Tylenol and Risk Of Liver Failure

The UGT1A1 gene provides instructions for making enzymes called UDP-glucuronosyltransferases which are primarily found in cells of the liver. Hundreds of different substances are metabolized by UGT enzymes, including bilirubin, a toxic substance produced when red blood cells are broken down; steroids such as testosterone and estrogen; and serotonin, an important hormone that transmits brain signals. UGT enzymes also metabolize certain drugs such as acetaminophen and morphine through a process known as Glucuronidation. Glucuronidation makes the affected substances dissolvable in water, which allows them to be removed from the body. Genetic variations in UGT genes can play a role in a person's response to these drugs.

Acetaminophen (Tylenol) is the leading worldwide cause of drug overdose and acute liver failure1. Single overdose ingestion may cause liver toxicity. Several factors, such as alcohol use, concurrent medications, genetic factors, and nutritional status, can influence the susceptibility and severity of Acetaminophen liver toxicity. Early clinical signs of Acetaminophen toxicity are nonspecific. N-acetylcysteine is a very effective antidote when giving within 8 hours.1

Related to:
Acetaminophen, Tylenol, Paracetamol, Panadol, Tylenol, Anacin, Feverall, Apap, UGT1A