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NAPQI therefore remains in its toxic form in the liver and reacts with cellular membrane molecules, resulting in widespread hepatocyte damage and death, leading to acute liver necrosis. [35] [40] In animal studies, the liver's stores of glutathione must be depleted to less than 70% of normal levels before liver toxicity occurs. [36]
NAPQI, also known as NAPBQI or N-acetyl-p-benzoquinone imine, is a toxic byproduct produced during the xenobiotic metabolism of the analgesic paracetamol (acetaminophen). [1] It is normally produced only in small amounts, and then almost immediately detoxified in the liver.
Hepatotoxicity (from hepatic toxicity) implies chemical-driven liver damage. Drug-induced liver injury (DILI) is a cause of acute and chronic liver disease caused specifically by medications and the most common reason for a drug to be withdrawn from the market after approval.
Paracetamol, [a] or acetaminophen, [b] is a non-opioid analgesic and antipyretic agent used to treat fever and mild to moderate pain. [13] [14] [15] It is a widely available over-the-counter drug sold under various brand names, including Tylenol and Panadol. Paracetamol relieves pain in both acute mild migraine and episodic tension headache.
The Rumack–Matthew nomogram, also known as the acetaminophen nomogram, is an acetaminophen toxicity nomogram. It plots serum concentration of acetaminophen against the time since ingestion, in order to predict possible liver toxicity and allow a clinician to decide whether to proceed with N-Acetylcysteine (NAC) treatment.
But for a small number of drugs that are very toxic to the intestine (e.g. irinotecan), these molecules which would not otherwise be very toxic can become so because of this process, and therefore inhibition of this step can be protective. For the majority of drugs which undergo enterohepatic circulation that are not toxic to the intestine ...
Data from Drug Induced Liver Injury Network reported the rates of liver injury due to botanical products has been on the rise from 7% in 2004-2005 to 20% in 2013-2014.
Centrilobular necrosis (CN) is a nonspecific histopathological observation brought on by hepatotoxins like acetaminophen (paracetamol), [1] thioacetamide, tetrachloride, [2] cardiac hepatopathy due to acute right sided cardiac failure, and congestive hepatic injury in veno-occlusive disease, [3] or hypoxic injury due to ischemia. [2]