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PubMed2003

[The value of platelet function tests].

Platelet function tests are used to detect patients with abnormal platelet function, which may be inborn or acquired or to detect increased platelet activation which may be accompanied by an increased risk of thrombosis. Platelet function tests are also used to monitor platelet function inhibitors as aspirin, clopidogrel or platelet membrane glycoprotein IIb/IIIa-inhibitors. Incorrect blood sampling is a major source of error in measuring platelet function. Global tests besides platelet count and bleeding time are thrombelastography, the platelet function analyzer (PFA) and possibly in the future the new Impact-system. Specific tests measure platelet spreading and adhesion to defined surfaces. In a series of methods platelets are counted before and after passage of a filter. Some of these tests are partially standardized. The most frequently measured platelet function is aggregation induced by ADP, collagen or other substances as first described by Gustav Born. Some newer methods to perform aggregometry are described. Platelet activation can be detected by measuring spontaneous aggregation as in the PAT-test. Prospective trials with this test have shown that enhanced spontaneous aggregation is a risk factor for new vascular occlusions in diabetics and for myocardial infarctions in healthy individuals. The Wu and Hoak-test and the measurement of released platelet factor 4 or betaglobulin are of limited value. Flow cytometric methods are frequently used to measure platelet activation markers as CD 62 and others. Platelet induced thrombin generation is an interesting function to measure drug effects. None of the presently available platelet function tests is well standardized, so there is much room for improvement.

Blood Platelet Disorders↗
PubMed1992

[Current status and problems of platelet function tests].

Platelet function tests have been utilized for a long time as a useful tool for the diagnosis of qualitative platelet disorders. However, recently reports suggest that platelet function tests currently available in routine laboratory do not necessarily reflect in vivo hemostatic states. First of all, bleeding time could sometimes be non-informative for the following reasons; 1) Duke method, the most popular method in Japan, has poor reproducibility, 2) there is no appropriate method for monitoring of aspirin ingestion, 3) prolongation of bleeding time does not correlate with the amount of blood loss during surgery. Platelet adhesion is still measured by the ability of platelets to be retained on glass beads. However, this test is unable to detect selectively platelet adhesion. Thus, the test in which platelets can exclusively adhere to subendothelial components such as collagen, may be required. Platelet aggregation has been mostly analyzed by the changes in light transmittance in platelet rich plasma (PRP) with a platelet aggregometer. However, this test totally depends on the platelet count in PRP or duration of time after taking blood from patients. Moreover, platelet aggregation in this system is optimally observed and is hardly detectable when the in vivo Ca++ concentration has been chelated. Furthermore, the test could not detect small platelet aggregates, thus being unable to measure the early phase of platelet aggregation. These observations suggest that more simple and specific tests should be developed and become available in routine laboratory.

Bleeding Time↗
PubMed2004

[Monitoring of tienopyridines or glycoprotein IIb/IIIa-receptor antagonists: simple platelet function tests].

Platelet function analyses were known as mystified, complicated, and time consuming laboratory investigations with a high coefficient of variation. Only in rare cases they led to precise interpretations under routine clinical laboratory conditions. In the first line they were focussed on bleeding tendencies. Only few were suited to evaluate the state of hyperaggregability of platelets. This short presentation of the GTH-Symposium 2004 gives a survey on the most simple and practicable tests for checking platelet function which may be used for the monitoring of therapy with tienopyridines and glycoprotein IIb/IIIa-receptor antagonists.

Blood Platelets↗
PubMed2003

Platelet function tests using platelet aggregometry: need for repetition of the test for diagnosis of defective platelet function.

