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What are normal liver enzyme counts: High, Low & Normal Results, Symptoms & Causes


Mistakes in liver function test abnormalities and how to avoid them | UEG

Ignoring nonhepatic causes of abnormal LFT results

None of the LFTs discussed in this article is 100% liver specific. The possibility of a nonhepatic origin of LFT abnormalities should, therefore, always be considered. This holds especially true for isolated LFT abnormalities.
ALT is more liver specific than AST, since the latter can also be found in skeletal and cardiac muscle, kidneys, brain, lungs, pancreas and red blood cells.3 A disproportionate or isolated AST elevation, therefore, should raise suspicion that the source is nonhepatic. Nonhepatic causes of AST elevation include injury to skeletal or cardiac muscle, hyperthyroidism or hypothyroidism, haemolysis, and (rarely) macro-aspartate aminotransferase. The latter condition is caused by the binding of AST to immunoglobulins, which results in delayed AST clearance.27

GGT is expressed in the kidney, pancreas, spleen, lung, heart and brain.13 In general, an isolated elevation of GGT levels is not a specific marker for liver disease, since it can be elevated in patients with diabetes, chronic obstructive pulmonary disease, myocardial infarction, pancreatic disease or renal failure. GGT levels can also be elevated in patients using enzyme inducers (CYP2C, CYP3A, CYP1A) such as phenobarbital, carbamazepine or alcohol.28

ALP consists of several isoenzymes that are located in liver (isoenzyme 1 and 2), bone, intestine and placenta. ALP can be fractionated in order to determine its origin.  Bone-derived ALP is increased in patients who suffer from bone disease (e.g. Paget’s disease, primary and metastatic bone tumours, osteomalacia, rickets, hyperparathyroidism), and in children due to rapid bone growth. Intestinally-derived  ALP is increased in patients with blood group O or B after fatty meals, and in those with familial ALP elevation.9 Raised intestinal ALP isoenzyme levels have also been reported in patients with liver cirrhosis, diabetes, chronic kidney disease, and bowel ischaemia.30 The placental ALP isoenzyme can be elevated in pregnant women, usually during the third trimester.9 The Regan isoenzyme, a rare variant of placental ALP, can be elevated in cancers that do not involve the bone, such as gonadal, urologic or lung cancer.31  Of note, after the age of 50 years, ALP levels (both hepatic and bone) tend to increase, especially in women.29

Hypoalbuminaemia can have various nonhepatic causes, such as a decrease in albumin synthesis (e.g. malnutrition, malabsorption), albumin dilution (e.g. pregnancy), albumin loss (e.g. nephrotic syndrome, protein-losing enteropathy), or a catabolic state (e.g. infection, trauma, malignancy). Hypoalbuminaemia without liver test abnormalities is usually not associated with liver disease.
The prothrombin time can be affected by various coagulation disorders in the absence of hepatic disease, such as disseminated intravasal coagulation and conditions that affect the function of vitamin K (which activates clotting factors II, VII and X of the intrinsic coagulation pathway). These conditions include the use of warfarin and vitamin K deficiency during cholestatic liver disease and cirrhosis, which occurs due to a decrease in its intestinal absorption.32

Liver function tests

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Liver function tests are blood tests used to help diagnose 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 normal 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.

Abnormal liver function test results don’t always indicate liver disease. Your doctor will explain your results and what they mean.

Why it’s done

Liver function tests can be used to:

  • Screen for liver infections, such as hepatitis
  • Monitor the progression of a disease, such as viral or alcoholic hepatitis, and determine how well a treatment is working
  • Measure the severity of a disease, particularly scarring of the liver (cirrhosis)
  • Monitor possible side effects of medications

Liver function tests check the levels of certain enzymes and proteins in your blood. Levels that are higher or lower than normal can indicate liver 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.
  • Aspartate transaminase (AST). AST is an enzyme that helps metabolize amino acids. Like ALT, AST is normally present in blood at low levels. An increase in AST levels may indicate liver damage, disease or muscle damage.
  • Alkaline phosphatase (ALP). ALP is an enzyme found in the liver and bone and is important for breaking down proteins. Higher-than-normal levels of ALP may indicate liver damage or disease, such as a blocked bile duct, or certain bone diseases.
  • 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-normal levels of albumin and total protein may indicate liver damage or disease.
  • Bilirubin. Bilirubin is a substance produced during the normal breakdown of red blood cells. Bilirubin passes through the liver and is excreted in stool. Elevated levels of bilirubin (jaundice) might indicate liver damage or disease or certain types of anemia.
  • Gamma-glutamyltransferase (GGT). GGT is an enzyme in the blood. Higher-than-normal levels may indicate liver or bile duct damage.
  • L-lactate dehydrogenase (LD). LD is an enzyme found in the liver. Elevated levels may indicate liver damage but can be elevated in many other disorders.
  • Prothrombin time (PT). PT is the time it takes your blood to clot. Increased PT may indicate liver damage but can also be elevated if you’re taking certain blood-thinning drugs, such as warfarin.


