Abstract
Nonsteroidal anti-inflammatory drugs (NSAIDs) are often the initial treatment for rheumatoid arthritis. NSAID-induced inhibition of cyclooxygenase-2 (COX2) and cyclooxygenase-1 appears to correlate with clinical efficacy and toxicity, respectively. Newer NSAIDs with greater COX2 selectivity offer the promise of less toxic therapy.
MeSH terms
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Animals
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Anti-Inflammatory Agents, Non-Steroidal / adverse effects
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Anti-Inflammatory Agents, Non-Steroidal / therapeutic use*
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Arthritis, Rheumatoid / drug therapy*
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Arthritis, Rheumatoid / enzymology
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Cyclooxygenase 1
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Cyclooxygenase 2
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Cyclooxygenase 2 Inhibitors
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Cyclooxygenase Inhibitors / adverse effects
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Cyclooxygenase Inhibitors / therapeutic use*
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Dose-Response Relationship, Drug
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Female
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Humans
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Isoenzymes / drug effects
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Isoenzymes / metabolism*
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Male
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Membrane Proteins
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Prognosis
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Prostaglandin-Endoperoxide Synthases / drug effects
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Prostaglandin-Endoperoxide Synthases / metabolism*
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Rats
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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Cyclooxygenase 2 Inhibitors
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Cyclooxygenase Inhibitors
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Isoenzymes
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Membrane Proteins
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Cyclooxygenase 1
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Cyclooxygenase 2
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PTGS1 protein, human
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PTGS2 protein, human
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Prostaglandin-Endoperoxide Synthases
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Ptgs1 protein, rat