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NSAIDS have antipyretic activity and can be used to treat fever. [75] [76] Fever is caused by elevated levels of prostaglandin E2 , which alters the firing rate of neurons within the hypothalamus that control thermoregulation. [75] [77] Antipyretics work by inhibiting the enzyme COX, which causes the general inhibition of prostanoid biosynthesis ( PGE2 ) within the hypothalamus . [75] [76] PGE2 signals to the hypothalamus to increase the body's thermal set point. [76] [78] Ibuprofen has been shown more effective as an antipyretic than paracetamol (acetaminophen). [77] [79] Arachidonic acid is the precursor substrate for cyclooxygenase leading to the production of prostaglandins F, D & E.

A person's history of taking paracetamol is somewhat accurate for the diagnosis. [38] The most effective way to diagnose poisoning is by obtaining a blood paracetamol level. A drug nomogram developed in 1975, called the Rumack-Matthew nomogram , estimates the risk of toxicity based on the serum concentration of paracetamol at a given number of hours after ingestion. [8] To determine the risk of potential hepatotoxicity, the paracetamol level is traced along the nomogram. Use of a timed serum paracetamol level plotted on the nomogram appears to be the best marker indicating the potential for liver injury. [17] A paracetamol level drawn in the first four hours after ingestion may underestimate the amount in the system because paracetamol may still be in the process of being absorbed from the gastrointestinal tract . Therefore, a serum level taken before 4 hours is not recommended. [16]

Paracetamol non steroidal

paracetamol non steroidal

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