Arachidonic acid ? Induced platelet aggregation and prostanoid formation in whole blood in relation to plasma concentration of indomethacin

1985 ◽  
Vol 28 (2) ◽  
pp. 163-169 ◽  
Author(s):  
E. Vinge
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Plasma Concentration ◽  
Whole Blood

scholarly journals Lipid peroxidation, prostacyclin and thromboxane A2 in pigs depleted of vitamin E and selenium and supplemented with linseed oil

1995 ◽  
Vol 74 (3) ◽  
pp. 369-380 ◽  
Author(s):  
Maeve R. Nolan ◽  
Seamus Kennedy ◽  
W. John Blanchflower ◽  
D. Glenn Kennedy
Keyword(s):  
Lipid Peroxidation ◽  
Arachidonic Acid ◽  
Vitamin E ◽  
Platelet Aggregation ◽  
Plasma Concentration ◽  
Linseed Oil ◽  
Thromboxane A2 ◽  
Dietary Factors ◽  
Biochemical Effects ◽  
Skeletal Myopathy

In a 2×2 balanced factorial experiment the biochemical effects on pigs of two dietary factors were investigated. The first factor was α-tocopherol and Se supplementation and the second factor was supplementation with α-tocopherol-stripped linseed oil. In pigs fed on diets depleted of α-tocopherol and Se, increases in concentrations of markers of lipid peroxidation (4-hydroxynonenal and hexanal) were observed. However, skeletal myopathy was only observed in those pigs fed on diets depleted of α-tocopherol and Se and supplemented with oil. In those pigs, increased lipid peroxidation was observed in heart and supraspinatus muscle. The plasma concentration of thromboxane B2 was increased in pigs fed on diets depleted of α-tocopherol and Se, suggesting an increased tendency towards platelet aggregation. However, this change was reversed in pigs depleted of α-tocopherol and Se, but supplemented with oil. This may have been a consequence of loss of arachidonic acid, the substrate for thromboxane formation, as a result of lipid peroxidation.

scholarly journals Comparison of effect of aloe Vera gel with aspirin and celecoxib on platelet aggregation.

2020 ◽  
Vol 27 (05) ◽  
pp. 973-978
Author(s):  
Sidra Mushtaq ◽  
Zobia Mushtaq ◽  
Javeria Arif ◽  
Mufakhara Fatima ◽  
Sadida Bahawal ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Whole Blood ◽  
Blood Count ◽  
Complete Blood Count ◽  
Platelet Rich Plasma ◽  
Aloe Vera ◽  
Medical Institute ◽  
Aloe Vera Gel ◽  
Study Setting

Objective: This study was designed to compare the effect of Aloe vera gel with aspirin and celecoxib on platelet aggregation. Study Design: Comparative Study. Setting: Post graduate Medical Institute Lahore, Children Hospital, Lahore. Period: September 2015 to September 2016. Material & Methods: Blood was withdrawn from anti-cubital vein, complete blood count was checked, platelet rich plasma was prepared by centrifuging citrated whole blood and then incubated with  Aloe vera low (AVL), Aloe vera high (AVH), aspirin and celecoxib for 30 minutes at 37C. After adding the agonist arachidonic acid, reading was then taken for 3 minutes and percentage aggregation was recorded. Results: Platelet aggregation with aspirin, AVH and AVL was statistically significantly lower as compared to control and celecoxib groups. Conclusion: This study has demonstrateda dose dependentanti-platelet effect of Aloe vera gel which is comparable to aspirin.

Rapid Assessment of Platelet Function Using Thromboelastography and Small Volumes of Citrated Whole Blood.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3995-3995 ◽  
Author(s):  
Fred G. Pluthero ◽  
Margaret L. Rand ◽  
Victor S. Blanchette ◽  
Walter H. Kahr
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Whole Blood ◽  
Function Analysis ◽  
Maximum Amplitude ◽  
Ease Of Use ◽  
Platelet Response ◽  
Platelet Function Disorders ◽  
Wide Range

