Rare but serious adverse effects include hypersensitivity, anaphylactic reactions, and serious and even fatal skin reactions. Increased bilirubin and alkaline phosphataseĪdditional adverse effects of acetaminophen administered intravenously include nausea, vomiting, constipation, pruritus, and abdominal pain. Other studies have suggested that acetaminophen or one of its metabolites, e.g., AM 404, also can activate the cannabinoid system e.g., by inhibiting the uptake or degradation of anandamide and 2-arachidonoylglyerol, contributing to its analgesic action. The analgesic properties may be due to a stimulating effect on the descending serotonergic pathways in the central nervous system (CNS). Regardless, the reduction of the COX pathway activity by acetaminophen is thought to inhibit the synthesis of prostaglandins in the central nervous system, leading to its analgesic and antipyretic effects. It also has been theorized that acetaminophen inhibits a splice variant of COX-1, also called COX-3, but this has not been confirmed in humans. Additionally, acetaminophen does not appear to bind to the active site of either the COX-1 or COX-2 enzyme instead, it reduces the activity of COX by a different mechanism. Acetaminophen may inhibit the COX pathway in the central nervous system but not peripheral tissues. However, studies have shown that acetaminophen lacks peripheral anti-inflammatory properties. Like NSAIDs, acetaminophen has analgesic and antipyretic properties. Although its exact mechanism of action remains unclear, it is historically categorized along with NSAIDs because it inhibits the cyclooxygenase (COX) pathways. Acetaminophen, also called N- acetyl para- amino phenol (APAP) or paracetamol, is one of the most widely used over-the-counter analgesic and antipyretic agents.

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