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Aspirin acts as an acetylating agent where an acetyl group is covalently attached to a serine residue in the active site of the COX enzyme. [1] This makes aspirin different from other NSAIDs (such as diclofenac and ibuprofen), which are reversible inhibitors; aspirin creates an allosteric change in the structure of the COX enzyme. [2]
In cases where ICH already has occurred, aspirin use results in higher mortality, with a dose of about 250 mg per day resulting in a relative risk of death within three months after the ICH around 2.5 (95% confidence interval 1.3 to 4.6). [224] Aspirin and other NSAIDs can cause abnormally high blood levels of potassium by inducing a ...
Lysine acetylsalicylate, also known as aspirin DL-lysine or lysine aspirin, is a more soluble form of acetylsalicylic acid (aspirin). As with aspirin itself, it is a nonsteroidal anti-inflammatory drug (NSAID) with analgesic, anti-inflammatory, antithrombotic and antipyretic properties. [ 1 ]
Non-steroidal anti-inflammatory drugs [1] [3] (NSAID) [1] are members of a therapeutic drug class which reduces pain, [4] decreases inflammation, decreases fever, [1] and prevents blood clots. Side effects depend on the specific drug, its dose and duration of use, but largely include an increased risk of gastrointestinal ulcers and bleeds ...
Nonsteroidal anti-inflammatory drugs (NSAIDs) alleviate pain by counteracting the cyclooxygenase (COX) enzyme. [1] On its own, COX enzyme synthesizes prostaglandins, creating inflammation. In whole, the NSAIDs prevent the prostaglandins from ever being synthesized, reducing or eliminating the inflammation and resulting pain. [citation needed]
Prostaglandin inhibitors are drugs that inhibit the synthesis of prostaglandin in human body. [1] There are various types of prostaglandins responsible for different physiological reactions such as maintaining the blood flow in stomach and kidney, regulating the contraction of involuntary muscles and blood vessels, and act as a mediator of inflammation and pain.
Aspirin-exacerbated respiratory disease (AERD), also called NSAID-exacerbated respiratory disease (N-ERD) or historically aspirin-induced asthma and Samter's Triad, is a long-term disease defined by three simultaneous symptoms: asthma, chronic rhinosinusitis with nasal polyps, and intolerance of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs).
[1] In pharmacology , the term mechanism of action ( MOA ) refers to the specific biochemical interaction through which a drug substance produces its pharmacological effect . [ 2 ] A mechanism of action usually includes mention of the specific molecular targets to which the drug binds, such as an enzyme or receptor . [ 3 ]