scholarly journals Unexpected Low Expression of Platelet Fibrinogen Receptor in Patients with Chronic Myeloproliferative Neoplasms: How Does It Change with Aspirin?

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 1794-1794
Author(s):  
Alessandro Lucchesi ◽  
Silvia Carloni ◽  
Martina Ghetti ◽  
Serena De Matteis ◽  
Gerardo Musuraca ◽  
...  
Keyword(s):  
Blood Flow ◽  
Platelet Count ◽  
Platelet Activation ◽  
Binding Capacity ◽  
Myeloproliferative Neoplasms ◽  
Positive Control ◽  
Vascular Events ◽  
Chronic Myeloproliferative Neoplasms ◽  
Fibrinogen Receptor ◽  
Microcirculatory Disorders

Abstract INTRODUCTION Patients affected by Philadelphia-negative chronic myeloproliferative neoplasms (MPNs) are considered at high risk of thrombo-haemorrhagic events, but the role of the platelet count in the assessment of the risk of vascular events is still controversial. A tight correlation was found between the platelet count and plasma sCD40L, which appears to be required for thrombus formation in vivo. However sCD40L is increased both in MPNs and reactive thrombocytosis. Intravascular aggregates of platelets and leukocytes, mediated by P-selectin and CD11b on the former and the latter, respectively, have been observed. Both of this processes should imply a perpetual - and measurable - platelet activation. Several studies on platelet function have been already proposed, nevertheless the mechanisms through which platelets are able to trigger vascular events, are not yet adequately clarified. A refined method for the determination of platelet activation appears to be the use of platelet PAC-1 antibody, able to identify the expression of the fibrinogen receptor of platelet glycoprotein IIb/IIIa. This expression is indeed unique in the process of platelet activation, and yet rarely analyzed. Moreover, since the platelet fibrinogen receptor exposure seems to be influenced by turbulence in blood flow, we have thought that its evaluation could provide important biological evidences to explain some clinical manifestations, such as microvascular disturbances. METHODS Blood samples from 40 consecutive MPNs patients who never received cytoreductive agents, were obtained. 28/40 patients were receiving a continuative antiplatelet prophylaxis with low dose aspirin (ASA, 75-100 mg) at the time of collection, while 12/40 of them were not on such therapy. Our aim was to verify the expression of platelet fibrinogen receptors (PFRs) in the two different groups of patients compared to healthy volunteers, using whole blood flow cytometry. In each experiment sodium citrate and heparin (positive control of platelet activation) tubes were collected from the same patient. Within 10 minutes from blood sampling, 5 ml of whole blood from each tube was incubated for 20 minutes at room temperature in the dark with saturating concentration of CD61 PerCP, CD62P PE and PAC-1 FITC. Positive control was also incubated with PAC-1 in the presence of Arg-Gly-Asp-Ser (RGDS) in order to test the specific antibody binding. Samples were fixed with paraformaldehyde 1% for 30 minutes at 4°C in the dark and analyzed on a flow cytometer. RESULTS Surprisingly, we have been able to verify a very low PAC-1 binding to platelets in patients with MPNs not receiving cytoreduction nor antiplatelet agents (33%) if compared to that observed in healthy subjects (61%; p<0.0001). The use of aspirin seems conversely to restore the expression of platelet fibrinogen receptor, as PAC-1 binding capacity is comparable to that of healthy volunteers (56%). No difference was found with respect to the JAK2 Val617Phe mutation and its allele burden. Interestingly, by focusing on the group of patients under antiplatelet prophylaxis and with no history of thrombosis, it was found that subjects with persistent microcirculatory disorders show a higher PAC-1 binding capacity if compared to the asymptomatic ones (67% vs 52%, p= 0.04). CONCLUSION In untreated MPNs, a large amount of platelets are resting in a conformation that is unable to bind fibrinogen, as demonstrated by the low PAC-1 expression in cytofluorimetry. This lack of activity can be reversed by administering ASA, which is also known for its fibrinolytic and hypoprothrombinemic effects. We hypotesize that the hypercoagulable states observed in these patient could depend on a primarly plasma-driven impairment of fibrin turnover and thrombin generation. Further investigations are going to be promoted by our Group. PAC-1 could be at the same time a good marker of aspirin resistance in patients experiencing microcirculatory disorders. Figure. Figure. Disclosures Martinelli: Janssen: Consultancy; Jazz Pharmaceuticals: Consultancy; Ariad/Incyte: Consultancy; Pfizer: Consultancy, Speakers Bureau; Celgene: Consultancy, Speakers Bureau; Amgen: Consultancy; Abbvie: Consultancy; Roche: Consultancy; Novartis: Speakers Bureau.

