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Liver function tests are blood tests used to help find the cause of your symptoms and monitor liver disease or damage. The tests measure the levels of certain enzymes and proteins in your blood.

Some of these tests measure how well the liver is performing its regular functions of producing protein and clearing bilirubin, a blood waste product. Other liver function tests measure enzymes that liver cells release in response to damage or disease.

Irregular liver function test results don't always mean liver disease. A member of your health care team will typically explain your results and what they mean.

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Why it's done

Liver function tests can be used to:

  • Screen for liver infections, such as hepatitis.
  • Monitor a disease, such as viral or alcoholic hepatitis, and determine how well a treatment is working.
  • Look for signs of serious disease, particularly scarring of the liver, called cirrhosis.
  • Monitor possible side effects of medicines.

Liver function tests check the levels of certain enzymes and proteins in your blood. Levels that are higher or lower than usual can mean liver problems. The pattern and degree of elevation of these tests along with the overall clinical picture can provide hints to the underlying cause of these problems.

Some common liver function tests include:

  • Alanine transaminase (ALT). ALT is an enzyme found in the liver that helps convert proteins into energy for the liver cells. When the liver is damaged, ALT is released into the bloodstream and levels increase. This test is sometimes referred to as SGPT.
  • Aspartate transaminase (AST). AST is an enzyme that helps the body break down amino acids. Like ALT , AST is usually present in blood at low levels. An increase in AST levels may mean liver damage, liver disease or muscle damage. This test is sometimes referred to as SGOT.
  • Alkaline phosphatase (ALP). ALP is an enzyme found in the liver and bone and is important for breaking down proteins. Higher-than-usual levels of ALP may mean liver damage or disease, such as a blocked bile duct, or certain bone diseases, as this enzyme is also present in bones.
  • Albumin and total protein. Albumin is one of several proteins made in the liver. Your body needs these proteins to fight infections and to perform other functions. Lower-than-usual levels of albumin and total protein may mean liver damage or disease. These low levels also can be seen in other gastrointestinal and kidney-related conditions.
  • Bilirubin. Bilirubin is a substance produced during the breakdown of red blood cells. Bilirubin passes through the liver and is excreted in stool. Higher levels of bilirubin might mean liver damage or disease. At times, conditions such as a blockage of the liver ducts or certain types of anemia also can lead to elevated bilirubin.
  • Gamma-glutamyltransferase (GGT). GGT is an enzyme in the blood. Higher-than-usual levels may mean liver or bile duct damage. This test is nonspecific and may be elevated in conditions other than liver disease.
  • L-lactate dehydrogenase (LD). LD is an enzyme found in the liver. Higher levels may mean liver damage. However, other conditions also may cause higher levels of LD .
  • Prothrombin time (PT). PT is the time it takes your blood to clot. Increased PT may mean liver damage. However, it also can be higher if you're taking certain blood-thinning drugs, such as warfarin.

More Information

  • Acute liver failure
  • Alcoholic hepatitis
  • Anorexia nervosa
  • Cholangiocarcinoma (bile duct cancer)
  • Ehrlichiosis and anaplasmosis
  • Enlarged spleen (splenomegaly)
  • Eye melanoma
  • Gilbert syndrome
  • Hemochromatosis
  • Hepatitis B
  • Hepatocellular carcinoma
  • Liver disease
  • Nonalcoholic fatty liver disease
  • Primary sclerosing cholangitis
  • Wilson's disease

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The blood sample for liver function tests is usually taken from a vein in your arm. The main risk associated with blood tests is soreness or bruising at the site of the blood draw. Most people don't have serious reactions to having blood drawn.

How you prepare

Certain foods and medicines can affect the results of your liver function tests. Your doctor will probably ask you to avoid eating food and taking some medicines before your blood is drawn.

What you can expect

During the test.

The blood sample for liver function tests is usually drawn through a small needle inserted into a vein in the bend of your arm. The needle is attached to a small tube, to collect your blood. You may feel a quick pain as the needle is inserted into your arm and have some short-term soreness at the site after the needle is removed.

After the test

Your blood goes to a laboratory for analysis. If the lab analysis happens on-site, you could have your test results within hours. If your doctor sends your blood to an off-site laboratory, you may get the results within several days.

Standard range blood test results for typical liver function tests include:

  • ALT . 7 to 55 units per liter (U/L).
  • AST . 8 to 48 U/L .
  • ALP . 40 to 129 U/L .
  • Albumin. 3.5 to 5.0 grams per deciliter (g/dL).
  • Total protein. 6.3 to 7.9 g/dL .
  • Bilirubin. 0.1 to 1.2 milligrams per deciliter (mg/dL).
  • GGT . 8 to 61 U/L .
  • LD . 122 to 222 U/L .
  • PT . 9.4 to 12.5 seconds.

These results are typical for adult men. Standard range results may be different from laboratory to laboratory. They also might be slightly different for women and children.

Your health care team uses the results to help diagnose your condition or decide on treatment you might need. Sometimes, additional blood tests and imaging may be used to help make a diagnosis. If you already have liver disease, liver function tests can help determine how your disease is progressing and if you're responding to treatment.

  • Diagnosing liver disease: Liver biopsy and liver function tests. American Liver Foundation. https://liverfoundation.org/liver-diseases/diagnosing-liver-disease. Accessed April 28, 2023.
  • Laboratory tests of the liver and gallbladder. Merck Manual Professional Version. https://www.merckmanuals.com/professional/hepatic-and-biliary-disorders/testing-for-hepatic-and-biliary-disorders/laboratory-tests-of-the-liver-and-gallbladder. Accessed April 28, 2023.
  • Friedman LS. Approach to the patient with abnormal liver biochemical and function tests. https://www.uptodate.com/contents/search. Accessed May 1, 2023.
  • Blood tests. National Heart, Lung, and Blood Institute. https://www.nhlbi.nih.gov/health/blood-tests. Accessed May 1, 2023.
  • ALT. Mayo Clinic Laboratories. https://www.mayocliniclabs.com/test-catalog/overview/8362#Clinical-and-Interpretive. Accessed May 1, 2023.
  • AST. Mayo Clinic Laboratories. https://www.mayocliniclabs.com/test-catalog/overview/8360#Clinical-and-Interpretive. Accessed May 1, 2023.
  • ALP. Mayo Clinic Laboratories. https://www.mayocliniclabs.com/test-catalog/overview/8340#Clinical-and-Interpretive. Accessed May 1, 2023.
  • ALB. Mayo Clinic Laboratories. https://www.mayocliniclabs.com/test-catalog/overview/8436#Clinical-and-Interpretive. Accessed May 1, 2023.
  • Total protein. Mayo Clinic Laboratories. https://www.mayocliniclabs.com/test-catalog/overview/8520#Clinical-and-Interpretive. Accessed May 1, 2023.
  • Bilirubin. Mayo Clinic Laboratories. https://www.mayocliniclabs.com/test-catalog/overview/8452#Clinical-and-Interpretive. Accessed May 1, 2023.
  • GGT. Mayo Clinic Laboratories. https://www.mayocliniclabs.com/test-catalog/overview/8677#Clinical-and-Interpretive. Accessed May 1, 2023.
  • LD. Mayo Clinic Laboratories. https://www.mayocliniclabs.com/test-catalog/overview/8344#Clinical-and-Interpretive. Accessed May 1, 2023.
  • PT. Mayo Clinic Laboratories. https://www.mayocliniclabs.com/test-catalog/Clinical+and+Interpretive/40934. Accessed May 1, 2023.
  • Khanna S (expert opinion). Mayo Clinic. May 12, 2023.

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Interpretation of Liver Function Tests (LFTs)

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Liver function tests (LFTs) are among the most commonly ordered blood tests and include:

  • Alanine transaminase (ALT)
  • Aspartate aminotransferase (AST)
  • Alkaline phosphatase (ALP)
  • Gamma-glutamyltransferase  (GGT)

This guide gives an overview of LFTs   and a structured approach to their interpretation.

Why check LFTs?

LFTs can be requested for multiple reasons: 1

  • To investigate patients with suspected liver disease
  • To monitor patients with confirmed liver disease (e.g. cirrhosis)
  • To monitor the effects of potentially hepatotoxic medications

LFTs are often sent as part of a ‘ baseline ’ screening panel of investigations for patients presenting with a wide range of symptoms, even where none of the above criteria is met. 

Reference ranges

Table 1 . Liver function test reference ranges

3-40 IU/L
3-30 IU/L
30-100 IU/L
8-60 IU/L
3-17 μmol/L
35-50 g/L

These reference ranges can vary between laboratories, so always check local guidelines. 

Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are enzymes found within liver cells at high concentrations.

Raised ALT / AST levels in the blood occur in pathologies that cause liver cell (hepatocyte) inflammation or damage. Therefore, raised ALT / AST levels are a marker of hepatocellular injury .

Common causes of hepatocellular injury include:

  • Hepatitis (viral, alcoholic, ischaemic)
  • Liver cirrhosis
  • Drug / toxin-induced liver injury (e.g. paracetamol overdose)
  • Malignancy (hepatocellular carcinoma)

Hint : The AST:ALT ratio can help determine the aetiology of hepatocellular injury, with a >2:1 ratio classical of alcoholic liver disease. 2

Serum alkaline phosphatase (ALP) is derived from biliary epithelial cells (cells lining the biliary tract) and bones . 3 Raised ALP levels can therefore be caused by cholestasis or bone disease .

  • Cholestasis

Cholestasis describes an interruption in the bile flow from hepatocytes to the small intestine. Common causes include gallstone disease , external compression of the biliary tract (e.g. pancreatic malignancy ) or medication side effects. Bilirubin may or may not be raised depending on the severity of cholestasis.

Gamma-glutamyltransferase (GGT) is found in hepatocytes and also biliary epithelial cells. 2 It is a non-specific but highly sensitive marker of liver damage and cholestasis.

ALP and GGT are interpreted together to localise the source of raised ALP in the blood:

  • An ALP rise with normal GGT suggests bone disease (e.g. Paget’s disease, vitamin D deficiency, bony metastases)
  • An ALP rise with associated GGT rise is more suggestive of cholestasis

Hint : An isolated GGT rise is classically associated with alcohol excess .

Bilirubin is a waste product of haemoglobin breakdown . It is predominantly metabolised and excreted by the liver . Raised levels of bilirubin in the blood will lead to a yellowing of the skin, known as jaundice .

Hint : Jaundice is usually absent until the bilirubin level exceeds 50 micromol/L .

Bilirubin metabolism

To understand the significance of raised bilirubin levels, it is essential to consider the bilirubin metabolism/excretion pathway:4

  • When red blood cells are broken down, unconjugated (insoluble) bilirubin is created as a waste product and binds to albumin in the bloodstream
  • Hepatocytes take up unconjugated bilirubin and metabolise it to form conjugated (soluble) bilirubin
  • Hepatocytes excrete conjugated bilirubin into the biliary tract, where it flows into the bowel lumen as bile
  • Gut bacteria further metabolise bilirubin in bile to form urobilinogen , which is eventually excreted in the stools as stercobilinogen
  • A small amount of urobilinogen is reabsorbed from the intestine into the portal venous system, and as urobilinogen is water-soluble, the kidney is able to excrete some of this into the urine.

Stercobilinogen gives stools their dark colour . Urobilinogen is colourless in the urine. However, if the urine is left exposed to the air, oxidation will occur, creating a dark colour. Under normal physiological conditions, urobilinogen will be present in the urine, however conjugated bilirubin will not be present.

Raised levels of bilirubin in the blood can be caused by:

  • Excess bilirubin production ( pre-hepatic jaundice )
  • A breakdown in bilirubin metabolism ( hepatocellular jaundice )
  • A blockage in the bile excretion pathway ( cholestatic jaundice )

Pre-hepatic jaundice

Pre-hepatic jaundice occurs when increased red blood cell breakdown produces excess bilirubin . This can overwhelm metabolism/excretion pathways, leading to jaundice .

The most common cause of increased red blood cell breakdown is haemolysis . Bilirubin is unconjugated in the blood, as the hepatocytes have not yet metabolised it. The remainder of LFTs are generally normal , as the liver is otherwise working well.

Hint : In pre-hepatic jaundice, patients are often anaemic due to excess red blood cell breakdown. The diagnosis may be Gilbert’s syndrome if no anaemia is present.

Gilbert’s syndrome

Gilbert’s syndrome is a congenital disorder present in up to 5% of the population. It results from a deficiency of glucosyltransferase , the enzyme responsible for the conjugation of bilirubin within hepatocytes.

Gilbert’s syndrome classically presents following viral infection with raised bilirubin but normal LFTs/ full blood count. The disease is benign and requires no specific management.

Hepatocellular jaundice

Hepatocellular jaundice occurs when hepatocytes are damaged and dysfunctional, leading to an inability to metabolise unconjugated bilirubin from the bloodstream. This leads to high levels of unconjugated bilirubin in the blood. There will generally also be very high ALT / AST levels , marking hepatocyte damage.

Hint : Common causes of hepatocellular injury are covered above (hepatitis, cirrhosis, malignancy, drug or toxin insult). When liver injury is severe, there are not enough functioning hepatocytes to metabolise bilirubin, and jaundice will develop.

Cholestatic (obstructive) jaundice

Cholestasis is an interruption in bile flow from hepatocytes to the gut. When this interruption is severe, bilirubin levels will build up in the blood. The bilirubin has been metabolised in the liver, and thus the bilirubin in the blood is predominantly conjugated bilirubin. There will generally also be high ALP levels with associated high GGT , marking dysfunction of the biliary system.

Obstructive jaundice will classically lead to dark urine and pale stools . Bilirubin cannot enter the gastrointestinal tract due to cholestasis, leading to low stercobilinogen excretion in stools .

The bilirubin in the blood is conjugated and can be filtered by the kidneys. The presence of conjugated bilirubin gives the urine a very dark colour .

Hint : Stools may also be pale in hepatocellular jaundice, as there is decreased bilirubin metabolism/excretion, however as the bilirubin in the blood is unconjugated, it will not be able to pass into the urine. Therefore, the urine should remain a normal colour.

Causes of cholestasis

Cholestasis can occur due to either intrahepatic or extrahepatic biliary obstruction.

Causes of intrahepatic obstruction (obstruction of the hepatic bile canaliculi):

  • Drugs (e.g. antibiotics, oral contraceptive pills, anabolic steroids)

Causes of extrahepatic obstruction (obstruction of hepatic ducts, or distal biliary tree):

  • Primary sclerosing cholangitis
  • Intraluminal malignancy: cholangiocarcinoma
  • Extraluminal malignancy causing duct compression: head of pancreas tumours

Split bilirubin

The split of conjugated/unconjugated bilirubin in the blood can be requested to give further clues as to the aetiology of jaundice.

Causes of predominantly unconjugated hyperbilirubinaemia :

  • Pre-hepatic jaundice (e.g. haemolysis)
  • Gilbert syndrome

Causes of predominantly conjugated hyperbilirubinaemia :

  • Hepatocellular jaundice*

*Hepatocellular jaundice can initially cause a mixed conjugated/unconjugated jaundice, but at its most severe, unconjugated hyperbilirubinaemia is seen.

Albumin is synthesised in the liver and helps to bind water, cations, fatty acids and bilirubin. It also plays a crucial role in maintaining the oncotic pressure of blood. Albumin is used as a non-specific marker of the  synthetic function of the liver.

Albumin levels can fall due to:

  • Decreased albumin production: malnutrition , severe liver disease
  • Increased albumin loss: protein-losing enteropathies, nephrotic syndrome

Hint : A decrease in the synthetic function of the liver indicates severe liver disease.

Albumin has a half-life of 20 days , so it will take time to decrease, even in severe liver disease. Further assessment of the synthetic function of the liver can be gained by ordering a coagulation screen , as the liver is also responsible for the synthesis of clotting factors .

Severe liver disease leads to decreased production of clotting factors and an increased prothrombin time (PT) / INR in the absence of other causes of coagulopathy.

The liver is also responsible for gluconeogenesis , and serum blood glucose assessment can also indirectly assess the liver’s synthetic function. However, gluconeogenesis tends to be one of the last functions to become impaired in liver failure.

LFT interpretation method

Determine the pattern of lft derangement.

The pattern of ALT to ALP rise can indicate whether the pathology is primarily cholestatic or hepatocellular:

  • A greater than 10-fold increase in ALT and a less than 3-fold increase in ALP suggests a predominantly hepatocellular injury
  • A less than 10-fold increase in ALT and a more than 3-fold increase in ALP suggests cholestasis
  • It is possible to have a mixed picture involving both hepatocellular injury and cholestasis

An isolated ALP rise without a GGT rise should raise your suspicion of bony pathology .

Assess the bilirubin

Bilirubin is a marker of severity in acute cholestatic pathology and acute hepatocellular liver injuries. The presence of clinical jaundice is generally an indication of severe disease requiring urgent referral to secondary care for prompt assessment and management.

An isolated bilirubin rise without further LFT derangement suggests pre-hepatic jaundice or Gilbert’s disease.

Assess synthetic function

In severe hepatocellular injuries, the synthetic functions of the liver also become impaired , leading to decreased albumin .

Coagulation studies may show prolonged prothrombin time, and in very severe disease, serum blood glucose may be low due to impaired gluconeogenesis.

Hint : In chronic hepatocellular pathology (e.g. cirrhosis), the ALT / AST may return to within the normal range, however synthetic function of the liver can be markedly impaired.

Summary table

The table below compares the typical LFT patterns associated with acute hepatocellular damage and cholestasis . A single arrow (↑) refers to a mild impairment, and a double arrow (↑↑) refers to severe impairment.



Normal or ↑


Normal or ↑

 Normal or ↑


 Normal or ↑




Further investigations

Once the pattern of LFT derangement has been established, it is essential to determine the underlying cause .

If cholestasis is suspected, an ultrasound should be arranged to assess the biliary tree for a potential site/cause of biliary obstruction .

If hepatocellular injury is suspected, a liver ultrasound is generally arranged to assess for any structural lesions that may give clues as to the diagnosis. If the cause is unclear, a ‘ liver screen’ may be ordered to investigate further.

