In 1893, the white, odourless crystalline compound with a bitter taste that became known as paracetamol was discovered. Initially, paracetamol was found in the urine of patients who had taken phenacetin and in 1889 it was demonstrated that paracetamol was a urinary metabolite of acetanilide. These discoveries, however, failed to attract much attention and were largely ignored at the time.
It was not until 1948, when Brodie and Axelrod established that paracetamol was a major metabolite of both acetanilide and phenacetin, that paracetamol experienced a resurgence of interest. As a derivative of p-aminophenol, paracetamol corresponds to the active principal metabolite phenacetin. It was commonly assumed at the time that their rapid conversion by the body into paracetamol was actually responsible for the therapeutic effects of both of these medicines. It was eventually ascertained that phenacetin had its own pharmacological action and was not dependent on paracetamol for its effects. Because a high proportion of phenacetin is converted into paracetamol in the liver, however, phenacetin required a large dosage to achieve any direct analgesic effect.
In 1956, 500mg tablets of paracetamol went on sale in the United Kingdom and its popularity as an over-the-counter analgesic rapidly increased. This popularity was partly explained by the fact that paracetamol was proven to be easier on the stomach than some other analgesics. Paracetamol gradually became combined with both analgesics and oral decongestants.
Paracetamol works as a weak prostaglandin inhibitor. It achieves this by blocking the production of prostaglandins, which are chemicals involved in the transmission of the pain message to the brain. In this regard, paracetamol is different from Aspirin and NSAIDs (non-steroidal anti-inflammatory drugs) in that it blocks the pain message at the brain and not at the source of the pain, as the others do.
Structually, paracetamol is similar to aspirin. They are both recognised by the same enzyme, which is called cyclo-oxygenase (COX). Cyclo-oxygenase serves as a pain activator, amplifying the degree of pain experienced in order to let the body know that there is a problem. It is this enzyme that is responsible for the biosynthesis of prostoglandins. By reducing the amount of prostaglandin available for synthesis, paracetamol helps relieve headache pain by reducing the dilation of the blood vessels that cause the pain. Paracetamol, however, only inhibits prostaglandin biosynthesis in the central nervous system (CNS) with little or no effect on peripheral tissues.
Paracetamol is used to relieve mild to moderate pain, including instances of tension headache, migraine headache, muscular aches, neuralgia, backache, joint pain, rheumatic pain, general pain, toothache, teething pain, and period pain. It is suitable for most people, including the elderly and young children, because it has very few side effects. Paracetamol is used to treat osteoarthritis, a type of non-inflammatory arthritis due to the "wear and tear" of the joints, because of its analgesic properties and its lack of gastrointestinal side effects. It can also help with the pain experienced by sufferers of arthritis.Paracetamol is an antipyretic that can reduce fever by affecting the part of the brain known as the hypothalamus that regulates the temperature of the body. This is why paracetamol is included in many cough, cold and flu medications. Specifically, paracetamol has been given to children after they have been given vaccinations in order to prevent them developing post-immunisation pyrexia, or fever.
Paracetamol
