Browse Prescribing Notes by Therapeutic Subcategory

For NSAIDs used for dysmenorrhea and pain see Dysmenorrhea and Nonnarcotic analgesics sections, respectively.
For other pain relievers, see Nonnarcotic analgesics, Narcotic analgesics, Migraine and headache, and Topical analgesics/anesthetics sections.

NONSTEROIDAL ANTIINFLAMMATORY DRUGS (NSAIDs) are important drugs used in the treatment of rheumatoid arthritis and other forms of arthritis. They exert their effects primarily through inhibition of prostaglandin synthesis. Osteoarthritis, rheumatoid arthritis, and related disorders cause the production and release of prostaglandins from cell membrane constituents. Prostaglandins cause edema, cellular exudation, and pain. NSAIDs inhibit cyclooxygenase (COX), the enzyme responsible for the conversion of arachidonic acid into prostaglandins. There are at least two forms of this enzyme. The COX-1 isoenzyme produces those prostaglandins that maintain the normal stomach lining. The COX-2 isoenzyme produces the prostaglandins that mediate an inflammatory response. The nonselective NSAIDs (eg, ibuprofen) inhibit the activity of both COX-1 and COX-2, so they treat pain and inflammation but may damage the stomach lining. Because of clinical data suggesting that the long-term use of naproxen may be associated with an increased risk of cardiovascular events, naproxen and other OTC nonselective NSAIDs should not be used for more than 10 days without a physician's advice, according to the FDA. At therapeutic concentrations, COX-2 inhibitors (eg, celecoxib), do not inhibit the activity of the COX-1 isoenzyme, and may therefore have a reduced potential to cause gastric side effects. Because of emerging data indicating that the COX-2 inhibitors celecoxib and valdecoxib may be associated with an increased risk of serious cardiovascular events (MI, TIA), especially when they are used for long periods of time or in very high risk settings (eg, immediately after heart surgery), the FDA has issued a recommendation that prescribers consider this emerging information when weighing risks vs. benefits for individual patients. According to the FDA, patients who are at a high risk of GI bleed, have a history of intolerance to nonselective NSAIDs, or are not doing well on nonselective NSAIDs may be appropriate candidates for COX-2 inhibitor therapy; and, individual patient risk for cardiovascular events and other risks commonly associated with NSAIDs should be considered for each prescribing situation. Rofecoxib and valdecoxib have been removed from the market. There is considerable variability among patients in both effectiveness and tolerance of NSAIDs. If one particular drug proves ineffective or unacceptable, benefit may be obtained by changing to a drug of a different class. The doses of these drugs should be individualized. The addition of the prostaglandin analogue, misoprostol (see Hyperacidity, GERD, and ulcers section), to NSAID therapy helps protect against gastroduodenal ulceration.
DISEASE MODIFYING ANTIRHEUMATIC DRUGS (DMARDs) include penicillamine, gold salts (auranofin, aurothioglucose), immunosuppressants and hydroxychloroquine. These drugs differ from the NSAIDs in that they may favorably alter the outcome of the disease and will reduce erythrocyte sedimentation rate (ESR) and rheumatoid factor titer, as well as improving the symptoms and signs of the disease. Long-term suppressive drugs work slowly, taking as long as 6 weeks to show benefit and 6 months for full improvement. The toxicity and side effects which accompany the use of these drugs means that careful monitoring is necessary.