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Acetaminophen, also known as paracetamol, is a non-steroidal anti-inflammatory drug (NSAID) with potent antipyretic and analgesic actions but with very weak anti-inflammatory activity. The mechanism of action of acetaminophen is still not clearly understood. It has no known endogenous high affinity binding sites. In addition, acetaminophen does not appear to share with NSAIDs the ability to inhibit peripheral cyclo-oxygenase (COX) activity.1 Although various biochemical studies point to inhibition of central COX-2 activity, the existence of a COX activity that is selectively susceptible to acetaminophen (COX-3?) is an alternative hypothesis.2 However, this may hold true only for the dog. Database analysis of human COX-1 showed a frame shift induced by intron 1, possibly showing COX-3 to be a virtual protein in humans.3
Our studies in osteoarthritis provide evidence of a clear effect of acetaminophen on β endorphin levels in plasma (fig 1) compared with rofecoxib 25 mg/day.4 Plasma β endorphin levels decreased in 10 patients with osteoarthritis after 1 month of treatment with up to 4 g/day acetaminophen orally (p = 0.017) as well as after 3 months of treatment (p = 0.028). Whereas, there were no changes in the rofecoxib group after 1 month (p = 0.73) and 3 months (p = 1.00), respectively.
Acetaminophen may play a part in the delivery of peripheral β endorphin to their receptors and thereby relieve pain.
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