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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.
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cause of acute and chronic liver disease caused specifically by medications and the most common reason for a drug to be withdrawn from the market after approval.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.
Enterohepatic circulation of drugs. Enterohepatic circulation is the circulation of biliary acids, bilirubin, drugs or other substances from the liver to the bile, followed by entry into the small intestine, absorption by the enterocyte and transport back to the liver.
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]
for liver transplantation in acute liver failure [25] Patients with paracetamol toxicity. pH < 7.3 or Prothrombin time > 100 seconds and serum creatinine level > 3.4 mg/dL (> 300 μmol/L) if in grade III or IV encephalopathy. Other patients. Prothrombin time > 100 seconds or Three of the following variables: Age < 10 yr or > 40 years; Cause ...
The increasing liver damage also changes biochemical markers of liver function; International normalized ratio (INR) and the liver transaminases ALT and AST rise to abnormal levels. [14] Acute kidney failure may also occur during this phase, typically caused by either hepatorenal syndrome or multiple organ dysfunction syndrome .
Patients with type 1 HRS are usually ill, may have low blood pressure, and may require therapy with drugs to improve the strength of heart muscle contraction or other drugs to maintain blood pressure (vasopressors). [5] Unlike type II, in type I hepatorenal syndrome the kidney failure improves with treatment and stabilizes.
UDP-glucuronic acid (glucuronic acid linked via a glycosidic bond to uridine diphosphate) is an intermediate in the process and is formed in the liver. One example is the N-glucuronidation of an aromatic amine, 4-aminobiphenyl, by UGT1A4 or UGT1A9 from human, rat, or mouse liver. [2]