lft

Liver Function Tests (LFTs)

A comprehensive guide to interpreting the key blood tests that assess liver health, function, and injury. Learn to recognize the patterns.

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Sample LFT Report

⚠️ DISCLAIMER: This is an example report for educational purposes ONLY. It shows a *specific pattern* of severe liver injury and is NOT representative of a normal or typical result. Do not use for self-diagnosis.

Liver Function Panel

PATIENT: DOE, JOHN (ID: 12345)

STATUS: FINAL
DATE: 2025-10-20

Test Name	Result	Flag	Reference Range	Units
ALT (SGPT)	1250	HIGH	10 - 40	U/L
AST (SGOT)	980	HIGH	10 - 34	U/L
ALP (ALK Phos)	110		40 - 120	U/L
GGT	65	HIGH	5 - 38	U/L
Bilirubin, Total	2.5	HIGH	0.2 - 1.2	mg/dL
Bilirubin, Direct	1.1	HIGH	0.0 - 0.3	mg/dL
Albumin	4.1		3.5 - 5.0	g/dL
Total Protein	7.2		6.0 - 8.3	g/dL
PT (Prothrombin Time)	10.8		9.5 - 13.5	sec
INR	1.0		0.9 - 1.1

IMPRESSION: Pattern suggests severe, acute hepatocellular injury (ALT/AST >> ALP). Synthetic function (Albumin, PT/INR) appears preserved, consistent with an acute process.

The Complete Guide to Liver Function Tests (LFTs): Interpretation and Clinical Significance

Learn to decode the LFT panel, move beyond isolated numbers, and recognize the critical patterns of liver injury and dysfunction.

The "Liver Function Test" or LFT panel is one of the most frequently ordered blood tests in all of medicine. It serves as a vital screening tool, helps in diagnosing specific liver diseases, monitors disease progression, and assesses responses to treatment. However, the name itself is a common source of confusion. The LFT panel contains a mix of tests, some of which measure liver injury (inflammation), while others measure true liver function (its ability to synthesize proteins or clear substances). Understanding this distinction is the single most important step in interpreting the results correctly.

The liver is the body's metabolic powerhouse. It's a complex factory that performs over 500 vital functions, including:

• Detoxification: Filtering toxins, medications, and byproducts like ammonia from the blood.
• Synthesis: Producing essential proteins (like albumin and clotting factors), cholesterol, and bile.
• Metabolism: Playing a central role in carbohydrate, fat, and protein metabolism.
• Storage: Storing glucose (as glycogen), vitamins, and minerals.
• Excretion: Excreting bilirubin (a breakdown product of red blood cells) into bile.

A standard LFT panel provides clues about which of these functions are affected. This guide will explore each component and, most importantly, how to interpret them in cohesive patterns.

Part 1: Markers of Hepatocellular Injury (The "Transaminases")

These are enzymes normally found inside hepatocytes (liver cells). When liver cells are damaged or inflamed, their membranes become leaky, and these enzymes spill out into the bloodstream, causing their levels to rise. High levels signal liver cell *injury* or *death*.

Alanine Transaminase (ALT)

Also known as SGPT (Serum Glutamic-Pyruvic Transaminase). ALT is an enzyme primarily found in the cytoplasm of liver cells. Because it is found in high concentrations almost exclusively in the liver, ALT is considered the most *specific* marker for hepatocellular injury. A rise in ALT is a very sensitive indicator of liver damage from causes like viral hepatitis, toxins (including alcohol or drugs), or ischemic injury ("shock liver").

Aspartate Transaminase (AST)

Also known as SGOT (Serum Glutamic-Oxaloacetic Transaminase). AST is also found in liver cells, but unlike ALT, it's present in both the cytoplasm and the mitochondria. Crucially, AST is also found in significant amounts in other tissues, including cardiac muscle, skeletal muscle, kidney, and brain. Therefore, an elevated AST is *less specific* for liver injury than an elevated ALT. If you see a high AST with a normal ALT, you must consider non-liver causes, such as a recent heart attack (myocardial infarction) or significant muscle injury (rhabdomyolysis).

Interpreting ALT and AST Together: The Ratio and Magnitude

The relationship between ALT and AST is often more informative than either value alone.