Abstract Platelet function disorders are a key cause of abnormal bleeding, and diagnosis is challenging because: platelet abnormalities are diverse, affecting many aspects of function; variability in platelet function testing in clinical laboratories makes it difficult to compare results; large blood volumes required for platelet function analysis make it difficult to perform in neonatal patients; manipulation of platelet rich plasma used for platelet aggregation can lead to test variability; platelet aggregation curves are difficult to interpret in thrombocytopenic patients. We describe a method of testing platelet function using citrated whole blood and thromboelastography (TEG) that overcomes some of these limitations. Commercially-available platelet mapping kits allow the effects of the platelet agonists adenosine diphosphate (ADP) and arachidonic acid (AA) to be assessed via a TEG assay where reptilase and activated factor XIII produce fibrin clots independent of thrombin in heparinized whole blood. The activation and aggregation of platelets is quantified by measuring the difference in maximum amplitude (MA) between unstimulated samples, which form weak fibrin-only clots, and samples with agonists added, which form stronger clots containing fibrin and activated/aggregated platelets. Platelet mapping was used as the basis for a TEG assay which can be used to assess platelet responses to a wide range of stimuli - including ADP, AA, epinephrine, collagen, U46619 (thromboxane-A2 receptor agonist), SFLLRN (PAR-1 thrombin receptor activating peptide) and AYPGKF (PAR-4 activating peptide) - in small samples (330μL) of citrated native (CN) blood or plasma to which heparin is added to a concentration of 20U/mL. Samples were recalcified by adding calcium chloride to 10mM (necessary for the function of reptilase and FXIIIa), and other reagent volumes were the same as in platelet mapping assays, with fibrin activator prepared at 1/2 regular strength. The concentrations of platelet agonists were: collagen 51μg/ml, epinephrine 0.27μM, ADP 5.4μM, arachidonic acid 135μg/mL, U46619 2.6μM, SFLLRN 6.76μM and AYPGKF 34μM. These concentrations produced TEG MA values in heparinated fibrin-activated CN blood from a panel of normal individuals comparable to those obtained from recalcified CN blood in the absence of heparin (the fibrin/platelet response control). The platelet response was rapid with maximum amplitudes reached within 10 minutes for all agonists except collagen, which required >30 minutes to produce maximum amplitude. We have found this TEG platelet-response assay to be useful in detecting platelet function abnormalities, producing results which correlate with and extend those of other platelet function tests. For example in one patient a weak response to epinephrine corresponded to similar platelet aggregation results, and in another the TEG assay detected a weak PAR-1 response not specifically detected in other tests. The assay has also proven useful in assessing platelet function in blood and plasma having low platelet concentrations (<50 x 10E9/L) from experimental or pathological causes (e.g. thrombocytopenia), in titrating platelet responses to agonists and in assessing the effects of antiplatelet agents in vivo and in vitro. Thus this TEG platelet function assay has the advantages of speed, ease of use, flexibility, adaptability to low platelet concentrations and sample economy, requiring small volumes of citrated blood which can be used for other coagulation assays and platelet response tests.

A Prostacyclin-sparing Effect of Indobufen vs. Aspirin

1996 ◽  
Vol 75 (03) ◽  
pp. 510-514 ◽  
Author(s):  
R De Caterina ◽  
D Giannessi ◽  
W Bernini ◽  
G Lazzerini ◽  
M Lavezzari ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Whole Blood ◽  
Ex Vivo ◽  
Blood Platelet ◽  
Tolerability Profile ◽  
Double Blind ◽  
Baseline Serum ◽  
Cyclooxygenase Inhibition ◽  
Blood Platelet Aggregation

