Drug-induced Liver Injury Due to Paracetamol Abuse

Abstract

Paracetamol is widely known to be one of the agents causing drug-induced acute liver injury (Drug-Induced Liver Injury). DILI is an unfavorable reaction to the body, one of the reasons is due to the presence of xenobiotics in the body. Xenobiotics are foreign substances that enter the body such as drugs, chemicals, insecticides, and other carcinogenic substances. Xenobiotics will be metabolized in the body, especially in the liver so as not to cause toxic effects in the body. Paracetamol is a xenobiotic in the body. Administration of high doses of paracetamol will result in increased formation of N-acetyl-para-benzoquinoneimine (NAPQI), and reduced hepatic glutathione stores. The formation of metabolites between NAPQI in large quantities and a decrease in the amount of liver glutathione, will result in necrosis or liver damage. The use of high doses of paracetamol will lead to the accumulation of N-acetyl-p benzoquinoneimine (NAPQI), which is a highly reactive metabolite and causes liver cell injury leading to centrilobular necrosis and subsequent liver failure. Damaged liver cells will release enzymes that mark the damage including SGOT, SGPT, and total serum bilirubin. An increase in liver damage markers indicates that there is liver damage caused by paracetamol. Elevated levels of the liver enzymes alanine transaminase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) are considered indicators of liver injury. N-acetylcysteine ​​therapy can treat paracetamol overdose. The use of curcumin as an antioxidant has been shown to optimize the gene expression of antioxidant enzymes that can prevent liver damage. Stopping consumption of drugs that cause liver damage and monitoring is an effort to manage DILI cause paracetamol.