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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.
Normal ranges for both ALT and AST vary by gender, age, and geography and are roughly 8-40 U/L (0.14-0.67 μkal/L). [4] Mild transaminesemia refers to levels up to 250 U/L. [ 1 ] Drug-induced increases such as that found with the use of anti-tuberculosis agents such as isoniazid are limited typically to below 100 U/L for either ALT or AST.
In pregnancy, ALT levels would rise during the second trimester. In one of the studies, measured ALT levels in pregnancy-related conditions such as hyperemesis gravidarum was 103.5 IU/L, pre-eclampsia was 115, HELLP syndrome was 149. ALT levels would reduce by greater than 50% in three days after child delivery.
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.
Aminotransferases AST and ALT are moderately elevated, with AST > ALT. However, normal aminotransferase levels do not preclude cirrhosis. [52] Alkaline phosphatase – slightly elevated but less than 2–3 times the upper limit of normal. [citation needed] Gamma-glutamyl transferase – correlates with AP levels. Typically much higher in ...
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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]