In Vivo Effects of Eltrombopag on Human Platelet Function.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 1301-1301 ◽  
Author(s):  
Bethan Psaila ◽  
James B. Bussel ◽  
Matthew D. Linden ◽  
You Fu Li ◽  
Marc R. Barnard ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Blood Flow ◽  
Platelet Count ◽  
Platelet Activation ◽  
Platelet Function ◽  
Whole Blood ◽  
Adult Patients ◽  
Platelet Surface ◽  
Integrin Αiibβ3

Abstract Eltrombopag, an orally-administered small-molecule agonist of the thrombopoietin receptor (c-Mpl), is under investigation as a treatment for immune thrombocytopenic purpura (ITP). Studies have indicated that eltrombopag does not ‘prime’ platelets for activation in vitro, and eltrombopag administration to healthy volunteers does not increase platelet surface P-selectin or activated integrin αIIbβ3 (Jenkins J. Blood 2007). However, the effects of eltrombopag on platelet function in thrombocytopenic patients in vivo, either by direct binding to c-Mpl receptors on platelets or indirectly by altering the dynamics of platelet production and causing an influx of young, large platelets, is unknown. Whole blood flow cytometry, unlike other assays of platelet function, enables measurement of platelet function in the setting of marked thrombocytopenia (Michelson. Platelets, Elsevier, 2007). As a substudy of larger treatment studies, 17 adult patients with chronic ITP received eltrombopag at a starting dose of 50 mg daily, with the possibility of an increase to 75 mg daily after 3 weeks. Blood samples were drawn pre-treatment, and after 7 and 28 days of therapy. Platelet count, mean platelet volume (MPV), and the immature platelet fraction (IPF, or reticulated platelet count) were measured using a Sysmex XE-2100. Platelet surface P-selectin and activated integrin αIIbβ3 (reported by monoclonal antibody PAC1) were measured by whole blood flow cytometry in the presence and absence of 0.5 μM ADP, 20 μM ADP, 1.5 μM thrombin receptor activating peptide (TRAP), or 20 μM TRAP. Bleeding was quantified by a comprehensive scale that allocates grades of 0 (no), 1 (minor) or 2 (marked) bleeding at 10 anatomical sites according to physical examination and/or history (Page, L.K. Br J Haematol 2007). Eleven of the 17 patients responded to eltrombopag with a rise in platelet count of >30 x 109/L. The IPF increased in responders but not non-responders (table 1). Response to eltrombopag was not predicted by pretreatment MPV or IPF. The ITP bleeding score decreased in responders over the study period in parallel with the increases in platelet count (table 1). As determined by platelet surface P-selectin and activated integrin αIIbβ3, eltrombopag did not result in platelet activation or augment ADP- or TRAP-induced platelet activation (table 2). In summary, eltrombopag increases the platelet count and reduces bleeding in responding adult patients with chronic ITP through the release of new platelets into the circulation. While bleeding is reduced in responders, eltrombopag does not result in platelet activation or augmentation of platelet activation by ADP or TRAP. This suggests that the newer platelets released by eltrombopag stimulation are not hyper-functional (or are only transiently so prior to day 7). Table 1 IPF (maximum absolute change, mean ± SEM x 109/L) Number in whom bleeding decreased Responders 57.0 ± 22.4 8/11 Non-responders 3.3 ± 1.5 1/6 Table 2 Study Day 0 7 28 MFI, mean fluorescence intensity, *P <0.05 compared with day 0 Activated αIIbβ3 MFI No agonist 11.4 11.3 9.2 Low ADP 180.3 159.4 98.4 High ADP 451.2 348.2* 251.8* Low TRAP 158.1 175.5 143.9 High TRAP 385.2 347.0 299.6 P-selectin MFI No agonist 5.5 6.6 6.2 Low ADP 48.6 43.4 38.8 High ADP 144.5 109.0 96.8 Low TRAP 113.8 114.9 107.8 High TRAP 457.3 396.3 330.9

scholarly journals Activated Immune Response in Ventricular Assist Device Implanted Patients Identified through a Platelet Activation Biomarker