Liver screen

A ‘liver screen’ is a batch of blood investigations to identify a wide range of potential causes of liver disease:

  • Hepatitis serology (A/B/C)
  • Epstein-Barr Virus (EBV)
  • Cytomegalovirus (CMV)
  • Anti-mitochondrial antibody (AMA)
  • Anti-smooth muscle antibody (ASMA)
  • Anti-liver/kidney microsomal antibodies (Anti-LKM)
  • Anti-nuclear antibody (ANA)
  • Immunoglobulins  –  IgM/IgG
  • Alpha-1 Antitrypsin (to rule out alpha-1 antitrypsin deficiency)
  • Serum Copper (to rule out Wilson’s disease)
  • Ceruloplasmin (to rule out Wilson’s disease)
  • Ferritin (to rule out haemochromatosis)

Dr Chris Jefferies

  • Coates P. Liver Function Tests. Australian Family Physician. March 2011. Available at [ LINK ].
  • UpToDate. Approach to the patient with abnormal liver biochemical and function tests. May 2023. Available at [ LINK ].
  • Patient.info Professional. Abnormal Liver Function Tests. July 2019. Available at [ LINK ].
  • UpToDate. Bilirubin metabolism. October 2022. Available at [ LINK ].

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liver function test essay

What Is a Liver Function Test?

A liver function test is one of a group of tests that check levels of certain enzymes and other proteins in your blood .

Some of the tests look for enzymes that you’d find in your blood only when your liver is damaged or has a disease. Others check that the organ is working the way it should.

Your liver does all kinds of work that’s crucial for your health. It helps break down food, clean your blood, make proteins, and store energy. If something goes wrong with it, you might have a number of symptoms, from yellow skin to slurred speech. That’s when you might need a liver test.

Why Are Liver Function Tests Done?

You might have this test to check for a liver disease such as hepatitis (an illness in which your liver swells and can cause serious issues). General symptoms of liver problems include:

  • Lack of appetite
  • Nausea or vomiting
  • Weakness or feeling very tired
  • Yellowish eyes or skin ( jaundice )
  • Dark urine or light-colored poop (less common)
  • Swelling in your belly (less common)

Often, however, you don’t notice any symptoms.

Your doctor may order a liver test if you’re more likely to have liver damage or disease, like if you:

  • Drink heavily or have an alcohol use disorder
  • Have a family member with liver disease
  • Are very overweight , especially if you also have diabetes or high blood pressure
  • Take medicine that can harm your liver
  • Have gallbladder disease or anemia

The liver test can also help your doctor learn whether an illness is getting worse or how well treatment is working.

Types of Tests and What They Measure

There are a number of liver tests, with lots of complex names. Some common ones include:

  • Alanine transaminase (ALT) test. ALT is an enzyme that helps break down proteins and is found mainly in your liver. High levels in your blood could mean you have liver damage.
  • Alkaline phosphatase (ALP) test. ALP is an enzyme in your liver, bile ducts, and bone . You might have high levels if you have liver damage or disease, a blocked bile duct, or bone disease.
  • Albumin and total protein test. Your liver makes two main proteins: albumin and globulin. Low levels might mean damage or disease. Keep in mind that your immune system also makes globulin.
  • Aspartate transaminase (AST) test. AST is another enzyme in your liver. High blood levels could be a sign of damage or disease.
  • Bilirubin test. Your body makes b ilirubin when it breaks down red blood cells. Usually, your liver cleans bilirubin out of your body. If you have high levels in your blood, a problem called jaundice, you may have liver damage.
  • Gamma-glutamyltransferase ( GGT ) test. High levels of the GGT enzyme could point to liver or bile duct damage.
  • Prothrombin time (PT) test. This test measures how long it takes your blood to clot. If it takes a long time, that could be a sign of liver damage. Medications that thin your blood, such as warfarin ( Coumadin ), can also lead to a longer PT. You probably won’t have this test until you have had other liver tests.

How to Prepare for a Liver Function Test

Make sure to tell your doctor about any medicines you’re taking, including over-the-counter medications and herbal supplements . They may tell you to stop eating the night before the test.

What Happens During a Liver Function Test?

Your doctor uses a thin needle to take a small amount of blood, usually from your arm near your elbow . You’ll feel a pinch or stinging when the needle goes in.

If there is liver damage, you’ll probably have these tests more than once over a few days or weeks. Your doctor can look at how levels change to be sure of your condition.

If you get your test at a clinic that has a lab on-site, you can get results in a few hours. If not, it might take a few days.

Liver Function Test Results

The results usually show normal values for the specific test, along with your numbers. Keep in mind that what’s normal can vary with different labs. It also depends on whether you’re male or female.

If your results aren’t normal, you’ll probably get more tests.

By itself, a liver test can’t tell for sure that you have a certain illness. Your doctor can help you understand what your results mean.

Liver Function Test Risks

Liver function tests are generally safe, with few risks. You may have some soreness or a bruise where the blood is taken. Call your doctor if it doesn’t get better after a couple of days.

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liver function test essay

Liver Function Tests

Liver function tests (also known as a liver panel) are blood tests that measure different enzymes, proteins, and other substances made by the liver. These tests check the overall health of your liver. The different substances are often tested at the same time on a single blood sample, and may include the following:

  • Albumin , a protein made in the liver
  • Total protein. This test measures the total amount of protein in the blood.
  • ALP (alkaline phosphatase), ALT (alanine transaminase), AST (aspartate aminotransferase), and gamma-glutamyl tansferase (GGT) . These are different enzymes made by the liver.
  • Bilirubin , a waste product made by the liver.
  • Lactate dehydrogenase (LD) , an enzyme found in most of the body's cells. LD is released into the blood when cells have been damaged by disease or injury.
  • Prothrombin time (PT) , a protein involved in blood clotting.

If levels of one or more of these substances are outside of the normal range, it may be a sign of liver disease .

Other names: liver panel, liver function panel, liver profile hepatic function panel, LFT

Liver function tests are most often used to:

  • Help diagnose liver diseases, such as hepatitis
  • Monitor treatment of liver disease. These tests can show how well the treatment is working.
  • Check how badly a liver has been damaged or scarred by disease, such as cirrhosis
  • Monitor side effects of certain medicines

You may need liver function testing if you have symptoms of liver disease. These include:

  • Jaundice , a condition that causes your skin and eyes to turn yellow
  • Nausea and vomiting
  • Abdominal pain
  • Dark-colored urine
  • Light-colored stool

You may also need these tests if you have certain risk factors. You may be at higher risk for liver disease if you:

  • Have a family history of liver disease
  • Have alcohol use disorder, a condition in which you have difficulty controlling how much you drink
  • Think you have been exposed to a hepatitis virus
  • Take medicines that may cause liver damage

A health care professional will take a blood sample from a vein in your arm, using a small needle. After the needle is inserted, a small amount of blood will be collected into a test tube or vial. You may feel a little sting when the needle goes in or out. This usually takes less than five minutes.

You may need to fast (not eat or drink) for 10-12 hours before the test.

There is very little risk to having a blood test. You may have slight pain or bruising at the spot where the needle was put in, but most symptoms go away quickly.

If one or more of your liver function test results were not normal, it may mean your liver is damaged or not working properly. Liver damage can be caused by a number of different conditions, including:

  • Hepatitis A
  • Hepatitis B
  • Hepatitis C
  • Alcohol use disorder, which includes alcoholism.
  • Liver cancer

If you have questions about your results, talk to your health care provider.

Learn more about laboratory tests, reference ranges, and understanding results .

If any of your liver function tests were not normal, your provider may need more tests to confirm or rule out a specific diagnosis. These tests may include more blood tests and/or a liver biopsy . A biopsy is a procedure that removes a small sample of tissue for testing.

  • Cleveland Clinic [Internet]. Cleveland (OH): Cleveland Clinic; c2019. Liver Function Tests: Overview; [cited 2019 Aug 26]; [about 3 screens]. Available from: https://my.clevelandclinic.org/health/diagnostics/17662-liver-function-tests
  • Cleveland Clinic [Internet]. Cleveland (OH): Cleveland Clinic; c2019. Liver Function Tests: Test Details; [cited 2019 Aug 26]; [about 3 screens]. Available from: https://my.clevelandclinic.org/health/diagnostics/17662-liver-function-tests/test-details
  • Kids Health from Nemours [Internet]. Jacksonville (FL): The Nemours Foundation; c1995–2019. Blood Test: Liver Function Tests; [cited 2019 Aug 26]; [about 3 screens]. Available from: https://kidshealth.org/en/teens/test-liver-function.html
  • Lab Tests Online [Internet]. Washington D.C.; American Association for Clinical Chemistry; c2001–2019. Biopsy; [updated 2017 Jul 10; cited 2019 Aug 26]; [about 2 screens]. Available from: https://labtestsonline.org/glossary/biopsy
  • Lab Tests Online [Internet]. Washington D.C.; American Association for Clinical Chemistry; c2001–2019. Lactate Dehydrogenase (LD); [updated 2018 Dec 20; cited 2019 Aug 26]; [about 2 screens]. Available from: https://labtestsonline.org/tests/lactate-dehydrogenase-ld
  • Lab Tests Online [Internet]. Washington D.C.; American Association for Clinical Chemistry; c2001–2019. Liver Panel; [updated 2019 May 9; cited 2019 Aug 26]; [about 2 screens]. Available from: https://labtestsonline.org/tests/liver-panel
  • Mayo Clinic [Internet]. Mayo Foundation for Medical Education and Research; c1998–2019. Liver Function Tests: About; 2019 Jun 13 [cited 2019 Aug 26]; [about 3 screens]. Available from: https://www.mayoclinic.org/tests-procedures/liver-function-tests/about/pac-20394595
  • Merck Manual Consumer Version [Internet]. Kenilworth (NJ): Merck & Co., Inc.; c2019. Liver Function Tests; [updated 2017 May; cited 2019 Aug 26]; [about 2 screens]. Available from: https://www.merckmanuals.com/home/liver-and-gallbladder-disorders/diagnosis-of-liver,-gallbladder,-and-biliary-disorders/liver-function-tests?query=liver%20panel
  • National Heart, Lung, and Blood Institute [Internet]. Bethesda (MD): U.S. Department of Health and Human Services; Blood Tests; [cited 2019 Aug 26]; [about 3 screens]. Available from: https://www.nhlbi.nih.gov/health-topics/blood-tests
  • UF Health: University of Florida Health [Internet]. Gainesville (FL): University of Florida Health; c2019. Liver function tests: Overview; [updated 2019 Aug 25; cited 2019 Aug 26]; [about 2 screens]. Available from: https://ufhealth.org/liver-function-tests
  • University of Rochester Medical Center [Internet]. Rochester (NY): University of Rochester Medical Center; c2019. Health Encyclopedia: Liver Panel; [cited 2019 Aug 26]; [about 2 screens]. Available from: https://www.urmc.rochester.edu/encyclopedia/content.aspx?ContentTypeID=167&ContentID=liver_panel
  • UW Health [Internet]. Madison (WI): University of Wisconsin Hospitals and Clinics Authority; c2019. Health Information: Liver Function Panel: Topic Overview; [updated 2018 Jun 25; cited 2019 Aug 26]; [about 2 screens]. Available from: https://www.uwhealth.org/health/topic/special/liver-function-panel/tr6148.html
  • UW Health [Internet]. Madison (WI): University of Wisconsin Hospitals and Clinics Authority; c2019. Health Information: Liver Function Tests: Exam Overview; [updated 2018 Jun 25; cited 2019 Aug 26]; [about 2 screens]. Available from: https://www.uwhealth.org/health/topic/testdetail/liver-function-tests/hw144350.html#hw144367
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Liver function tests

Peer reviewed by Dr Rosalyn Adleman, MRCGP Last updated by Dr Rachel Hudson, MRCGP Last updated 2 Jun 2023

Meets Patient’s editorial guidelines

In this series: Gilbert's syndrome Jaundice Cirrhosis Liver failure Primary biliary cholangitis Wilson's disease

Liver function tests are a set of blood tests commonly done to check on the health of your liver. Changes in liver function tests give a clue as to whether your liver is under strain, inflamed, infected or diseased, and how badly. The pattern of the liver function tests can give a clue to the cause and can allow early detection of unsuspected problems, and monitoring of known problems.

In this article :

What is a liver function test, what are liver function tests used for, what are the main liver function tests, where and what is the liver, and what does it do, what can cause liver function tests to be abnormal, what does the 'normal range' mean in liver function tests, what will my doctor do if i have abnormal liver function tests, what does an abnormal bilirubin level mean, what does an abnormal total protein level mean, what does an abnormal alt (sgpt), ast (sgot) or creatine kinase level mean, what does an abnormal gamma-glutamyl transferase level mean, what does an abnormal alkaline phosphatase level mean, what do abnormal calcium and corrected calcium levels mean, what do abnormal prothrombin time and inr mean, how do i keep my liver function healthy.

Continue reading below

Liver function tests measure a series of chemicals which relate to the way the liver works. They include substances that are made in the liver or affected by the health of the liver cells, chemicals which are processed or excreted by the liver, and hormones that the liver makes in order to do its work.

Liver function tests are aimed at giving a picture of the 'state' of your liver. They are a sensitive way of looking for liver strain or liver damage, as they often show this well before you get any symptoms or problems with your liver. This means that the cause of liver strain or damage can be diagnosed and, often, reversed.

Liver function tests are also used for monitoring in cases of known liver inflammation, injury or disease.

The usual liver function tests typically include the following:

Total protein.

Transferases (AST or SGOT and ALT or SGPT).

Creatine kinase.

Calcium and corrected calcium.

Prothrombin time or International Normalised Ratio (INR).

Each of these is discussed below. The liver performs hundreds of different functions, so there are many other possible tests that look at its health. These would normally be done if an abnormality is found with the basic liver function tests described here, or if a specific problem is suspected. They might include:

Virus tests - for example, for hepatitis A, B or C - to look for the cause of disease.

Autoantibody tests (to detect and monitor immune diseases ).

Immunoglobulins (antibodies made in response to various challenges including allergies , infections, some blood disorders and some cancers ).

Serum ferritin and transferrin saturation (measures of iron storage and management by your body).

Alpha-fetoprotein (maternal levels help look at the health of the baby during pregnancy, and levels are also raised in some cancers).

Copper/caeruloplasmin (measures of copper management by the body).

Alpha-1 antitrypsin (a hormone involved in protecting liver and lung cells from injury).

Clotting factors (particularly if there is a suspicion that your blood is not clotting well or you have severe liver disease).

The liver is your largest internal organ. It sits in the tummy (abdomen), under your diaphragm on the right-hand side. It is usually tucked under the ribs, which protect it, although in some people the edge of the liver protrudes slightly. If the liver is swollen, through inflammation or disease, it can swell out from under the ribs and make your tummy swollen.

Liver function

Liver function

The liver is a factory for the production and breakdown of carbohydrates, fats, proteins, hormones and other essential body chemicals, and helps dispose of waste products. This work is mainly carried out by liver cells (hepatocytes). Some of the most important functions include:

Production of these substances

Glycogen (a carbohydrate energy store), which it makes from glucose.

Glucose, made and released into the blood from glycogen, proteins and fats.

Many essential proteins and amino acids (building blocks of proteins).

Many of the clotting factors that help your blood to clot normally.

Plays a part in red blood cell production.

Albumin, one of the main proteins in your blood, which bulks out your serum and enables it to carry essential substances around the body.

Angiotensinogen, which plays a role in blood pressure control.

Thrombopoietin, which regulates some of the work of your bone marrow.

Cholesterol, triglycerides, lipoproteins and fats - as part of the management of fat stores in your body.

Bile, excreted into the intestine for absorbing fats and vitamin K.

Hormones that help children grow and that build muscle in adults.

Breakdown of these substances

Excess hormones, including insulin.

Bilirubin, which is a waste product from worn-out blood cells.

Many waste products.

A wide range of toxic substances and medicines, including alcohol.

Foreign proteins that reach it from the digestive system (trapped and destroyed by specialised immune cells in the liver).

Storage of these (and other) substances

Glucose (as glycogen).

Vitamin A (1-2 years' supply).

Vitamin D (1-4 months' supply).

Vitamin B12 (3-5 years' supply).

Iron and copper.

Your liver function tests can be abnormal because:

There is a build up of fat in the liver, due to being overweight or obese (called non-alcoholic fatty liver disease , or NAFLD). However this does not always cause abnormal liver function tests, and can also be picked up on an ultrasound scan of the liver. If NAFLD is diagnosed, further blood tests including NAFLD score, and ELF (enhanced liver fibrosis) test, and a fibroscan (a special type of ultrasound to look for more advanced signs such as fibrosis/cirrhosis) may be done to assess the severity of the condition.

Your liver is inflamed (for example, by infection, toxic substances like alcohol and some medicines, or by an immune condition).

Your liver cells have been damaged (for example, by toxic substances, such as alcohol, paracetamol , poisons).

Your liver is having to work harder to process medicines or toxic substances (for example, alcohol, paracetamol, poisons).

The bile drainage from your liver is blocked - for example, by a gallstone .

There is a swelling inside your liver (for example, an abscess or a tumour).

You have an underlying condition that affects the liver's production and storage abilities (for example, Wilson's disease , haemochromatosis , Gilbert's syndrome ). In these cases the abnormality of your liver tests will be a feature of your condition, and may be normal for you.

Your liver is physically injured (for example, trauma).

You fall just outside the normal limits (see below).

The 'normal range' is a range of values given by the local laboratory for liver function tests. The range varies slightly between laboratories according to the measurement methods that they use.

The 'normal' limits are defined by laboratories as the range of levels inside which 19 of every 20 people with healthy livers will fall. This means that, for any one liver function test, around 1 in 20 people with healthy livers will have a result that is slightly abnormal. There will, in the majority of cases, be nothing wrong with their liver; having a liver function test that's just over the edge usually means nothing, as long as - crucially - there is only one slight abnormality out of the whole range of tests. You should always discuss even a slightly abnormal result with your doctor.

It is important to remember that having normal liver function test results doesn't mean you aren't at risk of liver problems. For instance, if you are involved in harmful behaviour, such as drinking excess alcohol, you could have normal liver function test results but still be putting your liver under strain.

What should I do if my liver function tests are abnormal?

You are likely to find out that your liver function tests are abnormal from your healthcare provider, who will tell you what you need to do next. However, if you obtain your liver function test results without explanation, you should contact your healthcare provider to discuss them.

Doctors consider a slightly abnormal liver function test as one that is less than twice the upper limit of the 'normal' value. Doctors consider a very abnormal liver function test as one that is more than two or three the upper limit of the 'normal' value.

Your doctor is also likely to be looking at the rate of change of your liver function tests - if a test has increased very rapidly, it may be of more concern even though it is not that high.

If the liver function tests are very mildly abnormal, only one or two tests are affected and you are perfectly well, this would not normally need an urgent consultation. However, you should speak to a health professional for advice within a few days (in case more tests or monitoring need to be done).

If you have multiple abnormalities on your liver function tests, if some of the tests are very abnormal or if you are also unwell or in pain then you should seek medical advice more urgently.

