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      Effects of Antiplatelet and Nonsteroidal Anti-inflammatory Medications on Platelet-Rich Plasma: A Systematic Review

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          Abstract

          Background:

          Platelet-rich plasma (PRP) has wide applications in orthopaedic care. Its beneficial effects are attributed to the growth factor profile from the platelet secretome. In theory, these effects would be diminished by medications that inhibit platelet activation and/or the subsequent release of growth factors.

          Purpose:

          To determine whether commonly used antiplatelets, nonsteroidal anti-inflammatory drugs (NSAIDs), or anticoagulant medications affect platelet growth factor release in PRP.

          Study Design:

          Systematic review; Level of evidence, 2.

          Method:

          A systematic review of the literature related to antiplatelet, anti-inflammatory, and anticoagulant drugs was performed following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. We used the Downs and Black objective quality scoring system. The literature search consisted of PubMed and Cochrane Library databases. Search terms consisted of 1 item selected from “platelet-rich plasma,” “platelet-derived growth factor,” and “platelet-rich plasma AND growth factor” combined with 1 item from “antiplatelet,” “aspirin,” “anticoagulant,” and “NSAID.” Only studies published within the past 25 years were included.

          Results:

          A total of 15 studies met the inclusion criteria: 7 studies detected no significant decrease in growth factors or mitogenesis, whereas 6 detected a decrease with antiplatelet agents, 1 detected mixed results with an antiplatelet agent, and 1 had mixed results with an antiplatelet agent/vasodilator. In terms of PRP activation, all 3 studies assessing collagen, the 2 studies analyzing adenosine diphosphate alone, and the 1 study investigating arachidonic acid found a decrease in growth factor concentration.

          Conclusion:

          Antiplatelet medications may decrease the growth factor release profile in a cyclooxygenase 1– and cyclooxygenase 2–dependent manner. Eight of 15 studies found a decrease in growth factors or mitogenesis. However, more studies are needed to comprehensively understand antiplatelet effects on the PRP secretome.

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          Most cited references29

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          The levels of evidence and their role in evidence-based medicine.

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            Platelet Activation: The Mechanisms and Potential Biomarkers

            Beyond hemostasis and thrombosis, an increasing number of studies indicate that platelets play an integral role in intercellular communication, mediating inflammatory and immunomodulatory activities. Our knowledge about how platelets modulate inflammatory and immunity has greatly improved in recent years. In this review, we discuss recent advances in the pathways of platelet activation and potential application of platelet activation biomarkers to diagnosis and prediction of disease states.
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              Anti-platelet therapy: cyclo-oxygenase inhibition and the use of aspirin with particular regard to dual anti-platelet therapy.

              Aspirin and P2Y(12) antagonists are commonly used anti-platelet agents. Aspirin produces its effects through inhibition of thromboxane A(2) (TXA(2)) production, while P2Y(12) antagonists attenuate the secondary responses to ADP released by activated platelets. The anti-platelet effects of aspirin and a P2Y(12) antagonist are often considered to be separately additive. However, there is evidence of an overlap in effects, in that a high level of P2Y(12) receptor inhibition can blunt TXA(2) receptor signalling in platelets and reduce platelet production of TXA(2). Against this background, the addition of aspirin, particularly at higher doses, could cause significant reductions in the production of prostanoids in other tissues, e.g. prostaglandin I(2) from the blood vessel wall. This review summarizes the data from clinical studies in which dose-dependent effects of aspirin on prostanoid production have been evaluated by both plasma and urinary measures. It also addresses the biology underlying the cardiovascular effects of aspirin and its influences upon prostanoid production throughout the body. The review then considers whether, in the presence of newer, more refined P2Y(12) receptor antagonists, aspirin may offer less benefit than might have been predicted from earlier clinical trials using more variable P2Y(12) antagonists. The possibility is reflected upon, that when combined with a high level of P2Y(12) blockade the net effect of higher doses of aspirin could be removal of anti-thrombotic and vasodilating prostanoids and so a lessening of the anti-thrombotic effectiveness of the treatment. © 2011 The Authors. British Journal of Clinical Pharmacology © 2011 The British Pharmacological Society.
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                Author and article information

                Journal
                Orthop J Sports Med
                Orthop J Sports Med
                OJS
                spojs
                Orthopaedic Journal of Sports Medicine
                SAGE Publications (Sage CA: Los Angeles, CA )
                2325-9671
                29 April 2020
                April 2020
                : 8
                : 4
                : 2325967120912841
                Affiliations
                [* ]Baylor College of Medicine, Houston, Texas, USA.
                []H. Ben Taub Department of Physical Medicine and Rehabilitation, Baylor College of Medicine, Houston, Texas, USA.
                []Department of Orthopedic Surgery, Baylor College of Medicine, Houston, Texas, USA.
                [4-2325967120912841] Investigation performed at Baylor College of Medicine, Houston, Texas, USA
                Author notes
                [*] [§ ]Prathap Jayaram, MD, Baylor College of Medicine, 7200 Cambridge Street, 10 C, Houston, TX 77030, USA (email: prathap.jayaram@ 123456bcm.edu ).
                Article
                10.1177_2325967120912841
                10.1177/2325967120912841
                7218995
                db18c154-c9f4-4a2e-8308-6614b59a3e99
                © The Author(s) 2020

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 License ( https://creativecommons.org/licenses/by-nc-nd/4.0/) which permits non-commercial use, reproduction and distribution of the work as published without adaptation or alteration, without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

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                platelet-rich plasma,aspirin,growth factor,nonsteroidal anti-inflammatory,cyclooxygenase inhibitor,platelet

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