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 5001-5001
Author(s):  
Walter Jeske ◽  
Jeanine M. Walenga ◽  
Tania Torres ◽  
Vicki Escalante ◽  
Jeffrey Schwartz ◽  
...  
Keyword(s):  
Immune Response ◽  
Blood Flow ◽  
Platelet Count ◽  
Adverse Events ◽  
Platelet Activation ◽  
Innate Immune ◽  
Assist Device ◽  
Ventricular Assist ◽  
Pump Thrombosis

Abstract Introduction: Mechanical circulatory support using an implanted ventricular assist device (VAD) is an important means of enhancing or maintaining the quality of life for heart failure patients awaiting heart transplant (bridge to transplant), during the recovery of their own heart (bridge to recovery) or for long-term destination therapy (no transplant). The non-physiologic continuous blood flow of a VAD (CF-VAD) exposes blood and vasculature to abnormal shear stress and leads to a variety of hemostatic derangements that likely contribute to the development of bleeding complications, neurologic dysfunction and venous thromboembolism in these patients. Additionally, the implanted CF-VAD likely stimulates the body's natural innate immune response to a foreign object. We hypothesize that the continuous activation of platelets due to the non-physiologic blood flow and the foreign nature of the CF-VAD combine to stimulate an immune response. Previous studies have suggested thatanti-PF4/heparin antibodies [as targeted in a diagnosis of heparin-induced thrombocytopenia (HIT)] can develop in the absence of heparin. It is believed that these antibodies are not related to heparin per se but rather are generated as a physiological response by platelets, in their capacity to generate an innate immune response, reacting to non-self substances. This study evaluated the time course of anti-PF4/heparin titers in patients supported by CF-VADs. Methods: Blood samples were collected from 13 randomly selected patients prior to implantation of a HeartMate II CF-VAD and at routine clinic visits following implantation. Median follow-up was 183 days (range: 32-352 days). Anti-PF4/heparin antibody titers were determined by the PF4 Enhanced X-45 Assay (Immucor GTI Diagnostics, Waukesha, WI). Patients were treated with heparin at the time of implant; long-term anticoagulation was maintained with warfarin (INR 1.5-2.0) and low-dose aspirin. Results: Following CF-VAD implantation, there was an acute increase in median platelet count from 169,000 to 420,000/µl. With increasing time post-implant, the median platelet count returned to pre-implant levels; no patients became thrombocytopenic. Pre-implant, 6 of 13 patients had 'positive' anti-PF4/heparin titers (OD >0.4 using the HIT criteria); the median OD for all patients was 0.433. There was a progressive increase in median titer with increasing time post-implant. At 1 month the median OD was 0.54. By 2 months all patients had an OD >0.4 with a median value of 0.82 (>0.750 is high clinical thrombosis risk using the HIT criteria). The median OD continued to rise through 8 months post-implant. At 5 months and later OD values >1.5 were common. OD values >1.5 were present in some patients as early as 1 month post-implant. Discussion: The mechanism(s) associated with CF-VAD pump thrombosis and other adverse events remains unclear. The above data shows that long-term implant of a CF-VAD leads to the development of anti-PF4/heparin antibodies. Such a response may result from shear-induced platelet activation and subsequent release of PF4. This response is similar to a previous report in which patients who underwent total knee or hip arthroplasty and subsequently received dynamic mechanical thromboprophylaxis demonstrated an anti-PF4/heparin immune response even in the absence of heparin (Bito et al, Blood 2016). CF-VAD-related infection may also contribute to the generation of anti-PF4/heparin antibodies as PF4 bound to bacteria has previously been shown to induce antibody formation (Krauel et al, Blood 2011). Data from our lab has shown that patients with implanted CF-VADs are frequently in heightened states of inflammation (ASH 2016 abstract) with excessive levels of C-reactive protein in patients who develop pump thrombosis. CRP has been shown to activate platelets and accelerate thrombogenesis (Xu et al, BMC Immunology 2015). Thus, it is plausible that the development of anti-PF4/heparin antibodies may be an indicator of an early activation mechanism of adverse events in CF-VAD implanted patients through the cross-talk between the hemostatic and immune systems. Larger studies are required to determine whether the presence of such antibodies confers any risk to LVAD patients. The presence of anti-PF4/heparin antibodies may be of particular concern for LVAD patients undergoing a subsequent surgery for pump replacement or heart transplant. Disclosures No relevant conflicts of interest to declare.

scholarly journals Unexpected low expression of platelet fibrinogen receptor in patients with chronic myeloproliferative neoplasms: how does it change with aspirin?