If you have known liver disease and your liver function tests have altered significantly since the last time they were checked, you should seek medical advice the same day unless you have a standing instruction to do something different.

Sometimes an abnormal liver function test is normal for you. If you already know this is the case then it may be that no action is needed. A common example of this is Gilbert's syndrome , when you have a naturally raised level of bilirubin but other liver function tests are normal and you are well. Your doctor will tell you if you have Gilbert's syndrome.

All abnormal liver function tests need explanation, even if that explanation is that you are one of the 5% who fall outside the 'normal' range. In many cases, a single, isolated, slightly abnormal liver function test in a well patient will not signify an underlying problem. However, some liver disorders, including early signs of overuse of alcohol, can produce slight changes (especially at first), so it's important to be sure.

Your doctor will want to do further liver tests and to see, question and examine you, to determine the reason for the blood test abnormality. If you are otherwise well, this will initially be done in primary care. Options include:

Repeating the blood test.

Further blood tests in order to discover or rule out particular causes.

An ultrasound scan of your liver and gallbladder.

Depending on the severity and suspected cause, referral to a liver specialist for advice, more specialist tests and liver biopsy.

If you are very unwell, you may need referral or admission to hospital.

Can my doctor make a diagnosis from my liver function test?

Sometimes. Single abnormalities in the liver function tests do not give diagnoses on their own but the pattern of abnormalities can point to the most likely cause of the problem. When this is combined with speaking to and examining you, your doctor may be able to make a clear diagnosis.

Once the cause of the abnormality has been determined, your doctor will discuss what you need to do next.

What do unusually low levels on my liver function tests mean?

Note that in most cases (except albumin and calcium) it is a raised (rather than a lowered) level in the liver function test which may indicate a problem. In the following descriptions, where low levels can be significant for your health they are also described.

Bilirubin comes from the breakdown of red blood cells in the body. The liver processes (conjugates) bilirubin so that it can be excreted via the kidneys. A high bilirubin level can make you appear jaundiced (with a yellow tinge to the skin and to the whites of the eyes).

The most likely cause of raised bilirubin depends on whether the rise is in bilirubin that the liver has already processed (conjugated bilirubin), in the bilirubin that the liver has not yet processed (unconjugated bilirubin), or in both.

A rise in both types of bilirubin

Conjugated bilirubin tends to rise if the flow of bile in the tiny tubes within the liver is blocked, and unconjugated bilirubin tends to rise if the liver calls cannot do their work (or there is too much work for them to do). If the liver is both damaged (not working properly) and swollen or scarred (blocking the drainage system) then both types of bilirubin will tend to rise.

An isolated rise in unconjugated bilirubin

Unconjugated bilirubin may increase because the liver can't process the bilirubin, or because the body is making an excess of bilirubin by breaking down too many blood cells, and the liver is normal but can't keep up.

In adults, the most common causes are breakdown of blood cells (haemolysis) and Gilbert's syndrome .

Haemolysis is a condition of the blood. Further tests will be needed to identify the cause and you may need to see a haematologist. Causes can include reactions to medicines, lifelong (congenital) blood cell abnormalities such as hereditary spherocytosis and, in babies, breast milk jaundice , severe infection ( sepsis ) and haemolytic disease of the newborn .

An isolated rise in conjugated bilirubin

Increased conjugated bilirubin suggests that the liver is conjugating the bilirubin properly (the job of liver cells) but not excreting it properly via the bile ducts. Causes include:

Reactions to some medicines, including common ones such as blood pressure tablets, hormones (for example, oestrogen), antibiotics (particularly erythromycin and flucloxacillin ), tricyclic antidepressants and anabolic steroids.

Some autoimmune diseases that affect bile excretion.

Blockage of the bile ducts - for example, by a gallstone.

Dubin-Johnson syndrome and Rotor's syndrome.

In babies a rise in conjugated bilirubin can signify rare but serious problems with the development of the bile drainage system in the liver, such as biliary atresia .

What does an abnormal albumin level mean?

Albumin is the main protein in your serum, and its level is a good guide to long-term liver health. Albumin levels that are abnormally low have the greatest significance for the liver.

Low levels of albumin

This can be due to:

Severe liver disease.

Poor nutrition.

Malabsorption of protein (for example, in Crohn's disease or in coeliac disease ).

Bowel conditions which result in leakage of protein (for example, severe bowel inflammation or infection such as cholera ).

Protein loss through kidney problems (for example, nephrotic syndrome ).

Failure of protein manufacture through severe liver inflammation.

Albumin levels also fall if you lose protein through your skin (for example, in extensive skin inflammation and widespread burns ).

Albumin levels decrease during pregnancy, when your blood is more dilute.

High levels of albumin

This is usually due to having the tourniquet on for too long before your blood sample is taken. Sometimes it can be due to a very high-protein diet, as in bodybuilders, or to lack of fluid in the body (dehydration), when the blood is more concentrated.

Total protein measures the total of albumin and globulins. It is usually normal in liver disease even if albumin levels are low, as globulin levels tend to increase as albumin levels fall.

High values of total protein are seen in chronic active hepatitis and alcoholic hepatitis .

High values of total protein are also seen in conditions outside the liver which increase globulins (such as myeloma ) and conditions involving overactivity of the immune system (such as severe infection and chronic inflammatory disease).

Low levels of total protein can sometimes be seen in severe liver disease, in conditions of severe protein loss (such as widespread burns) and in severe malnutrition.

These substances are also called transferases. They are liver hormones (proteins which help do the work of the liver) which are normally found inside liver cells rather than in the blood.

ALT stands for alanine transaminase and is also called SGPT (serum glutamic-pyruvic transaminase).

AST stands for aspartate transaminase and is also called SGOT (serum glutamic oxaloacetic transaminase).

Creatine kinase is sometimes checked along with AST and ALT.

If blood levels of transaminases go up this suggests leakage from damaged liver cells due to inflammation or cell death. AST and ALT tend to be high in liver disease and very high in liver inflammation.

ALT is mainly found in the liver. AST is also found in muscle and red blood cells.

ALT rises more than AST in acute liver damage eg, viral hepatitis.

In chronic liver disease (for example, alcoholic cirrhosis ), AST is higher than ALT.

Lower-than-normal levels of transaminases do not signify disease.

Creatine kinase comes mainly from muscle, so if it is raised alongside AST and ALT it suggests that the liver may not be the main source of the problem. Creatine kinase can be very raised if you have a heart attack . However, a different blood test called troponin is now used if you have a suspected heart attack.

Causes of mild rises in transferases

These include:

Non-alcoholic fatty liver disease (the most common cause).

Chronic hepatitis C infection.

Coeliac disease .

Haemochromatosis (a genetic condition that tends to come on in your 40s or 50s).

Autoimmune hepatitis .

Causes of marked increases in transferases

Marked increases are usually caused by acute injury to the liver by viruses, shortage of oxygen (ischaemia) or toxic substances. Causes include:

Acute alcoholic hepatitis .

Viral ( hepatitis A , hepatitis B , hepatitis C , hepatitis D or hepatitis E). Hepatitis A and B tend to have the greatest increases.

Chronic hepatitis and liver cirrhosis .

Very high levels (>75 times upper reference limit) suggest ischaemic or toxic (poison or medicine-related) injury to the liver.

Ischaemic liver damage is mostly seen in patients with other serious illnesses such as septicaemia or collapse.

Gamma-glutamyl transferase (GGT) levels increase in most liver diseases. This liver function test is very sensitive, although it also goes up in some heart, lung and kidney conditions.

The most common reason for GGT increasing as a single abnormality is drinking more alcohol than your liver can easily cope with. GGT levels can be 10 times normal. The rise is a sign your liver is under strain and is at risk of being damaged by alcohol.

GGT rises to 2-3 times the upper limit of normal in non-alcoholic fatty liver disease (NAFLD) . This condition is increasingly common and can progress to scarring or inflammation of the liver. Transaminase levels also tend to rise in NAFLD.

Some prescribed and over-the-counter medicines can increase GGT levels.

GGT rises in some patients with chronic hepatitis C infection.

In chronic liver disease, a rise in GGT suggests bile duct damage and scarring.

Alkaline phosphatase (ALP) comes mainly from the cells lining bile ducts and from bones - particularly growing bones. Therefore it is commonly raised during childhood and puberty. It rises if there is slow or blocked flow in the bile ducts, if the bile ducts are damaged and in bone disorders. If the cause is in the liver, the GGT is also abnormal, whereas if it's the bone, the GGT is usually normal. ALP is also raised during the third trimester of pregnancy.

Common causes of raised ALP with other abnormalities on your liver function tests include:

Gallstones .

Hepatitis of any cause.

Cirrhosis .

Bile duct blockage of any cause.

Isolated raised ALP can occur in:


Bone fractures.

Paget's disease of bone .

Osteomalacia .

Primary sclerosing cholangitis .

Primary biliary cholangitis .

Cancer in bones or in the liver.

99% of the body's calcium is stored in the bones, with the remaining 1% stored in other tissues, including the blood plasma. The calcium test measures the total calcium in the blood plasma. About half of this is tightly attached to the protein, albumin, which forms the bulk of the protein in your plasma. The calcium level that really counts is the 'free', or unbound, calcium that floats unattached in the plasma.

If you have low albumin levels, the total calcium in your blood will be lower. However, because the amount attached to the albumin is reduced (because there is less albumin), the actual free levels of calcium may be normal (or even raised). Corrected calcium corrects the figure to give the actual, free amount of calcium.

Causes of low (corrected) calcium levels

Calcium levels are regulated by the kidney, thyroid and parathyroid glands, using the hormones parathyroid hormone, calcitonin and vitamin D. Low levels are uncommon. Causes include:

Hypoparathyroidism (your parathyroid glands do not make enough of their hormone).

Just after parathyroid surgery.

Severe chronic kidney disease .

Pancreatitis .

Severe vitamin D deficiency .

High phosphate ingestion (we can take in phosphate from enemas, from baby milks and from some flours - for example, chapati flour).

Magnesium deficiency (often due to dietary deficiency and to prescribed medicines, including some antibiotics, diuretics and painkillers).

Causes of raised (corrected) calcium levels

Primary hyperparathyroidism (overactive parathyroid glands) cause 8 out of 10 cases.

Cancer of many different kinds can increase calcium levels, and accounts for about 2 out of 10 cases.

Rarer causes of hypercalcaemia (raised calcium levels) include:

Overconsumption of antacids .

Pulmonary tuberculosis .

Addison's disease .

Prolonged bed rest - especially in teenagers whose bones are growing fast.

Vitamin A and/or D overdose.

A number of medicines, including lithium, tamoxifen and diuretics.

Kidney dialysis.

Prothrombin time (PT) or International Normalised Ratio (INR) are sometimes measured as a part of standard liver function tests.

PT and INR are ways of measuring the ability of your blood to clot. Conditions which impair this clotting (prolonging the PT and increasing the INR) include:

Acute and severe liver disease (including liver failure and severe paracetamol overdose ).

Use of anticoagulant medicines (in this case, lengthening the prothrombin time and increasing the INR is the intention).

There is a difference between what you need to do to keep your liver healthy most of the time and what you need to do if your liver is inflamed or damaged.

The liver does not need a detox diet, which will not help it and will often (if it is very low-calorie, for instance) make it work harder. The liver is a digesting, storage and detoxing organ. If you are well, the way to look after your liver is by:

A balanced diet with a good fibre content.

Regular exercise.

Keeping your weight within healthy limits.

Avoiding 'fad' diets (which can challenge the kidneys and liver hard).

Avoiding unnecessary medicines and supplements including paracetamol

Stopping smoking.

Saying within the recommended limits for alcohol (both daily and weekly).

If your liver is inflamed and injured (for example, you have hepatitis and are jaundiced) or you have advanced liver disease (for example, cirrhosis) then, depending on the severity, you may be advised to have a special diet. This involves using carbohydrates as your major source of calories, eating fat moderately and cutting down on protein. You may be advised to take vitamin supplements, and if you are retaining fluid you should reduce your salt consumption to less than 1500 milligrams per day.

A few things to remember about abnormal liver function tests

Liver function tests are not a diagnosis; they are a set of clues which help doctors make a diagnosis.

Liver function tests are a sensitive early warning system for problems in the liver and, in some cases, elsewhere.

Because 'normal ranges' used by laboratories are the levels between which about 19 out of 20 of people's tests will fall, about 1 person in 20 will have an abnormal test without cause. About half of these people will have slightly high tests and about half will have slightly low tests, but their levels either way should not be extreme.

The most likely cause of any particular pattern of abnormal liver function tests varies between patients (because of difference in age and sex) and between populations (because of variations in genetics and because different things are more common in different parts of the world).

Almost any pattern of liver function test abnormality can be caused by medicines (including over-the-counter medications), by herbal remedies and traditional medicines from other cultures, and by poisonous substances.

Many liver conditions cause no symptoms, at least at first; so, if you have several abnormal tests (or one test is markedly abnormal), it is very important to follow this up.

Although single, mildly abnormal tests are not usually significant, any unexplained abnormality generally needs a check that you are well and may need a repeat test.

Abnormal liver function tests in a person who is also sick are more worrying than those in a person who is well.

Dr Mary Lowth is an author or the original author of this leaflet.

Further reading and references

  • Cirrhosis in over 16s - assessment and management ; NICE Guideline (July 2016 - last updated September 2023)
  • Liver disease ; NICE Quality standard, June 2017
  • Hepatitis B ; NICE CKS, February 2022 (UK access only)
  • Non-alcoholic fatty liver disease (NAFLD) ; NICE CKS, October 2023 (UK access only)
  • Non-alcoholic fatty liver disease (NAFLD): Risk factors ; NICE CKS, October 2023 (UK access only)
  • Autoimmune Hepatitis Association
  • Hepatitis C ; NICE CKS, September 2022 (UK access only)
  • Hepatitis A ; NICE CKS, May 2021 (UK access only)

Article history

The information on this page is written and peer reviewed by qualified clinicians.

Next review due: 12 May 2028

2 jun 2023 | latest version.

Last updated by

Dr Rachel Hudson, MRCGP

Peer reviewed by

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Liver blood tests (formerly known as liver function tests – LFTs)

What are liver blood tests.

Liver blood tests look at how well the liver is functioning and can indicate whether there is any damage or inflammation inside the liver.

Until recently, liver blood tests were referred to as liver function tests, or LFTs.

However, as most patients with abnormal liver blood tests actually have normal function of the liver, this term was felt to be unhelpful and often led to unnecessary concern. Therefore the term liver function tests, or LFTs, has been replaced by liver blood tests. This is a very important change, and the medical profession is working hard to ensure the new term is widely accepted and used.

Calling these tests liver blood tests is a more accurate way of describing what the test actually does and uses less frightening language.

The British Liver Trust does not recommend home liver tests offered by private companies. The results of these tests do not provide a comprehensive assessment for determining the presence of liver disease. If you have concerns about your liver health, we recommend that you consult your GP. They will conduct a range of tests, consider your medical history, and integrate all the results to make an informed decision about the necessity of additional tests or potential treatment.

liver function test essay

In this section and useful links

  • Liver blood test FAQs
  • Liver disease tests, screening and diagnosis
  • Liver conditions
  • Support for you
  • Useful words glossary
  • Cost of living support

What is a liver blood test looking for?

A liver blood test looks at the chemicals (enzymes), proteins and other substances made by the liver to assess whether levels of any of these are abnormal. The main ones are:

Alanine aminotransferase (ALT) and aspartate aminotransferase (AST)

ALT and AST are enzymes found in the liver cells (hepatocytes) which leak into the blood stream when the liver cells are damaged. They indicate the degree of inflammation present in the liver. Levels of ALT and AST are usually high in conditions such as hepatitis – possibly twenty to fifty times higher than normal. The ALT ‘value’, or level, is more specific to the liver than the AST value because the AST value may also be high if there is muscle damage elsewhere in the body.

Monitoring levels of these enzymes can help doctors assess how much liver scarring (fibrosis) there is in conditions such as non-alcohol related fatty liver disease (NAFLD) and alcohol-related liver disease.

Alkaline phosphatase (ALP) and y-Glutamyltransferase (GGT)

These are enzymes found mainly in the bile ducts of the liver. Increases in ALP and another liver enzyme called y-Glutamyltransferase (GGT) can indicate obstructive or cholestatic liver disease, where the flow of bile from the liver is blocked because of an obstruction of the bile duct. GGT levels are also a potential indicator of how much alcohol a patient drinks and can also be higher in those with non-alcohol related fatty liver disease (NAFLD).

Bilirubin is produced when red blood cells break down, and is the main pigment in bile (a yellow/green substance made by your liver that aids digestion). An increase of bilirubin causes jaundice, characterised by a yellowing of the eyes and skin in liver disease.

This is a protein made by the liver that makes up about 60 per cent of total protein in the blood, helping to maintain tissue growth and repair. It stops fluids from leaking out of blood vessels and carries nutrients and hormones around the body. Albumin levels may decrease if the liver is damaged.

The levels of each of these will be given in numbers and values. The laboratory where the blood is being tested provides a ‘normal value’ or ‘reference value’ against which your test results are measured. This is a broad range into which people without liver disease will fall. An abnormal liver blood test result is defined as being below or above the normal range.

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Liver blood tests faqs, if i have concerns about my liver what initial tests should i request.

The first thing to do is discuss with your GP why you have concerns – are you worried about past or present lifestyle risk factors, such as drinking too much alcohol, being overweight or a risk of viral hepatitis? Do you have a familyhistory of liver disease or symptoms you’re worried about? If your GP thinks it’s appropriate, they will perform a panel of routine liver blood tests and relevant care or treatment can be discussed from there. If there is an additional family history for a condition such as haemochromatosis, in which the body stores too much iron, your doctor will organise additional specialist tests.

What happens when I have a liver blood test?

When you have a liver blood test, a syringe with a fine needle is used to remove a small amount of blood from a vein in your arm. The sample can be taken by your GP or a nurse at your local clinic, or by hospital staff (a person who is specially trained to take blood is called a phlebotomist). It will then be sent to a laboratory to be tested.

If I receive ‘abnormal’ blood test results, what should happen next?

Abnormal liver blood test results are relatively common and most people with these results have normal liver function. An infection or a reaction to medication might affect your blood test results and sometimes a repeat liver blood test is all that’s needed. However, any abnormality does need to be investigated to find out what the cause is.

Scans may be performed to help understand the cause of the abnormality and also to assess how significant any damage is.