• Degree of Elevation:
  • Mild Elevation (< 5x normal): Very non-specific. Can be seen in almost any liver disease, most commonly NAFLD (Non-Alcoholic Fatty Liver Disease), chronic viral hepatitis (B or C), or medication-related.
  • Moderate Elevation (5-15x normal): Often seen in acute or chronic hepatitis.
  • Severe Elevation (> 15x normal, often in the 1,000s to 10,000s): This signals massive, acute hepatocellular necrosis. The differential is narrow:
    1. Acute Viral Hepatitis (e.g., Hepatitis A, B, or E)
    2. Toxin- or Drug-Induced Liver Injury (especially Acetaminophen/Paracetamol overdose)
    3. Ischemic Hepatitis ("Shock Liver"): Caused by severe hypoperfusion of the liver (e.g., after cardiac arrest or in septic shock). This typically causes the most rapid and highest spike, which also falls quickly.
• The AST:ALT Ratio:
  • Most Liver Disease (ALT > AST): In most cases of liver injury (like viral hepatitis, NAFLD, acute toxins), ALT is higher than AST, or they are roughly equal.
  • Alcoholic Liver Disease (AST > ALT, usually 2:1 or 3:1): This is a classic, high-yield pattern. An AST:ALT ratio greater than 2:1 is highly suggestive of alcohol-related liver damage. This occurs for two reasons: 1) Alcohol is a mitochondrial toxin, causing more release of the mitochondrial AST. 2) Alcoholic patients are often deficient in Vitamin B6 (pyridoxine), which is a necessary cofactor for making ALT, thus suppressing the ALT level. It's rare for the AST to be > 500 in alcoholic hepatitis.

Part 2: Markers of Cholestasis (The "Obstructive" Pattern)

Cholestasis refers to any condition where bile flow from the liver is impaired. This can be due to a problem *inside* the liver (intrahepatic, e.g., primary biliary cholangitis, drug reactions) or a blockage *outside* the liver (extrahepatic, e.g., a gallstone or tumor blocking the common bile duct). When bile flow is blocked, it "backs up" and causes the following enzymes, found in the bile duct lining, to rise.

Alkaline Phosphatase (ALP or ALK Phos)

ALP is an enzyme found in high concentrations in the cells lining the bile ducts. When bile ducts are irritated or blocked, the synthesis of ALP increases, and it is released into the blood. Therefore, a high ALP is the key marker of a cholestatic pattern.

However, like AST, ALP is not specific to the liver. It is also found in:

• Bone:** Osteoblasts (bone-building cells) produce ALP. (Causes of high ALP: bone growth in children/adolescents, fractures, Paget's disease, bone cancers/metastases).
• Placenta:** ALP levels are naturally very high during the third trimester of pregnancy.
• Intestine:** Can cause a mild rise after a fatty meal.

Because of this, an elevated ALP requires a follow-up test to confirm its origin.

Gamma-Glutamyl Transferase (GGT or GGTP)

GGT is another enzyme found in bile duct cells. It is extremely sensitive to biliary tract disease. Its primary clinical use is to confirm the origin of an elevated ALP.

• High ALP + High GGT:** Confirms the problem is hepatobiliary (liver or bile duct-related).
• High ALP + Normal GGT:** Points to a non-liver source, most commonly bone disease.

GGT is also independently very sensitive to alcohol consumption and certain medications. It can be elevated after even moderate alcohol intake, often long before other LFTs become abnormal. However, it is not specific, so it can't be used alone to diagnose alcohol abuse.

Part 3: Markers of Excretory Function (Bilirubin & Jaundice)

Bilirubin is the yellow pigment that causes jaundice. It's a waste product from the breakdown of heme, a component of hemoglobin from old red blood cells. The liver's job is to "process" this waste product and excrete it.

The Bilirubin Pathway (Simplified):

1. Old red blood cells are broken down, releasing heme, which becomes unconjugated bilirubin (UB). UB is fat-soluble and toxic, so it circulates in the blood bound to albumin.
2. The albumin-bound UB is delivered to the liver.
3. Liver cells (hepatocytes) take up the UB and use an enzyme (UGT) to attach a glucuronide molecule, "conjugating" it. This makes it conjugated bilirubin (CB), which is water-soluble and non-toxic.
4. The liver excretes this water-soluble CB into the bile ducts, which then drain to the gallbladder and small intestine.

