Acetaminophen and NSAIDs are two of the most popular types of medications that people take for pain and fever relief.
NSAIDs work by limiting the body's production of prostaglandins. In addition to reducing fever, body aches, and pain caused by prostaglandins, NSAIDs reduce inflammation.
NSAIDs act as reversible, competitive inhibitors of cyclooxygenase. Two unique cyclooxygenases have been described in mammals:
- The constitutive cyclooxygenase, COX-1, synthesizes prostaglandins necessary for normal gastrointestinal and renal function.
- The inducible cyclooxygenase, COX-2, generates prostaglandins involved in inflammation.
Traditional NSAIDs block the actions of both COX-1 and COX-2: Inhibition of COX-1 is thought to be associated with gastrointestinal and renal toxicity while inhibition of COX-2 provides anti-inflammatory activity.
Among the NSAIDs, aspirin is unique in that it not only has analgesic (pain), antipyretic (fever) and anti-inflammatory effects but it also exerts beneficial effects on the cardiovascular system. Low doses of Acetylsalicylic acid block platelet production of thromboxane A2 and thereby, platelet activation and aggregation. This property accounts for its use in the long-term prevention of heart attacks.
NSAIDs are associated with stomach distress and can also cause reversible damage to the kidneys. The risk of kidney damage may increase in people who are over 60, have high blood pressure, heart disease or pre-existing kidney disease and people who are taking a diuretic.
Acetaminophen lowers fever and reduces aches and pains. Unlike NSAIDs, it doesn't reduce inflammation.
Acetaminophen works primarily in the central nervous system, attacking a slightly different form of the enzyme called COX-3
In large doses, acetaminophen can lead to liver damage.