Four hundred and ninety seven patients were referred to our center for platelet aggregation studies because of spontaneous mucocutaneous bleeds. All these patients had normal complete blood count, platelet count and peripheral smears except in ten patients of Bernard Soulier Syndrome where platelet count was marginally reduced in the presence of giant platelets. Two hundred and eighty patients were found to have normal platelet aggregation to ADP, collagen, ristocetin and arachidonic acid. Out of the remaining 217 patients, 62 patients were diagnosed to have Glanzmanns thrombasthenia, 10 Bernard Soulier Syndrome, 6 storage pool deficiencies, 7 cyclooxygenase deficiencies and 72 von Willebrand disease. In all the patients with GT and BSS, diagnosis was confirmed with flow cytometry using multiple monoclonal antibodies to GPIIb-IIIa and GPIb-IX. There were sixty patients where initial platelet aggregation studies showed reduced (<30%) aggregation to either ADP, collagen, ristocetin or arachidonic acid in its various combination, however in 12 such patients (20%) the platelet aggregation studies were normal on repetition. All our platelet aggregation studies were done only after assuring that the patient is not taking any medicine for at least 7-10 days which may affect the platelet function tests. The present study shows that single atypically abnormal platelet aggregation studies should always be repeated. Finally in 48/217 patients (22%) some aggregation abnormality to one or more of the agonists persisted, although we could not categorize these patients into any clear-cut platelet disorder. None of these 48 patients platelet associated immunoglobulin was increased by flow cytometry. It is possible that large number of patients from that disorder will finally prove to be some form of platelet secretory defect. In north India similar group of defect in a large number of patients have been reported as isolated PF3 abnormality or thrombasthenic thrombopathy.

Adenosine Diphosphate↗
PubMed1980

Platelets in myeloproliferative disorders. I. A comparative evaluation with certain platelet function tests.

Certain platelet functions were evaluated in 24 patients with secondary polycythaemia (SP) and in a large number of patients suffering from myeloproliferative disorders (MD'S): 89 patients with chronic myeloid leukaemia (CML) at different stages of development, 58 with polycythaemia vera (PV), 23 with essential thrombocythaemia (ET), and 25 with agnogenic myeloid metaplasia (AMM). Bleeding time, epinephrine-induced platelet aggregation and adhesiveness agreed with those generally reported in the literature; they are independent of thrombocytosis, the haemoglobin level and the leucocyte count. Macrothrombocytosis, evaluated by an electronic method, was only found in CML, mainly during acute blast crisis. An increased percentage of light platelets was a constant feature in all groups except in the SP and in 20% of the PV. The most severe abnormalities were observed in AMM and CML in the acute stage; in the chronic phase of CML there is no correlation between the severity of platelet abnormalities and the survival of the patients.

Blood Platelets↗
PubMed1981

A review of platelet function and testing.

Platelet function testing is an area of recent growth and development in clinical laboratories. Additions to classical testing procedures include aggregation and retention tests and measurement of platelet release products. The necessity exists for understanding platelet structure and function. In this paper, the various platelet structures are demonstrated, their composition is described, and their individual contribution to platelet activation discussed. Platelet activation is described in four phases: adhesion, reversible contraction, aggregation, and release. Each is described in relationship to the others and laboratory test procedures marking each are described. The question of the relationship of measurement of platelet release markers to clinical condition is reviewed.

Blood Platelets↗
PubMed2002

Platelet activation markers in patients with nephrotic syndrome. A comparative study of different platelet function tests.

BACKGROUND/AIM: Enhanced platelet reactivity may play a significant role in the genesis of the hypercoagulable state of nephrotic syndrome. However, the role of platelet function testing in nephrosis is controversial, partly because the methods used to assess platelet function (platelet aggregation and immunoassays of plasma beta-thromboglobulin and platelet factor 4) have such marked methodological problems. In the present study, we evaluated several tests assessing platelet function in 18 adult patients with idiopathic nephrotic syndrome and normal renal function. METHODS: Platelet function was assessed by measurement of plasma beta-thromboglobulin (enzyme-linked immunosorbent assay, ELISA), plasma P-selectin (ELISA), circulating platelets exposing the activation-dependent antigens P-selectin (CD62P) and lysosomal GP53 (CD63) (flow cytometry), and by aggregation response to agonists such as ADP and collagen. Results were compared to those obtained in a group of 16 age- and gender-matched healthy subjects. RESULTS: Levels of plasma beta-thromboglobulin (p = 0.001), plasma P-selectin (p < 0.001), and CD62P/CD63-positive platelets (p < 0.001 for both) were increased in nephrotic patients as compared to healthy controls. Platelet hyperaggregability in vitro was found in 13/18 patients. The reproducibility of platelet activation markers, as assessed by blood sample collection a week later from all patients, was found to be higher for plasma P-selectin (Spearman correlation coefficient, R = 0.99) and circulating activated platelets (CD62P: R = 0.97; CD63: R = 0.96) than for plasma beta-thromboglobulin (R = 0.78). CONCLUSIONS: Pronounced platelet activation takes place in nephrotic syndrome and may contribute to the hypercoagulability of nephrosis. Whole blood flow cytometry assay of platelet activation and plasma P-selectin assay may represent useful tests to assess the hypercoagulable state in nephrotic patients.

