Elevated transaminases
In medicine, the presence of elevated transaminases, commonly the transaminases alanine transaminase (ALT) and aspartate transaminase (AST), may be an indicator of liver damage.[1] Other terms employed include transaminasemia,[2] transaminitis (which some sources consider pathologically meaningless[3]) and elevated liver enzymes (though they are not the only enzymes in the liver). Normal ranges for both ALT and AST are 8-40 U/L with mild transaminesemia noted to the upward numerical limit of 250 U/L. 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. 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. Elevated transaminases that persist less than six months are termed "acute" in nature, and those values that persist for six months or more are termed "chronic" in nature.
Elevated transaminases | |
---|---|
Alanine transaminase is one of the two transaminases measured (Aspartate transaminase is the other). |
Pathophysiology
The liver has transaminases to synthesize and break down amino acids and to convert energy storage molecules. The concentrations of these transaminases in the serum (the non-cellular portion of blood) are normally low. However, if the liver is damaged, the liver cell (hepatocyte) membrane becomes more permeable and some of the enzymes leak out into the blood circulation.
The two transaminases commonly measured are alanine transaminase (ALT) and aspartate transaminase (AST).[1] These levels previously were called serum glutamate-pyruvate transaminase (SGPT) and serum glutamate-oxaloacetate transaminase (SGOT). Elevated levels are sensitive for liver injury, meaning that they are likely to be present if there is injury. However, they may also be elevated in other conditions such as thyroid disorders, celiac disease, and muscle disorders.[4]
ALT is usually found only in the liver. AST is most commonly found in the liver, but also in significant amounts in heart (cardiac) and skeletal muscle.
Measurement of ALT and AST were used in diagnosing heart attacks, although they have been replaced by newer enzyme and protein tests that are more specific for cardiac damage.
Possible causes for high ALT levels are liver inflammation (hepatitis A, B, C, infectious mononucleosis, acute viral fever, alcohol, pancreatic disorder), injury to muscles (trauma, myocardial infarction, congestive heart failure, acute kidney failure), and many toxins and drugs.
Role in diagnosis
In general, any damage to the liver will cause medium elevations in these transaminases, but diagnosis requires synthesis of many pieces of information, including the patient's history, physical examination, and possibly imaging or other laboratory examinations. 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.
Levels over 1000 can be associated with ischemic hepatitis.[5]
See also
References
- Giboney PT (March 2005). "Mildly Elevated Liver Transaminase Levels in the Asymptomatic Patient". Am Fam Physician. 71 (6): 1105–10. PMID 15791889.
- "Transaminasemia: semantic confusion of a clinical dilemma". Calif Med. 114 (6): 45–7. June 1971. PMC 1501958. PMID 5578107.
- Maddrey, Willis C.; Schiff, Eugene R.; Sorrell, Michael F. (2007). Schiff's diseases of the liver. Hagerstwon, MD: Lippincott Williams & Wilkins. p. 924. ISBN 978-0-7817-6040-9.
- Oh, RC; Hustead, TR (1 November 2011). "Causes and evaluation of mildly elevated liver transaminase levels". American Family Physician. 84 (9): 1003–8. PMID 22046940.
- Raurich JM, Pérez O, Llompart-Pou JA, Ibáñez J, Ayestarán I, Pérez-Bárcena J (July 2009). "Incidence and outcome of ischemic hepatitis complicating septic shock". Hepatol. Res. 39 (7): 700–5. doi:10.1111/j.1872-034X.2009.00501.x. PMID 19473435.