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 medications can affect the results of your liver function tests. Your doctor will probably ask you to avoid eating food and taking some medications 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 experience some short-term discomfort at the site after the needle is removed.

After the test

Your blood will be sent to a laboratory for analysis. If the lab analysis is done on-site, you could have your test results within hours. If your doctor sends your blood to an off-site laboratory, you may receive the results within several days.


Normal 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. Normal results vary from laboratory to laboratory and might be slightly different for women and children.

Your doctor will use these results to help diagnose your condition or determine treatment you might need. If you already have liver disease, liver function tests can help determine how your disease is progressing and if you’re responding to treatment.

Liver enzyme tests and others | Guides

Liver enzyme tests: ALT and AST

Liver enzymes are proteins with specific functions (and difficult long names).

If the liver becomes damaged, some of these enzymes leave the liver and enter the blood.

Many things can cause liver enzyme levels to increase. These include:

  • Prescription and over-the-counter medicines.
  • Herbs, vitamins and supplements.
  • Toxic fumes.
  • High alcohol intake or coming off drugs and/or alcohol.
  • New or existing hepatitis infection.

HIV drugs can cause liver enzymes to increase, though usually not to dangerous levels. In some cases, these drugs need to be stopped or switched.

People taking HIV drugs (or other drugs processed by the liver) need to have liver enzymes routinely measured with other blood tests. This is especially important with HCV coinfection.

Raised liver enzymes do not always mean there is liver damage. But persistently high levels can be a sign of ongoing damage that needs to be treated.


Two important enzymes are ALT (alanine aminotransferase) and AST (aspartate aminotransferase).

ALT is produced in the liver and Increases are usually a sign of liver inflammation or damage. However, ALT is not a good marker of either liver damage or changes in liver health. This is because HCV itself causes levels to go up and down.

Up to a third of people with chronic HCV always have a normal ALT, even with serious liver damage.

If an increase in ALT continues to rise, or is getting worse, it may mean continued HCV related inflammation which may eventually lead to scarring (fibrosis).

AST is an enzyme that is made in the heart, intestines, and muscles. AST is only used to monitor liver inflammation and damage in combination with other tests.

  • Normal liver enzymes, even over time, do not mean there is no liver damage.
  • Raised liver enzymes do not always mean there is liver damage, but if they are persistently high this can be a sign of ongoing damage, and that treatment may be a good idea.

ALP, GGT, bilirubin, albumin and prothrombin time

Routine monitoring in coinfection also includes ALP, GGT, bilirubin, albumin and prothombin time (PT).

ALP (alkaline phosphatase) is an enzyme that is present throughout the body, including the liver. If blood levels of ALP increase, this can be a sign of tissue disease or damage. Your doctor can also test specifically for ALP from the liver. Some medications, including the HIV protease inhibitor atazanavir, can increase ALP. Elevated ALP from the liver is a sign of blocked bile ducts caused by liver disease.

GGT (gamma glutamyl transferase) is an enzyme involved in metabolism that is produced in the bile ducts. Any liver disease, heavy drinking, and some medications can all increase GGT.

Bilirubin is a waste product from the breakdown of red blood cells. Before it passes through the liver, where it is mixed with sugars to become water-soluble, it is called indirect or unconjugated bilirubin. Once it has been processed through the liver it is called direct or conjugated bilirubin.

A damaged liver may be unable to process bilirubin, causing an increase in the total bilirubin levels. Usually, a laboratory will subtract the amount of direct bilirubin from the total amount of bilirubin in the bloodstream; the leftover is indirect bilirubin.

Jaundice is an increased level of bilirubin and common signs include a yellowing of the skin and eyes, dark urine or pale stools. Some drugs, including the HIV protease inhibitor atazanavir, and HCV protease inhibitors, can increase bilirubin.

Albumin is a protein made by the liver. It carries drugs, hormones and waste products through the blood and maintains fluid levels within the body. An abnormally low level of albumin is a sign of serious liver damage.

Last updated: 17 August 2017.

Liver Disease, Tests

This sheet describes tests that may be done for liver problems. Your healthcare provider will tell you which tests you need.

