Recognizing a cholestatic pattern on a liver function panel

Learn how to recognize a cholestatic pattern of an abnormal liver function panel. Click here to read more!
Last update26th Jan 2021

Three abnormal patterns can be recognized when interpreting the results of a liver testing panel. These include the hepatocellular pattern, the cholestatic pattern, and the isolated hyperbilirubinemia pattern. Now, let’s focus on the cholestatic pattern.

How can I recognize a cholestatic pattern?

The cholestatic pattern of liver function test abnormalities indicates biliary obstruction. The pattern occurs when there is a disproportionate elevation in alkaline phosphatase (ALP) compared to alanine aminotransferase (ALT) and aspartate aminotransferase (AST).

Serum bilirubin can also be elevated. Tests for synthetic function, such as prothrombin time (PT) and albumin, may be abnormal.

Table 1. Liver function testing abnormalities that are common with the cholestatic pattern.

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What causes biliary obstruction?

Biliary obstruction or cholestasis can be due to intrahepatic or extrahepatic obstruction. Causes of intrahepatic obstruction include primary sclerosing cholangitis, primary biliary cholangitis, drugs (e.g., steroids or chlorpromazine), toxins, and infiltrative diseases (e.g., tuberculosis, sarcoidosis, or lymphoma). On the other hand, causes of extrahepatic obstruction include gallstones in the common bile duct, tumors blocking the bile ducts, pancreatitis, and strictures.

Figure 1. Intrahepatic obstruction can be caused by primary sclerosing cholangitis, primary biliary cholangitis, medications, toxins, or infiltrative diseases. Extrahepatic obstruction can be caused by gallstones in the common bile duct, tumors blocking the bile ducts, pancreatitis, or strictures.

How do you determine the possible cause of a biliary obstruction?

There are four additional tests to consider when determining the cause of biliary obstruction:

  1. Further serum testing
  2. Ultrasound
  3. Magnetic resonance imaging (MRI) or x-ray
  4. Biopsy

Further serum testing

Biliary obstruction is characterized by elevated levels of ALP, typically three times the normal level. Remember that there are three sources of alkaline phosphatase—the liver, bone, and placenta.

Whenever the source of elevated ALP is the liver, gamma-glutamyl transpeptidase (GGT) levels are also raised. Thus, gamma-glutamyl transpeptidase can be tested if there is a doubt about the source of the elevated ALP.

In addition to elevated ALP, antimitochondrial antibody (AMA) levels are also raised in primary biliary cholangitis.

Table 2. With biliary obstruction, alkaline phosphatase (ALP) is typically elevated three times higher than normal and gamma-glutamyl transpeptidase (GGT) is also elevated. With primary biliary cholangitis, ALP and antimitochondrial antibody (AMA) levels are elevated.


The next best test for determining the cause of biliary disease in individuals with significantly elevated levels of ALP is imaging such as ultrasonography of the abdomen. Gallstones in the common bile duct and pancreatic lesions are easily diagnosed on ultrasound.

Magnetic resonance imaging or x-ray

Further testing by magnetic resonance cholangiopancreatography or endoscopic retrograde cholangiopancreatography may be required to diagnose differential causes of intrahepatic obstruction.


Lastly, a liver biopsy may be required if the cause of the biliary obstruction remains undetermined.

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. 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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