Adult↗
PubMed2004

Platelet function testing to assess effectiveness of platelet transfusion therapy.

BACKGROUND: Posttransfusion corrected count increments (CCI) following administration of platelets is the standard method for assessing effectiveness of platelet transfusion therapy. However, improvement in platelet count following transfusion may not necessarily indicate improvement in platelet function or restoration of primary hemostatic capacity. To address this possibility, we investigated the effectiveness of platelet transfusion based on results of the Platelet Function Analyzer (PFA-100) and post-transfusion CCI. INVESTIGATION DESIGN AND METHODS: Platelet transfusion requests with different indications received at the blood bank were evaluated for inclusion in the investigation. Pre-transfusion, the following laboratory tests were performed: (1) PFA-100 assays (blood collected in 3.2% buffered sodium citrate) performed with CEPI and CADP test cartridges; (2) complete blood count (in EDTA) and platelet count; and (3) routine coagulation profile including PT, PTT, fibrinogen and D-Dimer. Only patients with normal coagulation profiles were included. The same set of tests were performed on a new blood sample collected 10-60 min post-transfusion. Chart review and clinical evaluation for response to platelet therapy were performed on each occasion of transfusion. RESULTS: Thirty-one patients, five of whom were transfused on more than one occasion were evaluated. Thirty-five transfusion incidents were included. Posttransfusion outcomes were divided into two groups--those that resulted in shortening (>40 s) or normalization of the closure time (Group A) and those that had no change or greater prolongation of the closure time (Group B) when compared to the pre-transfusion value. Seventeen and eighteen transfusion episodes were categorized as Groups A and B, respectively. In Group A with improved PFA testing, nine patients had bleeding as indication for transfusion and six of these had concomitant improvement in their clinical picture as confirmed by control of hemorrhage. In contrast in Group B with no improvement in PFA testing, seven patients had bleeding as indication for transfusion and none showed cessation of hemorrhagic symptoms. These findings were statistically significant (p=0.0114). Similar evaluation using the post-transfusion CCI showed no correlation to bleeding symptoms in these patients (p-=0.500). CONCLUSIONS: In this evaluation, platelet function testing using the PFA-100 provided a better indication of transfusion outcome than did the post-transfusion CCI. Using this approach, PFA-100 may be an effective aid for supporting platelet transfusion decisions and may further aid in improving management of the hospital blood bank platelet inventory.

Adult↗
PubMed2001

Testing platelet activation with a shear-dependent platelet function test versus aggregation-based tests: relevance for monitoring long-term glycoprotein IIb/IIIa inhibition.

