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This is a good reminder that AST and ALT are not good measures of liver function when other sources may influence AST or ALT, because they do not reliably reflect the synthetic ability of the liver, and they may come from tissues other than liver (such as muscle). [10] For example, intense exercise such as weight lifting can increase ALT to 50 ...
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.
[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]
Alanine transaminase (ALT), also known as alanine aminotransferase (ALT or ALAT), formerly serum glutamate-pyruvate transaminase (GPT) or serum glutamic-pyruvic transaminase (SGPT), is a transaminase enzyme (EC 2.6.1.2) that was first characterized in the mid-1950s by Arthur Karmen and colleagues. [1]
Serum AST level, serum ALT (alanine transaminase) level, and their ratio (AST/ALT ratio) are commonly measured clinically as biomarkers for liver health. The tests are part of blood panels. The half-life of total AST in the circulation approximates 17 hours and, on average, 87 hours for mitochondrial AST. [4]
AST and ALT blood levels are both elevated, but at less than 300 IU/liter, with an AST:ALT ratio > 2.0, a value rarely seen in other liver diseases. [52] In the United States, 40% of cirrhosis-related deaths are due to alcohol. [33] In non-alcoholic fatty liver disease (NAFLD), fat builds up in the liver and eventually causes scar tissue. [53]