Blood tests to check the liver

A simple blood test can show how your liver is working.

A small amount of blood may be taken and tested for one or more of the following:

  • AFP (alpha fetoprotein). This is a protein made by the liver. A high level in the blood can be a sign of liver cancer or liver injury and regeneration in adults.
  • Albumin. This is a liver function test. It measures a protein made by the liver. When a person has liver disease, the level of albumin in the blood (serum albumin) is often low.
  • Alk phos (alkaline phosphatase). This is an enzyme that is mostly made in the liver and bones. It’s measured with a blood test. A high level suggests a problem with the bile ducts in the liver.
  • ALT (alanine aminotransferase). ALT is an enzyme made by the liver. When the liver is damaged, ALT leaks into the blood. If a blood test finds a high level of ALT, this can be a sign of liver problems such as inflammation, scarring, or a tumor.
  • Ammonia. This is a liver function test that shows when a harmful substance is left behind in the blood after digestion. Normally the liver removes ammonia from the blood and turns it into urea. This leaves the body with urine. If a blood test shows that the ammonia level is too high, this process isn’t happening as it should. This test is very inaccurate for liver function and should rarely be used.
  • AST (aspartate aminotransferase). AST is another enzyme made by the liver as well as by other organs such as muscle. It too is measured with a blood test. High levels of AST may be a sign of liver injury, especially if the ALT level is also high.
  • Bilirubin. This is a liver function test. It measures the yellow substance made when the body breaks down red blood cells. Bilirubin is collected by the liver to be sent out of the body with stool. When something is wrong with the liver or bile ducts, bilirubin may build up in the body. This causes yellowing of the skin and the whites of the eyes (jaundice). Two measurements may be taken from this test: total bilirubin and direct bilirubin. A high bilirubin level may be the result of liver disease or a blockage in the bile ducts. A high indirect bilirubin can mean a condition called Gilbert syndrome. Only a small portion of people have Gilbert syndrome. Gilbert syndrome is not a sign of disease. A high indirect bilirubin can also be a sign of rapid red blood cell breakdown.
  • CBC (complete blood count). This is a test that measures all the parts of the blood. These are red blood cells, white blood cells, and platelets. Problems with these counts can mean infection or illness. They can also be a sign of a problem with the spleen. The spleen is an organ close to the liver that can be affected by liver disease. A low platelet count is common with advanced fibrosis of the liver. It also happens when the spleen becomes enlarged and begins to absorb platelets.
  • GGT (gamma-glutamyl transpeptidase). This is a liver enzyme that’s often measured along with other enzymes to gauge liver problems. GGT is measured with a blood test. If alk phos and GGT are both higher than normal, it may be a sign that the bile ducts in the liver may be diseased or blocked. It also can be a sign of fatty liver or alcohol damage.
  • Glucose. This is a sugar in the blood and the body’s most important source of energy. A healthy liver helps the body maintain a normal glucose level. If a blood test shows that glucose is low, this may mean the liver is not working properly.
  • Infectious hepatitis. This is a disease and can be found with antibody and antigen tests for Hepatitis A, B, C, D, and E.
  • PT (prothrombin time) or INR (international normalized ratio). This checks how long it takes for blood to form clots. The liver makes a protein that helps with clotting. Problems with clotting can be a sign of liver disease. 
  • 5NT (5′-nucleotidase). This is enzyme is made is several organs, but only released into the blood by the liver. A high or low level may be a sign of liver disease.
  • SBA (serum bile acid). This test measures the amount of bile acid in the blood. A high level may mean that bile ducts are blocked or that the liver is unable to excrete bile acid. This test is rarely done.
  • Vitamins A, D, E, and K. These vitamins are stored in the liver and fat and released over time (fat-soluble). They are absorbed by the liver, with help from bile. If a blood test shows that these vitamin levels are low, this could mean the liver is not absorbing them properly.
  • Zinc. This is a nutrient that is absorbed by the liver. If a blood test shows a low zinc level, this could mean the liver isn’t absorbing zinc properly. This can worsen conditions brought on by high levels of ammonia.

Several other lab tests may be done to check for specific liver problems once liver damage is found. These include:

  • Autoimmune antibodies
  • Ceruloplasmin (Wilson disease)
  • An iron panel (hemochromatosis)
  • Alpha-1-antitrypsin (alpha-1-antitrypsin deficiency)

Other tests to check the liver

The tests below may be done to check the liver’s condition or function. These tests can also check related organs, such as the gallbladder or bile ducts.