SummaryIndobufen ((±)-2-[p-(l-oxo-2-insoindolinyl)-phenyI]-butyric acid, indo) is a drug inhibiting platelet function by a reversible block of the arachidonic acid metabolism at the level of cyclooxygenase. Since tolerability profile of such drugs is mostly linked to extra-platelet cyclooxygenase inhibition, we prospectively evaluated the extent of platelet and extra-platelet cyclooxygenase inhibition by in vivo administration of indo in comparison with ASA. We assessed the effects of the two drugs on the ex vivo generation of TXB2 and 6-keto-PGFlΑ in whole blood, as indices of the production of TXA2 and PGI2 (prostacyclin), respectively, either after spontaneous clotting at 37° C for 1 h (Study 1) or after the addition of 2 Μg/ml collagen (Study 2). Generation of 6-keto-PGFlΑ in whole blood is a mixed index of platelet and extra-platelet cyclooxygenase activity, deriving from both platelet and white blood cell arachidonic acid metabolization. Fifteen patients with ischemic heart disease and baseline serum TXB2 levels > 300 ng/ml were allocated to receiving one single administration of either indobufen 200 mg (n = 6) or aspirin 500 mg (n = 9). Whole blood prostanoid generation was assessed at 0,1,2,4,6, 8,12 and 24 h after drug administration (Study 1). Ten healthy male volunteers were allocated to a double-blind, randomized crossover comparison of indo 200 mg b.i.d. vs. ASA 300 mg/d for 7 days (Study 2). Prostanoid generation and whole blood platelet aggregation were performed before and at the end of each study period (Day 0 and Day 7). At each time-point after single dose administration (Study 1), indobufen caused less % inhibition of whole blood 6-keto-PGFlΑ than of TXB2. At 2 h, TXB2 was reduced to a similar extent after ASA (98 ± 4%) and indo (97 ± 6%) (p = N.S.), while inhibition of 6-keto-PGFla was clearly different (> 98% after ASA, 81 ± 2.5% after indo, p < 0.01). After one week of ASA or indo (Study 2) the maximum extent of whole blood platelet aggregation was similarly inhibited (from 17.2 ± 1.4 ohms to 3.6 ± 1.3 ohms with ASA; from 18.3 ± 1.0 ohms to 1.6 ± 0.7 ohms with indo (p ASA vs. indo = N. S.). Despite equal inhibition of whole blood TX production after collagen (from 49.0 ± 4.3 ng/ml to 1.1 ± 0.6 ng/ml with ASA, from 49.8 ± 1.3 ng/ml to 1.4 ± 0.6 ng/ml with indo), again, however, 6-keto-PGFlΑ production was less affected by indo than by ASA (from 409 ± 30 pg/ml to 37 ± 13 pg/ml with ASA, inhibition = 91%; from 396 ± 35 to 318 ± 40 with indo, inhibition = 20%). These differential effects of indo and ASA might lead to a better platelet selectivity, tolerability and benefit/risk profile of indo vs. ASA, which are worthy of further assessment.

Influence of Fibrinogen Split Products on Platelets

1967 ◽  
Vol 17 (01/02) ◽  
pp. 078-098 ◽  
Author(s):  
M. I Barnhart ◽  
D. C Cress ◽  
R. L Henry ◽  
J. M Riddle
Keyword(s):  
Platelet Aggregation ◽  
Plasma Concentration ◽  
Whole Blood ◽  
Platelet Rich Plasma ◽  
Platelet Response ◽  
Transient Nature ◽  
Platelet Morphology ◽  
Platelet Aggregates

SummaryBreakdown products of fibrinogen and fibrin can play a role in hemostasis and also may be of consequence in thrombosis. β2 fibrinogen derivative D is an electropositive terminal proteolysis product of fibrinolysis which has the ability to aggregate platelets. The normal plasma concentration of such nonclottable fibrinogen relatives is 0.2 mg/ml. During fibrinolysis this concentration may reach 5 mg/ml plasma. Addition of β 2 fibrinogen D (raising the plasma concentration 0.1 to 5 mg/ml) either in vivo or in vitro induced platelet aggregations. Moreover, alterations in platelet morphology occurred which were obvious by electron microscopy.Platelet depletion was a consistent response to the infusion of purified β2 fibrinogen D (8 to 55 mg/kg body weight) into dogs. Circulating platelets decreased as much as 85% but were only temporarily aggregated and reappeared in the circulation within 1 to 5 hrs. Small platelet aggregates circulated while large aggregates were trapped in the microcirculation. Thrombin was not responsible for the platelet aggregations as neither prothrombin nor clottable fibrinogen were changed significantly. The transient nature and morphological features of the platelet response according to microscopic criteria were prominent during and after infusion of β2 fibrinogen D.In vitro studies included 3 systems; washed platelets, platelet rich plasma and whole blood. Positive results were obtained with all, but platelets in whole blood were most responsive. The magnitude of platelet aggregation and morphology correlated with the concentration of β2 fibrinogen D. Platelet aggregation induced by ADP (10~5 mg/ml) was compared with that induced by β2 fibrinogen D (0.09 to 0.72 mg/ml). With either reagent aggregates were of dendritic forms. Combination of the 2 reagents was additive but did not further change the morphology. Additional factors seem necessary for development of viscous metamorphosis.

