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Macronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Thromboxane A2 (TXA2) is metabolite of arachidonic acid through thromboxane A synthase 1 action. Thromboxane B2 (TXB2) outcomes from TXA2 degradation and plays an important role in the acetaminophen hepatotoxicity. TxA2 is released by macrophages, neutrophils, and endothelial cells, and has prothrombotic properties such as the activation of platelets and platelet aggregation (102).
Dermal filler complications and management
Published in Michael Parker, Charlie James, Fundamentals for Cosmetic Practice, 2022
Aspirin prevents platelet aggregation and prevents blood clotting by inhibiting thromboxane A2. It is therefore a useful emergency therapy in the context of impending necrosis and should be given to the patient immediately as long as there are no contraindications. It is currently advised to advise a patient to take 300 mg of aspirin daily for at least seven days pending your continued review. It is also worth writing a letter to their general practitioner to inform them you have given them this advice as they are likely to know the patient’s history better than you and be well aware of any potential contraindications.
Resource-Limited Environment Plastic Surgery
Published in Mansoor Khan, David Nott, Fundamentals of Frontline Surgery, 2021
Johann A. Jeevaratnam, Charles Anton Fries, Dimitrios Kanakopoulos, Paul J. H. Drake, Lorraine Harry
Prostaglandin F2-alpha and thromboxane A2 cause platelet aggregation and vasoconstriction. As long as there are no contraindications, a systemic prostaglandin inhibitor should be administered, such as oral ibuprofen, at a dose of 12 mg/kg−1 twice daily (up to a maximum of 2400 mg day−1), or aspirin at 300 mg once a day.
What can we learn from the platelet lipidome?
Published in Platelets, 2023
Gaëtan Chicanne, Jean Darcourt, Justine Bertrand-Michel, Cédric Garcia, Agnès Ribes, Bernard Payrastre
Another important pathway in platelets involves PLA2. Among the fatty acyls generated by PLA2, arachidonic acid is a major precursor for oxidative transformation to eicosanoids by lipoxygenase and cyclooxygenase pathways. Following stimulation, platelets produce a number of eicosanoids, including thromboxane A2 (TXA2), a proaggregatory lipid. T×A2 released by activated platelets acts as an auto- and paracrine molecule through the G-protein coupled receptor TP-receptor [7,8]. The calcium-sensitive cytosolic PLA2α isoform (cPLA2α) has a major role in human platelets as demonstrated in a rare inherited human deficiency of this enzyme leading to impaired platelet eicosanoid generation associated with platelet dysfunction [21]. A platelet lipidomic profiling study has highlighted the importance of PLA2α (cPLA2α) in platelet activation and clarified the substrates of this PLA2 isoform [22]. Moreover, the lysophospholipids generated by cPLA2 were identified but their role in platelet remains poorly understood. This study also suggested the involvement of cPLA2 in the production of a unique eicosanoid downstream of PAR4 and GPVI triggering.
Effects of aspirin and statin use on venous thromboembolism prophylaxis and survival in patients with endometrial cancer
Published in Expert Opinion on Drug Safety, 2022
Shinya Matsuzaki, Heather Miller, Tsuyoshi Takiuchi, Maximilian Klar, Koji Matsuo
Aspirin continues to be manufactured since the end of the 19th century and is widely used as an analgesic and anti-inflammatory agent as well as for the prevention of cardiovascular diseases[36]. It directly inhibits the activities of both cyclooxygenase (COX)-1 and COX-2 enzymes (Figure 1)[37]. COX-1 produces thromboxane A2 that induces platelet aggregation and thrombus formation. COX-2 is induced in various tissues by the action of inflammatory cytokines and lipopolysaccharides[38]. Although aspirin inhibits the activities of both COX-1 and COX-2 enzymes, this inactivation of COX activity can be rapidly reversed by the synthesis of new proteins in proliferating cells[37]. It has been reported that a higher dose of aspirin is necessary to inhibit COX-2 compared to the dose required to inhibit COX-1, owing to the differences in the sensitivity of the target cells of aspirin. Therefore, a low dose (100 mg/day) of aspirin is needed to inhibit COX-1 activity, whereas frequent (3–4 times/day) and high doses (approximately 2000 mg/day) of aspirin are needed to inhibit COX-2 activity[37].
Nonsteroidal anti-inflammatory drugs in end-stage kidney disease: dangerous or underutilized?
Published in Expert Opinion on Pharmacotherapy, 2021
The predominant mechanism of action of NSAIDs is the inhibition of COX enzymes, prohibiting prostanoid synthesis from arachidonic acid (Figure 1) [1,15,16]. Arachidonic acid metabolism is a multi-step enzymatic process that follows platelet aggregation and activation of membrane phospholipases. Thromboxane A2 (TXA2), a platelet prostanoid product of arachidonic acid metabolism, acts as a vasoconstrictor and platelet aggregant. This platelet-activating cascade is initiated by COX-1, an enzyme that is constituently expressed in mature platelets as well as various organ tissues including the gastric mucosa, kidneys, and vascular endothelium [17]. In contrast, COX-2 is only transiently expressed in immature platelets [18] or in vascular endothelial cells during inflammatory states and is largely involved in the production of prostaglandins, most notably prostacyclin (PGI2). Inhibition of prostacyclin’s vasodilatory and platelet anti-aggregant effects contribute to increased risk for adverse cardiovascular events in patients taking NSAIDs and selective COX-2 inhibitors [19,20].