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Synthesis of a Borylated Ibuprofen Derivative Through Suzuki Cross-Coupling and Alkene Boracarboxylation Reactions
Published on: November 30, 2022
[Renal and cardiovascular effects of non-steroidal anti-inflammatories and selective cox 2 inhibitors]
1Service de néphrologie, Groupe hospitalier Pitié-Salpêtrière, 83 boulevard de l'Hôpital, 75013 Paris, France. gilbert.deray@psl.ap-hop-paris.fr
Abstract:
HYPERKALIEMIA AND RENAL FAILURE: Nonsteroidal anti-inflammatory drugs (NSAIs) may induce hyperkaliemia and renal failure. With regard to these complications, the notion of a risk factor is fundamental. Selective cyclooxygenase-2 inhibitors (Cox-2) do not provide any notable advantages with regard to the incidence of hyperkaliemia and renal failure. OEDEMA AND BLOOD PRESSURE: The NSAIs provoke salt-water retention which is responsible for oedema in 2 to 5% of patients (here again the notion of a risk factor is important). The salt-water retention is implied in the increase in blood pressure and the decompensation of heart failure. It has been shown that the incidence of oedema and the increase in blood pressure was significantly reduced with celecoxib compared with rofecoxib. This might have a crucial impact on the mean and long term follow-up of cardiovascular risk in these patients.
Cardiovascular Risk:
The results of the VIGOR study that demonstrated an increase in risk of myocardial infarction with rofecoxib, can probably be explained by an anti-thrombotic effect of naproxene, the high dose of rofecoxib used, the type of patients included or the fact that aspirin had been contraindicated. A recent study suggested that the cardiovascular risk was greater with rofecoxib than with celecoxib and with NSAIs when the dose of rofecoxib used was greater than 25mg/day. In this case control study, the cardiovascular risk was identical with celecoxib and NSAIs, whatever the dose used, but increased with a relative risk rate of 1.7 with the doses of rofecoxib greater than 50mg/day. In cases treated with aspirin Some NSAIs can reduce the anti-aggregant effects of aspirin whereas this effect is not observed with Cox-2 selective inhibitors. Hence, the latter should be the pharmacological agents of choice in patients treated with aspirin.
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