Comparison of Rapid Platelet Function Assay with Whole Blood Platelet Impedance Aggregometry for the Definition of Aspirin Resistance.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4018-4018
Author(s):  
Anna M. Dyszkiewicz-Korpanty ◽  
Anne Kim ◽  
James D. Burner ◽  
Eugene P. Frenkel ◽  
Ravindra Sarode
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Whole Blood ◽  
Platelet Rich Plasma ◽  
Blood Platelet ◽  
Aspirin Resistance ◽  
Impedance Aggregometry ◽  
Definition Of ◽  
Induced Aggregation

Abstract The reported incidence of aspirin (ASA) resistance ranges from 5 to 30%. Various platelet function assays have been employed to detect aspirin resistance in patients with cardio- and cerebrovascular disease. Such a high proposed incidence of ASA resistance poses a critical need for a rapid point-of -care (POC) platelet function test. Unfortunately, no uniformly accepted definition of ASA resistance exists. Platelet aggregation studies that have been used to define ASA resistance are time consuming and require special technical expertise. The Ultegra Rapid Platelet Function -ASA (RPFA-ASA) has been developed as a POC test that is performed without sample processing. This optical method measures agglutination of fibrinogen-coated beads upon platelet activation with arachidonic acid. In the presence of aspirin effect, however, the agglutination of the beads is inhibited. The described cutoff of ≥ 550 Aspirin Reaction Units (ARU) is termed non-responsiveness to ASA based on a preclinical study and subsequent correlation with epinephrine-induced platelet aggregation in platelet rich plasma. Since RPFA-ASA uses whole blood, we validated its performance characteristics against a classic whole blood platelet aggregation assay (WBA). We studied 50 healthy volunteers, aged 25–75 (24 men, 26 women) with normal CBC, who had not ingested anti-platelet drugs for 14 days prior to the study. Baseline studies included WBA (dual channel aggregometer, Chrono-log Inc., Havertown, PA) using both arachidonic acid (AA -0.5; 0.25 mM) and collagen (1; 2 μg/mL) as well as an RPFA-ASA assay (Accumetrics Inc., San Diego, CA). These studies were repeated after 3 days of ASA (325 mg/d) intake. Based on a review of the literature, we defined an adequate ASA response as a completely inhibited AA-induced platelet aggregation and at least 30% inhibition of collagen-induced aggregation (both concentrations of the agonist). Thus, those with &lt; 30% inhibition of aggregation response to collagen were considered ASA resistant. Eleven subjects were ASA resistant by WBA (20%; 8 females and 3 males (aged 25–63). In contrast, since all 50 subjects achieved ARU values of &lt; 550 ARU, none were recognized as an ASA non-responder by the RPFA-ASA. While the current cutoff of &lt; 550 ARU posed by the Ultegra RPFA-ASA does identify those who have taken ASA, the assay is unable to recognize ASA non-responders. Thus, based on these data, the appropriate cutoff for the recognition of ASA resistance by the RPFA-ASA should be re-adjusted to a significantly lower level to ensure appropriate assay results.

scholarly journals The Role of Whole Blood Platelet Aggregation Studies in the Diagnosis of Unexplained Bleeding Tendencies

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 2260-2260
Author(s):  
Nicole De Simone ◽  
Ravi Sarode ◽  
Sean Yates ◽  
Karen Matevosyan ◽  
Manasa Reddy ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Whole Blood ◽  
Selective Serotonin ◽  
Impedance Method ◽  
Platelet Dysfunction ◽  
Atp Secretion ◽  
Abnormal Results

