Toxic liver failure in paracetamol poisoned patient abusing ethyl alcohol – case study

Abstract

Paracetamol is a drug which is commonly used in pain and fever therapy. Its composition includes many single and multiple ingredient medications. When used in therapeutic doses, it is considered to be quite safe. However, its common availability and low public awareness concerning the risk of overdose can be the reason of uncontrolled ingestion and may lead to poisoning resulting in severe liver failure. About 5% of paracetamol is metabolized in the liver by CYP2E1 into a toxic metabolite called N-acetyl-p-benzoquinoneimine (NAPQI). In healthy organisms, this metabolite is caught by sulfhydryl groups of hepatic glutathione and removed from the body. Ethyl alcohol is also metabolized by CYP2E1, ethanol induces its activity. Chronic ingestion of ethanol increases the level of this enzyme. When the ingestion of ethanol is stopped, the level of CYP2E1 is significantly increased. In such cases, the dosage of paracetamol results in increased level of NAPQI that cannot be removed by hepatic glutathione. NAPQI creates a covalent bond with hepatocyte macromolecules which may end in the demise of these cells. During paracetamol treatment, drinking alcohol is not allowed because of the higher risk of hepatotoxicity. It especially concerns people who drink alcohol regularly (chronic alcohol addicts). Alcoholism in Central and Eastern European countries is based on the tradition of drinking large amounts of strong liquors. A headache caused by misuse of alcohol often becomes the reason of painkillers overdose. However, paracetamol poisonings linked to suicide attempts have become commonplace.