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Aspartate transaminase (AST) or aspartate aminotransferase, also known as AspAT/ASAT/AAT or (serum) glutamic oxaloacetic transaminase (GOT, SGOT), is a pyridoxal phosphate (PLP)-dependent transaminase enzyme (EC 2.6.1.1) that was first described by Arthur Karmen and colleagues in 1954.
[11] [12] [13] Levels in the third trimester can be as much as 2-fold greater than in non-pregnant women. [11] As a result, ALP is not a reliable marker of hepatic function in pregnant women. [11] In contrast to ALP, levels of ALT, AST, GGT, and lactate dehydrogenase are only slightly changed or largely unchanged during pregnancy. [11]
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.
Cirrhosis, also known as liver cirrhosis or hepatic cirrhosis, chronic liver failure or chronic hepatic failure and end-stage liver disease, is an acute condition of the liver in which the normal functioning tissue, or parenchyma, is replaced with scar tissue and regenerative nodules as a result of chronic liver disease.
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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.