Higher levels indicate possible hepatotoxicity.

A level ≤ 150 mcg/mL ( ≤ 990 micromol/L) and absence of toxic symptoms indicate that hepatotoxicity is very unlikely. For a single acute overdose of traditional acetaminophen or rapid-relief acetaminophen (which is absorbed 7 to 8 minutes faster), levels are measured ≥ 4 hours after ingestion and plotted on the nomogram.

If the time of acute ingestion is known, the Rumack-Matthew nomogram is used to estimate likelihood of hepatotoxicity if the time of acute ingestion is unknown, the nomogram cannot be used. Likelihood and severity of hepatotoxicity caused by an acute ingestion can be predicted by the amount ingested or, more accurately, by the serum acetaminophen level. However, therapeutic doses of acetaminophen in alcoholic patients are not associated with hepatic injury. read more could increase risk of toxicity because hepatic enzyme preconditioning may increase formation of NAPQI and because undernutrition (also common among alcoholics) reduces hepatic glutathione stores. (Malnutrition also includes overnutrition.) Undernutrition can result from inadequate ingestion of nutrients, malabsorption, impaired metabolism, loss. read more or undernutrition Overview of Undernutrition Undernutrition is a form of malnutrition. According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), 8.5% of US adults are estimated to. Theoretically, alcoholic liver disease Alcohol-Related Liver Disease Alcohol consumption is high in most Western countries. As a result, NAPQI accumulates, causing hepatocellular necrosis and possibly damage to other organs (eg, kidneys, pancreas). An acute overdose depletes glutathione stores in the liver. The principal toxic metabolite of acetaminophen, N-acetyl- p-benzoquinone imine (NAPQI), is produced by the hepatic cytochrome P-450 enzyme system glutathione stores in the liver detoxify this metabolite.

Mucomyst antidote