ABSTRACT
Gout and gouty arthritis are among the most common of rheumatic disorders. The
medical community is fortunate to have a variety of medical approaches available
to treat acute gouty arthritis and acute arthritis induced by other crystals.
Although corticosteroids, colchicine, opiates, and other analgesics and anti-
inflammatory drugs are effective therapies for acute crystal-induced arthritis,
non-aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs) remain the most
commonly used agents for the therapy of gout and pseudogout. As a class,
NSAIDs have been in widespread clinical use for many years; their mechanism of
action is well understood, and their limitations and toxicities are widely known
and appreciated by both primary care and specialist physicians. Both patients and
physicians feel comfortable with the use of NSAIDs for the treatment of acute
gouty arthritis as these drugs are used in the treatment of so many other rheumatic
and non-rheumatic conditions. Indeed, textbooks of medicine and rheumatology
suggest using NSAIDs as first-line therapy for most patients with acute gouty
arthritis and reserve high-dose oral and intravenous colchicine, oral and intra-
articular corticosteroids, and injections of ACTH for patients who are not likely
to tolerate or respond to NSAIDs (1-4). This chapter reviews the pharmacologic
basis for the anti-inflammatory effects of NSAIDs on acute pain and
inflammation and the evidence supporting their use in the treatment of acute
gouty arthritis.
