COX-2 inhibitor


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COX-2 inhibitor

A drug class that relieves inflammation and pain by inhibiting the action of cyclooxygenase-2.

Prostanoids that mediate inflammation, pain, and fever are synthesized through the action of cyclooxygenase-2 (COX-2), an enzyme that is constitutively expressed in the brain but can be induced in other tissues by cytokines. In both osteoarthritis and rheumatoid arthritis, COX-2 inhibitors have been shown to be superior in pain relief to acetaminophen and placebo, and equivalent to nonselective nonsteroidal antiinflammatory drugs (NSAIDs) such as ibuprofen and naproxen. In rheumatoid arthritis, COX-2 inhibitors are not disease-modifying drugs. Because nonselective NSAIDs inhibit not only COX-2 but also inhibit COX-1, which plays a role in platelet aggregation and gastric mucosal protection, their use is associated with a higher risk of gastrointestinal bleeding than that of selective COX-2 inhibitors. Like NSAIDs, however, the selective agents can cause liver and kidney toxicity, fluid retention, and hypertension. One of them (rofecoxib) was withdrawn by the manufacturer after 5 years on the market because of an unacceptably high incidence of heart attack and thrombotic stroke in patients receiving it for 18 months or more. For these reasons and because they are more expensive than NSAIDs, COX-2 inhibitors are indicated chiefly in patients who are at increased risk of gastrointestinal bleeding.

COX-2 inhibitor

n.
Any of a class of nonsteroidal anti-inflammatory drugs that selectively block prostaglandin formation so as to cause minimal gastrointestinal side effects.

COX-2 inhibitor

Cyclooxygenase-2 inhibitor Pain management A class of analgesics with fewer side effects than those of conventional NSAIDs–which inhibit both cyclooxygenases–COX-1 and COX-2; COX-1 protects the gastric mucosa, preventing ulcers, bleeding, and other digestive tract problems. See COX-2, Prostaglandin.

COX-2 in·hib·i·tor

(in-hibi-tŏr)
A drug class that relieves inflammation and pain by inhibiting the action of cyclooxygenase-2.
References in periodicals archive ?
After its withdrawal in 2004, following the emergence of evidence of increased cardiovascular morbidity in the APPROVe (Adenomatous Polyp Prevention on Vioxx) study, COX-2 inhibitors represented less than 16% of the NSAID prescriptions.
These proxy variables are the percent of all the physician's monthly office visits that are to OA patients and the percent of all the physician's monthly visits to OA patients that are associated with a COX-2 inhibitor prescription, respectively.
Recipients with low to moderate risk for serious GI events were not allowed to receive a COX-2 inhibitor under the PAR program.
1) The claim of decreased gastrointestinal bleeding with long-term use of COX-2 inhibitors has also been questioned.
26 in the journal Circulation, an AHA expert panel wrote that further studies have reinforced concerns about COX-2 inhibitors and also have found an increased risk of cardiovascular events with conventional, nonselective COX-2 NSAIDs, including ibuprofen (Motrin, Advil) and diclofenac (Cataflam, Voltaren).
The latest study showed that, as expected, COX-2 inhibitors doubled the risk of an attack - but so did the two non-steroidal anti-inflammatories.
The risk of giving a COX-2 inhibitor that has been most widely discussed over the last several years would be the cardiovascular risk.
The controversy over COX-2 inhibitors has prompted many consumers to find alternative pain relief options.
Among them were 27, 000 patients who had been taking Vioxx, which belongs to a family of drugs known as Cox-2 inhibitors.
But Bextra, Pfizer's other COX-2 inhibitor, did not register as many new prescriptions because of concerns over its safety.
Celecoxib was the first selective cox-2 inhibitor to be approved for treating osteoarthritis and rheumatoid arthritis.