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Muscle sources of the enzymes, such as intense exercise, are unrelated to liver function and can markedly increase AST and ALT. [5] Cirrhosis of the liver or fulminant liver failure secondary to hepatitis commonly reach values for both ALT and AST in the >1000 U/L range; however, many people with liver disease have normal transaminases.
Patients with liver cirrhosis develop liver cancer at a rate of 1.5% per year. [11] In total, 70% of those with alcoholic hepatitis will go on to develop alcoholic liver cirrhosis in their lifetimes. [10] Infection risk is elevated in patients with alcoholic hepatitis (12–26%).
Risk factors known as of 2010 are: Quantity of alcohol taken: Consumption of 60–80 g per day (14 g is considered one standard drink in the US, e.g. 1 + 1 ⁄ 2 US fl oz or 44 mL hard liquor, 5 US fl oz or 150 mL wine, 12 US fl oz or 350 mL beer; drinking a six-pack of 5% ABV beer daily would be 84 g and just over the upper limit) for 20 years or more in men, or 20 g/day for women ...
The proportion of AST to ALT in hepatocytes is about 2.5:1, but because AST is removed from serum by the liver sinusoidal cells twice as quickly (serum half-life t 1/2 = 18 hr) compared to ALT (t 1/2 = 36 hr), so the resulting serum levels of AST and ALT are about equal in healthy individuals, resulting in a normal AST/ALT ratio around 1.
The alcohol tolerance is also connected with activity of alcohol dehydrogenases (a group of enzymes responsible for the breakdown of alcohol) in the liver, and in the bloodstream. High level of alcohol dehydrogenase activity results in fast transformation of ethanol to more toxic acetaldehyde. Such atypical alcohol dehydrogenase levels are less ...
Because liver enzyme function is based on the relative function of liver cells (hepatocytes) [31] liver disease caused by chronic alcohol use can lead to poor metabolism of alcohol overtime, due to improper function of enzymes that would otherwise process alcohol.
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