Practice Therapeutics

Non-steroidal anti-inflammatory drugs (NSAIDs)

BMJ 2013; 346 doi: http://dx.doi.org/10.1136/bmj.f3195 (Published 27 June 2013) Cite this as: BMJ 2013;346:f3195

This article has a correction. Please see:

  1. Richard O Day, professor of clinical pharmacology12,
  2. Garry G Graham, professorial visiting fellow12
  1. 1Department of Pharmacology, University of New South Wales, Sydney, Australia
  2. 2Department of Clinical Pharmacology and Toxicology, St Vincent’s Hospital, Sydney, Australia
  1. Correspondence to: R O Day r.day{at}unsw.edu.au

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). 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). 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 …

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