Abstract
Pain (dolor), swelling (tumor), erythema (rubor), and warmth (calor), the cardinal features of inflammation, are present in most patients with rheumatic diseases. Therapeutic strategies to reduce inflammation have been used for centuries, beginning with botanical treatments in both Western and Eastern medical traditions (1). The first isolated plant constituent to be tested as an anti-inflammatory drug was salicylic acid from willow bark, which was chemically altered to acetyl salicylic acid to improve its pharmacologic properties. Acetyl salicylic acid became “aspirin” in 1899, one of the first drugs to be widely marketed, and aspirin remains one of the most widely used drugs today. Other drugs that share the anti-inflammatory, analgesic, and antipyretic properties of aspirin are termed nonsteroidal anti-inflammatory drugs (NSAIDs), and are a chemically diverse group of compounds (Table 41-1). It was established in 1971 that salicylates and other NSAIDs act by blocking the synthesis of prostaglandins (PGs), products of the metabolism of the membrane-associated fatty acid arachidonic acid. This finding demonstrated conclusively that PGs play an important role in mediating symptoms and signs of inflammation. However, PGs play a role in normal physiology as well as in disease. As a consequence, all NSAIDs possess predictable therapeutic and adverse effects that must be understood in order to use these drugs safely.
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Crofford, L.J. (2008). Nonsteroidal Anti-Inflammatory Drugs. In: Klippel, J.H., Stone, J.H., Crofford, L.J., White, P.H. (eds) Primer on the Rheumatic Diseases. Springer, New York, NY. https://doi.org/10.1007/978-0-387-68566-3_41
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