2019 ◽  
Vol 189 (2) ◽  
pp. 335-338 ◽  
Author(s):  
Alessandro Lucchesi ◽  
Silvia Carloni ◽  
Serena De Matteis ◽  
Martina Ghetti ◽  
Gerardo Musuraca ◽  
...  
Keyword(s):  
Myeloproliferative Neoplasms ◽  
Chronic Myeloproliferative Neoplasms ◽  
Fibrinogen Receptor ◽  
Low Expression

scholarly journals Increased Thromboxane in Patients with Polycythemia Vera and Thrombosis: Evidence for Aspirin-Unsuppressible Platelet Activation In Vivo

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 5372-5372
Author(s):  
Rossella Rosari Cacciola ◽  
Elio Gentilini Cacciola ◽  
Veronica Vecchio ◽  
Emma Cacciola
Keyword(s):  
Platelet Count ◽  
Platelet Activation ◽  
Platelet Function ◽  
Conflicts Of Interest ◽  
Myeloproliferative Neoplasm ◽  
Vascular Events ◽  
Platelet Factor ◽  
Thrombotic Risk ◽  
Closure Time ◽  
The Mean

Polycyhemia vera (PV) is a myeloproliferative neoplasm characterized by increased thromboxane (TX) production and thrombotic risk. It is reported that serum TXB2 concentrations in PV patients are twofold higher than healthy controls and that low-dose aspirin (ASA) therapy reduces the risk of major vascular events by 50 to 60%. To evaluate this unusual size of the effect of ASA we have studied platelet count, hematocrit (HCT), β-thromboglobulin (β-TG) and platelet factor 4 (PF4), as markers of platelet activation, TXB2, as primary indicator of platelet activation, the platelet function activity (PFA), as indicator of ASA platelet sensitivity, and the clotting time (CT), as parameter of thrombin formation. We studied 60 patients (38 men, 22 women; mean age 51 years, range 32-70) with PV according to WHO criteria. The mean duration of disease was 12 years. All patients were on ASA 100 mg once daily. All patients were on phlebotomy. None had inherited or acquired thrombotic risk factors. Of 60 patients, 30 had thrombosis (20 men, 10 women) and 30 had no thrombosis. Of 30 with thrombosis, 15 developed nonfatal myocardial infarction (10 men, 5 women) defined by chest pain of typical intensity and duration and ST-segment elevation in any limb lead on electrocardiography, 10 had nonfatal stroke (8 men, 2 women) confirmed with the use of magnetic resonance imaging, and 5 (2 men , 3 women) had deep venous thrombosis confirmed by ultrasonography. Platelet count and HCT were measured by automated analyzer. β-TG and PF4 were determined by ELISA. TXB2 was measured by radioimmunoassay technique. ASA platelet sensitivity was measured by Platelet Function Analyzer (PFA-100). CT was measured by thromboelastometry. The mean platelet count was 430±170x109/L. The mean HCT value was 42±3%. The patients with thrombosis had high β-TG, PF4 and TXB2 (110±45 IU/ml, 45±21 IU/ml, and 1.700±1.990 nmol/L, respectively), shortened C/EPI closure time (T, unit: s, n.v. 84-160 s) (55±10 s) and shortened CT (CT, unit: s. n.v. 100-240 s) (45±20 s) whereas the patients without thrombosis had normal β-TG, PF4 and TXB2 (20±11 IU/ml, 6±2 IU/ml, and 800±280 nmpl/L, respectively), prolonged C/EPI closure time (249±40 s) and normal CT (110±20 s). These findings might suggest that in PV patients and thrombotic complications might need a platelet-selective dosage of ASA. Disclosures No relevant conflicts of interest to declare.

