The in vitro effect of antirheumatic drugs on platelet function
Several antirheumatic drugs lower the cardiovascular risk among rheumatoid arthritis patients. It is, however, unknown whether inhibition of platelet function contributes to this risk reduction. Only few studies have investigated the potential role of platelets as a target of antirheumatic drugs. In...
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Format: | Article |
Language: | English |
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Taylor & Francis Group
2020-02-01
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Series: | Platelets |
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Online Access: | http://dx.doi.org/10.1080/09537104.2019.1609665 |
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author | Camilla Brødsgaard Nielsen Christian Nielsen Mads Nybo Søren Andreas Just Pernille Just Vinholt |
author_facet | Camilla Brødsgaard Nielsen Christian Nielsen Mads Nybo Søren Andreas Just Pernille Just Vinholt |
author_sort | Camilla Brødsgaard Nielsen |
collection | DOAJ |
description | Several antirheumatic drugs lower the cardiovascular risk among rheumatoid arthritis patients. It is, however, unknown whether inhibition of platelet function contributes to this risk reduction. Only few studies have investigated the potential role of platelets as a target of antirheumatic drugs. In this study, platelet function was tested in vitro in samples from 24 healthy individuals spiked with antirheumatic drugs in clinically relevant concentrations or vehicle. Platelet aggregation was tested with 96-well light transmission aggregometry (LTA), and when an effect ≥20% compared to vehicle was observed, flow cytometric platelet aggregation and activation were evaluated and closure time was measured by Platelet Function Analyzer (PFA-200). When evaluated by LTA, teriflunomide (the active metabolite of leflunomide), tocilizumab, and prednisolone reduced ADP- and collagen-induced platelet aggregation ≥20%, while adalimumab increased TRAP-induced platelet aggregation ≥20%. Using flow cytometry, agonist-induced platelet aggregation with teriflunomide or vehicle was mean ± standard deviation (SD); 30.7% ± 5.8 vs. 41.7% ± 6.5, p = 0.02 using ADP, and 34.7% ± 13.9 vs. 55.8% ± 3.9, p = 0.01 using collagen. Results indicate that teriflunomide, prednisolone, and tocilizumab inhibit, and adalimumab increases platelet aggregation. The study suggests that the majority of antirheumatic drugs mainly reduced cardiovascular risk through indirect effects (e.g., reducing inflammation). |
first_indexed | 2024-03-12T00:26:47Z |
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institution | Directory Open Access Journal |
issn | 0953-7104 1369-1635 |
language | English |
last_indexed | 2024-03-12T00:26:47Z |
publishDate | 2020-02-01 |
publisher | Taylor & Francis Group |
record_format | Article |
series | Platelets |
spelling | doaj.art-0efa9e209eee4487bfc368997e695b3c2023-09-15T10:32:01ZengTaylor & Francis GroupPlatelets0953-71041369-16352020-02-0131224825710.1080/09537104.2019.16096651609665The in vitro effect of antirheumatic drugs on platelet functionCamilla Brødsgaard Nielsen0Christian Nielsen1Mads Nybo2Søren Andreas Just3Pernille Just Vinholt4Odense University HospitalOdense University HospitalOdense University HospitalOUH Svendborg SygehusOdense University HospitalSeveral antirheumatic drugs lower the cardiovascular risk among rheumatoid arthritis patients. It is, however, unknown whether inhibition of platelet function contributes to this risk reduction. Only few studies have investigated the potential role of platelets as a target of antirheumatic drugs. In this study, platelet function was tested in vitro in samples from 24 healthy individuals spiked with antirheumatic drugs in clinically relevant concentrations or vehicle. Platelet aggregation was tested with 96-well light transmission aggregometry (LTA), and when an effect ≥20% compared to vehicle was observed, flow cytometric platelet aggregation and activation were evaluated and closure time was measured by Platelet Function Analyzer (PFA-200). When evaluated by LTA, teriflunomide (the active metabolite of leflunomide), tocilizumab, and prednisolone reduced ADP- and collagen-induced platelet aggregation ≥20%, while adalimumab increased TRAP-induced platelet aggregation ≥20%. Using flow cytometry, agonist-induced platelet aggregation with teriflunomide or vehicle was mean ± standard deviation (SD); 30.7% ± 5.8 vs. 41.7% ± 6.5, p = 0.02 using ADP, and 34.7% ± 13.9 vs. 55.8% ± 3.9, p = 0.01 using collagen. Results indicate that teriflunomide, prednisolone, and tocilizumab inhibit, and adalimumab increases platelet aggregation. The study suggests that the majority of antirheumatic drugs mainly reduced cardiovascular risk through indirect effects (e.g., reducing inflammation).http://dx.doi.org/10.1080/09537104.2019.1609665cardiovascular diseaseexperimental studypharmacologyplatelet functionrheumatoid arthritis |
spellingShingle | Camilla Brødsgaard Nielsen Christian Nielsen Mads Nybo Søren Andreas Just Pernille Just Vinholt The in vitro effect of antirheumatic drugs on platelet function Platelets cardiovascular disease experimental study pharmacology platelet function rheumatoid arthritis |
title | The in vitro effect of antirheumatic drugs on platelet function |
title_full | The in vitro effect of antirheumatic drugs on platelet function |
title_fullStr | The in vitro effect of antirheumatic drugs on platelet function |
title_full_unstemmed | The in vitro effect of antirheumatic drugs on platelet function |
title_short | The in vitro effect of antirheumatic drugs on platelet function |
title_sort | in vitro effect of antirheumatic drugs on platelet function |
topic | cardiovascular disease experimental study pharmacology platelet function rheumatoid arthritis |
url | http://dx.doi.org/10.1080/09537104.2019.1609665 |
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