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A 70 year old obese woman asks if more can be done for her knee and low back pain, due to osteoarthritis. She used to smoke and has type 2 diabetes. Her orthopaedic surgeon does not consider the clinical presentation and radiographic changes in her knees severe enough for surgery. Her height is 160 cm, weight 85 kg, blood pressure 130/80 mm Hg, with normal renal function, plasma cholesterol concentration 5.5 mmol/L, and HDL cholesterol concentration 0.9 mmol/L. Her present drug treatment is paracetamol (4 g daily) and metformin.
What are non-steroidal anti-inflammatory drugs (NSAIDs)?
NSAIDs act by inhibiting cyclo-oxygenase-1 (COX-1) and COX-2 enzymes, which are involved in prostaglandin synthesis, resulting in their analgesic, anti-inflammatory, and antipyretic effects (figure 1). Although the boundary is blurred, there are two broad groups of NSAIDs—the older, traditional, non-selective NSAIDs that inhibit both COX-1 and COX-2 and the newer, selective COX-2 inhibitors that predominantly inhibit COX-2 (figure 1). The non-selective NSAID aspirin is used primarily for its antiplatelet effect, thus reducing the risk of myocardial re-infarction and stroke.
Arachidonic acid is metabolised by the cyclo-oxygenase isoenzymes COX-1 and COX-2 to intermediate prostaglandins (PGG2, then PGH2), which are then converted to other prostaglandins that are mediators of pain, inflammation, and fever, and are gastroprotective. Thromboxane A2 causes platelet aggregation, and prostacyclin produces vasodilation. By blocking COX enzymes, NSAIDs inhibit the synthesis and thus the effects of prostaglandins, prostacyclin, and thromboxane A2. The clinical effects of NSAIDs depend largely on their selectivity for these enzymes. Aspirin works by irreversibly inhibiting COX-1 mediated synthesis of thromboxane A2, and is used to inhibit platelet aggregation.
How well do NSAIDs work?
Table 1 shows the indications and effectiveness of the various NSAIDs. There is little difference in their mean efficacy, although a review of individual patient data indicates that patients vary in their responses to different NSAIDs.7 Effectiveness …
Footnotes
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▸ This article is an abridged version of a paper that was published on bmj.com. Cite this article as: BMJ 2013;346:f3195
This is one of a series of occasional articles on therapeutics for common or serious conditions, covering new drugs and old drugs with important new indications or concerns. The series advisers are Robin Ferner, honorary professor of clinical pharmacology, University of Birmingham and Birmingham City Hospital, and Albert Ferro, professor of cardiovascular clinical pharmacology, King's College London. To suggest a topic for this series, please email us at practice{at}bmj.com.
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Contributors: Both authors contributed equally to the conceptualisation and writing ofthis article. ROD has expertise in medicine, clinical pharmacology, and toxicology. GGG has expertise in basic and clinical pharmacology. ROD is guarantor.
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Competing interests: We have read and understood the BMJ Group policy on declaration of interests and declare the following interests: ROD has been involved with consultancies with several drug companies on patents and advice on paracetamol, ibuprofen, selective COX-2 inhibitors, and other drugs used for osteoarthritis; all payments for consultancies were made to a trust fund at St Vincent's Hospital. Payment to ROD was made for expert testimony regarding a veterinary anti-arthritic product unrelated to NSAIDs. We acknowledge the assistance ofthe National Health and Medical Research Council programme grant (568612) for general research relating to patient safety.
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Provenance and peer review: Commissioned; externally peer reviewed.
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Patient consent: Not required (patient anonymised, dead, or hypothetical).
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