These may include imaging scans such as ultrasound, elastography scans such as FibroScan, CT or MRI scans , which help doctors get a better picture of the extent of any damage to the liver. In certain cases a liver biopsy (where a tiny piece of tissue is taken from the liver for examination) may be considered to specifically diagnose a condition or provide information on the extent of scarring inside the liver.

If you are very unwell, you may be referred or admitted to hospital, although this is unusual – only a very small number of people with abnormal liver blood tests require admission.

How do I work out what my liver blood test results mean?

Your doctor will explain your test results to you. If they are abnormal, your doctor will also explain the most likely cause, and how severely affected your liver may be.

I’ve heard doctors talk about a ‘standard liver screen’. What tests are involved in this?

When a patient has been found to have an abnormal liver blood test, the next step is to establish the cause. This requires a second panel (set) of blood tests that look for potential causes such as viruses, problems with the immune system and rarer inherited conditions.

If I am found to have non-alcohol related fatty liver disease (NAFLD), what tests should I have next?

NAFLD is very common and 30-40% of the population have it. If you have NAFLD, the next step is to investigate the extent of the condition and if the liver is scarred or damaged. The level of scarring can be assessed using specialist scans or blood tests and your doctor can explain these to you.

If these tests are not able to assess any damage accurately, a liver biopsy may be considered to provide more detailed information.

What can I do about my NAFLD?

Because NAFLD is commonly associated with being overweight, there is evidence to suggest that losing weight through diet and exercise helps reduce the amount of fat in the liver and damage done to it.

How do I know if I’m drinking too much alcohol and it’s affecting my liver?

The Government advises that both men and women should not regularly drink more than 14 units in a week. It is also important to have 2-3 consecutive days off drinking a week to allow your liver to recover.

However, the National Institute for Clinical Excellence (NICE) guidelines recommend that if you drink alcohol in a harmful way, defined as more than 50 units of alcohol per week for men (around 15 pints of beer) and 35 units for women (about 3.5 bottles of wine), and have done so for several months, you should have a non-invasive test for cirrhosis.

Should I see a specialist if I have abnormal liver blood tests?

Not necessarily. If your results are abnormal your GP can advise you on the next steps to determine the cause and assess how serious the problem and any associated damage is.

If I am found to have evidence of advanced liver disease what should my doctors be doing next?

You need to see specialists at this point, which your doctor will arrange. A specialist team will then do more tests to get a better idea of what’s wrong with your liver, and how best to treat it.

Please download the Liver Disease Tests Explained publication for further information.

Liver disease tests explained

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  • Clin Liver Dis (Hoboken)
  • v.18(Suppl 1); 2021 Oct

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A History of the Assessment of Liver Performance

Omar Y. Mousa

1 Division of Gastroenterology and Hepatology, Department of Internal Medicine, Mayo Clinic, Rochester MN

Patrick S. Kamath

Associated Data

Short abstract.

Content available: Author Interview and Audio Recording


Watch the interview with the author.

Listen to an audio presentation of this article.

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History From Ancient To Modern

In antiquity, inspection of the liver, hepatoscopy ( hēpatoskōpia , from the Greek ηπατοσκόπια), was a common method among Babylonians, Etruscans, Greeks (Fig. ​ (Fig.1), 1 ), and Romans to use the liver to seek knowledge of the future using supernatural means, 1 but not for the purpose of assessing the performance of this royal organ. Ezekiel, the sixth century BCE biblical prophet who lived during the Babylonian captivity and had warned earlier about the impending destruction of Jerusalem, documented the popular Babylonian practice of hepatomancy ( ηπατομανία ) that is divination of the will of the gods via hepatoscopy of the livers of carefully selected sheep. In this context, the venerable prophet reported that “the king of Babylon (i.e., Nebuchadnezzar) has stood at the fork of the road, at the crossroad of the two ways, to perform divination, to shake out arrows, to inquire of the household gods, to inspect the liver. On its right lobe was the omen of Jerusalem…” 2 Hepatoscopy convention ordained that signs on the right side (later called the pars familiaris ) of the liver that were deemed favorable, such as gallbladder swelling, paradoxically predicted success of the enemy when present on the left ( pars hostilis ) side. 1 Guided by the omens, Nebuchadnezzar went to Jerusalem and not Rabbah (modern Amman in Jordan), with devastating effect. How different might the Middle East have looked today had the configuration of that ovine liver been different? Was the clue a tight embedding of the gallbladder in the substance of the liver on the left or deep enclosure of the hepatic duct in the porta hepatis? 1 We can only speculate.

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Greek inspection of the liver, depicted on a big‐bellied amphora decorated with red figures by the Kleophrades Painter (510‐470 BCE). Müler K. 1967 Die Leberschau in der Antike. Deutsche Laevosan‐Gesellschaft, Mannheim.

Since Paleolithic times, the liver was appreciated to be a highly vascular organ, as evidenced by the remarkable cave art of prehistoric hunters, found at Lascaux in Southern France. 3 Moreover, the liver was also long considered to be the source of blood—the basis of life itself—described by the most esteemed of all Roman physicians, Aelius (alternatively Claudius) Galen (c. 130‐210 CE; Fig. ​ Fig.2) 2 ) of Pergamon (modern‐day Bergama, in Izmir Provence, Western Turkey), as the sanguifactionis officina , 4 “the factory of the blood,” that is the site of sanguification . It is not surprising, therefore, that the liver was chosen for inspection as a natural consequence of the deep‐grounded belief that the soul, which was the jurisdiction of priests in those civilizations, resided there along with the source of emotions, feelings and desires, and even sexual potency. Later, of course, the heart usurped the liver’s claim as the seat of the soul. 1 A Babylonian priest, known as a  Bārû , was trained to recognize the predictive signs in the liver, and thus was collected a mountain of omens called the  Bārûtu . These priests recognized that livers from similar animals never looked alike, which in Mesopotamia led to the use of clay liver models, 5 examples of which are held in the Middle East Department of the British Museum (Fig. ​ (Fig.3) 3 ) and date back to the Temple of Marduk in Babylon in 2000 BCE, in the age of Hammurabi (perhaps better written phonetically as Hammurapi 6 ). These historic details were revealed in a trove of some 800 fragments of medical texts out of tens of thousands of potsherds excavated at Mound Kouyunjik, opposite the site of ancient Nineveh (modern Mosul), among the vast library of King Ashurbanapal of Assyria (668‐626 BCE). 6 A clay model of an ox liver, dating from the 15th century BCE, was also found at the archeological site of Tel Hazor in the Upper Galilee, Israel, at the site of the Middle Bronze Age fortified city of Hazor. 7 Subsequently, durable Etruscan bronze models were produced (Fig. ​ (Fig.4 4 ), 8 in which inscriptions on the liver surface showed divisions into regions assigned to specific deities of the Etruscan religion.

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Galen of Pergamon. Lithograph by Pierre Roche Vigneron.

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Clay model of sheep liver held at the Middle East Department of the British Museum, London. This teaching model dates from 1900‐1600 BCE, probably from the ancient Sumerian/Babylonian city of Sippar, 30 km southwest of modern Baghdad. The surface is divided into boxes in which are described the implications of blemishes found in this region of the sacrificed sheep’s liver; wooden pegs were inserted into the holes to record the blemishes that were found, for later divination. Reproduced with permission. © Board of Trustees at the Middle East Department of the British Museum, London.

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The famous Bronze Liver (Iecur Placentinum) of Piacenza is held in the Musei Civici Di Palazzo Farnese, Piacenza, Italy. This teaching model or memory aid that dates from the early second/late first century BCE Etruscan period was found in 1877 by a peasant working in his field, in nearby Decima di Gossolengo, presumably having been lost there by a haruspex during the 80s BCE civil wars of Lucius Cornelius Sulla. The inscriptions on the surface of the liver (below right) indicate the domains of the Etruscan gods. Photograph reproduced with permission from Musei Civici Di Palazzo Farnese, Piacenza, Italy.

In the Etruscan tradition that was practiced in Ancient Rome (and which even persisted to the Middle Ages 9 ), divination was performed by a haruspex (Fig. ​ (Fig.1), 1 ), who was trained to look for omens by performing haruspicy , from the Latin haruspicina meaning “inspecting entrails,” and especially the livers, of sacrificed animals (after the archaic word haru and the root spec , “to observe”). Perhaps the most famous haruspex in ancient Rome was the soothsayer Spurinna, at whose warnings about the Ides of March * Julius Caesar scoffed to his cost, at least according to Suetonius. 10 Haruspicy contrasts with divination performed by an augur, who interprets the will of the gods by “taking the auspices,” that is, studying the flight of birds.

It was not until the Renaissance dawned, 1000 years after the fall of Rome, that there was any advance in understanding the anatomy and function of the liver. Throughout the Dark Ages and even in the latter part of the Middle Ages, the spiritual soul was more important than the physical body. Leonardo da Vinci (1452‐1519) studied the anatomy of the human liver thoroughly 11 (Fig. ​ (Fig.5), 5 ), and apparently he even described different liver diseases, including cirrhosis, but his work in hepatology was relatively unknown until the latter half of the 18th century. Andreas Vesalius (1514‐1564) mistakenly portrayed the liver as having five lobes in his famed anatomical drawings ( Tabulae Anatomicae Sex, Venice 1538 ) based on his earlier dissection of a baboon (Fig. ​ (Fig.6A), 6A ), but he later derided that representation in his 1543 De Humani Corporis Fabrica Septum and accurately described the anatomy of the human liver and biliary tree in detail 12 (Fig. ​ (Fig.6B), 6B ), while yet perpetuating his errors of its portal venous anatomy. 13 He may have even found a correlation between excessive alcohol consumption and cirrhosis. 14 Galen and his adherents believed that the major function of liver was to convert digested food from the intestines into blood by concoction ( pepsis ) and to separate the light (yellow) bile for excretion via the biliary tree from the heavy (black) bile that would pass via the spleen to the stomach. Yet, even up to the late Middle Ages, there was still no inkling that the liver had any function other than bile production. 15 Several centuries elapsed before the celebration of the liver by Dutch anatomist Thomas Bartholin, † as “the body’s master cook and engineer” that “cooks and stews for us…” 16

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“The Vessels of the Liver” by Leonardo da Vinci in Dell'Anatomia Fogli B circa 1508. From the Leonardo da Vinci Anatomical Drawings Collection held in the Royal Library, Windsor Castle. RCIN 91905v, Royal Collection Trust/© Her Majesty Queen Elizabeth II 2018. (Top) Intrahepatic branches of the hepatic artery and portal vein. (Bottom left) Branches of the umbilical vein, portal vein, hepatic artery, and bile duct, with both the gallbladder and bile duct. (Bottom right) The hepatic veins and their junction with the inferior vena cava. See Video 1 (watch here), a video animation of liver blood flow, as portrayed in a drawing by Leonardo Da Vinci and devised by the renowned British heart surgeon Francis Wells, Royal Collection Press Office. Reprinted with permission from © ATS Heritage.

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Liver illustrations by Andreas Vesalius (A) from Tabulae Anatomicae Sex, Venice (1538) showing a five‐lobed liver and (B) from De Humani Corporis Fabrica Libri Septum , Basel (1543) showing a two‐lobed liver reflected upward to display its visceral surface.

In 1654, Francis Glisson (1597‐1677 CE), a young colleague of William Harvey and a founder of both the Royal Society (of Great Britain) and the Royal College of Physicians, London, declared in his authoritative monograph on the liver that the hepatic parenchyma was responsible for the liver’s function, 17 namely, the separation of bile from the blood by the mechanisms of so‐called affinity. A finding published in 1666 by Marcello Malpighi (1628‐1694), 18 using primitive microscopy, albeit antedated a couple of years earlier by Johan Jacob Wepfer, 19 that the parenchyma was arranged into grape‐like out‐budding structures that he termed lobules , comprising lobuli and glandulosi acini , convinced him that there had to be a functional connection between the hepatic parenchyma and adjacent vascular structures. The architecture of the hepatic lobule in humans was elegantly demonstrated by Kiernan in 1833 using only a hand lens. 20

There are intriguing links between the appreciation of liver function and Glisson’s pivotal demonstration of intravascular channels in the liver 21 (Fig. ​ (Fig.7), 7 ), which he proved by injecting “warm water, coloured with a little milk” into the portal vein of a fresh human cadaver, using an ox bladder attached to a siphon (such as was used for administrating enemas). With the result of this perfusion experiment, Glisson vindicated the renowned physician‐anatomist, Erasistratus of Chios (310‐250 BCE), 22 who postulated the existence of intrahepatic vascular channels and who had actually coined the term parenchyma (παρέγχυμα, meaning “adjoining infusion”) that in Glisson’s mind was the locus of the liver’s function. It is likely that, in common with Glisson, Erasistratus considered that in anatomy, as in architecture, “Form follows function,” thereby presciently espousing the 1896 views of the renowned Chicago architect Louis Sullivan (1856‐1924) that the latter published over the course of 1901 as his Kindergarten Chats in the Interstate Architect and Builder . ‡ Or, as Sullivan’s most distinguished apprentice, Frank Lloyd Wright (1867‐1959), later paraphrased in his Dear Master’s ordinance, “Form and function are one.” 23 Galen did not ignore the impressive body of anatomical discoveries of his Alexandrian predecessor, but he was bitterly critical of the latter’s inference about an organ’s function, based on its anatomy. Incidentally, Francis Glisson’s experiment also provided crucial evidence for the hypothesis by that Man of Kent from Folkestone, United Kingdom, William Harvey (1578‐1657 CE), 24 that blood flows through the lungs, because the milky water he injected into the portal vein passed sequentially through the right heart, the lungs, and the left heart into the systemic arterial circulation. It was reasoned that if blood could pass through a dense organ like the liver from the portal vein to the vena cava seemingly without any propulsive force, then blood could surely flow through the delicate spongy lungs driven by the contraction of the heart’s right ventricle.

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One of Glisson's drawings of a cast of the intrahepatic vessels, from his Anatomia Hepatis. London: Typis Du‐Gardiani; 1654. 17

Cirrhosis was described in detail from the 17th century onward, although the notion that a “hard” liver was a bad sign, especially in association with jaundice, can be traced back to Greek and Roman medicine from Hippocrates 25 and Aulus Cornelius Celsus 26 to Aretæeus the Cappadocian 27 and Caelius Aurelianus, 28 over a span of almost 1000 years (from 400 BCE though 500 CE). However, the terminology was not always unequivocally lucid, making interpretation of early clinicopathological entities difficult. Swelling that probably meant inflammation (i.e., hepatitis) was thought to progress to hardness , which we presume to equate with cirrhosis, and then to a scirrhus state that we interpret as carcinoma. Confusion was compounded by the widespread application of the label tubercle that was introduced by Giovanni Battista Morgagni (1682‐1771) in his 1761 seminal mechanistic book, De sedibus et causis morborum per anatomen indagatis (Fig. ​ (Fig.8 8 ) 29 , to refer to any discrete liver mass that George Budd later referred to as nodules, often the size of peas, while scarring gave the surface of the liver a “hob‐nailed appearance.” 31 In the years before Laennec and Budd, livers were described as being tubercular and even tuberculated , despite there being no hint of tuberculosis. Further, Morgagni’s failure to distinguish between cirrhosis and carcinoma 30 only contributes more uncertainty.

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Title page of the 1765 second edition of Morgagni’s De sedibus et causis morborum per anatomen indagatis.

St Thomas’s Hospital London surgeon John Browne (1642‐1702) has long been credited with being the first to publish an illustration of a cirrhotic liver 32 (Fig. ​ (Fig.9) 9 ) that was drawn by the distinguished crayon artist and engraver William Faithorne the Elder, § from an autopsy that the artist witnessed and was carried out by Browne himself. Although Browne attended both Charles II and his nephew William III (of Orange), and had an impressive list of innovations and achievements, it is sad to report that his reputation was stigmatized by brazenly copying from others, an apparently common practice in his time that was called piracy but which now would be plagiarism, an act that was not yet illegal in those days. 33 Matthew Baillie (1761‐1823), 34 a Scottish physician, nephew of William and John Hunter (from each of whom he inherited a substantial museum of pathological specimens) and Physician in Ordinary to George III, was credited with having published the first systematic study of pathology and the first publication in English on pathology as a separate subject. 35 Oddly enough, he did not publish the accompanying illustrations from his own specimens and those from his uncles’ considerable inheritance until much later, in a separate volume. 36 His description of cirrhosis is vivid, graphic, and almost lyrical, 37 but the name he chose for this pathological entity, namely, Common tubercle of the liver (Fig. ​ (Fig.10), 10 ), is a startling throwback to Morgagni. Tubercles of the liver include ordinary cirrhotic nodules, presumed neoplasms, and lesions related to scrofula or syphilitic gumma, and these Baillie carefully distinguished from tubercles that were “commonly produced by a long habit of drinking spirituous liquors.” 37 Most notable, Baillie had recognized an association between drinking alcohol and liver disease.

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John Browne’s illustration of a glandulous‐appearing (i.e., cirrhotic) liver. 32 Key: (A) left lobe; (B) concave part of the right lobe; (C) cut surface of the right lobe; (D) black spots, possibly representing divided vessels; (E) gallbladder; (F) portal vein together with the bile duct; (G) liver tissue lying between the vena cava and the portal vein and bile duct; (H) vena cava.

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Matthew Baillie’s illustration of a cirrhotic liver. From A series of engravings accompanied with explanations which are intended to illustrate the morbid anatomy of some of the most important parts of the human body, 36 Fascicle 5, Plate II. Portion of the external surface (top) and cross section (bottom) of the liver studded with tubercles. Line drawings by William Clift (John Hunter’s former assistant), and engraving by James Basire.

Since the opportunity to give this multifaceted clinicopathological entity an enduring name was passed up by liver luminaries from antiquity to Browne and Baillie, the nomenclator’s baton was taken up 25 years later by a tuberculous Parisian physician from Normandy, 38 who delighted in Latin and Greek. In what must surely be the all‐time most celebrated footnote 39 in the History of Hepatology, René Theophile Hyacinthe Laennec (1781‐1826), who had invented the stethoscope and made major contributions to the pathological understanding and diagnosis of diseases of the chest, coined the neologism “cirrhosis” that as a devoted classicist he derived from the Greek kirrhos (κιρρός), meaning “tawny yellow.” The orange‐yellow color referred to the appearance of the nodules in the diseased liver of the patient (whose pleurisy was the main focus of the famous 1819 case report), which he had in fact already described in a little known 16‐page essay on Les Cirrhoses that was part of his incomplete Treatise on Pathological Anatomy (1804‐1808) from 15 years earlier. 38 Whether the Laennec eponym that is popular in the United States, less so in Great Britain, and hardly at all in France is deserved for alcoholic cirrhosis, the memory of Laennec will surely prevail for devising the generic nomenclature itself, cirrhosis , for the clinicopathological entity that pervades our chosen field. It should come as no surprise that Laennec’s moniker was not universally applauded; none other than Baron Carl (Freiherr) von Rokitansky (1804‐1878), the renowned Bohemian Viennese pathologist, humanist philosopher, and liberal politician, preferred terms like granular atropy ( atrophie in German) and tuberculization . 40 Parenthetically, in a later edition of Traite de l'Auscultation , Laennec cautions that the nodules of cirrhosis may be mistaken for malignant tumors ( squirrhe in French).

