Liver enzymes and the liver function panel
Several liver enzymes are commonly measured in blood serum, and each one has a normal range in healthy patients.
Now, let’s take a look at what we can learn from each of these liver enzymes.
What can serum alanine aminotransferase and aspartate aminotransferase testing tell us?
The breakdown of hepatocytes results in the release of aminotransferases such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST) into the blood. Therefore, elevated levels of these enzymes indicate liver injury.
Alanine aminotransferase is a cytosolic enzyme only found in hepatocytes and is specific to liver disease. Aspartate aminotransferase is a mitochondrial enzyme in the liver, but it is also found in the heart, muscle, kidney, and brain. So, AST is nonspecific to liver disease.
What can serum alkaline phosphatase testing tell us?
Alkaline phosphatase (ALP) is present in the liver, bone, intestine, and placenta. Production of ALP is increased during cholestasis, which is a decrease in bile flow due to intrahepatic or extrahepatic causes.
It is important to determine if the source of ALP is the liver or another organ. If gamma-glutamyl transpeptidase (GGT) or 5’-nucleotidase levels are increased alongside ALP, we can assume that the source of the ALP is the liver.
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What can serum GGT testing tell us?
Gamma-glutamyl transpeptidase is a microsomal enzyme produced by the biliary epithelium. Gamma-glutamyl transpeptidase is elevated in the liver, biliary tract, and pancreas diseases as well as common bile duct obstruction. When seen in conjunction with the transaminases (e.g., ALT and AST), GGT is also a marker of alcohol abuse.
What can serum 5’-nucleotidase testing tell us?
The serum 5'-nucleotidase enzyme is derived from the plasma membranes of liver cells. It is elevated in hepatobiliary diseases.
In cholestatic conditions, ALP, GGT, and 5’-nucleotidase levels are all elevated.
So, there you have it! Elevated liver enzymes, whether alone or in combination, can provide information that helps clarify the clinical picture of your patient.
That’s it for now. If you want to improve your understanding of key concepts in medicine, and improve your clinical skills, make sure to register for a free trial account, which will give you access to free videos and downloads. We’ll help you make the right decisions for yourself and your patients.
Recommended reading
- Chalasani, N, Younossi, Z, Lavine, JE, et al. 2012. The diagnosis and management of non-alcoholic fatty liver disease: practice guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology. Gastroenterology. 142: 1592–1609. PMID: 22656328
- Fuchs, S, Bogomolski-Yahalom, V, Paltiel, O, et al. 1998. Ischemic hepatitis: clinical and laboratory observations of 34 patients. J Clin Gastroenterol. 26: 183–186. PMID: 9600366
- Lok, ASF and McMahon, BJ. 2007. Chronic hepatitis B. Hepatology. 45: 507–539. PMID: 17256718
- Moussavian, SN, Becker, RC, Piepmeyer, JL, et al. 1985. Serum gamma-glutamyl transpeptidase and chronic alcoholism. Influence of alcohol ingestion and liver disease. Dig Dis Sci. 30: 211–214. PMID: 2857631
- Myers, RP, Cerini, R, Sayegh, R, et al. 2003. Cardiac hepatopathy: clinical, hemodynamic, and histologic characteristics and correlations. Hepatology. 37: 393–400. PMID: 12540790
- Rej, R. 1978. Aspartate aminotransferase activity and isoenzyme proportions in human liver tissues. Clin Chem. 24: 1971–1979. PMID: 213206
- van de Steeg, E, Stránecký, V, Hartmannová, H, et al. 2012. Complete OATP1B1 and OATP1B3 deficiency causes human Rotor syndrome by interrupting conjugated bilirubin reuptake into the liver. J Clin Invest. 122: 519–528. PMID: 22232210