Interpreting Bilirubin Levels:

The LFT panel measures Total Bilirubin and Direct Bilirubin (which is a close estimate of conjugated bilirubin). Indirect Bilirubin = Total - Direct.

• Isolated High Indirect (Unconjugated) Bilirubin:** This pattern means the liver is either *overwhelmed* with bilirubin (pre-hepatic) or *unable to conjugate* it (intra-hepatic).
  • Pre-Hepatic Cause:** Too much bilirubin is being made, usually from hemolysis (rapid breakdown of red blood cells). The liver is healthy but can't keep up.
  • Intra-Hepatic Cause:** The liver's conjugation machinery is broken. The most common cause is Gilbert's syndrome, a harmless genetic condition causing mildly elevated UB. Rare, severe causes include Crigler-Najjar syndrome.
  In both cases, ALT/AST and ALP/GGT are typically normal.
• High Direct (Conjugated) Bilirubin:** This pattern means the liver *successfully conjugated* the bilirubin, but it *cannot excrete it*. The "drain" is clogged. The conjugated bilirubin "leaks" back into the blood. This *always* indicates a problem with the liver or bile ducts (hepatobiliary disease). It is often seen alongside high ALP/GGT in cholestatic injury (e.g., gallstones, pancreatic cancer) or high ALT/AST in severe hepatocellular injury (e.g., acute hepatitis), as the damaged liver cells can't transport the bile out.

Part 4: True Markers of Synthetic Function (The "Function" Tests)

These tests measure substances *produced* by the liver. A drop in these levels indicates the liver's "factory" is failing, which is a sign of severe, often chronic, liver disease (like cirrhosis). These markers change slowly.

Albumin

Albumin is the most abundant protein in the blood, and it is made exclusively by the liver. Its functions include maintaining oncotic pressure (keeping fluid inside blood vessels) and transporting hormones, drugs, and other substances. The liver has a large reserve capacity for making albumin. Furthermore, albumin has a long half-life of about 20 days.
Clinical Significance:** Because of its long half-life, albumin levels are normal in acute liver failure. A low albumin level (hypoalbuminemia) is a sign of a chronic process, such as:

• Chronic Liver Disease (Cirrhosis):** The damaged liver can no longer produce enough albumin.
• Nephrotic Syndrome:** The kidneys leak large amounts of albumin into the urine.
• Severe Malnutrition:** Not enough protein intake to make albumin.
• Severe Systemic Inflammation:** Albumin is a "negative acute phase reactant" and levels can drop during severe illness.

Prothrombin Time (PT) and INR (International Normalized Ratio)

The PT measures how long it takes for blood plasma to clot, specifically assessing the "extrinsic" pathway. The liver synthesizes most of the key clotting factors, including Factor VII, which has a very short half-life of only ~6 hours.
**Clinical Significance:** Because Factor VII is depleted so quickly, the PT/INR is the single best marker of acute liver synthetic function. If a patient has acute liver failure (e.g., from an acetaminophen overdose), a rising PT/INR is the first and most critical sign that the liver's synthetic factory is shutting down. It is also elevated in chronic liver disease (cirrhosis) and is a key component of prognostic scores like the MELD score.

Note: The PT/INR is *also* elevated in Vitamin K deficiency (as factors II, VII, IX, X need Vitamin K for activation). In a patient with liver disease, a doctor may give a shot of Vitamin K. If the PT/INR corrects, the problem was vitamin deficiency; if it *does not* correct, it means the liver itself is failing and cannot make the factors.

Putting It All Together: Recognizing Common LFT Patterns

The real power of LFTs comes from pattern recognition. No single value tells the whole story.

Pattern 1: The Hepatocellular Pattern

• Signature:** Dramatically elevated ALT and AST (hundreds to thousands).
• Other Tests:** ALP/GGT are normal or only mildly elevated. Bilirubin may be normal or high (both conjugated and unconjugated). PT/INR may be high if the injury is severe (acute failure). Albumin is almost always normal.
• Think:** "Acute liver cell death."
• Top Causes:** Acute Viral Hepatitis (A, B, E), Toxin/Drug Injury (Acetaminophen), Ischemic Hepatitis (Shock Liver).