BACKGROUND: Tests developed to monitor glycoprotein (GP) IIb/IIIa blockade do not properly reflect platelet function in vivo and need a baseline (pretreatment) value. Because GP IIb/IIIa is essential in platelet aggregation and thrombosis under shear conditions, a flow-dependent approach to monitor its inhibition can be used. METHODS AND RESULTS: We compared a test based on flow-dependent platelet deposition, the Cone and Platelet Analyzer (CPA), with in vitro platelet aggregometry and the Rapid Platelet Function Assay (RPFA) on platelet function after GP IIb/IIIa inhibition. In vitro, increasing concentrations of abciximab (0% to 100% receptor occupancy) were tested. Ex vivo, platelet function was monitored with the CPA and with aggregometry for up to 1 week after abciximab administration. The CPA was better correlated with the percentage of free GP IIb/IIIa receptors than was aggregometry or the RPFA. Only the RPFA, when expressed as a ratio over baseline (pretreatment), was comparable to the CPA. Ex vivo, the CPA, but not aggregometry, showed prolonged platelet inhibition with gradual recovery from GP IIb/IIIa receptor blockade in the first week after abciximab administration. CONCLUSIONS: Platelet function assessment by shear-induced deposition is a reliable test to monitor a wide range of GP IIb/IIIa inhibition. Its accuracy does not require a baseline reference. The effects of GP IIb/IIIa blockade on platelet function should be examined under high shear conditions.

Abciximab↗
PubMed2006

Current options in platelet function testing.

The variable response to antiplatelet therapy has led to the use of platelet function tests to monitor the effects of antiplatelet drugs in cardiovascular diseases. The goal is to guide antiplatelet therapy to the optimal dose for the prevention or treatment of thrombosis while minimizing hemorrhagic side effects. The bleeding time is no longer recommended for use because of its nonspecificity and lack of clinical correlations. The current de facto "gold standard" test of platelet function is turbidometric platelet aggregometry. Although this method has been successful in measuring the aggregation of platelets in a glycoprotein (GP) IIb/IIIa (integrin alpha(IIb)beta(3))-dependent manner, it has several limitations, including poor reproducibility, high sample volume, requirement for sample preparation, length of assay time, requirement for a skilled technician, and cost. Therefore, new options for platelet function testing have been developed to address these disadvantages and to meet the need for point-of-care testing that can be performed at or near a patient's bedside without requiring a high degree of technical expertise. The new tests include VerifyNow (Accumetrics, San Diego, CA); Plateletworks (Helena Laboratories, Beaumont, TX); Thrombelastograph PlateletMapping System (Haemoscope Corporation, Niles, IL); Impact cone and plate(let) analyzer (DiaMed, Cressier, Switzerland); and Platelet Function Analyzer 100 (PFA-100; Dade Behring, Newark, DE). In patients treated with antiplatelet drugs, the degree of platelet inhibition, as determined by several of these new platelet function assays, has been shown to predict major adverse cardiac events.

Cardiovascular Diseases↗
PubMed1970

Relationships between platelet function tests in normal and uraemic subjects.

IN TESTS OF PLATELET FUNCTION IN NORMAL SUBJECTS, THE FOLLOWING RELATIONSHIPS WERE FOUND: the greater the platelet adhesiveness the less the ability to disaggregate after challenge with adenosine diphosphate (ADP), and the greater the disaggregation after ADP, the longer the clotting time in the test for platelet factor 3 availability. Such correlations were disturbed in uraemic patients.

Adenine Nucleotides↗
PubMed2004

[Platelet function tests for monitoring of acetylsalicylic acid: clinical significance in antiplatelet treatment].

Several studies have demonstrated with the use platelet function tests (PFT) that subgroups of patients under acetylsalicylic acid (ASA) fail to produce the anticipated antiplatelet effect. This phenomenon as well as the clinical failure of ASA to protect patients from thromboembolic complications has been termed ASA resistance (AR) or ASA nonresponsiveness. Several subtypes of AR can be distinguished by PFT. The following PFT were used to characterize AR: optical aggregometry, platelet aggregation in whole blood, platelet function analyzer (PFA-100), platelet reactivity test or platelet aggregate ratio, flow cytometry and thromboxane B(2) generation. All PFT have in common that their widespread clinical use is substantially limited due to complex preanalytic factors, reduced specificity and poor reproducibility. PFT are not interchangeable for monitoring antiplatelet treatment. Three prospective clinical trials revealed a possible relationship between AR and subsequent cardiovascular events. There is a need for a simple and reliable assay for predicting the clinical efficacy of antiplatelet therapy. Recent data demonstrate that none of the currently available assays including the PFA-100 system are capable to accomplish these objectives.

