NSAIDs combat arthritis by interfering with the inflammatory process.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are a large group of drugs commonly used to treat arthritis because of their:
NSAID Categories
There are three types of NSAIDs:
salicylates (both acetylated, such as aspirin, and nonacetylated)
traditional NSAIDs
COX-2 selective inhibitors
NSAIDs commonly used for arthritis include:
Ansaid
(generic name flurbiprofen)
Arthrotec (generic name diclofenac with misoprostol)
Aspirin
(acetylated / non-acetlyted salicylates)
Cataflam
(generic name diclofenac potassium)
Celebrex (generic name celecoxib)
Clinoril
(generic name sulindac)
Daypro
(generic name oxaprozin)
Disalcid (generic name salsalate)
Dolobid
(generic name diflunisal)
Feldene
(generic name piroxicam)
Ibuprofen (brand names include Motrin, Advil, Mediprin, Nuprin, Motrin IB)
Indocin
(generic name indomethacin)
Ketoprofen (brands names include Orudis, Oruvail, Actron, Orudis KT)
Lodine
(generic name etodolac)
Meclomen (generic name meclofenamate sodium)
Mobic (generic name meloxicam)
Nalfon
(generic name fenoprofen)
Naproxen
(brand names include Naprosyn, Aleve, Naprelan, Anaprox)
Ponstel
(generic name mefanamic acid)
Relafen
(generic name nabumetone)
Tolectin (generic name tolmetin sodium)
Trilisate (generic name choline magnesium trisalicylate)
Voltaren (generic name diclofenac sodium)
How NSAIDs Work
The mechanism of action of NSAIDs is the inhibition of the enzyme cyclooxygenase, which catalyzes arachidonic acid to prostaglandins and leukotrienes. Arachidonic acid is released from membrane phospholipids as a response to inflammatory stimuli. Prostaglandins establish the inflammatory response. NSAIDs interfere with prostaglandin production by inhibiting cyclooxygenase.
This mechanism may relate to the variation in response between patients. Scientific studies have shown a correlation between concentration of the drug and effect, but do not explain the differences in individual patient responses. It is thought that the pharmacokinetic (process by which a drug is absorbed, distributed, metabolized, and eliminated) differences among the various NSAIDs may account for the variability in response.
Inflammation - Test Your Knowledge
The Enzyme Cyclooxygenase
Further research of the enzyme cyclooxygenase, also known as COX, has revealed that there are two forms, known as COX-1 and COX-2. NSAIDs affect both forms of cyclooxygenase. COX-1 is involved in maintaining healthy tissue, while COX-2 is involved in the inflammation pathway.
COX-2 selective inhibitors became the newest subset of NSAIDs born of this research.
FDA Actions For All NSAIDs
In April 2005, The U.S. Food and Drug Administration announced actions which will be taken regarding the marketing of NSAIDs. The actions include changes for COX-2 inhibitors, as well as prescription and non-prescription (over-the-counter) NSAIDs. The actions by the FDA follow scrutiny of NSAIDs and COX-2 inhibitors provoked by the voluntary withdrawal of the COX-2 selective inhibitor Vioxx in September 2004.
FDA Announces Changes For All NSAIDs
Questions And Answers: FDA Regulatory Actions On COX-2 Inhibitors And NSAIDs
Other Facts About NSAIDs
Pain and inflammation sometimes occur in a circadian rhythm (daily rhythmic cycle based on a 24 hour interval). Therefore NSAIDs may be more effective at certain times.NSAIDs can be divided into two groups: those with plasma (blood) half-lives less than 6 hours (i.e. aspirin, diclofenac, ibuprofen) and those with half-lives greater than 10 hours (i.e. diflunisal, piroxicam, and sulindac). Since it takes three to five half-lives to stabilize blood levels, NSAIDs with longer half-lives require a loading dose to be given (large dose given initially). The "half-life" is the time it takes a drug to go down to half of its initial level.Prostaglandins, which are inhibited by NSAIDs, function in the body to protect the stomach lining, promote clotting of the blood, regulate salt and fluid balance, and maintain blood flow to the kidneys when kidney function is reduced. By decreasing prostaglandins, NSAIDs can cause stomach irritation, bleeding, fluid retention, and decreased kidney function.Synovial fluid (joint fluid) concentrations are 60% of plasma concentrations regardless of type of NSAID or its half-life. Synovial fluid is mostly the site of action of NSAIDs.NSAIDs are 95% albumin (protein) bound. The unbound fraction of the NSAID is increased in patients with low albumin concentrations such as in active rheumatoid arthritis and the elderly.
