombin time (TT), platelet count, platelet function tests (platelet adhesiveness and microthrombus index) and plasma fibrinogen levels were performed in 30 patients of coronary artery disease (14 myocardial infarction, 16 angina pectoris) and 20 age and sex matched controls. There was no statistically significant difference in platelet adhesiveness and mean microthrombus index in patients and controls. The BT, PT, PTTK and TT were normal in all patients and controls. Stepwise logistic regression analysis showed that plasma fibrinogen was an independent risk factor in the production of CAD.

Adult↗
PubMed1997

Rapid assessment of platelet function with a modified whole-blood aggregometer in percutaneous transluminal coronary angioplasty patients receiving anti-GP IIb/IIIa therapy.

BACKGROUND: The glycoprotein (GP) IIb/IIIa receptor antagonist abciximab (c7E3 Fab, ReoPro) is approved for use in high-risk percutaneous transluminal coronary angioplasty (PTCA). At present, no "point of care" exists for measuring pharmacological GP IIb/IIIa blockade. To address this need, the Chrono-log Whole Blood Aggregometer, which measures platelet aggregation by electrical impedance, was adapted to test platelet function at the bedside. METHODS AND RESULTS: GP IIb/IIIa receptor blockade, impedance (5 microg/mL collagen), and turbidimetric aggregation (5 and 20 micromol/L ADP) measurements were obtained on 14 PTCA patients who received the standard bolus plus a 12-hour infusion of abciximab. During abciximab administration, mean GP IIb/IIIa receptor blockade was > 91%, and both impedance and turbidimetric aggregation were inhibited by > or = 90%. At 12 hours after abciximab treatment, the mean inhibition of turbidimetric platelet aggregation to 5 and 20 micromol/L ADP was 65+/-20% and 49+/-14%, respectively, and inhibition of impedance aggregation was 69+/-12%. GP IIb/IIIa receptor blockade was 67+/-8%. At 36 hours after abciximab treatment (n=8), the mean inhibition of turbidimetric platelet aggregation to 5 and 20 micromol/L ADP was 44+/-21% and 30+/-14%, respectively, whereas impedance aggregation was inhibited by 60+/-14%. GP IIb/IIIa receptor blockade was 57+/-7%. CONCLUSIONS: During and at 12 hours after abciximab therapy, impedance and turbidimetric platelet aggregation to 5 micromol/L ADP were comparable and closely correlated with GP IIb/IIIa receptor blockade. However, at 36 hours after abciximab treatment, impedance platelet aggregation more closely paralleled GP IIb/IIIa receptor blockade and indicated a slower recovery of platelet function than turbidimetric aggregometry.

Abciximab↗
PubMed1983

Storage of platelets for tests of platelet function: effects of pH on platelet aggregation and liberation of beta-thromboglobulin.

Platelet aggregation responses are influenced by conditions of storage of platelet-rich plasma (PRP). The aim of the present study was to further define the necessity for pH control during storage of PRP for tests of platelet function. Aliquots of citrated PRP were maintained at different pH levels by alteration of the CO2 content of the atmosphere in an incubation chamber. At intervals over 2-2 1/2 hours, plasma beta-thromboglobulin and 14C-serotonin were measured as well as platelet aggregation induced by ADP and collagen. At each time a dose response curve was studied for aliquots stored at each pH level. When two aliquots were maintained at different pH levels in the range 6.85-7.90, there was a significant increase in aggregation at the higher pH, even when the pH difference was as small as 0.2 units. In this range, pH did not influence the rate of deterioration of the aggregation response, but when pH was above 8.0, there was marked deterioration of the response. Increased pH was associated with an increase in plasma levels of beta-thromboglobulin and 14C-serotonin, which was more marked when pH was above 8.0. It appears that increases in pH are harmful to platelets and even small pH changes should be avoided during storage of platelet-rich plasma for tests of platelet function.

Adenosine Diphosphate↗
PubMed1987

Effect of monoclonal antibodies against von Willebrand factor and platelet glycoproteins IIb/IIIa on the platelet retention test.

The platelet retention test provides a measure of the number of platelets retained in a column of glass beads and is one of the few in vitro platelet function tests that is abnormal in von Willebrand's disease (vWd). In a two-stage test, 1 mL of blood (designated A) was passed through the column, followed by 5 mL of isotonic saline and then 5 mL of blood (B) in which platelet retention was measured. With normal blood as A and B, retention is very high in all 5 mL of blood B. In the first stage, platelets adhere to the glass beads; this requires fibrinogen but not von Willebrand factor (vWf). The platelet-platelet adhesion in the second stage requires vWf, is dependent on release of ADP, and fails to occur if thrombasthenic platelets are tested. Retention was normal when blood from a patient with afibrinogenemia was used as blood B. We have now used monoclonal antibodies to elucidate further the mechanism of platelet retention. Five antibodies to different epitopes on vWf essentially abolished retention in the one-stage test and in the second stage of the two-stage test, but had no effect on the first stage. Thus, the entire vWf molecule must be free of antibody to function in the platelet-platelet adhesion of the second stage of this test. Binding of the antigen-antibody complex to the platelet Fc receptor was not responsible, as Fab and F(ab')2 fragments of one of the antibodies were as effective as intact antibody, and as neither heat-aggregated IgG nor a polyclonal antibody to plasma factor IX inhibited retention. F(ab')2 fragments of 6D1, an antibody to platelet GP Ib that prevents binding of vWf to platelets, also inhibited the second phase of retention. An antibody that inhibits binding of fibrinogen and vWf to GP IIb/IIIa (LJ-CP8) inhibited both the first and second stages of retention, whereas LJ-P5, an antibody that inhibits only the binding of vWf to GP IIb/IIIa, caused slight inhibition of retention when normal or afibrinogenemic blood was used as blood B and was reported to cause only partial inhibition of ADP-induced platelet aggregation in this afibrinogenemic patient. The results suggest that vWf is altered during rapid passage of blood through the glass-bead column so that it attaches to GP Ib, exposing GP IIb/IIIa, which then binds the altered vWf or fibrinogen, either of which can induce platelet aggregation (platelet-platelet adhesion) and thus retention in the column.