Jaundice, the yellowing of the eyes, skin, mucous membranes and secretions, was perhaps the earliest appreciated expression of liver dysfunction to be recognized in all ancient systems of medicine—in the clay tablets of Mesopotamia, repeatedly in The Old Testament and Talmud, 41 in exquisite detail in the Hippocratic Corpus , 42 and in Ayurvedic 43 and Chinese 44 sources, where a plethora of traditional remedies were offered. Thus was created the need for one of the foremost early tests of liver function, which survives to this day. Once it had been determined that the function of the liver parenchyma was bile formation, the liver dysfunction responsible for jaundice (otherwise named morbus regius by Celsus 45 because of its gold color, or perhaps because of cure by the touch of a king or because only a king could afford its costly therapy) was deduced by Erasistratus to be due to impaired bile secretion. Yet in Letter 37 in the 1769 edition of The seats and causes of diseases, investigated by anatomy …, Morgagni attributed jaundice to constriction of the liver by hepatic nerves caused by passion or emotional disturbance, for which Celsus some 1800 years previously had already recommended rest in a “good bed in a tasteful room” and emotional support. 45

Encephalopathy and ascites also featured prominently in times of yore as manifestations of chronic liver dysfunction and, even now, together with jaundice, are included in a time‐honored index that purports to assess liver performance. 46 For the first, we must distinguish the sudden delirium of acute liver injury, which had been observed and described by Hippocrates, Celsus, Galen, and their successors, in which there is fairly abrupt impairment or loss of true liver function, that is, the syndrome of acute liver failure (ALF; also known as fulminant hepatic failure)—as reviewed elegantly elsewhere in this series by Will Bernal and the late Roger Willims 47 —from the neuropsychiatric syndromes of disturbed behavior and reduced consciousness associated with portosystemic shunting in cirrhosis, that is, portosystemic encephalopathy. The History of Encephalopathy is the subject of a lively forthcoming essay in this series by Nathan Bass.

The challenge of ascites to the well‐being of the individual was appreciated by the ancient Egyptians, the Hebrews, the Greeks, and the Mayans (Fig. ​ (Fig.11) 11 ) alike. 48 Hippocrates observed pithily that “when the belly becomes full of water, death follows.” 49 Methods were devised early on to alleviate ascites, including physical drainage and the early introduction of dietary salt restriction. The obvious expeditious remedy for massive ascites was to drain the offending fluid rapidly by tapping the barrel‐shaped distended abdomen—a practice that Celsus favored and for which he even designed a lead or bronze tube with a retaining collar. 49 Erasistratus cautioned against rapid paracentesis, which he had abandoned in favor of opening the abdomen and inserting a catheter 50 (in his hands an implement shaped like a Roman S), as had been performed since the Hippocratists. Adherence to Erasistratus’s counsel against the rapid removal of ascites (which Paul of Ægena thought would prove immediately fatal because it also “evacuates the vital spirit” 51 ) persisted until the group in Barcelona documented that it is safe when performed in conjunction with intravenous (IV) albumin as a plasma expander. 52 As far back as Erasistratus, paracentesis was usually effected via the umbilicus (as described by Ambroise Paré 53 ), but this site would scarcely be countenanced nowadays, 54 because of the risks for permanent leakage from the hernia sac and of puncture of portal hypertensive collateral veins (varices) even in the absence of a visible caput Medusa.

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(A) Abdominal distension caused by ascites, showing an everted umbilicus and fine dilated superficial abdominal wall paraumbilical veins in which cephalad flow can be demonstrated by expelling blood between two fingers and observing the direction of return. Photograph provided by Dr. A. Reuben, Series Editor (B) Figurine from the Mayan burial site on the Island of Jaina (off the Yucatan Peninsula) depicting a man with massive ascites and eversion of the umbilicus. The Mayans of the classic period (300‐900 CE) were familiar with the physical signs of massive ascites. 101 Reproduced with permission from Annals of Internal Medicine . Copyright 1994, Annual College of Physicians.

In the 18th and 19th centuries, additional observations were made in hepatobiliary disease regarding gallstones, liver tumors, fatty liver, hepatic congestion, and acute hepatic necrosis; coincidentally, several formidable tomes (now of historic hepatological interest) devoted exclusively to liver disease were published by William Saunders, 55 George Budd, 31 Friedrich Theodor von Frerichs, 56 and Charles Murchison. 57 The 20th century was the beginning of the modern era of hepatology, spurred on by the exponential progress in the physical and biological sciences, epidemiology, immunology, microbial discovery, pathology, and light and electron microscopy. Among a plethora of anatomic features studied were the lobules of the human liver and its microcirculatory units, 58 along with a host of physiological, pathophysiological, and biochemical functions for which tests had already been devised in the early decades of the century, 59 including heme catabolism to bilirubin; bile composition and function; glycogenesis, gluconeogenesis, and other facets of carbohydrate metabolism; urea synthesis as the end stage of protein metabolism; detoxification processes; and aspects of deranged hepatic lipid metabolism that underlie microvesicular and macrovesicular fatty degeneration. Many scientists, in the tradition of Hippocrates and Galen, reported on jaundice caused by biliary obstruction, the infective hepatitides, ‖ and other causes of dysregulated bilirubin metabolism and transport. Autoimmune hepatitis and primary biliary cirrhosis (later updated to primary biliary cholangitis) were recognized, and hemochromatosis and Wilson disease were differentiated from other causes of liver disease. ¶ Compared with these sublime scientific pursuits, clinical interest in “tight‐lace” or “corset” liver, as a consequence of the capricious fashion of wearing barbarously rigid corsets to achieve an hourglass waist, 60 now appears almost comical. Yet an unexpected benefit of the end of the First World War, namely, the welcome demise of this misogynistic torture, is ostensibly not yet complete. 61 , 62 , 63

The recognition of different classes and etiologies of liver disease, their influence on patient morbidity and mortality, and the development of medical and surgical therapies demanded the introduction of techniques not only for diagnosis but also for assessment of disease severity, as judged by the impairment of overall liver performance and ultimately its impact on prognosis. The early decades of the 20th century witnessed the development of a serum bilirubin test, 64 utilization of Bauer’s 1906 galactose test, 65 hippuric acid synthesis assays 66 based on the research of Armand J. Quick (of Quick Test fame 67 ), and tests based on the disposal by the body of a rainbow of dyes: indigo carmine, Congo red, methylene blue, Evans blue, Rose Bengal, indocyanine green (ICG), and arguably the most popular, the now‐obsolete bromsulphalein (BSP) that is gloriously purple in alkaline solution. The clinical importance of the 1913 van den Bergh reaction for bilirubin estimation in the blood 64 was endorsed by many clinicians. 68 Serum bilirubin measurement subsequently became an important tool for distinguishing the different causes of scleral icterus —the equivalent Greek term for the Latin/French descriptor jaundice that refers to the yellow discoloration of the sclera, mucous membranes, the skin, and even cerebrospinal fluid—that Galen inferred as being either obstructive, concomitant, or hemolytic. 15 This included the detection of latent jaundice, 68 meaning an elevation of serum bilirubin below a level of ~3 mg/dL that should be evident on careful clinical inspection in a good light. The linguistic origins of both jaundice and icterus are discussed elsewhere in this series, as well as the ancient Greek and Jewish beliefs that placing a golden thrush or pigeon near the umbilicus would cure jaundice/icterus 69 —a practice that was fatal to the bird and that Celsus might have considered to be “complementary and alternative medicine.”

It was not until the 1950s that the diagnostic value of the serum transaminases (officially referred to as aminotransferases since 1961 70 ) was appreciated in the diagnosis of viral hepatitis. 71 There are many clinical applications for liver‐associated serum biochemical tests that include aminotransferases, bilirubin, alkaline phosphatase, and albumin, 72 which are usually bundled together with the Quick prothrombin time (i.e., the number of seconds that it takes plasma to clot in a test tube)—a major facet of blood coagulation in which the liver has a near monopoly. 67 Such blood test bundles are popularly but, as Gerald Klatskin pointed out in 1948, 73 erroneously denoted as “liver function tests” (LFTs), yet they are widely used essential noninvasive tools of hepatology. It is not commonly known that the term liver function test had been in use since the 1930s 59 at least and included some curious laboratory procedures that are reminiscent of alchemy and witchcraft, in which the flocculation of negatively charged colloids of gold by serum globulin or the precipitation of gammaglobulins from serum by heavy metals, pungent phenols, or mixtures of sheep brain cephalin and cholesterol was relied on to distinguish among different etiologies of jaundice and other liver afflictions. 74 Yet it must be conceded that, like Voltaire’s quip about the Holy Roman Empire, # LFTs are neither liver ‐restricted, nor measures of its function , nor really tests of tolerance or performance 73 (in the sense that a glucose tolerance test assesses glucose handling quantitatively or that creatinine clearance and cardiac output reflect the percent of kidney and heart performance, respectively). Be that as it may, LFTs are widely used to: (1) screen for liver disease, including injury caused by a wide spectrum of medical, surgical, radiological, and radiation interventions, and by medicinal and recreational agents, including herbal and dietary supplements and other complementary and alternative medicines; (2) assess its severity; (3) monitor disease progression; and (4) measure the efficacy of various therapies. Despite the obvious limitations, LFTs are indeed often interpreted as global tests of liver function.

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Title page of an 1835 edition of Voltaire’s Essai sur les mœurs et l'esprit des nations , with a portrait of the author.

Assessment of Global Liver Function

Biochemical tests by themselves or combined with complications of portal hypertension like ascites and encephalopathy have been used to assess global hepatic function. Incorporation of both biochemical and clinical information to determine prognosis was the basis of the Child‐Turcotte classification that was developed, using actuarial statistics for the first time in surgical research, by Jeremiah G. Turcotte 76 (1933‐2020), who was an instructor in the Department of Surgery chaired by Prof. G.C. Child 3rd (1908‐1991) at the University of Michigan (Fig. ​ (Fig.13). 13 ). The Child‐Turcotte classification used preoperative serum albumin, serum bilirubin, the severity of ascites and encephalopathy, respectively, and an assessment of nutritional status. Using these variables, patients with cirrhosis who had undergone portosystemic shunting under Child’s care were designated as class A, B, or C 75 (according to a liver disease stratification scheme published 3 years previously by Wantz and Payne 77 ); patient survival was compared among these three classes. 76

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(A) C.G. Child 3rd. HS1015, Medical School (University of Michigan) records, Bentley Historical Library, University of Michigan. Reproduced with permission. (B) J.G. Turcotte. HS9059. Photo by Peter Yates, News and Information Services (University of Michigan) Faculty and Staff Files, Bentley Historical Library, University of Michigan. CC BY 4.0.

Child‐Turcotte class A patients were determined to be the best surgical candidates. With time, unfortunately, the designation often came to be abbreviated as the “Child Class,” as Turcotte’s name was rather unceremoniously dropped. In a follow‐up study published by Pugh, a medical resident, and others from the late Roger Williams’s group in the United Kingdom, 46 nutritional status was thought to be difficult to define and was replaced by the prothrombin time (and later the international normalized ratio [INR]); the ensuing Child‐Turcotte‐Pugh ** (CTP) classification became the standard to determine operative risk for portosystemic shunt surgery. Scores of 1 to 3 were assigned to the values of the five individual variables, namely, prothrombin time (or INR), bilirubin, albumin, ascites, and hepatic encephalopathy, and the sum of the five individual scores was then used to score the severity of liver disease (Table ​ (Table1). 1 ). Patients with scores of 5 to 6 points were classified as CTP class A, 7 to 9 points as CTP class B, and 10 to 15 points as CTP class C.

CTP Classification: Grading the Severity of Liver Disease 46 , 77

Biochemical and Clinical Variables
Total bilirubin, mg/dL1‐22‐3>3
Albumin, g/dL>3.52.8‐3.5<2.8
Prothrombin time, seconds1‐44‐6>6
Encephalopathy gradeNone1 and 23 and 4

Transjugular intrahepatic portosystemic shunts (TIPSs) were described in 1989 78 and started becoming widely used in the 1990s, but some patients were at high risk for procedure‐related mortality. Similar to the development of the CTP score and using data from four centers in the United States, investigators at the Mayo Clinic developed a prognostic model to predict survival after TIPS. 79 The variables in the model were the serum total bilirubin, INR (for prothrombin time), serum creatinine, and etiology of liver disease. Later this model was also found to predict survival among patients with cirrhosis not undergoing TIPS. 79 The model, originally termed the Mayo End‐Stage Liver Disease Model (MELD), was validated in hospitalized patients with cirrhosis and ambulatory patients with cirrhosis of varying etiologies, including primary biliary cirrhosis, as it was then known; it was independently validated in an inception cohort of patients with cirrhosis in Italy. 80 Although developed as a prognostic tool to determine mortality risk after TIPS, the MELD score received widest recognition as a tool to prioritize organ allocation for liver transplantation.

Organ allocation for liver transplant in the United States was prioritized in the 1990s largely on waiting time on the transplant waiting list. Patients with ALF received the highest priority (Status 1). Patients with CTP scores ≥10 were assigned to Status 2, and the rest of patients to Status 3. Patients in the intensive care unit (ICU) were subclassified as Status 2A, and the rest of the patients in Status 2 as Status 2B. There were two downsides to this approach. The first was that patients were sometimes admitted to the ICU even if they were ambulatory outpatients solely so that they could receive an early transplant. The second anomaly was that for the large number of Status 3 patients, time on the waiting list became the deciding factor for who would receive a transplant. Moreover, among the variables in the CTP score, determining severity of ascites and hepatic encephalopathy was subjective, and the prothrombin time (INR) can vary between laboratories depending on the sensitivity of the thromboplastin used in the assay. 81 Recognizing the problems in the then prevailing system for organ allocation for liver transplants, the Department of Health and Human Services in the United States came up with the “Final Rule” in 1998, 82 namely, that prioritization for liver transplantation should be based on objective criteria and waiting time should be de‐emphasized. It was considered then that the MELD would be the prognostic tool to prioritize organ allocation because it was based purely on easily measured objective criteria and had a range of scores wide enough apart that waiting time could be de‐emphasized. MELD was subsequently termed “Model for End‐Stage Liver Disease,” delinking the institution from the score for wider acceptability. Etiology of liver disease was also dropped to avoid misclassification when the etiology was unclear. In February 1992, the MELD score was established as the tool to prioritize organs for liver transplantation. Benefits of this change included reduction in mortality on the waiting list, higher numbers of patients being transplanted, a reduction in the number of patients admitted to the ICU before transplant, and ethnic minority patients no longer being disadvantaged. The MELD score, as shown in Table ​ Table2, 2 , has subsequently been shown to be predictive of mortality in ALF, 83 alcoholic hepatitis, 84 drug‐induced liver injury, 85 and patients with cirrhosis undergoing surgery. 86 However, over the years since its introduction in the United States for prioritizing patients on the liver transplant waitlist, a number of modifications have been proposed, 87 such as the MELD‐sodium (MELD‐Na) that is used to adjust the score in transplant candidates with significant hyponatremia.

MELD 80 and MELD‐Na 87 Scores

MELD Score Calculations
Biochemical variables
Total bilirubin
MELD score: 3.8 × log (bilirubin mg/dL) + 11.2 × log (INR) + 9.6 × log (creatinine mg/dL) + 6.4
MELD‐Na modification: (0.025 × MELD × [140 – Na]), where Sodium is limited in a range of 125‐140, and if outside of these bounds, is set to the nearest limit.

Dynamic Tests

The classic tests of hepatic clearance, also called “dynamic tests,” are rarely used nowadays (Fig. ​ (Fig.14). 14 ). These tests were initially used in the assessment of residual liver function in hospitalized patients with shock requiring vasopressors for hemodynamic support, patients with sepsis, and patients undergoing liver resection or awaiting liver transplantation. 88 , 89 These tests reflect the liver’s ability to clear endogenous or exogenous substances from the circulation, a function known as hepatic clearance. The key determinants are organ perfusion and the functional unit of the hepatocytes. 90 , 91 To measure hepatic clearance, the compound used should have the liver as the sole route of departure from the plasma, and if there are other routes, they should be negligible. The compound should remain in the plasma before extraction by the liver, and equilibrium should be rapidly established if other fluid compartments are used. In addition, clearance should be independent of the concentration of plasma. 91 Examples of dyes used in clearance tests include sulphobromophthalein (also known as BSP) in 1913 and ICG in 1957. BSP binds to plasma proteins until it is excreted by the liver, and therefore the test results can be affected by abnormal concentrations of plasma albumin or by disturbed hepatic blood flow. ICG has a more predictable distribution volume because it is avidly bound to plasma proteins, which helps it measure the blood flow. The plasma level of ICG reflects hepatic uptake because there is low nonhepatic removal, along with great hepatic clearance. 89 , 90 , 91

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(A) Dynamic tests of liver performance. (B) Examples of a few dynamic tests that were studied to assess the liver function preoperatively, showing the function measured and the principle of the test. Table reproduced with permission from New England Journal of Medicine . 89 Copyright 2007, Massachusetts Medical Society.