Abstract Introduction: Platelet aggregation studies (PAS) are an important and underutilized diagnostic test (due to non-availability in most clinical laboratories and the requirement to be performed within 4 hours of sample collection) used in the evaluation of unexplained mucocutaneous type of bleeding after ruling out von Willebrand disease. Platelet aggregation studies are typically performed by one of two methods: impedance method using whole blood aggregometry (WBA) and light transmission aggregometry (LTA) using platelet rich plasma (PRP). WBA confers several advantages over LTA. First, it does not require centrifugation, which not only reduces testing time by half, but also avoids platelet activation and loss of giant thrombocytes. Second, in vivo conditions are better replicated reflecting the natural milieu including red and white blood cells, which are known to affect platelet function in vivo. In addition, WBA requires smaller blood volume making testing feasible for neonates and pediatric patients. Lastly, simultaneous assessment of platelet ATP release is performed to assess secretion defects. Despite these advantages, WBA is not commonly used. Aims: To analyze our data to further support the diagnostic utility of WBA in identifying platelet dysfunction as the etiology of bleeding tendencies. Methods: A retrospective chart review of patients on whom PAS were performed between June 2011 and September 2014. Results: We performed 202 PAS on 162 patients. 82% of patients were females and the average age was 28 years (range 9 months-87 years). 24 (15%) patients were pediatric (range 9 months-18 years). 83 of 162 (51%) patients had abnormal results (52% of adults and 50% of the pediatric cases). 26 of the 162 (16%) patients had repeat studies performed. Of these patients, 77% (20/26) had reproducible findings that confirmed the previous results. 8% (2/26) had normalized platelet function after discontinuation of medications (e.g. statins, fish oil, selective serotonin reuptake inhibitor) known to induce platelet dysfunction. 15% (4/26) had different responses to agonists on repeat testing. Abnormal WBA studies revealed decreased to absent responses to various agonists described in table 1. In patients on selective serotonin release inhibitors (SSRIs), there was a spectrum of responses to agonists; the most common abnormality was global dysfunction. Abnormalities to single agonists, such as ADP and AA, were also seen in patients taking SSRIs. Non-steroidal anti-inflammatory drugs affected aggregation with arachidonic acid (AA) and AA+ADP. Statins affected aggregation with AA alone, AA+ADP and AA+ATP secretion. 3 patients had platelet dysfunction consistent with Acquired Glanzmann's Syndrome due possibly to autoantibodies in the setting of chronic lymphocytic leukemia. Conclusion: Over 50% patients tested by WBA had abnormal platelet function giving high positive predictive value for this test in a selected group of patients who otherwise would have carried a non-specific bleeding diagnosis with non-specific treatment. Table 1. Distribution of Agonists Eliciting Impaired Responses Agonists Eliciting Impaired Response Number of Studies with Abnormal Results AA+Collagen (Aspirin like defect) 27 (23%) AA+Collagen+ADP 22 (18%) AA+ADP 21 (17%) AA+Collagen+ADP+Ristocetin (Global dysfunction) 19 (15%) ADP 11 (9%) AA 7 (6%) ADP+Collagen 4 (3%) AA+ADP+Ristocetin 3 (2%) Decreased ATP Secretion 8 (7%) AA=Arachidonic Acid Disclosures No relevant conflicts of interest to declare.

Aspirin Resistance - A Comparison of Platelet Functions and 11-Dehydro Thromboxane B2 and 8-epi Prostaglandin F2α Plasma Concentration.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4005-4005
Author(s):  
Krystyna Zawilska ◽  
Marcin Zytkiewicz ◽  
Ewelina Hanszke ◽  
Liwia Gielwanowska ◽  
Piotr Psuja ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Ischemic Stroke ◽  
Platelet Aggregation ◽  
Plasma Concentration ◽  
Laboratory Tests ◽  
Prostaglandin F2α ◽  
Aspirin Resistance ◽  
Thromboxane B2 ◽  
Closure Time ◽  
Induced Aggregation