Pattern 2: The Cholestatic (Obstructive) Pattern

• Signature:** Dramatically elevated ALP and GGT.
• Other Tests:** ALT/AST are normal or only mildly elevated. Bilirubin is often high (mostly conjugated).
• Think:** "Blocked bile flow."
• Top Causes:** Gallstone in the common bile duct, Pancreatic cancer head, Primary Biliary Cholangitis (PBC), drug-induced cholestasis.

Pattern 3: The Chronic Disease / Cirrhosis Pattern

• Signature:** Low Albumin, High PT/INR, often a reversed Albumin/Globulin (A/G) ratio.
• Other Tests:** ALT/AST may be normal or only mildly elevated (the liver may be "burned out" and have few cells left to leak enzymes). Bilirubin often rises as the disease progresses. Platelet count is often low (thrombocytopenia) due to portal hypertension and hypersplenism.
• Think:** "Chronic liver failure / scarring."
• Top Causes:** Chronic Hepatitis C or B, Alcoholic Liver Disease (long-term), Advanced NAFLD (NASH cirrhosis).

Conclusion: A Powerful Diagnostic Panel

Liver Function Tests are a cornerstone of modern diagnostics. By understanding the role of each component—distinguishing between markers of *injury* (ALT, AST), *cholestasis* (ALP, GGT), *excretion* (Bilirubin), and true *synthetic function* (Albumin, PT/INR)—a clinician can build a powerful hypothesis. Remember, LFTs rarely provide a final diagnosis on their own. They are patterns that, when combined with a thorough history, physical exam, and further investigations like viral serologies and imaging (ultrasound, CT, MRI), allow you to effectively diagnose and manage the vast spectrum of liver disease.

LFT FAQs

Your common questions about Liver Function Tests, answered.

Do I need to fast for a Liver Function Test (LFT)?

It is often recommended, but not always mandatory. A fatty meal can sometimes slightly increase triglycerides or cause mild turbidity in the sample, which *can* interfere with some lab assays. However, for most of the core LFTs (ALT, AST, Bilirubin), fasting is not strictly necessary. It's best to follow the instructions provided by your doctor or the lab.

My LFTs are slightly elevated. Am I in trouble?

Not necessarily. Mild, transient elevations in liver enzymes (especially ALT and AST) are very common. They can be caused by strenuous exercise (raises AST), minor viral illnesses, certain medications, or even a fatty meal. The key is the *pattern*, the *degree* of elevation, and whether it's *persistent*. Your doctor will interpret the results in context and likely repeat the test to see if the elevation is temporary or requires further investigation.

What is NAFLD (Non-Alcoholic Fatty Liver Disease)?

NAFLD is the most common cause of mildly elevated LFTs in many parts of the world. It's characterized by the buildup of excess fat in liver cells (steatosis) in people who drink little to no alcohol. It is strongly associated with metabolic syndrome (obesity, type 2 diabetes, high cholesterol). While simple fatty liver can be benign, it can progress to inflammation (called NASH - Nonalcoholic Steatohepatitis), which can lead to fibrosis, cirrhosis, and liver cancer.

Can medications cause my LFTs to be abnormal?

Yes, absolutely. This is extremely common and is called Drug-Induced Liver Injury (DILI). Hundreds of drugs can affect LFTs, from common over-the-counter pain relievers (like acetaminophen/paracetamol in high doses), to statins (for cholesterol), antibiotics, anti-tuberculosis drugs, and herbal supplements. It's crucial to tell your doctor *all* medications and supplements you are taking.

What's the difference between "liver enzymes" and "liver function"?

This is a key concept. Liver Enzymes (like ALT and AST) are markers of *liver injury or inflammation*. When liver cells are damaged, these enzymes leak into the blood. True "Liver Function" Tests measure the liver's *synthetic or excretory ability*. These include Albumin and PT/INR (which test synthetic function) and Bilirubin (which tests excretory function). It's possible to have severe acute liver injury (very high enzymes) but still have normal function (normal albumin/PT) if the injury is new. Conversely, it's possible to have end-stage cirrhosis (poor function) with normal enzymes because the liver is too scarred to leak them.