In addition, the liver’s capacity to transport organic anions as suggested by measurement of serum levels of bilirubin and bile acids, or to metabolize drugs and exogenous compounds (such as lidocaine metabolite formation or breath tests with 14 CO 2 / 13 CO 2 exhalation) can help determine its function. 89 , 90 , 91 These tests may allow assessment of liver functionality and guide the management strategy and treatment response, 92 but they are not helpful when screening for liver disease, are difficult and expensive to perform, and therefore have all but completely fallen out of routine use. However, newer high‐tech stable‐isotope versions of some breath tests, which are semiautomated and simple to administer and assay, are showing great promise. Table ​ Table3 3 describes some of the older dynamic liver tests. Other research projects investigating liver function assessment include the HepQuant SHUNT test 93 and hepatobiliary scintigraphy 94 (and signal intensity on gadolinium‐ethoxybenzyl‐diethylenetriaminepentaacetic acid–enhanced magnetic resonance imaging during the interstitial and hepatobiliary phases. 95 Finally, mention must be made of a simple but powerful test that is being used increasingly in clinical hepatology, one that predicts well the outcome of various complications and therapies of cirrhosis, that is, the measurement of the hepatic venous pressure gradient (HVPG), 96 which incidentally also provides the opportunity to perform a transvenous liver biopsy. The pathophysiological underpinning of the HVPG is, in a sense, arguably one of the most vital of the liver’s functions, which so many of the histories retold in this essay embody: normal blood flow through the liver. Unfortunately, HVPG measurement is invasive and requires fastidious technique. 97 In this context, it is to be hoped that the results of comparing HVPG with the 13 C‐methacetin breath test, 98 , 99 or indeed any of the other noninvasive dynamic tests currently available (including various elastography modalities 100 ), will be successful, allowing for the simultaneous evaluation of liver performance and portal hypertension, and thereby eradicating a duality of endothermic feathered vertebrates using a singular particle of a naturally occurring crystalline composite.

Examples of Dynamic Tests of Liver Performance 88 , 89

Clearance tests
Sulphobromophthalein (or BSP)

Summary of the test:

Clinical application:


Summary of the test:

, and its plasma disappearance rate is >18%/min

Clinical application:

Caffeine testUseful in severe liver lesions
Correlates with BSP and the CO breath elimination test
Mechanism: quantifies hepatic microsomal activity

Summary of test:

Clinical application:

Breath tests
C‐Aminopyrine test


Clinical application:

Metabolic capacity
Monoethylglycineexylilide (MEGX) test

Clinical application:

Tests rarely performed in clinical practice
Amino acid clearance testEvaluate periodic plasma clearance of amino acids after standardized infusion dose.
Galactose elimination capacity

In summary, liver performance assessment requires a noninvasive test that is well tolerated, reproducible, operator independent, able to assess early and late stages of liver disease, is possibly linked to its pathogenesis, and predicts outcomes. To date, there is an unmet need in hepatology for such a noninvasive test of dynamic liver performance, but, fortunately, there are now admirable candidates for this role. Until the ideal noninvasive tests for assessing both liver performance and the natural history and treatment of disease and treatments materialize, it should not be overlooked that prognostic indices, however imperfect, already exist for these same almost all acute and chronic liver diseases, such as ALF, alcoholic hepatitis, autoimmune hepatitis, causality of drug‐induced liver injury, and complications of cirrhosis, and therapies such as liver transplantation, relief of Budd‐Chiari syndrome, and many others. Many of these indices can be calculated easily nowadays on handheld and desktop devices with the aid of individual applications (“apps”) that have been developed by investigators in their respective fields (e.g., for MELD, Transplant‐Free Survival from ALF, etc.) or using collections of apps, such as HelpCalc (available from the App Store), which was created and especially designed for hepatology by Dr. Gary Poleynard, with some assistance from Michael Davies.

Series Editor’s Postscript

The current essay by Drs. Mousa and Kamath is by far the longest yet in the History of Hepatology series, and rightly so. Whereas other authors in this series have elegantly and informatively reviewed the history of the respective chosen topics of their expertise, in this essay, the authors from WFMC (The World‐Famous Mayo Clinic) have provided a long‐overdue overview of the history of liver studies as a fitting backdrop to efforts made over the centuries to assess the performance of the liver. In antiquity, the liver was used to predict the future, but then the impetus quickly changed to devising means to predict the future of the liver disease and its impact on the owner of that diseased organ. Hepatologists are at a disadvantage compared with their pulmonary, cardiology, and nephrology colleagues, because the functions of their organs of interest, so to say, are monothematic. A simple alliterative mnemonic sums up the global function of the lungs, heart, and kidneys—the lungs Puff, the heart Pumps, and the kidneys Pee. The liver has no such unitary global function; therefore, there cannot be a global LFT. Instead, we have a battery of tests related to the different functions of the liver—catabolic, anabolic, excretory, secretory, detoxifying, etc.—as well as measures of liver performance that predict outcomes, which are summarized here. Incidentally, it is probably a forlorn hope that the time‐honored but specious term liver function tests will ever be expunged from the hepatological dictionary, as it trips easily off the tongue even though it erroneously seems meaningful.

In the context of the purpose of the present essay, who better could be charged with the responsibility of describing the evolution of liver function assessment than the senior author Patrick Kamath—who devised an innovative simple arithmetic index of liver performance with global impact (calculated from readily available serum variables), namely, the MELD score—and his junior colleague Omar Mousa. In addition to his clinical practice and clinical research achievements, Patrick is a legendary teacher, for which he has been repeatedly recognized and honored by the Mayo Clinic College of Medicine (upward of a dozen times), the Mayo Clinic Foundation, and the American Gastroenterology Association, culminating in the presentation of the Distinguished Clinician Education/Mentor Award of the American Association for the Study of Liver Diseases in 2018. The readers of the current series are fortunate to have access to the mentorship embodied in this essay.

Supporting information

Supplementary Material

Potential conflict of interest: Nothing to report.

* Et immolantem haruspex Spurinna monuit, caveret periculum, quod non ultra Martias Idus proferretur.  "Again, when he was offering sacrifices, the soothsayer Spurinna warned him to beware of danger, which would come not later than the Ides of March." ( De Vitis Caesarum, Divus Iulius  ch. LXXXI).

† As expressed in his Latin dirge on the death of the liver, which was published in 1653: Bartholinus T. Vasa lymphatica, nuper Hafniae in animalibus inventa et hepatis exsequiae. Paris.

‡ These essays were not published in book form until 1934, a decade after Sullivan’s death.

§ During the English Civil War, Faithorne was imprisoned as a monarchist and briefly exiled to France.

‖ All five human viral hepatitides have already been reviewed in this series by Drs. Shouval, Gish, Alter, Rizzetto, and Seth and Sherman, respectively.s

¶ The history of these entities and many others have already been published in this series (see essays by Albert Czaja on Autoimmune Hepatitis [Clin Liver Dis (Hoboken) 2020;15(suppl 1):S72‐S81] and Paul Adams on Hemochromatosis [Clin Liver Dis (Hoboken) 2020;16(suppl 1):83‐90]; others are scheduled to be covered in due course.

# In his 1756 Essay on Customs ( Essai sur les mœurs et l'esprit des nations ; Fig. ​ Fig.12), 12 ), Voltaire (the nom de plume of François‐Marie Arouet, 1694‐1778; Fig. ​ Fig.12) 12 ) joked sarcastically of the Holy Roman Empire, that “It was… ni saint, ni romain, ni empire ” (neither Holy, nor Roman, nor an Empire). 75

** All too often, the score or class is known as Child‐Pugh, once again denying Turcotte his eponymous due.

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AST and ALT Liver Enzymes Tests

When They're Needed and What the Results Mean

  • Indications for Testing
  • Purpose of Testing
  • Interpreting Results
  • What Can Affect Results

Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are two enzymes measured in a blood test to check the health of your liver . High AST and ALT levels are a general sign of a liver problem.

Based on which enzyme is elevated—or if both are elevated—healthcare providers can make an educated guess as to the underly cause of the liver problem and order additional tests. This may help diagnose diseases ranging from hepatitis and cirrhosis to liver cancer and liver failure.

This article explains what ALT and AST liver enzymes are, why they are tested, and what the results of the blood tests mean.

Verywell / Elise Degarmo

When ALT and AST Testing Is Used

ALT and AST are enzymes produced by the liver. These enzymes are used by the body to facilitate metabolism (the conversion of food into energy).

When the liver is damaged, ALT and AST can leak into the bloodsteram. High levels of ALT and AST in the blood are reliable markers for liver disease.

ALT and AST are part of a comprehensive panel of tests known as a liver function test (LFT) . An LFT may be ordered:

  • If you have symptoms of liver disease , including jaundice (yellowing of the skin or eyes), dark urine, pale stools, nausea, vomiting, and fatigue
  • To monitor the progression of a liver disease
  • To determine when drug treatments should be started
  • To check your response to treatment

Why ALT and AST Are Important

High ALT and AST are strong indications of liver disease, but what they tell us individually and together can be very different. This is because ALT is produced mainly in the liver, while AST is produced in the liver, brain, pancreas , heart, kidneys , lungs, and muscles.

As such, a high ALT is a pretty clear indication of liver disease. On the other hand, a high AST may be a sign of liver disease or conditions affecting the brain, pancreas, heart, kidneys, lungs, or muscles.

This shouldn't suggest that the AST is any less important in diagnosing liver disease. This is because other organs are commonly affected by liver disease, and a high ALT accompanied by a high AST can tell us how advanced the liver disease is.

Results of ALT and AST Testing

ALT and AST are measured in international units per liter (U/L). The normal range of values (meaning the values between which levels are normal) are:

  • ALT: Between 4 and 36 U/L
  • AST: Between 8 and 33 U/L

The high end of the reference range is referred to as the upper limit of normal (ULN)

High ALT and AST levels may indicate a problem with your liver, but it doesn't necessarily mean that you have a condition requiring treatment. This is because there is a wide gap between the ULN and what is considered to be dangerously high levels.

Mild elevations are generally two to three times that of the ULN. With some liver diseases, the level can be more than 50 times that of the ULN. Levels this high are considered deranged (dangerous).

Very elevated ALT and AST levels can indicate:

  • Fatty liver disease (liver injury caused by the buildup of fat in the liver)
  • Alcoholic liver disease (fatty liver disease caused by alcohol)
  • Viral hepatitis (liver inflammation caused by a virus)
  • Cirrhosis (loss of liver function due to severe liver scarring)
  • Hepatoxicity (liver injury caused by medications or toxins)
  • Liver cancer (most commonly a type called hepatocellular carcinoma )
  • Liver failure (the inability of the liver to service the body's needs)

It may also be due to any number of other medical conditions, such as infectious mononucleosis, heart problems, or pancreatitis


While it may seem that a high ALT is all that is needed to diagnose liver disease, its relationship to AST can tell whether the condition is acute (sudden and severe) or chronic (persistent).

For instance, if the liver experiences an acute injury, you can expect a sudden spike in the ALT and a relatively normal (or only mildly elevated) AST.

On the other hand, if liver disease is chronic, the damage will gradually affect other organs. As these organs are damaged, the AST will begin to rise.

The relationship is described with the AST/ALT ratio (also known as the De Ritis ratio).

The AST/ALT ratio is important because the pattern can tell much about the underlying condition. By way of example:

  • An AST/ALT ratio of less than 1 (where the ALT is higher than the AST) is a general indication of fatty liver disease.
  • An AST/ALT ratio equal to 1 (where the ALT is equal to the AST) may indicate acute viral hepatitis or hepatotoxicity.
  • An AST/ALT ratio higher than 1 (where the AST is higher than ALT) indicates cirrhosis.
  • An AST/ALT ratio higher than 2:1 (where the AST is more than twice as high as the ALT) is a common sign of alcoholic liver disease.

What Can Affect AST/ALT Results?

High or low ALT or AST results do not always indicate a health problem. Certain factors can cause a temporary increase or decrease in levels, such as:

  • Recent heavy alcohol use
  • Extreme physical activity
  • Recent cocaine use (which is hepatotoxic)
  • Recent fasting or extreme weight loss

Obesity, sex, and age can also influence ALT or AST levels, meaning that what is considered "normal" overall may need to be adjusted if you are overweight or underweight, male or female, or older or younger. Labs will generally take these factors into account.

ALT and AST are liver enzymes produced by the liver. If you have high levels of ALT and AST in your blood, it could be a sign of liver disease. The ratio of ALT to AST can help diagnose the underlying cause.

MedlinePlus. Liver function tests .

MedlinePlus. Alanine transaminase (ALT) blood test .

MedlinePlus. Aspartate aminotransferase (AST) blood test.

MedlinePlus. ALT blood test .

MedlinePlus. AST test .

Oh RC, Hustead TR, Ali SM, Pantsari MW. Mildly elevated liver transaminase levels: causes and evaluation . Am Fam Physician . 2017;96(11):709–15.

Newsome P, Cramb R, Davison S, et al.  Guidelines on the management of abnormal liver blood tests .  Gut.  2018;67:6-19. doi:10.1136/gutjnl-2017-314924

Stanford Health Care. Liver function tests .

By Charles Daniel  Charles Daniel, MPH, CHES is an infectious disease epidemiologist, specializing in hepatitis.

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This is an updated version of the article that appeared in print.

Am Fam Physician. 2020;102(9):603-612

Related letter: NAFLD in Children and Adolescents

Related letter: Updated Statistics for Liver Biopsy Risk

Patient information: See related handout on nonalcoholic fatty liver disease , written by the authors of this article.

Author disclosure: No relevant financial affiliations.

Nonalcoholic fatty liver disease (NAFLD) is the most common form of liver disease in the United States, affecting up to 30% of adults. There are two forms of NAFLD: nonalcoholic fatty liver (NAFL), defined as 5% or greater hepatic steatosis without hepatocellular injury or fibrosis, and nonalcoholic steatohepatitis (NASH), defined as 5% or greater hepatic steatosis plus hepatocellular injury and inflammation, with or without fibrosis. Individuals with obesity are at highest risk of NAFLD. Other established risk factors include metabolic syndrome and type 2 diabetes mellitus. Although NAFLD is common and typically asymptomatic, screening is not currently recommended, even in high-risk patients. NAFLD should be suspected in patients with elevated liver enzymes or hepatic steatosis on abdominal imaging that are found incidentally. Once other causes, such as excessive alcohol use and hepatotoxic medications, are excluded in these patients, risk scores or elastography tests can be used to identify those who are likely to have fibrosis that will progress to cirrhosis. Liver biopsy should be considered for patients at increased risk of fibrosis and when other liver disorders cannot be excluded with noninvasive tests. Weight loss through diet and exercise is the primary treatment for NAFLD. Other treatments, such as bariatric surgery, vitamin E supplements, and pharmacologic therapy with thiazolidinediones or glucagon-like peptide-1 analogues, have shown potential benefit; however, data are limited, and these therapies are not considered routine treatments. NAFL typically follows an indolent course, whereas patients with NASH are at higher risk of death from cardiovascular disease, cancer, and end-stage liver disease.

Nonalcoholic fatty liver disease (NAFLD) comprises a continuum of fatty liver disease that occurs in the absence of alcohol use or other secondary causes of hepatic steatosis. There are two manifestations of NAFLD ( Figure 1 ) . 1 One is nonalcoholic fatty liver (NAFL), which is defined as 5% or greater hepatic steatosis without evidence of hepatocellular injury or fibrosis. The other is nonalcoholic steatohepatitis (NASH), which is defined as 5% or greater hepatic steatosis with hepatocellular injury and inflammation, with or without fibrosis. 1


It is projected that 100 million people in the United States will have nonalcoholic fatty liver disease by 2030, with direct medical costs of about $103 billion annually.

By 2030, nonalcoholic steatohepatitis is predicted to become the leading indication for liver transplantation in U.S. adults, surpassing hepatitis C.

Consensus guidelines; lack of evidence surrounding diagnosis, treatment, and benefit of screening
, Consensus guidelines
, Limited-quality disease-oriented evidence
, , , Moderate-quality disease-oriented evidence
Consensus guideline and usual practice
Consensus guidelines
, , , , , Low- to high-quality disease-oriented evidence from randomized controlled trials and expert opinion
, Consensus guidelines and usual practice

liver function test essay

Differentiating NAFL from NASH is important because they have different prognoses. NAFL follows a more indolent course, whereas patients with NASH are at risk of progression from fibrosis to cirrhosis and development of hepatocellular carcinoma.

NAFLD is the most common form of liver disease in the United States and other developed countries, with rates in the adult population estimated to be between 10% and 30%. 2 About one-third of people with NAFLD have NASH. 3 The prevalence of NAFLD increases with age, and it is more common in males and those of Hispanic descent. 4

It is projected that 100 million people in the United States will have NAFLD by 2030, with direct medical costs of about $103 billion annually. 5 , 6 Having tripled since 2004, NASH is predicted to become the leading indication for liver transplantation in U.S. adults by 2030, surpassing hepatitis C. 7

Who Is at Risk of NAFLD?

People with obesity are at the highest risk of NAFLD. Metabolic syndrome and type 2 diabetes mellitus are other established risk factors. Emerging evidence shows that other conditions, such as genetic factors, sleep apnea, and hypothyroidism, are contributors ( Table 1 ). 2 , 8 – 13

Obesity (highest risk)
Metabolic syndrome ( )
Type 2 diabetes mellitus
Genetic variation of the gene
Obstructive sleep apnea
Polycystic ovary syndrome


Although not all individuals with NAFLD are overweight, 14 the prevalence of NAFLD is directly proportional to body weight, with 37% to 93% of those undergoing bariatric surgery having NAFLD and 26% to 44% having NASH. 8 However, any of the components of metabolic syndrome ( Table 2 15 ) increase the risk of NAFLD. 2 , 15

Blood pressure
≥ 130 mm Hg systolic or ≥ 85 mm Hg diastolic, or antihypertensive pharmacotherapy needed in a patient with a history of hypertension
Fasting glucose level
≥ 100 mg per dL (5.55 mmol per L) or pharmacotherapy needed for elevated glucose level
HDL cholesterol level
< 50 mg per dL (1.29 mmol per L) in women or < 40 mg per dL (1.04 mmol per L) in men, or pharmacotherapy needed for reduced HDL cholesterol level
Triglyceride level
≥ 150 mg per dL (1.69 mmol per L) or pharmacotherapy needed for elevated triglyceride level
Waist circumference
≥ 35 in (89 cm) in women or ≥ 40 in (102 cm) in men

For example, some studies suggest that 33% to 66% of patients with type 2 diabetes develop NAFLD, often accompanied by advanced fibrosis. Likewise, those with NAFLD are at higher risk of developing type 2 diabetes. This bidirectional relationship makes the data on prevalence difficult to interpret because each can occur concurrently. 9 , 10 In patients with NAFLD, having type 2 diabetes is a risk factor for progression to NASH, cirrhosis, and death, and poor glycemic control is also associated with poorer outcomes. 2

Dyslipidemia is another metabolic risk factor for NAFLD. A study of 44,000 patients with dyslipidemia found the prevalence of NAFLD was 54% in this population, and this increased to 78% among those with the highest triglyceride to high-density–lipoprotein cholesterol ratios. 11

Genetic factors are also involved in the risk of NAFLD. A study of 339 adults found that those with NAFLD who had the high-risk allele of the patatin-like phospholipase domain-containing protein 3 ( PNPLA3 ) gene had a twofold greater risk of advanced fibrosis ( P = .006). 12 The PNPLA3 gene is responsible for making a protein found in adipocytes and hepatocytes.