Abstract Introduction. Laboratory tests do not reveal any changes due to administration of aspirin (75 – 150 mg/d) in about 25% of patients. The definition of aspirin resistance and parameters of different laboratory tests for its identification have not yet been established. Aim. The aim of our study was to compare the results of platelet aggregation studies, the closure times in PFA-100, the plasma concentrations of 11-dehydro thromboxane B2 (11-d TxB2) and 8-epi prostaglandin F2α (8-epi PgF2α) in patients receiving aspirin chronically. Material. The study group consisted of 22 patients taking aspirin for the secondary prevention of ischemic stroke (IS). All patients were at least 6 months after the acute onset, and had a diminished intraplatelet concentration of malonyldialdehyde due to aspirin ingestion. Methods. Following parameters have been evaluated: Platelet aggregation induced by either ADP (3,5 and 5,0 μM), collagen (2 μg/ml) or arachidonic acid (AA) (0,6 mM); Closure time in PFA-100 (collagen/epinephrine and collagen/ADP cartridges); Plasma 11-d TxB2 and 8-epi PgF2α concentration measured by ELISA method (Cayman Chemicals). Aspirin resistance has been determined by the following criteria: the intensity of ADP induced platelet aggregation ≥ 60%, collagen induced aggregation ≥ 70%, AA induced aggregation ≥ 20%, PFA-100 closure time ≤ 165 s, 11-d TxB2 concentration ≥ mean of the control group ± 2 SD. Results. The frequency of aspirin resistance in patients after ischaemic stroke Aggregation ADP 3,5 μM ADP 5,0 μM Collagen Arachidonic acid PFA-100 11-d TxB2 63,6% 45,5% 18,2% 13,6% 54,5% 50,0% Statistically significant correlations have been found between the plasma concentration of 11-d TxB2 and PFA-100 (Col/Epi) closure times and between plasma concentration of 8-epi PgF2α and PFA-100 (Col/Epi) closure times. There was no difference in mean plasma concentration of 8-epi PgF2α between the group of patients and controls. Conclusions. The most valid laboratory method of aspirin resistance identification in ischemic stroke patients (besides a mesurement of 11-dehydro thromboxane B2) seems to be PFA-100 closure time. Our PFA-100 studies reveal a much higher percentage of aspirin resistance as compared to former studies. The plasma concentration of 8-epi prostaglandin F2α remains in the normal range in patients taking aspirin for the secondary prevention of ischemic stroke.

scholarly journals Whole Blood Platelet Aggregation and Release Reaction Testing in Uremic Patients

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Jay Zeck ◽  
Jason Schallheim ◽  
Susie Q. Lew ◽  
Louis DePalma
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Whole Blood ◽  
Low Dose ◽  
Reference Range ◽  
Atp Release ◽  
Blood Platelet ◽  
Ckd Stage ◽  
Uremic Patients ◽  
Blood Platelet Aggregation

Background. Platelet function analysis utilizing platelet-rich plasma and optical density based aggregometry fails to identify patients at risk for uremia associated complications.Methods. We employed whole blood platelet aggregation analysis based on impedance as well as determination of ATP release from platelet granules detected by a chemiluminescence method. Ten chronic kidney disease (CKD) stage 4 or 5 predialysis patients underwent platelet evaluation. Our study aims to evaluate this platform in this patient population to determine if abnormalities could be detected.Results. Analysis revealed normal aggregation and ATP release to collagen, ADP, and high-dose ristocetin. ATP release had a low response to arachidonic acid (0.37 ± 0.26 nmoles, reference range: 0.6–1.4 nmoles). Platelet aggregation to low-dose ristocetin revealed an exaggerated response (20.9 ± 18.7 ohms, reference range: 0–5 ohms).Conclusions. Whole blood platelet analysis detected platelet dysfunction which may be associated with bleeding and thrombotic risks in uremia. Diminished ATP release to arachidonic acid (an aspirin-like defect) in uremic patients may result in platelet associated bleeding. An increased aggregation response to low-dose ristocetin (a type IIb von Willebrand disease-like defect) is associated with thrombus formation. This platelet hyperreactivity may be associated with a thrombotic diathesis as seen in some uremic patients.

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