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Inflammation is a complex response to cell injury that primarily occurs in vascularized connective tissue and often involves the immune response. The mediators of inflammation function to eliminate the cause of cell injury and clear away debris, in preparation for tissue repair. Unfortunately, inflammation also causes pain and, in instances in which the cause of cell injury is not eliminated, can result in a chronic condition of pain and tissue damage such as that seen in rheumatoid arthritis. The nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen are often effective in controlling inflammatory pain. Other treatment strategies applied to the reduction of inflammation are targeted at immune processes. These include glucocorticoids and disease-modifying antirheumatic drugs (DMARDs). Gout is an inflammatory joint disease caused by precipitation of uric acid crystals. Treatment of acute episodes targets inflammation, whereas treatment of chronic gout targets both inflammatory processes and the production and elimination of uric acid.

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AntipyreticA drug that reduces fever (eg, aspirin, NSAIDs, acetaminophen)
Cyclooxygenase (COX)The enzyme at the head of the enzymatic pathway for prostaglandin synthesis (Figure 36–2)
Cytotoxic drugDrugs that interfere with essential metabolic processes, especially DNA maintenance and replication and cell division. Such drugs generally kill rapidly dividing cells and are used for cancer chemotherapy and immunosuppression (Chapters 54 and 55)
Disease-modifying antirheumatic drugs (DMARDs)Diverse group of drugs that modify the inflammatory processes underlying rheumatoid arthritis; they have a slow (weeks to months) onset of clinical effects
Nonsteroidal anti-inflammatory drugs (NSAIDs)Inhibitors of cyclooxygenase; the term nonsteroidal differentiates them from steroid drugs that mediate anti-inflammatory effects through activation of glucocorticoid receptors (eg, cortisol; Chapter 39)
Reye's syndromeA rare syndrome of rapid liver degeneration and encephalitis in children treated with aspirin during a viral infection
Tumor necrosis factor-α (TNF-α)A cytokine that plays a central role in inflammation
Uricosuric agentA drug that increases the renal excretion of uric acid
Xanthine oxidaseA key enzyme in the purine metabolism pathway that converts hypoxanthine to xanthine and xanthine to uric acid
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Classification and Prototypes

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Aspirin (acetylsalicylic acid) is the prototype of the salicylates and other NSAIDs (Table 36–1). The other older nonselective NSAIDs (ibuprofen, indomethacin, many others) vary primarily in their potency, analgesic and anti-inflammatory effectiveness, and duration of action. Ibuprofen and naproxen have moderate effectiveness; indomethacin has greater anti-inflammatory effectiveness; and ketorolac has greater analgesic effectiveness. Celecoxib was the first member of a newer NSAID subgroup, the cyclooxygenase-2 (COX-2)-selective inhibitors, which were developed in an attempt to lessen the gastrointestinal toxicity associated with COX inhibition while preserving efficacy. Unfortunately, clinical trials involving some of the highly selective COX-2 inhibitors have shown a higher incidence of cardiovascular thrombotic events than the nonselective drugs.

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