About 1 in 4 patients with hepatotoxicity experience marked renal impairment, rising to 1 in 2 of those with fulminant liver failure. The other major organ to be affected to any clinically significant degree is the kidney. This results in free NAPQI very quickly binding to and arylating key cellular proteins, such that cell death ensues 3. Post overdose, the amount of NAPQI in the liver may overwhelm the ability of the glutathione system to neutralise this toxic metabolite. In adults, 7.5 g, or 150 mg/kg in children, are thought to be the minimum acute doses (taken all at once, not over a day) associated with toxicity 3. Indeed, some have stated that acetaminophen would not receive a commercial licence today if it was a new agent 1. Unfortunately, acetaminophen is associated with significant acute hepatotoxicity even with small and/or "staggered" overdoses, which is not uncommonly fatal. ChronicĪlthough historically acetaminophen was considered to be a very safe agent, it has now been fairly well-established that long term treatment-range dosing is associated with increased risk of cardiovascular morbidity, which is thought to be related to their effects on the cyclooxygenases ( cf. Rarely, an allergic skin reaction may be seen. With short-term use at treatment doses, acetaminophen is extremely well tolerated and most people experience no side effects whatsoever. Clinical usageĪcetaminophen produces a mild analgesic effect, similar in degree to that of aspirin 3. The systematic IUPAC name is N-(4-hydroxyphenyl)acetamide. Indeed, the American brand name, Tylenol®, is also derived from N-ace tyl-para-aminoph enol. acetaminοphen from N- acetyl-para- aminophenol.paracetamοl from N-a cetyl- para- aminophen ol.Chemically the agent is known as N-acetyl-para-aminophenol, the name from which both the generic British and American names derive:
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