REVERSIBLE BLOCKADE OF PLATELET ACTIVATION DURING CARDIO-PUIMONAR BYPASS IN DOGS AFTER IV ADMINISTRATION OF AJOENE

1987 ◽  
Author(s):  
R Apitz Castro ◽  
E Ledezma ◽  
A Jorquera ◽  
M K Jain
Keyword(s):  
Platelet Count ◽  
Platelet Activation ◽  
Platelet Function ◽  
Ex Vivo ◽  
Platelet Reactivity ◽  
Shape Change ◽  
Postoperative Bleeding ◽  
Direct Interaction ◽  
Platelet Surface ◽  
Fibrinogen Receptor

Surgery with extracorporeal circulation (ECC) is associated with platelet activation, which greatly contribute to prolonged postoperative bleeding and increased blood loss after surgery. Antiplatelet ccnpounds which induce rapid and reversible inhibition of platelet function, without affecting platelet adhesiveness would be potentially useful in the management of the platelet-dependent hemostatic disorder observed in ECC. Ajoene, an organosulfur originally obtained from garlic, inhibits platelet release and aggregation induced ex vivo by all know agonists. It does not affect shape change or adhesion to collagen nor interfere with metabolic pathways relevant to the platelet reaction. Ajoene action is related to its direct interaction with the fibrinogen receptor on the platelet surface which irrpairs fibrinogen binding to stimulated or chymotrypsin treated platelets. IV administration of ajoene (15 mg/Kg) to mongrel dogs, inhibits platelet aggregation induced ex vivo by collagen (2-5 g/ml) or ADP (10 M). Ccnplete inhibition is attained after 20-35min and recuperation of platelet reactivity is obtained after 2.5-3.5 hours. To study the potential benefit of ajoene for the prevention of platelet activation during cardio-pulnonary bypass, ajoene was administered to anesthesized (heparin-anticoagulated) dogs, as described above, 40min before establishing the ECC. Circulation was mantained at 1.5L/min for a period of lOOmin Platelet count, and aggregation induced esc vivo by ADP or collagen were meassured immediately before ajoene administration, lOmin after the end of ECC and thereafter, hourly. Platelet count lOmin after end of ECC, in ncn-treated dogs fell to about 57% of prepump values, while in ajoene-treated animals circulating platelets represented 80% of pre-ECC values. Recovery of platelet function in ajoene-treated dogs started 2 hr after end of ECC (about 4 hr. after ajoene administration) reaching 70% 4 hr after end of ECC. Surgical bleeding in treated-dogs was not different frrm controls. Moderate bradicardia and hypotension, which in atrqpi-nized dogs returned to normal values within 3 min was observed. Although detailed pharmacological studies are still needed, our results suggest that ajoene is a potentially useful drug for the prevention of platelet activation induced by ECC.

Increased Thromboxane Biosynthesis in Essential Thrombocythemia

1995 ◽  
Vol 74 (05) ◽  
pp. 1225-1230 ◽  
Author(s):  
Bianca Rocca ◽  
Giovanni Ciabattoni ◽  
Raffaele Tartaglione ◽  
Sergio Cortelazzo ◽  
Tiziano Barbui ◽  
...  
Keyword(s):  
Platelet Count ◽  
Platelet Activation ◽  
Essential Thrombocythemia ◽  
Therapeutic Strategy ◽  
Low Dose ◽  
Thrombotic Risk ◽  
Dose Aspirin ◽  
Gender And Age ◽  
Low Dose Aspirin

