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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.
However, very high elevations of the transaminases suggests severe liver damage, such as viral hepatitis, liver injury from lack of blood flow, or injury from drugs or toxins. Most disease processes cause ALT to rise higher than AST; AST levels double or triple that of ALT are consistent with alcoholic liver disease. [citation needed]
[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]
Hepatic artery thrombosis may cause severe elevations in serum aminotransferases, alanine transaminase (ALT) and aspartate transaminase (AST). [4] Often the AST is greater than the ALT. [ 4 ] Hepatic artery thrombosis is usually diagnosed with ultrasound with doppler , although it may be diagnosed using computed tomography (CT) or magnetic ...
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.