The most frequently reported adverse effect associated with paracetamol is hepatotoxicity, which occurs after acute overdosage (usually doses greater than 10 to 15g are needed) and, very rarely, during long term treatment with doses at the higher levels of the therapeutic range. The lack of any significant influence on peripheral cyclo-oxygenase would explain the absence of anti-inflammatory activity.Īt therapeutic doses paracetamol is well tolerated and produces fewer side effects than aspirin.
The mechanism of action of paracetamol is poorly defined, although it has been speculated that it may selectively inhibit prostaglandin production in the central nervous system, which would account for its analgesic/antipyretic properties. Since a major portion of a dose of phenacetin is rapidly metabolised to paracetamol, it seems possible that phenacetin owes some of its therapeutic activity to its main metabolite, paracetamol, whereas its most troublesome side effect (methaemoglobinaemia) is due to another metabolite, p-phenetidine. This marked increase in the wide approval attained by paracetamol has been accompanied by the virtual commercial demise of phenacetin because of its role, albeit somewhat circumstantial, in causing analgesic nephropathy.īoth paracetamol and phenacetin are effective mild analgesics, suitable for treating mild to moderate pain, and their actions are broadly comparable with those of aspirin and related salicylates, although they do not appear to possess significant anti-inflammatory activity. Today the opposite is true, and paracetamol, along with aspirin, has become one of the two most popular ‘over-the-counter’ non-narcotic analgesic agents. Initially, paracetamol was discarded in favour of phenacetin because the latter drug was supposedly less toxic. Since their synthesis in the late 1800s paracetamol (acetaminophen) and phenacetin have followed divergent pathways with regard to their popularity as mild analgesic/antipyretic drugs.
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