The non-steroidal anti-inflammatory drugs (NSAIDs), are a large class of chemically heterogenous drugs used in the management of inflammation, pain, and fever. They are widely prescribed for conditions ranging from mild pain and fever, to dysmenorrhea and arthritis. Paracetmaol is a drug with pharmacological similarities to the NSAIDs but which exhibits no clinically significant anti-inflammatory action.
The principal pharmacological action of the NSAIDs is the inhibition of cyclooxygenase (COX), the enzyme that produces prostaglandins (PGs). PGs are important chemical mediators in the processes of inflammation, pain transmission, and temperature regulation. The ability to interfere with the activity of COX allows the NSAIDs to reduce inflammation, pain, and body temperature elevated by fever. Paracetamol appears to act by inhibiting COX selectively in the central nervous system and so can control fever and pain through central mechanisms but has little or no anti-inflammatory action at clinical doses.
However, PGs are also important mediators in many physiological processes in the body, e.g. the maintenance of the protective mucus layer in the stomach and duodenum and blood flow in the kidneys. NSAIDs also interfere with the production of the PGs involved in these physiological processes. This results in the adverse effects associated with NSAID use, e.g. gastric ulceration and bleeding, and renal toxicity. The discovery that COX exists in isozymic forms has resulted in the production of new selective COX-2 inhibitors (coxibs), supposedly able to inhibit the production of PGs associated with pain and inflammation, while not interfering with the PGs involved in physiological processes. While COX-2 selective inhibitors do have better adverse effects profiles than nonselective COX inhbitors, they do not live up to the promise of completely sparing all physiological processes involving PGs.