Paracetamol has analgesic and antipyretic effects. It is only a weak inhibitor of prostaglandin biosynthesis, although there is some evidence to suggest that it may be more effective against enzymes in the CNS than those in the periphery. This fact may partly account for its ability to reduce fever (a central action) and to induce analgesia. Dihydrocodeine is a centrally acting analgesic which produces its effects by its action at opioid binding sites within the CNS.
Paracetamol is well absorbed from the gastrointestinal tract, peak plasma concentrations occurring 0.5-2 hours after ingestion. It is metabolised in the liver and excreted in the urine mainly as glucuronide and sulphate conjugates – less than 5% is excreted as unmodified paracetamol. The plasma half-life is between 1 and 4 hours. Binding to plasma proteins is minimal as therapeutic concentrations but increases as plasma concentrations increase.
Oral dihydrocodeine undergoes considerable presystemic metabolism, but its subsequent metabolism is uncertain. The pharmacokinetics of dihydrocodeine may be similar to those of codeine.
Conventional studies using the currently accepted standards for the evaluation of toxicity to reproduction and development are not available.
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