Antibodies, Monoclonal↗
PubMed1991

Characteristics of platelet concentrates, with particular reference to Autopheresis C Plateletcell: correlation between dMPV and other tests for platelet function.

The quality of platelet concentrates (PC) collected by the Autopheresis C cell separator was assessed in two Regional Transfusion Centres taking part in a multicentre study. This study also enabled the assessment of a new simple, rapid test of platelet function and comparison with more established tests, such as aggregation to adenosine diphosphate, as a tool for the quality testing of PC. The new test, based upon the measurement of mean platelet volume using automated haematological cell analysers, is rapid and uses the same samples as those used to estimate the platelet and leucocyte content of the concentrates. The high correlation between this test and the other tests of platelet function used in the study suggests that it is an ideal tool in the quality testing of platelet concentrates.

Antigens↗
PubMed2000

Monitoring antiplatelet therapy: What is the best method?

Platelet function tests measure different aspects of platelet function, which include adherence, activation, aggregation and secretion. Clinically, the goal of platelet function testing is to provide information about the platelet contribution to the risk of thrombotic or haemorrhagic events and the optimisation of antiplatelet therapy. The important clinical questions are whether an antiplatelet agent is having the desired effect on platelet inhibition (effectiveness) and whether the patient has sufficient residual platelet function to avoid bleeding (safety). The role of aspirin (acetylsalicylic acid) and thienopyridines is well established in the management of patients with coronary artery disease and in the setting of coronary interventions. The last several years have demonstrated the unequivocal effectiveness of intravenously administered platelet glycoprotein (GP) IIb/IIIa antagonists in the management of acute coronary syndromes and in the setting of percutaneous coronary interventions. With the increasing use of these GPIIb/IIIa antagonists, it is becoming more important clinically to measure platelet inhibition with these agents. This paper reviews major techniques and instrumentation for platelet monitoring and discusses the goals of the best method.

Humans↗
PubMed2004

[Platelet Adhesion Assay (PADA), a new quantitative test for assessment of platelet function and therapeutic drug monitoring of GPIIb/IIIa and ADP receptor antagonists].

Platelet ADhesion Assay (PADA) is a POCT capable method for quantitative determination of platelet adhesiveness. Using special polymer particles and test conditions adjusted to the physiologic conditions, the current functional state of blood platelets is determined directly from a whole blood sample. Within a short time, using little technical equipment and small sample volume, a therapeutic drug monitoring of GP IIb/IIIa and ADP receptor antagonists is possible, too. Whereas in healthy volunteers dose/effect curves of GP IIb/IIIa antagonists vary only slightly, in thrombopilic patients there are big variations. Differences in efficacy up to drug resistance may occur also in use of the ADP receptor antagonist clopidogrel. A therapeutic drug monitoring of GP IIb/IIIa- and ADP receptor antagonist therapy is essential and becomes feasible using PADA, also as long-term drug monitoring of ADP receptor antagonists and detection of drug resistance. Additionally, an individual ex vivo dose estimation for GP IIb/IIIa antagonists is possible. PADA allows diagnostics of pathological platelet function in thrombophilic patients as well as long-term therapeutic drug monitoring due to its simple handling.

Blood Specimen Collection↗
PubMed2005

Platelet aggregation testing in platelet-rich plasma: description of procedures with the aim to develop standards in the field.

Platelet function testing consisting of platelet aggregation and secretion often is requested in the clinical evaluation of patients with bleeding problems. At present, there are no uniform clinical laboratory standards for the performance or interpretation of these studies. The present report describes one laboratory's methods and interpretations of platelet aggregation and secretion studies of platelet-rich plasma using each of the common platelet agonists. Diagnostic categories for the evaluation of the platelet function testing are presented. The diagnostic categories then are applied to the evaluation of 61 patients referred to our medical center for these studies. The aims of this report are to present clinical platelet aggregation and secretion studies and to provide a working schema to evaluate these results. Our intent is to stimulate interest in the development of professional guidelines for platelet function testing in the clinical laboratory.

Adenosine Diphosphate↗
PubMed2005

Platelet adhesion assay--a new quantitative whole blood test to measure platelet function.

At this time no practical laboratory method for the measurement of the current functional state of blood platelets is available. A new innovative platelet adhesion assay (PADA) is described here. With only a short time requirement and minimal equipment, the PADA provides quantitative measurements of platelet adhesiveness. Only 0.5 mL of freshly drawn citrated whole blood is needed, to which special polymer particles are added. A defined shear grade is induced by a short period of shaking the sample. Proteins of the blood sample, especially fibrinogen, and thereafter also activated platelets, bind to the specific polymer surface. Following platelet counts both in the sample and in a control (blood without particles), the adhesion index (AI) is calculated as a quantitative measure of platelet adhesiveness. In healthy volunteers, a mean AI of 52+/-12 was measured. AI was shown to be nearly independent of the number of platelets in the sample (100 to 350 k/ microL), the hematocrit (44 to 25%), and the fibrinogen content (1.5 to 5 g/L). Age of the volunteers had only a minor influence on the AI. PADA was shown to be a simple reliable laboratory method for the detection of disturbed platelet function. The test requires low analytical efforts compared with other diagnostic platelet function tests.

Adult↗