Recognizing a hepatocellular pattern on a liver function panel

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

An abnormality in a single liver function test provides us with limited diagnostic information. But, if we can recognize a pattern of abnormality in our findings, it can help us to determine the origin of the abnormality. Liver test abnormalities can be divided into three patterns:

  1. Hepatocellular (indicating hepatocellular disease)
  2. Cholestatic (indicating intrahepatic or extrahepatic biliary obstruction)
  3. Isolated hyperbilirubinemia (indicating conjugated or unconjugated hyperbilirubinemia)

Each of these may be acute (e.g., present for less than 6 weeks), subacute (e.g., present for 6 weeks–6 months), or chronic (e.g., present for more than 6 months).

Figure 1. The three abnormal patterns that can be detected in liver function tests include the hepatocellular pattern, cholestatic pattern, and isolated hyperbilirubinemia pattern, each of which can be acute, subacute, or chronic in presentation.

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How do you recognize a hepatocellular pattern?

Let’s discuss the hepatocellular pattern of liver test abnormalities. With the hepatocellular pattern, serum aminotransferases, such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST), are significantly elevated. Alkaline phosphatase (ALP) levels are mildly elevated (typically less than three times the normal level), and serum bilirubin levels are also elevated.

Tests for synthetic function, such as prothrombin time (PT) and albumin levels, may also be abnormal. If they are abnormal, PT and albumin levels are typically decreased.

Table 1. Liver function testing abnormalities that are common with hepatocellular diseases.

Common causes of hepatocellular diseases include viral hepatitis, drug-induced liver damage, and chronic liver disease. The most common chronic liver disease is cirrhosis resulting from alcohol abuse or autoimmune hepatitis.

Figure 2. A hepatocellular pattern on a liver testing panel could indicate viral hepatitis, drug-induced liver damage, or chronic liver disease.

What do relative levels of AST and ALT tell us in a clinical setting?

Let’s outline a few key points that may be clinically useful when it comes to identifying a hepatocellular pattern on a liver function panel.

If ALT and AST values are 8 times greater than the upper limit of the normal range, a hepatocellular pattern of disease is more likely. If ALT and AST values are 25 times greater than normal, the diagnosis is likely viral hepatitis or drug-induced liver damage. However, if ALT and AST are 50 times greater than normal, it suggests ischemic hepatic damage from insufficient blood flow secondary to shock or low blood pressure. With nonalcoholic steatohepatitis, ALT and AST are less than 4 times the upper limit of normal. Lastly, an AST to ALT ratio that is greater than 2:1 suggests alcoholic liver disease.

Table 2. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) testing results and their implications.

What should you do if you recognize this pattern in your patients?

In individuals with hepatocellular patterns of liver function test abnormalities (e.g., significant elevation of ALT and AST), there are seven tests you should consider running to help diagnose the cause:

  1. Acetaminophen levels
  2. Viral hepatitis serology
  3. Toxicology screen
  4. Autoimmune markers (if indicated)
  5. Antinuclear antibodies
  6. Anti-smooth muscle antibodies
  7. Anti-liver kidney microsomal type 1 antibodies

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
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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