Aspirin↗
PubMed1981

Standardization of platelet function tests.

Methods for the standardization of several currently used platelet function tests (bleeding time, capillary fragility, platelet retention, platelet aggregation, platelet factor 3, and platelet volume profiles) are presented, Different variables than may interfere with the reproducibility of the results of each assay were identified and standardized. Using the standardized techniques, the range of normal values for each test was determined in a large population of normal volunteers and used to identify disease states by comparing patient results with those of the normal population. A format for presenting the entire profile of platelet function parameters is proposed.

Adult↗
PubMed1989

[Effect of short-term hypoxia on blood platelet function tests of normal subjects].

We studied how smoking and hypoxia affected blood platelet functions. Eighteen normal subjects (ten nonsmokers and eight smokers) inspired 13% oxygen gas and underwent platelet function tests (blood platelet count, MPV, maximum platelet aggregation rate, plasma beta-TG, plasma PF-4) measured just before inspiration and 30 minutes and 60 minutes after inspiration of the gas. Four principal results were obtained. First, breathing room air, blood platelet count and maximum platelet aggregation rate of smokers were significantly increased compared to those of non-smokers. Second, platelet counts and MPV were not affected by hypoxia in either group. Third, the maximum platelet aggregation rate of smokers was significantly decreased by hypoxia. Fourth, in both groups, the plasma levels of beta TG and PF-4 were decreased 30 minutes after inspiration of the 13% oxygen gas. In non-smokers, 60 minutes after inspiration, these plasma levels recovered to the primary levels. Our study showed that blood platelet functions of normal subjects were affected by hypoxia, and the effects of hypoxia on these functions in these two groups were markedly different.

Adult↗
PubMed2006

Impact--the cone and plate(let) analyzer: testing platelet function and anti-platelet drug response.

The Impact [cone and plate(let) analyzer (CPA) Technology]is testing whole blood platelet adhesion and aggregation under arterial flow conditions. The adhered platelets are stained and the percentage of surface covered (SC) by the stained objects and the average size (AS) of the objects are determined by image analyzer. The system allows screening of congenital primary hemostasis abnormalities, including adhesion as well as aggregation defects. The observation that exposure of blood to suboptimal concentrations of platelet agonists for 1 min prior to the Impact test causes platelet adhesion refractoriness led to the development of Impact aggregation tests and of specific tests for the determination of platelet response to aspirin and clopidogrel.

Blood Platelet Disorders↗
PubMedDate not supplied

Platelet function tests in thrombotic cerebrovascular disorders.

A variety of platelet function tests were performed in patients with four forms of obstructive cerebrovascular disease (CVD); transient ischemic attacks (TIA), reversible ischemic neurological deficit (RIND), cerebral infarct, and cerebral embolism of cardiac source in rheumatic valvular heart disease (RVHD). Platelet studies included platelet aggregation induced by ADP and ristocetin, spontaneous platelet aggregation, von Willebrand factor (VIII:vWF), platelet aggregation enhancing factor (PAEF), and percentage of large platelets (megathrombocytes). Serial testing was carried out in acute stroke patients. The effect of aspirin therapy was also evaluated. A clear difference in results was observed between patients with cardiogenic embolism and those with other forms of CVD. In patients with TIA, RIND, and cerebral infarct, platelet aggregation, both induced and spontaneous, was enhanced along with elevation of plasma VIII:vWF and PAEF, and increased percentage of megathrombocytes. In patients with cardiogenic embolism, however, these studies were negative except for percent megathrombocytes. This value was increased in the embolic patients with RVHD in comparison with non-embolic patients with RVHD. Increase in platelet aggregation to ADP and percent megathrombocytes developed slowly over a week following stroke. Induced and spontaneous platelet aggregation, and percent megathrombocytes could be normalized with 600 mg aspirin p.o. These studies suggest that a systemic increase of hyperaggregable platelets and of plasma activators of platelet function exists in thrombotic CVD and may be related to its pathogenesis, while local hemodynamic factors may be more important in the thrombogenesis of cardiogenic embolism.

Adult↗