Overview of the liver function panel

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Last update26th Jan 2021

The liver is the largest internal organ in the body. It is involved in processing dietary amino acids, carbohydrates, lipids, and vitamins. It also metabolizes cholesterol and toxins, produces clotting factors, and stores glycogen. As well, the liver is the principal site for the synthesis of all circulating proteins (except gamma globulins).

Four biomarkers are routinely measured on a liver function panel:

  1. Bilirubin
  2. Liver enzymes
  3. Prothrombin and partial thromboplastin time
  4. Albumin

Let’s look at each of these tests in a bit more detail.


Bilirubin is a waste product that is produced from the breakdown of red blood cells. Heme (derived from the breakdown of hemoglobin) ultimately becomes unconjugated bilirubin, which is a water-insoluble molecule that is bound to serum albumin in the blood.

Unconjugated bilirubin is taken up by the liver, where it is converted to conjugated bilirubin. Conjugated bilirubin is water-soluble and can be excreted in bile.

Figure 1. Heme is a waste product that is produced from the breakdown of red blood cells. It ultimately becomes unconjugated bilirubin and is converted to conjugated bilirubin by the liver.

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Liver enzymes

Six liver enzymes are commonly measured in a liver function panel:

  1. Alanine aminotransferase (ALT)
  2. Aspartate aminotransferase (AST)
  3. Alkaline phosphatase (ALP)
  4. Gamma-glutamyl transpeptidase (GGT)
  5. 5’-nucleotidase
  6. Lactate dehydrogenase (LDH)
Figure 2. Liver enzymes that are commonly tested on a liver function panel include alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (GGT), 5’-nucleotidase, and lactate dehydrogenase (LDH).

Prothrombin and partial thromboplastin time

The coagulation cascade is divided into the extrinsic, intrinsic, and common pathways. Prothrombin time (PT) is one way of measuring how long it takes a patient’s blood to form a clot. It is a common measurement included in a liver function panel and assesses the integrity of the extrinsic and common coagulation pathways.

Partial thromboplastin time (PTT) is another coagulation test. It measures the integrity of the intrinsic and common coagulation pathways.

Except for factor VIII, all blood clotting factors are produced in the liver—including prothrombin (which is also called factor II). Therefore, when liver function is significantly impaired (in the acute or chronic setting), clotting factor levels will be reduced.

Figure 3. The coagulation cascade consists of intrinsic, extrinsic, and common pathways. Prothrombin time (PT) measures the integrity of the extrinsic and common pathways, while partial thromboplastin time (PTT) measures the integrity of the intrinsic and common pathways.


Albumin is the most common protein found in the blood. It is used by the body for growth and tissue repair. When liver function is impaired over a prolonged period, albumin synthesis is also impaired, which results in low levels of albumin in the blood. For this reason, hypoalbuminemia is a common finding in chronic (but not acute) liver failure.

Figure 4. Albumin is the most common protein found in the blood. It is used for growth and tissue repair, and levels are low with chronic (but not acute) liver disease.

What do these liver function tests tell us?

Biomolecules such as ALT, AST, ALP, and bilirubin are markers of liver injury. So, a change in their levels suggests a pathological process causing liver damage or injury.

In contrast, albumin, bilirubin, PT, and PTT are markers of hepatocellular function. This means that changes in these biomarkers suggest an altered or reduced function of the liver cells.

Table 1. Abnormal levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and bilirubin may suggest a pathological process that is causing liver damage or injury. Abnormal albumin, bilirubin, prothrombin time (PT), or partial thromboplastin time (PTT) levels may suggest reduced or altered hepatocellular function.

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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. Gastroenterology142: 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 Gastroenterol26: 183–186. PMID: 9600366
  • Lok, ASF and McMahon, BJ. 2007. Chronic hepatitis B. Hepatology45: 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 Sci30: 211–214. PMID: 2857631
  • Myers, RP, Cerini, R, Sayegh, R, et al. 2003. Cardiac hepatopathy: clinical, hemodynamic, and histologic characteristics and correlations. Hepatology37: 393–400. PMID: 12540790
  • Rej, R. 1978. Aspartate aminotransferase activity and isoenzyme proportions in human liver tissues. Clin Chem24: 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 Invest122: 519–528. PMID: 22232210

About the author

Amer Wahed, MD FRCPath
Amer is a Professor and Vice Chair (Clinical Pathology) and Associate Residency Program Director in the Department of Pathology and Laboratory Medicine at the University of Texas, Health Science Center at Houston, USA.
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