Liver Function Tests ("LFT's")
LFT's are useful for detecting a broad range of abnormalities. As a general rule, they indicate one of three
broad categories of liver dysfunction:  Direct damage to hepatic tissue;  Problems with the synthetic capabilities of the liver;
and  Disorders of bile metabolism. By understanding these basic distinctions, you can interpret LFT's more accurately.
Damage to hepatic tissue
- ALT (Alanine Aminotransferase) - formerly SGPT is an enzyme that is found primarily in hepatic
cells. Increased ALT is fairly specific for liver damage.
- AST (Aspartate Aminotransaminase) - formerly SGOT is an enzyme found in the liver, but also in
cardiac and other muscle cells, in renal cells, and brain tissue, as well as in red blood cells. Increases in AST can therefore
indicate cardiac or other muscle damage, renal or brain injury, red blood cell damage, or hepatic injury.
AST > ALT is commonly seen in alcoholic liver disease.
ALT > AST is commonly seen in viral hepatitis or in toxin ingestion.
Any of the following can cause increases in transaminases (particularly AST): acetominophen (Tylenol), NSAIDs, ACE inhibitors,
Isoniazid, Sulfonamides, Erythromycin, Griseofulvin, Fluconazole, Nicotinic Acid.
- Other conditions:
Increased transaminases are also seen in both hypo- and hyper-thyroidism, and in NASH (Non-Alcoholic SteatoHepatitis), which is
associated with diabetes, obesity, and the use of TPN or Amiodarone.
- Alkaline Phosphatase is an enzyme that is used to detect hepatic damage or injury to the biliary tree.
However, there are 5 isoenzymes of Alk Phos:
To confirm that the fraction responsible for the increase is primarily hepatic, you should check GGT
(Gamma-GlutamylTransferase) - if increased, it confirms the origin as hepatic.
- Liver (this fraction is sythesized by bile duct epithelial cells)
- Bone (including during adolescent growth spurt)
A hepatic origin indicates cholestasis, which can have various causes:
Increased alk phos can also indicate hyperthyroidism, cardiac failure, lymphoma, and hypernephroma.
- Extrahepatic blockage, such as in gallstones or tumors
- Localized liver blockage, such as in hepatocellular carcinoma
- Patchy liver blockage, such as in granulomatous disease
- Diffuse liver blockage, such as in intrahepatic cholestasis
The only reliable results are from those patients who have been fasting, are not pregnant, and are not growing children.
Damage to the Synthetic Capabilities of the Liver
- INR (PT) - The International Normalized Ratio (INR) is the accepted way to describe the Prothrombin
Time (PT), a measure of clotting ability. Increases in INR (>1.2) can indicate Vitamin K deficiency (PT measures prothrombin, a.k.a.
Factor II, a Vitamin K-dependent clotting factor - II, VII, IX, X), or in hepatocellular disease. The gastroenterologists will tell
you that INR is the most sensitive assay for evaulating the liver's synthetic function.
- Albumin is made solely by the liver, but circulates for up to 3 weeks. It is also considered a
"negative acute phase reactant" - meaning that it goes down in acute disease. [Other negative acute phase
reactants include cholesterol, total protein, transferrin, iron, pre-albumin, and many others. Positive acute phase reactants
- lab values that go UP in acute disease - include ferritin, neutrophils, platelets, c-reactive protein, d-dimer, fibrinogen,
alpha-1 antitrypsin, alpha-2 macroglobulin, haptoglobin, and many others.]
A decreased albumin is consistent with long-standing (>3 weeks) liver disease.
- Cholesterol is also synthesized by the liver, so liver disease (such as cirrhosis, for example) will
lead to cholesterol. Often, cholesterol is used as a marker of returning liver synthesis after
Disorders in Bile Metabolism
A brief review: Red cells contain hemoglobin, and red cells are constantly leaking, lysing, &/or being recycled, so hemoglobin is
always running around. It breaks down into bilirubin, which binds to albumin - together, they are transported to the liver. Before
the liver processes them, the bilirubin is unconjugated. The liver is responsible for processing the unconjugated bilirubin
into the conjugated form, which is water-soluble. The conjugated form is excreted by the liver as bile into the gall
bladder, which empties through the biliary tree into the intestine. Conjugated bilirubin is acted upon by intestinal flora to form
urobilinogen (which colors urine yellow) and stercobilinogen (which colors stool brown).
Bile metabolism is one of the most sensitive markers of hepatic dysfunction.
- Unconjugated Bilirubin ("indirect") will increase under two conditions: either there is excessive heme
breakdown (causing increased hemoglobin to be released), or there is a primary liver disease, which makes the liver unable to
function properly to conjugate the bilirubin. Suspect hemolysis or Gilbert's Syndrome.
- Conjugated Bilirubin ("direct") increases when there is cholestasis present, or if there is
hepatocellular dysfunction. Useful for helping to diagnose biliary tree obstruction.
General Disease Profiles
- Metastatic Disease: AST & ALT normal. bili & alk phos.
- EtOH: AST > ALT. May have bili &/or alk phos.
- Viral Hepatitis: ALT > AST. May have completely normal enzymes.
- Muscle Damage: Large in AST.
- Cirrhosis: ALT & AST normal or low because parenchyma damaged. albumin. INR, alk phos, & bili.
- Extrahepatic Obstruction: AST & ALT (+/-). alk phos, conj bili. Possibly delta bili.
- Toxins: ALT & AST.
- Morphine or Opiate Use: Opiates cause biliary stasis. Expect conj bili.