aspirin resistance

aspirin resistance

The inability of aspirin to reduce platelet production of thromboxane A2 and consequently platelet activation and aggregation. Possible causes of aspirin resistance include inadequate dosage, interaction with other drugs, increased platelet turnover and mutations of genes concerned with thromboxane synthesis.
References in periodicals archive ?
The issue of Aspirin resistance, Prof.Shahbaz Kureshi stated has been over emphasized but it is because of non-compliance and some of the patients may be non-responders to Aspirin just like other drugs.
The antiplatelet mechanism of aspirin is to make arachidonic acid lose its ability to transform into prostaglandin endoperoxide and hindering the formation of prostaglandin E2 and thromboxane A2 through inhibiting the activity of cyclooxygenase in platelets.17 However, a study shows that aspirin resistance exists in a few patients although aspirin has a good therapeutic effect in the treatment of acute myocardial infarction,18 that is, acute thrombosis may occur even after taking aspirin, and the incidence of adverse reactions increases with the increase of dosage.
Aspirin is more active in male platelets, and aspirin resistance is more frequent in women.
But the underlying reason for aspirin resistance in compliant patients has long been questioned.
Pirmohamed, "Aspirin resistance: effect of clinical, biochemical and genetic factors," Pharmacology and Therapeutics, vol.
This phenomenon, called aspirin resistance (AR), remains still an important clinical problem.
Despite adequate aspirin therapy, many patients still experience cardiovascular events, the phenomenon named as aspirin resistance (AR) [2].
Some patients prescribed aspirin suffer recurrent thromboembolic vascular events, giving rise to the term "aspirin resistance." Recently, a number of studies have examined the association between aspirin resistance and several receptors on the surface of platelets, [sup][21] such as genetic polymorphisms of platelet membrane glycoproteins, genetic mutations of TBXA2R, the platelet-activating factor acetylhydrolase, and coagulation factor XIII.
Aspirin resistance is defined as persistent platelet activation (i.e.
Testing aspirin resistance using the platelet function analyzer-100: some methodological caveats and considerations.
Given that previous studies have shown that the use of aspirin is associated with lower stroke severity and decreased infarction growth, the current study's findings may help to define the effect of aspirin resistance (AR) on stroke severity, since previous studies had provided inconclusive results, Dr.
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