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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 ...
An AST/ALT ratio >5 necessarily involves extrahepatic tissue, as death of hepatocytes alone would produce an AST/ALT ratio no greater than 2.5. [9] Because the primary cause is extrahepatic, typically an isolated elevated AST is seen, with no change in ALT. Common causes include bone disease, chronic renal failure, lymphoma, and congestive ...
When ALT rises to more than 500 IU/L, causes are usually from the liver. It can be due to hepatitis, ischemic liver injury, and toxins that causes liver damage. The ALT levels in hepatitis C rises more than in hepatitis A and B. Persistent ALT elevation more than 6 months is known as chronic hepatitis.
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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.
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]
It is the major cause of liver disease in Western countries, and is the leading cause of death from excessive drinking. [ 2 ] [ 3 ] Although steatosis ( fatty liver disease ) will develop in any individual who consumes a large quantity of alcoholic beverages over a long period of time, this process is transient and reversible. [ 1 ]
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