Main articles: Paracetamol toxicity and Analgesic nephropathy
Paracetamol hepatotoxicity is, by far, the most common cause of acute liver failure in both the United States and the United Kingdom.[6][65] Paracetamol overdose results in more calls to poison control centers in the US than overdose of any other pharmacological substance.[66] Signs and symptoms of paracetamol toxicity may initially be absent or vague. Untreated, overdose can lead to liver failure and death within days. Treatment is aimed at removing the paracetamol from the body and replacing glutathione. Activated charcoal can be used to decrease absorption of paracetamol if the patient presents for treatment soon after the overdose. While the antidote, acetylcysteine, (also called N-acetylcysteine or NAC) acts as a precursor for glutathione, helping the body regenerate enough to prevent damage to the liver, a liver transplant is often required if damage to the liver becomes severe.[3]
There are tablets available (brandname in the UK Paradote) which combine paracetamol with an antidote (methionine), to protect the liver in case of an overdose.
In June 2009, an FDA advisory committee recommended that new restrictions should be placed on paracetamol usage in the United States to help protect people from the potential toxic effects. The maximum dosage to be consumed at any given time would be decreased from 1000 mg to 650 mg, while combinations of paracetamol and narcotic analgesics would be prohibited. Committee members were particularly concerned by the fact that the present maximum dosages of paracetamol had been shown to produce alterations in hepatic function.[67] The FDA has not implemented their recommendations as of March 2010.[68]
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