A 2019 review showed that obstructive sleep apnea is associated with more severe forms of NAFLD, and treating the apnea may improve associated liver injury. 13 Higher rates of NAFLD are also observed in patients with polycystic ovary syndrome or hypothyroidism. Low thyroid function may worsen the progression of liver damage, whereas thyroid replacement therapy may improve liver function. 13

Does Routine Screening of Asymptomatic Adults at Risk of NAFLD Improve Health?

Routine screening for NAFLD is not recommended, even in high-risk adults, because of uncertainties surrounding diagnostic tests and treatment options, and the lack of knowledge related to the long-term benefits and cost-effectiveness of screening. However, physicians should be alert for incidental findings suggestive of NAFLD in high-risk patients and initiate prompt evaluation when such findings are noted .

Routine screening is not recommended in the United States, even in high-risk patients, because liver enzyme levels are often normal in patients with NAFLD. Additionally, screening tools such as liver ultrasonography are not reliable at the low hepatic steatosis levels (less than 20%) often seen in early NAFLD. 1

A 2015 cost-effectiveness analysis compared no screening with one-time ultrasound screening in a hypothetical cohort of 50-year-olds with type 2 diabetes. Participants with NASH received pioglitazone (Actos; 30 mg daily) to prevent cirrhosis. Those who were screened had a 1.32% decrease (10.22% to 8.90%) in cirrhosis and a 0.61% decrease (5.12% to 4.51%) in liver-related deaths compared with those who were not screened. However, in addition to the small reductions in cirrhosis and death, there was also a small reduction in quality-adjusted life-years because of weight gain, the most common adverse effect of pioglitazone therapy. 16

What Is the Characteristic Presentation of NAFLD?

Except in late-stage disease when patients may have manifestations of overt hepatic insufficiency, there are no typical or characteristic symptoms of NAFLD. Rather, patients are often asymptomatic, and elevated liver enzymes or evidence of hepatic steatosis is incidentally found on testing performed for unrelated reasons. Occasionally, patients with NAFLD report fatigue, abdominal right upper quadrant fullness or pain, or pruritus. 6

Abnormal findings on liver function tests can be clues to the presence of NAFLD. Normal alanine transaminase (ALT) and aspartate transaminase (AST) levels are typically defined as 0 to 35 U per L (0 to 0.58 μkat per L). 17 Hepatic steatosis caused by excessive alcohol use is often associated with an AST:ALT ratio greater than 1.5, whereas patients with NAFLD tend to have a ratio less than 0.8, especially early in the disease. However, as NAFLD progresses to NASH with fibrosis, the AST:ALT ratio increases. 18

What Is Included in the Initial Evaluation of a Patient with Suspected NAFLD?

The first step is to obtain a detailed history to exclude other causes of hepatic steatosis such as alcohol use or exposure to hepatotoxic medications. If these are excluded, the next step is to test for hepatitis B surface antigen and hepatitis C virus antibody and measure ferritin, iron, lipid, and fasting glucose or A1C levels. Abdominal ultrasonography is the first-line imaging test for patients with suspected NAFLD and should be ordered if not already performed. If the test or ultrasound results point to alternative or coexisting causes of liver disease, additional testing should be performed .

Excessive alcohol use is defined as more than 21 standard drinks per week (or more than 30 g per day) for men and more than 14 standard drinks per week (or more than 20 g per day) for women. 1 , 19 Drugs known to cause hepatic steatosis are shown in Table 3 . 20

Chemotherapy drugs (fluorouracil, tamoxifen, irinotecan [Camptosar], cisplatin, asparaginase [Erwinaze])
Nonsteroidal anti-inflammatory drugs
Valproic acid

The National Institute for Health and Care Excellence (NICE) recommends assessing patients with suspected NAFLD for metabolic risk factors and obtaining lipid and fasting glucose or A1C levels. 21 Testing for hepatitis B surface antigen and hepatitis C virus antibody and measurement of ferritin and iron are also recommended because chronic viral hepatitis and hereditary hemochromatosis are common causes of chronic liver disease that are found incidentally. 1 Testing should be considered for less common alternative or coexisting causes of chronic liver disease ( Table 4 22 ) as indicated based on clinical findings. 1 , 23

Alpha -antitrypsin deficiencyHepatomegaly and elevated liver enzyme levelsAlpha -antitrypsin level, phenotyping, and liver biopsy
Autoimmune hepatitisMore common in women and in people with a history of thyroid diseaseAntinuclear antibody, smooth muscle antibody, and liver/kidney microsomal antibody testing
Hereditary hemochromatosisBronze diabetes, arthritis, congestive heart failure, impotence, and family historyComplete blood count, ferritin level, transferrin saturations, genetic testing ( gene), liver biopsy with staining for iron, and magnetic resonance imaging
Wilson diseaseNeurologic and psychological presentation in addition to liver disease at a young age (younger than 40 years) and family history24-hour urinary copper measurement, ceruloplasmin level, liver biopsy, and genetic testing

A 2011 meta-analysis concluded that ultrasonography is the imaging test of choice in the evaluation of patients with suspected NAFLD because of its low cost, safety, and accessibility, although sensitivity and specificity of ultrasonography, computed tomography, and magnetic resonance imaging are similar. 24 A 2017 retrospective study of 352 patients with chronic liver disease found that combining standard ultrasound with various scoring systems (Hamaguchi score, ultrasound fatty liver index, or hepatorenal steatosis index) increases sensitivity and specificity for detection of hepatic steatosis. 25 , 26 It should be noted that when ultrasonography is performed, sensitivity and specificity are higher at greater levels of fat infiltration.

What Noninvasive Testing Is Available to Determine Which Patients with NAFLD Are at High Risk of Fibrosis?

Clinical decision aids, such as the NAFLD Fibrosis Score ( http://gihep.com/calculators/hepatology/nafld-fibrosis-score ) and the Fibrosis-4 Score ( http://gihep.com/calculators/hepatology/fibrosis-4-score ), and liver stiffness measurements using vibration-controlled elastography (Fibroscan) or magnetic resonance elastography are clinically useful noninvasive tools for identifying patients with NAFLD that has a higher likelihood of progressing to fibrosis or cirrhosis . Table 5   summarizes these noninvasive tests. 27 – 30 Figure 2   is an algorithm for the evaluation of patients with suspected NAFLD. 1 , 22 , 31 , 32

AST:ALT ratioAST, ALT≥ 1.0 (sensitivity = 82%; PPV = 48%)< 1.0 (specificity = 72%; NPV = 93%)Best at excluding advanced fibrosis (as opposed to mild disease) because of lower specificity (44%) in patients with normal ALT levels
Fibrosis-4 Score Age, platelets, AST, ALT> 3.25 (specificity = 98%; PPV = 80% to 85%)< 1.45 (sensitivity = 82%; NPV = 92% to 95%)Specificity is high in those with normal or abnormal ALT levels (77% and 72%, respectively)
NAFLD Fibrosis Score Age, blood glucose, body mass index, platelets, albumin, AST: ALT ratio> 0.676 (specificity = 97% to 98%; PPV = 82% to 88%)< −1.455 (sensitivity = 82% to 90%; NPV = 88% to 92%)Better at excluding advanced fibrosis because of lower specificity (57%) in patients with normal ALT levels
Magnetic resonance elastographyProbe placed on the patient's back emits low-frequency vibrations that can be measured to quantify fibrosis> 3.62 kPa (specificity = 83.2%; PPV = 61.8%)≤ 3.62 kPa (sensitivity = 82.5%; NPV = 93.5%)Higher sensitivity at less fibrosis severity
Vibration-controlled elastography (Fibroscan)Uses mild amplitude and low-frequency elastic shear T waves propagating through the liver, which is directly related to tissue stiffness> 9.9 kPa (specificity = 77%; PPV = 46.5%)≤ 9.9 kPa (sensitivity = 95%; NPV = 98.7%)Unreliable results in patients with body mass index > 36.65 kg per m if using the M probe

liver function test essay

Liver biopsy is the diagnostic standard for fibrosis in NAFLD. Although the mortality associated with liver biopsy is low, ranging from 0.01% to 0.3%, the invasiveness of the procedure and potential for serious complications such as major bleeding (0.1% to 4.6%) leads most clinicians to utilize noninvasive tests for initial evaluation. 58 , 59 , 60 [updated]

Treatment guidelines consistently recommend that adults with NAFLD undergo risk stratification using the NAFLD Fibrosis Score or the Fibrosis-4 Score. 1 , 18 , 19 , 30 , 35 A 2016 study demonstrated that these scores are better than other indices and as good as magnetic resonance elastography for predicting advanced fibrosis. 27

If more advanced noninvasive testing is used, a 2019 systematic review and pooled analysis of 230 patients found that magnetic resonance elastography has a significantly higher diagnostic accuracy than vibration-controlled elastography, especially when identifying early (stage 1 or 2) fibrosis. 28 Other studies have shown that the tests are comparable in identifying stage 3 disease (advanced fibrosis) or stage 4 disease (cirrhosis). 29 , 30 , 36

When Should Liver Biopsy Be Considered in Patients with NAFLD?

Liver biopsy should be considered for patients with NAFLD who are at increased risk of NASH or advanced fibrosis based on noninvasive test results. It should also be considered if other possible causes of chronic liver disease ( Table 4 22 ) cannot be excluded with noninvasive tests .

The American Association for the Study of Liver Diseases (AASLD) recommends biopsy when the etiology of liver disease is unclear and in those who are at increased risk of NASH or advanced fibrosis. 1 For instance, liver biopsy should be considered in a patient with persistently elevated serum ferritin and transferrin levels, which may suggest hereditary hemochromatosis, especially if genetic testing is positive. Likewise, biopsy should be considered when high serum titers of autoantibodies are present in association with other features of autoimmune liver disease. 1 A liver biopsy can also distinguish between NAFL and NASH ( Figure 1 ) . 1

How Is NAFLD Treated?

Weight loss through diet and exercise is the primary treatment for NAFLD. Bariatric surgery, vitamin supplements, thiazolidinediones (pioglitazone), and glucagon-like peptide-1 analogues (liraglutide [Victoza]) may be beneficial for some patients, but there is insufficient evidence to support their use as first-line or primary treatments . Table 6   summarizes the treatment options for NAFLD. 1 , 22

Weight loss via diet and exerciseImprovedImprovedRCTsStandard primary treatment for NAFLD
Bariatric surgeryImprovedImprovedRetrospective and prospective cohort studiesConsider foregut bariatric surgery in patients with NAFLD only when indicated based on obesity
GLP-1 analogue (liraglutide [Victoza])ImprovedImprovedRCTPremature to recommend as routine therapy
Thiazolidinediones (pioglitazone [Actos])ImprovedInconsistentRCTLimit use to patients with biopsy-proven NASH; may cause weight gain
Vitamin EImprovedImprovedRCTConsider in patients without diabetes mellitus who have biopsy-proven NASH; discuss the risks and benefits with patients

A meta-analysis of eight randomized controlled trials (RCTs) and a prospective trial demonstrated that a loss of 3% to 5% of total body weight is needed to improve hepatic steatosis, and a loss of 7% to 10% of total body weight is needed to improve the histopathologic abnormalities in the liver associated with NAFLD. 1 A 2017 review of the association between the Mediterranean diet and NAFLD found that the Mediterranean diet consistently reduced liver fat independent of weight loss. 37 The European Associations for the Study of the Liver, Diabetes, and Obesity recommend the Mediterranean diet for patients with NAFLD. 38

Bariatric Surgery . Several prospective studies of disease-oriented outcomes found resolution of NASH after bariatric surgery. One of these studies reported that NASH resolved in 85% (95% CI, 75.8% to 92.2%) of the 109 participants within one year of bariatric surgery. 39 Although bariatric surgery can be recommended for patients with NAFLD when indicated based on obesity, it is premature to consider bariatric surgery as an option to specifically treat NAFLD. 1

Vitamin E . Because of its antioxidant potential, vitamin E has also been evaluated as a potential treatment for NAFLD. A large clinical trial showed that nearly all patients receiving 800 IU of vitamin E daily had histologic improvements of NASH (96% vs. 19% with placebo; P < .001). 6 However, some studies have shown an association between vitamin E and an increased risk of prostate cancer and hemorrhagic stroke; one study demonstrated a reduction in thrombotic stroke. 40 – 43 The AASLD recommends use of vitamin E in patients without diabetes who have biopsy-proven NASH only after discussing the risks and benefits with the patient. 1

Omega-3 Fatty Acids . Because studies of omega-3 fatty acids have not demonstrated a therapeutic benefit, the AASLD and NICE recommend against using omega-3 fatty acids in the treatment of NAFLD. 1 , 21 A 2017 Cochrane review found insufficient evidence to recommend vitamin D as a treatment for liver disease; however, only four of the 16 trials specifically evaluated its use in NAFLD. 44

Prescription Medications . Although no prescription medications have been approved by the U.S. Food and Drug Administration to treat NAFLD, interventions should be aimed at treating the patient's comorbid metabolic conditions. For example, although statins do not treat NAFLD directly, they should be used to treat dyslipidemia in patients with NAFLD because these patients have an inherently higher risk of cardiovascular disease. The AASLD recommends use of a statin for dyslipidemia in these patients, noting that there is no increased risk of serious liver injury in those with NAFLD. 1 NICE also recommends that statin medications be continued in patients with NAFLD and discontinued only if liver enzymes double within three months of initiation. 21

In two RCTs, metformin did not lead to improvement in liver histology in patients with NAFLD. Thus, metformin should not be prescribed to patients with NAFLD in the absence of type 2 diabetes. 1

The thiazolidinedione pioglitazone and the glucagon-like peptide-1 analogue liraglutide have shown some promise, although data are limited. In a trial involving 101 patients with prediabetes, 51% of patients taking pioglitazone had resolution of biopsy-proven NASH compared with 19% taking placebo ( P < .001). 45 In another trial, resolution of NASH was also achieved in more patients taking pioglitazone than those taking placebo (n = 247; 47% vs. 21%; P < .001). 46 A more recent systematic review found a similar benefit. 47 However, pioglitazone use increases the risk of weight gain and should not be used to treat NAFLD in patients without biopsy-proven NASH until further data are available. 1

In a small RCT (n = 52), liraglutide demonstrated greater resolution of NASH compared with placebo (39% vs. 9%; P = .019). 48 Several other studies have also found improvement in the histologic features of NAFLD with liraglutide therapy. 47 Nonetheless, it is premature to recommend glucagon-like peptide-1 analogues such as liraglutide as routine treatment for NAFLD or NASH. 1

What Monitoring Is Recommended for NAFLD?

Although there is no consensus on monitoring, it is reasonable for primary care clinicians to initiate intensive lifestyle changes and repeat liver enzyme measurements and ultrasonography in six to 12 months. If abnormalities persist and the patient is at low risk of fibrosis, the patient should be monitored every 12 to 24 months with a complete blood count; measurement of liver enzyme, lipid, and fasting glucose or A1C levels; and calculation of fibrosis risk scores (NAFLD Fibrosis Score or Fibrosis-4 Score). High-risk patients should be referred to a specialist .

Based on expert consensus, guidelines recommend an annual reassessment for low-risk patients with abnormal liver enzyme levels and every two years for those with normal liver enzyme levels but hepatic steatosis noted on imaging. 49 – 51

What Is the Prognosis for Those with NAFLD?

Most patients with NAFL will have a benign, nonprogressive disease course. Only 20% develop NASH, and 20% of those with NASH develop cirrhosis. Patients with a higher degree of fibrosis have a higher risk of death, mainly from cardiovascular disease, cancer, and end-stage liver disease .

Two cohort studies found that 80% of patients with NAFLD had no progression to NASH. Of those who developed cirrhosis, 31% progressed to hepatic decompensation. About 2% of patients with NAFLD developed hepatocellular carcinoma. 52

A community-based study of 420 patients with NAFLD found that these patients had a 34% higher risk of death (standard mortality ratio = 1.34; 95% CI, 1.003 to 1.76; P = .03) than would be expected in the general population; the three main causes of death were cancer, ischemic heart disease, and liver disease. 53 A study of 817 patients with NAFLD echoed these results (hazard ratio = 1.038; 95% CI, 1.036 to 1.041; P < .0001), with liver disease as the third leading cause of death after cardiovascular disease and malignancy. 54 A meta-analysis also showed higher overall mortality in patients with NAFLD (odds ratio = 1.57; 95% CI, 1.18 to 2.10; P = .002). 55 Further studies that stratified patients' risk using fibrosis scoring tools found higher disease-specific mortality in those with NASH, indicating that fibrosis is the most important predictor of long-term outcomes. 56

When Should Patients with NAFLD Be Referred to a Specialist?

Referral to gastroenterology should be considered in patients who have a high likelihood of NASH fibrosis because of the presence of metabolic syndrome or type 2 diabetes, who have progression to fibrosis as indicated by an AST:ALT ratio greater than 1.0, who have an NAFLD Fibrosis Score or Fibrosis-4 Score showing high risk, who have abnormal results on noninvasive testing (magnetic resonance elastography or vibration-controlled elastography), or who have imaging or clinical evidence of cirrhosis .

An AST:ALT ratio greater than 1.0 is concerning for other causes of liver disease or advanced fibrosis in patients with NAFLD. One study determined that this cutoff ratio provided the best negative predictive value for advanced fibrosis. 57 Based on expert opinion, referral should be considered for adults with fibrosis and cirrhosis because they may benefit from aggressive monitoring for esophageal varices, signs of decompensation of hepatic function (international normalized ratio, bilirubin level, and albumin level), and hepatocellular carcinoma or referral for liver transplantation. 6 , 21

This article updates previous articles on this topic by Wilkins, et al. 22 ; and Bayard, et al. 14

Data Sources: A targeted PubMed search was completed in Clinical Queries using the key terms nonalcoholic fatty liver disease, fatty liver disease, fatty liver, and NASH. The search included meta-analyses, randomized controlled trials, clinical trials, and reviews. Also searched were POEMs, Cochrane reviews, clinical decision rules, the Agency for Healthcare Research and Quality Effective Healthcare reports, Guidelines.org, and Essential Evidence Plus. Search dates: May 2019 through April 2020.

The authors thank Angela Buffington, PhD, ABPP-CN, LP, University of Minnesota Department of Family Medicine and Community Health, for assistance with proofreading and editing the manuscript.

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Musso G, Gambino R, Cassader M, et al. Meta-analysis: natural history of non-alcoholic fatty liver disease (NAFLD) and diagnostic accuracy of non-invasive tests for liver disease severity. Ann Med. 2011;43(8):617-649.