SummaryIn order to investigate the in vivo thromboxane (TX) biosynthesis in essential thromboeythemia (ET), we measured the urinary exeretion of the major enzymatic metabolites of TXB2, 11-dehydro-TXB2 and 2,3-dinor-TXB2 in 40 ET patients as well as in 26 gender- and age-matched controls. Urinary 11-dehydro-TXB2 was significantly higher (p <0.001) in thrombocythemic patients (4,063 ± 3,408 pg/mg creatinine; mean ± SD) than in controls (504 ± 267 pg/mg creatinine), with 34 patients (85%) having 11-dehydro-TXB2 >2 SD above the control mean. Patients with platelet number <1,000 × 109/1 (n = 25) had significantly higher (p <0.05) 11 -dehydro-TXB2 excretion than patients with higher platelet count (4,765 ± 3,870 pg/mg creatinine, n = 25, versus 2,279 ± 1,874 pg/mg creatinine, n = 15). Average excretion values of patients aging >55 was significantly higher than in the younger group (4,784 ± 3,948 pg/mg creatinine, n = 24, versus 2,405 ± 1,885 pg/mg creatinine, n = 16, p <0.05). Low-dose aspirin (50 mg/d for 7 days) largely suppressed 11-dehydro-TXB2 excretion in 7 thrombocythemic patients, thus suggesting that platelets were the main source of enhanced TXA2 biosynthesis. The platelet count-corrected 11-dehydro-TXB2 excretion was positively correlated with age (r = 0.325, n = 40, p <0.05) and inversely correlated with platelet count (r = -0.381, n = 40, p <0.05). In addition 11 out of 13 (85%) patients having increased count-corrected 11-dehydro-TXB2 excretion, belonged to the subgroup with age >55 and platelet count <1,000 × 1099/1. We conclude that in essential thrombocythemia: 1) enhanced 11-dehydro-TXB2 excretion largely reflects platelet activation in vivo;2) age as well as platelet count appear to influence the determinants of platelet activation in this setting, and can help in assessing the thrombotic risk and therapeutic strategy in individual patients.

Changes in Platelet Aggregability after Ovariectomy

1979 ◽  
Vol 42 (04) ◽  
pp. 1332-1339 ◽  
Author(s):  
Hiroh Yamazaki ◽  
Takeshi Motomiya ◽  
Minoru Sonoda ◽  
Noboru Miyagawa
Keyword(s):  
Platelet Count ◽  
Platelet Activation ◽  
Ovarian Hormones ◽  
Control Group ◽  
Platelet Aggregability ◽  
Appearance Rate ◽  
Before And After ◽  
The Difference ◽  
Induced Aggregation ◽  
Observation Period

SummaryChanges in platelets in 48 patients with uterine myoma before and after hysterectomy with and without ovariectomy were examined. Bilateral ovariectomy in 25 cases (ovariec-tomized group) and unilateral or non-ovariectomy in 23 cases (control group) were performed at the hysterectomy. Platelet count and an appearance rate of secondary aggregation decreased at one day after and increased at one week after the operation, similarly in both the ovariectomized and the control group. The appearance rate of secondary aggregation was reflected in an intensity of aggregation at 5 min after the addition of reagent to PRP. At one month after the operation, the appearance rate of secondary aggregation induced by 3 μM ADP showed a statistically significant decrease in comparison with the preoperation value (P <0.05) and the enhancement of 5-min aggregation was still observed in the control group, while ceased in the ovariectomized group. The difference between the two groups was significant (P < 0.05). There was almost no change in the speed and intensity of primary and secondary aggregation during the observation period. No significant differences in collagen-induced aggregation were noted between the two groups. The results suggest that ovarian hormones, mainly estrogen, facilitate platelet activation which is mediated by the so-called secondary aggregation.

A Simple and Rapid Method to Determine GPIIb/IIIa-Receptor Inhibitor Activity in Whole Blood

1999 ◽  
Vol 19 (03) ◽  
pp. 134-138
Author(s):  
Gitta Kühnel ◽  
A. C. Matzdorff
Keyword(s):  
Flow Cytometry ◽  
Platelet Count ◽  
Blood Sample ◽  
Platelet Activation ◽  
Whole Blood ◽  
Receptor Occupancy ◽  
Aggregate Formation ◽  
Inhibitor Activity ◽  
Receptor Inhibitor

SummaryWe studied the effect of GPIIb/IIIa-inhibitors on platelet activation with flow cytometry in vitro. Citrated whole blood was incubated with increasing concentrations of three different GPIIb/IIIa-inhibitors (c7E3, DMP728, XJ757), then thrombin or ADP were added and after 1 min the sample was fixed. Samples without c7E3 but with 0.1 U/ml thrombin had a decrease in platelet count. Samples with increasing concentrations of c7E3 had a lesser or no decrease in platelet count. The two other inhibitors (DMP 725, XJ757) gave similar results. GPIIb/IIIa-inhibitors prevent aggregate formation and more single platelets remain in the blood sample. The agonist-induced decrease in platelet count correlates closely with the concentration of the GPIIb/IIIa inhibitor and receptor occupancy. This correlation may be used as a simple measure for inhibitor activity in whole blood.

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