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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cause of acute and chronic liver disease caused specifically by medications and the most common reason for a drug to be withdrawn from the market after approval. The liver plays a central role in transforming and clearing chemicals and is susceptible to the toxicity from these agents.
Hy's law is a rule of thumb that a patient is at high risk of a fatal drug-induced liver injury if given a medication that causes hepatocellular injury (not Hepatobiliary injury) with jaundice. [1] The law is based on observations by Hy Zimmerman, a major scholar of drug-induced liver injury.
Analogous terms such as "drug-induced" or "toxic" liver disease are also used to refer to disorders caused by various drugs. [7] Fatty liver disease (hepatic steatosis) is a reversible condition where large vacuoles of triglyceride fat accumulate in liver cells. [8]
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.
Liver regeneration is the process by which the liver is able to replace damaged or lost liver tissue. The liver is the only visceral organ with the capacity to regenerate. [ 1 ] [ 2 ] The liver can regenerate after partial hepatectomy or injury due to hepatotoxic agents such as certain medications, toxins, or chemicals. [ 3 ]
(Reuters) -The U.S. Food and Drug Administration on Wednesday approved Gilead Sciences' liver disease treatment, Livdelzi, which it gained through a $4.3 billion buyout of CymaBay Therapeutics ...
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]
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