Which medications in the drug class Nonsteroidal Anti-inflammatory Drugs are used in the treatment of Rheumatoid Arthritis (RA)?

Updated: Feb 07, 2020
  • Author: Howard R Smith, MD; Chief Editor: Herbert S Diamond, MD  more...
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Answer

Nonsteroidal Anti-inflammatory Drugs

NSAIDs interfere with prostaglandin synthesis through inhibition of the enzyme cyclooxygenase (COX), thus reducing swelling and pain. However, they do not retard joint destruction and therefore are not sufficient to treat RA when used alone. Like corticosteroids, NSAIDs can be reduced in dose or discontinued with successful DMARD therapy. These agents decrease intraglomerular pressure and decrease proteinuria.

The several dozen NSAIDs available can be classified into several different groups of compounds. Commonly used NSAIDs include ibuprofen, naproxen, ketoprofen, celecoxib, and diclofenac.

Ibuprofen (Advil, Motrin)

Ibuprofen is indicated for patients with mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Naproxen (Naprosyn, Aleve, Anaprox, Anaprox DS, Naprelan)

Naproxen is used to relieve mild to moderate pain. This agent inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, which is responsible for prostaglandin synthesis.

Diclofenac (Voltaren, Cambia)

Diclofenac is one of a series of phenylacetic acids that have demonstrated anti-inflammatory and analgesic properties in pharmacologic studies. It is believed to inhibit COX, which is essential in the biosynthesis of prostaglandins.

Ketoprofen

Ketoprofen is used to relieve mild to moderate pain and inflammation. It reversibly inhibits cyclooxygenase-1 and 2 (COX-1 and 2) enzymes, which results in decreased formation of prostaglandin precursors.

Celecoxib (Celebrex)

Celecoxib is approved for the relief of signs and symptoms of RA. It primarily inhibits COX-2, which is considered an inducible isoenzyme (induced during pain and inflammatory stimuli). Inhibition of COX-1 may contribute to NSAID gastrointestinal (GI) toxicity. At therapeutic concentrations, celecoxib does not inhibit COX-1, thus potentially resulting in decreased GI toxicity. Administer the lowest possible dose for each patient. Use of celecoxib has been associated with an increased risk of cardiovascular toxicity.


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