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Aspirin resistance likely does not exist when defined as the inability to inhibit COX-1, as reported cases are usually due to noncompliance, inadequate dosing, or nonspecific platelet function tests.
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True aspirin resistance likely does not exist; apparent resistance is typically due to noncompliance, underdosing, or nonspecific testing methods.
Aspirin irreversibly inhibits platelet cyclooxygenase-1 (COX-1). Aspirin sensitivity can be measured easily by its inhibition of arachidonic acid (AA) -induced platelet aggregation. Aspirin resistance has to be defined by its inability to inhibit COX-1. By using this definition, aspirin resistance very likely does not exist. A specific rapid laboratory test using either AA-induced platelet aggregation or AA-induced malondialdehyde production in platelet-rich plasma is needed to test aspirin sensitivity. The reports on so-called aspirin resistance are usually due to noncompliance of aspirin intake or consumption of inadequate doses of aspirin. In addition, data generated from using nonspecific platelet function tests have added confusion to this observed phenomenon of aspirin resistance.
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Rao et al. (2007) conducted a review in Aspirin resistance. Aspirin was evaluated. Aspirin resistance likely does not exist when defined as the inability to inhibit COX-1, as reported cases are usually due to noncompliance, inadequate dosing, or nonspecific platelet function tests.
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