Goh GB, McCullough AJ. Natural history of nonalcoholic fatty liver disease. Dig Dis Sci. 2016;61(5):1226-1233.

McPherson S, Stewart SF, Henderson E, et al. Simple non-invasive fibrosis scoring systems can reliably exclude advanced fibrosis in patients with non-alcoholic fatty liver disease. Gut. 2010;59(9):1265-1269.

West J, Card TR. Reduced mortality rates following elective percutaneous liver biopsies. Gastroenterology. 2010;139(4):1230-1237. [Added as part of update]

Midia M, Odedra D, Shuster A, et al. Predictors of bleeding complications following percutaneous image-guided liver biopsy: a scoping review. Diagn Interv Radiol. 2019;25(1):71-80. [Added as part of update]

Boyum JH, Atwell TD, Schmit GD, et al. Incidence and risk factors for adverse events related to image-guided liver biopsy. Mayo Clin Proc. 2016;91(3):329-335. [Added as part of update]

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Medical terms in lay language.

Please use these descriptions in place of medical jargon in consent documents, recruitment materials and other study documents. Note: These terms are not the only acceptable plain language alternatives for these vocabulary words.

This glossary of terms is derived from a list copyrighted by the University of Kentucky, Office of Research Integrity (1990).

For clinical research-specific definitions, see also the Clinical Research Glossary developed by the Multi-Regional Clinical Trials (MRCT) Center of Brigham and Women’s Hospital and Harvard  and the Clinical Data Interchange Standards Consortium (CDISC) .

Alternative Lay Language for Medical Terms for use in Informed Consent Documents

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ABDOMEN/ABDOMINAL body cavity below diaphragm that contains stomach, intestines, liver and other organs ABSORB take up fluids, take in ACIDOSIS condition when blood contains more acid than normal ACUITY clearness, keenness, esp. of vision and airways ACUTE new, recent, sudden, urgent ADENOPATHY swollen lymph nodes (glands) ADJUVANT helpful, assisting, aiding, supportive ADJUVANT TREATMENT added treatment (usually to a standard treatment) ANTIBIOTIC drug that kills bacteria and other germs ANTIMICROBIAL drug that kills bacteria and other germs ANTIRETROVIRAL drug that works against the growth of certain viruses ADVERSE EFFECT side effect, bad reaction, unwanted response ALLERGIC REACTION rash, hives, swelling, trouble breathing AMBULATE/AMBULATION/AMBULATORY walk, able to walk ANAPHYLAXIS serious, potentially life-threatening allergic reaction ANEMIA decreased red blood cells; low red cell blood count ANESTHETIC a drug or agent used to decrease the feeling of pain, or eliminate the feeling of pain by putting you to sleep ANGINA pain resulting from not enough blood flowing to the heart ANGINA PECTORIS pain resulting from not enough blood flowing to the heart ANOREXIA disorder in which person will not eat; lack of appetite ANTECUBITAL related to the inner side of the forearm ANTIBODY protein made in the body in response to foreign substance ANTICONVULSANT drug used to prevent seizures ANTILIPEMIC a drug that lowers fat levels in the blood ANTITUSSIVE a drug used to relieve coughing ARRHYTHMIA abnormal heartbeat; any change from the normal heartbeat ASPIRATION fluid entering the lungs, such as after vomiting ASSAY lab test ASSESS to learn about, measure, evaluate, look at ASTHMA lung disease associated with tightening of air passages, making breathing difficult ASYMPTOMATIC without symptoms AXILLA armpit

BENIGN not malignant, without serious consequences BID twice a day BINDING/BOUND carried by, to make stick together, transported BIOAVAILABILITY the extent to which a drug or other substance becomes available to the body BLOOD PROFILE series of blood tests BOLUS a large amount given all at once BONE MASS the amount of calcium and other minerals in a given amount of bone BRADYARRHYTHMIAS slow, irregular heartbeats BRADYCARDIA slow heartbeat BRONCHOSPASM breathing distress caused by narrowing of the airways

CARCINOGENIC cancer-causing CARCINOMA type of cancer CARDIAC related to the heart CARDIOVERSION return to normal heartbeat by electric shock CATHETER a tube for withdrawing or giving fluids CATHETER a tube placed near the spinal cord and used for anesthesia (indwelling epidural) during surgery CENTRAL NERVOUS SYSTEM (CNS) brain and spinal cord CEREBRAL TRAUMA damage to the brain CESSATION stopping CHD coronary heart disease CHEMOTHERAPY treatment of disease, usually cancer, by chemical agents CHRONIC continuing for a long time, ongoing CLINICAL pertaining to medical care CLINICAL TRIAL an experiment involving human subjects COMA unconscious state COMPLETE RESPONSE total disappearance of disease CONGENITAL present before birth CONJUNCTIVITIS redness and irritation of the thin membrane that covers the eye CONSOLIDATION PHASE treatment phase intended to make a remission permanent (follows induction phase) CONTROLLED TRIAL research study in which the experimental treatment or procedure is compared to a standard (control) treatment or procedure COOPERATIVE GROUP association of multiple institutions to perform clinical trials CORONARY related to the blood vessels that supply the heart, or to the heart itself CT SCAN (CAT) computerized series of x-rays (computerized tomography) CULTURE test for infection, or for organisms that could cause infection CUMULATIVE added together from the beginning CUTANEOUS relating to the skin CVA stroke (cerebrovascular accident)

DERMATOLOGIC pertaining to the skin DIASTOLIC lower number in a blood pressure reading DISTAL toward the end, away from the center of the body DIURETIC "water pill" or drug that causes increase in urination DOPPLER device using sound waves to diagnose or test DOUBLE BLIND study in which neither investigators nor subjects know what drug or treatment the subject is receiving DYSFUNCTION state of improper function DYSPLASIA abnormal cells

ECHOCARDIOGRAM sound wave test of the heart EDEMA excess fluid collecting in tissue EEG electric brain wave tracing (electroencephalogram) EFFICACY effectiveness ELECTROCARDIOGRAM electrical tracing of the heartbeat (ECG or EKG) ELECTROLYTE IMBALANCE an imbalance of minerals in the blood EMESIS vomiting EMPIRIC based on experience ENDOSCOPIC EXAMINATION viewing an  internal part of the body with a lighted tube  ENTERAL by way of the intestines EPIDURAL outside the spinal cord ERADICATE get rid of (such as disease) Page 2 of 7 EVALUATED, ASSESSED examined for a medical condition EXPEDITED REVIEW rapid review of a protocol by the IRB Chair without full committee approval, permitted with certain low-risk research studies EXTERNAL outside the body EXTRAVASATE to leak outside of a planned area, such as out of a blood vessel

FDA U.S. Food and Drug Administration, the branch of federal government that approves new drugs FIBROUS having many fibers, such as scar tissue FIBRILLATION irregular beat of the heart or other muscle

GENERAL ANESTHESIA pain prevention by giving drugs to cause loss of consciousness, as during surgery GESTATIONAL pertaining to pregnancy

HEMATOCRIT amount of red blood cells in the blood HEMATOMA a bruise, a black and blue mark HEMODYNAMIC MEASURING blood flow HEMOLYSIS breakdown in red blood cells HEPARIN LOCK needle placed in the arm with blood thinner to keep the blood from clotting HEPATOMA cancer or tumor of the liver HERITABLE DISEASE can be transmitted to one’s offspring, resulting in damage to future children HISTOPATHOLOGIC pertaining to the disease status of body tissues or cells HOLTER MONITOR a portable machine for recording heart beats HYPERCALCEMIA high blood calcium level HYPERKALEMIA high blood potassium level HYPERNATREMIA high blood sodium level HYPERTENSION high blood pressure HYPOCALCEMIA low blood calcium level HYPOKALEMIA low blood potassium level HYPONATREMIA low blood sodium level HYPOTENSION low blood pressure HYPOXEMIA a decrease of oxygen in the blood HYPOXIA a decrease of oxygen reaching body tissues HYSTERECTOMY surgical removal of the uterus, ovaries (female sex glands), or both uterus and ovaries

IATROGENIC caused by a physician or by treatment IDE investigational device exemption, the license to test an unapproved new medical device IDIOPATHIC of unknown cause IMMUNITY defense against, protection from IMMUNOGLOBIN a protein that makes antibodies IMMUNOSUPPRESSIVE drug which works against the body's immune (protective) response, often used in transplantation and diseases caused by immune system malfunction IMMUNOTHERAPY giving of drugs to help the body's immune (protective) system; usually used to destroy cancer cells IMPAIRED FUNCTION abnormal function IMPLANTED placed in the body IND investigational new drug, the license to test an unapproved new drug INDUCTION PHASE beginning phase or stage of a treatment INDURATION hardening INDWELLING remaining in a given location, such as a catheter INFARCT death of tissue due to lack of blood supply INFECTIOUS DISEASE transmitted from one person to the next INFLAMMATION swelling that is generally painful, red, and warm INFUSION slow injection of a substance into the body, usually into the blood by means of a catheter INGESTION eating; taking by mouth INTERFERON drug which acts against viruses; antiviral agent INTERMITTENT occurring (regularly or irregularly) between two time points; repeatedly stopping, then starting again INTERNAL within the body INTERIOR inside of the body INTRAMUSCULAR into the muscle; within the muscle INTRAPERITONEAL into the abdominal cavity INTRATHECAL into the spinal fluid INTRAVENOUS (IV) through the vein INTRAVESICAL in the bladder INTUBATE the placement of a tube into the airway INVASIVE PROCEDURE puncturing, opening, or cutting the skin INVESTIGATIONAL NEW DRUG (IND) a new drug that has not been approved by the FDA INVESTIGATIONAL METHOD a treatment method which has not been proven to be beneficial or has not been accepted as standard care ISCHEMIA decreased oxygen in a tissue (usually because of decreased blood flow)

LAPAROTOMY surgical procedure in which an incision is made in the abdominal wall to enable a doctor to look at the organs inside LESION wound or injury; a diseased patch of skin LETHARGY sleepiness, tiredness LEUKOPENIA low white blood cell count LIPID fat LIPID CONTENT fat content in the blood LIPID PROFILE (PANEL) fat and cholesterol levels in the blood LOCAL ANESTHESIA creation of insensitivity to pain in a small, local area of the body, usually by injection of numbing drugs LOCALIZED restricted to one area, limited to one area LUMEN the cavity of an organ or tube (e.g., blood vessel) LYMPHANGIOGRAPHY an x-ray of the lymph nodes or tissues after injecting dye into lymph vessels (e.g., in feet) LYMPHOCYTE a type of white blood cell important in immunity (protection) against infection LYMPHOMA a cancer of the lymph nodes (or tissues)

MALAISE a vague feeling of bodily discomfort, feeling badly MALFUNCTION condition in which something is not functioning properly MALIGNANCY cancer or other progressively enlarging and spreading tumor, usually fatal if not successfully treated MEDULLABLASTOMA a type of brain tumor MEGALOBLASTOSIS change in red blood cells METABOLIZE process of breaking down substances in the cells to obtain energy METASTASIS spread of cancer cells from one part of the body to another METRONIDAZOLE drug used to treat infections caused by parasites (invading organisms that take up living in the body) or other causes of anaerobic infection (not requiring oxygen to survive) MI myocardial infarction, heart attack MINIMAL slight MINIMIZE reduce as much as possible Page 4 of 7 MONITOR check on; keep track of; watch carefully MOBILITY ease of movement MORBIDITY undesired result or complication MORTALITY death MOTILITY the ability to move MRI magnetic resonance imaging, diagnostic pictures of the inside of the body, created using magnetic rather than x-ray energy MUCOSA, MUCOUS MEMBRANE moist lining of digestive, respiratory, reproductive, and urinary tracts MYALGIA muscle aches MYOCARDIAL pertaining to the heart muscle MYOCARDIAL INFARCTION heart attack

NASOGASTRIC TUBE placed in the nose, reaching to the stomach NCI the National Cancer Institute NECROSIS death of tissue NEOPLASIA/NEOPLASM tumor, may be benign or malignant NEUROBLASTOMA a cancer of nerve tissue NEUROLOGICAL pertaining to the nervous system NEUTROPENIA decrease in the main part of the white blood cells NIH the National Institutes of Health NONINVASIVE not breaking, cutting, or entering the skin NOSOCOMIAL acquired in the hospital

OCCLUSION closing; blockage; obstruction ONCOLOGY the study of tumors or cancer OPHTHALMIC pertaining to the eye OPTIMAL best, most favorable or desirable ORAL ADMINISTRATION by mouth ORTHOPEDIC pertaining to the bones OSTEOPETROSIS rare bone disorder characterized by dense bone OSTEOPOROSIS softening of the bones OVARIES female sex glands

PARENTERAL given by injection PATENCY condition of being open PATHOGENESIS development of a disease or unhealthy condition PERCUTANEOUS through the skin PERIPHERAL not central PER OS (PO) by mouth PHARMACOKINETICS the study of the way the body absorbs, distributes, and gets rid of a drug PHASE I first phase of study of a new drug in humans to determine action, safety, and proper dosing PHASE II second phase of study of a new drug in humans, intended to gather information about safety and effectiveness of the drug for certain uses PHASE III large-scale studies to confirm and expand information on safety and effectiveness of new drug for certain uses, and to study common side effects PHASE IV studies done after the drug is approved by the FDA, especially to compare it to standard care or to try it for new uses PHLEBITIS irritation or inflammation of the vein PLACEBO an inactive substance; a pill/liquid that contains no medicine PLACEBO EFFECT improvement seen with giving subjects a placebo, though it contains no active drug/treatment PLATELETS small particles in the blood that help with clotting POTENTIAL possible POTENTIATE increase or multiply the effect of a drug or toxin (poison) by giving another drug or toxin at the same time (sometimes an unintentional result) POTENTIATOR an agent that helps another agent work better PRENATAL before birth PROPHYLAXIS a drug given to prevent disease or infection PER OS (PO) by mouth PRN as needed PROGNOSIS outlook, probable outcomes PRONE lying on the stomach PROSPECTIVE STUDY following patients forward in time PROSTHESIS artificial part, most often limbs, such as arms or legs PROTOCOL plan of study PROXIMAL closer to the center of the body, away from the end PULMONARY pertaining to the lungs

QD every day; daily QID four times a day

RADIATION THERAPY x-ray or cobalt treatment RANDOM by chance (like the flip of a coin) RANDOMIZATION chance selection RBC red blood cell RECOMBINANT formation of new combinations of genes RECONSTITUTION putting back together the original parts or elements RECUR happen again REFRACTORY not responding to treatment REGENERATION re-growth of a structure or of lost tissue REGIMEN pattern of giving treatment RELAPSE the return of a disease REMISSION disappearance of evidence of cancer or other disease RENAL pertaining to the kidneys REPLICABLE possible to duplicate RESECT remove or cut out surgically RETROSPECTIVE STUDY looking back over past experience

SARCOMA a type of cancer SEDATIVE a drug to calm or make less anxious SEMINOMA a type of testicular cancer (found in the male sex glands) SEQUENTIALLY in a row, in order SOMNOLENCE sleepiness SPIROMETER an instrument to measure the amount of air taken into and exhaled from the lungs STAGING an evaluation of the extent of the disease STANDARD OF CARE a treatment plan that the majority of the medical community would accept as appropriate STENOSIS narrowing of a duct, tube, or one of the blood vessels in the heart STOMATITIS mouth sores, inflammation of the mouth STRATIFY arrange in groups for analysis of results (e.g., stratify by age, sex, etc.) STUPOR stunned state in which it is difficult to get a response or the attention of the subject SUBCLAVIAN under the collarbone SUBCUTANEOUS under the skin SUPINE lying on the back SUPPORTIVE CARE general medical care aimed at symptoms, not intended to improve or cure underlying disease SYMPTOMATIC having symptoms SYNDROME a condition characterized by a set of symptoms SYSTOLIC top number in blood pressure; pressure during active contraction of the heart

TERATOGENIC capable of causing malformations in a fetus (developing baby still inside the mother’s body) TESTES/TESTICLES male sex glands THROMBOSIS clotting THROMBUS blood clot TID three times a day TITRATION a method for deciding on the strength of a drug or solution; gradually increasing the dose T-LYMPHOCYTES type of white blood cells TOPICAL on the surface TOPICAL ANESTHETIC applied to a certain area of the skin and reducing pain only in the area to which applied TOXICITY side effects or undesirable effects of a drug or treatment TRANSDERMAL through the skin TRANSIENTLY temporarily TRAUMA injury; wound TREADMILL walking machine used to test heart function

UPTAKE absorbing and taking in of a substance by living tissue

VALVULOPLASTY plastic repair of a valve, especially a heart valve VARICES enlarged veins VASOSPASM narrowing of the blood vessels VECTOR a carrier that can transmit disease-causing microorganisms (germs and viruses) VENIPUNCTURE needle stick, blood draw, entering the skin with a needle VERTICAL TRANSMISSION spread of disease

WBC white blood cell

liver function test essay

Food & Function

Latilactobacillus sakei qc9 alleviates hyperglycaemia in a high-fat diet and streptozotocin-induced type 2 diabetes mellitus mice via the microbiota-gut-liver axis.

Probiotics have been considered a promising option for mitigating the progression of type 2 diabetes mellitus (T2DM). Here, Latilactobacillus sakei QC9 ( L. sakei QC9) with a hypoglycemic effect was screened out from 30 food-derived strains through α-glucosidase and α-amylase activity inhibition tests in vitro and a 4-week in vivo preliminary animal experiment. To further understand its alleviating effect on long-term hyperglycaemia occurring in T2DM, we conducted an experiment that lasted for 8 weeks. The results showed that taking L. sakei QC9 can regulate glucose and lipid metabolism while improving antioxidant capacity and alleviating chronic inflammation. In addition, our results demonstrated that L. sakei QC9 may mediate the microbiota-gut-liver axis by regulating the composition of intestinal flora (increasing the abundance of butyrate-producing bacteria) and increasing the content of short-chain fatty acids (especially butyrate), affecting the PI3K/Akt signalling pathway in the liver, thereby achieving the purpose of alleviating the development of T2DM. In summary, our work is the first to prove the long-term hypoglycemic effect of L. sakei in high-fat diet (HFD) and streptozotocin (STZ)-induced T2DM mice and supports the possibility of L. sakei QC9 being used as a new treatment for alleviating T2DM.

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liver function test essay

M. Chen, P. Pan, H. Zhang, R. Li, D. Ren and 斌. 姜, Food Funct. , 2024, Accepted Manuscript , DOI: 10.1039/D4FO02316A

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