  • Liver biopsy. This is a test to look for damage in liver tissue. A needle is used to take a small amount of tissue from the liver. The tissue is sent to a lab, where it is checked for signs of inflammation, scarring, or other problems.
  • CT scan. A CT scan is a series of X-rays that make a 3-D picture of the liver and gallbladder. This can show gallstones, abscesses, abnormal blood vessels, or tumors.
  • ERCP (endoscopic retrograde cholangiopancreatography). This test can show if the bile ducts are blocked or narrowed. It can also take pictures of the gallbladder. During this test, a small flexible tube (endoscope) is put into the mouth. The tube is moved down the esophagus and stomach to the top of the small intestine. This is where the bile ducts are. Dye is released through the tube to make the bile ducts show up on an X-ray. The healthcare provider may also use small tools to take tiny samples of tissue or fluid. These are sent to a lab to be studied.
  • HIDA scan. This test checks gallbladder and liver function. A small amount of radioactive fluid is put into the body. This fluid will be seen on a scan as it travels through the liver to the gallbladder and into the intestine. It can show if bile ducts are missing or blocked. It can show if the gallbladder is working properly. It can also show other problems in the bile ducts.
  • MRI. This test uses magnets, radio waves, and a computer to create an image of the organs and tissues in your body.
  • MRCP (magnetic resonance cholangipancreatography). This is a type of MRI that is more detailed than a standard MRI. It can show abnormal or narrow bile ducts, tumors, gallstones, or all three.
  • Ultrasound (sonogram). This test uses harmless sound waves and a computer to create a picture of the liver, gallbladder, and bile ducts. It can show gallstones, tumors, or fat in the liver. It is also used to check the condition of the blood vessels and look for bile collections where bile may leak out of the liver. A special ultrasound called elastography gives more information about scarring in the liver (cirrhosis.)

StayWell last reviewed this educational content on 3/1/2020

© 2000-2020 The StayWell Company, LLC. All rights reserved. This information is not intended as a substitute for professional medical care. Always follow your healthcare professional’s instructions.

Analysis and Interpretation of Classic Liver Enzymes

Symptoms and signs of liver disease are often seen late in the disease. As a result laboratory testing helps in identifying and characterizing liver disease. For the purposes of this article, the liver chemistries that will be focused on will be bilirubin, alkaline phosphatase, aminotransferases and gamma-glutamyl transferase. In addition, albumin and prothrombin time will be discussed briefly. Following discussion of these tests, this article will focus on different patterns of abnormalities that relate to different disease processes.

Archana Kulkarni, MD1 Mrinal Garg, MD2 Rad M. Agrawal, MD3 Michael Babich, MD4 1Department of Internal Medicine 2Division of Gastroenterology, Department of Internal Medicine 3Professor Emeritus, Division of Gastroenterology, Department of Internal Medicine 4Associate Professor of Medicine, Division of Gastroenterology, Department of Internal Medicine, Allegheny General Hospital, Pittsburgh, PA


Accessibility, ease of collection, and relatively low cost give serum chemistries an integral initial role in medical diagnosis. With the liver being a critical organ in the metabolism of carbohydrates, lipids and proteins as well as in first pass metabolism of exogenous medications, a great deal can be learned about hepatobiliary processes by having an appropriate grasp of specific liver chemistry tests. Liver enzymes are also commonly ordered for evaluation of other non-hepatic diagnoses and as part of health screening, which makes it imperative for all primary care physicians and specialists to have an accurate understanding of their normal values and an ability to interpret abnormal levels. Symptoms and signs of liver disease are often seen late in the disease. As a result laboratory testing helps in identifying and characterizing liver disease.

The term “liver function tests” is a misnomer, as many of these tests do not naturally reflect hepatobiliary function and are rather used as a determinant of liver injury. Furthermore, the origin of these tests may not be specific to the liver and, as such, abnormal results may be related to alternative organ injury. It is vital to use these test results in the context of patient history and physical examination in order to form an accurate diagnosis. For the purposes of this article, the liver chemistries that will be focused on will be bilirubin, alkaline phosphatase, aminotransferases and gamma-glutamyl transferase. In addition, albumin and prothrombin time will be discussed briefly. It will also provide a reference of normal laboratory values for an average adult male of individual tests based on information provided by the Mayo Clinic. Furthermore, as clinicians will be ordering these tests on a routine basis, the cost is relevant and Medicare pricing guidelines will be provided for each laboratory test. Following discussion of these tests individually, this article will focus on different patterns of abnormalities that relate to different disease processes.


Bilirubin is a product of the digestion of hemoglobin. During the catabolism of erythrocytes, an initial unconjugated or “indirect” form of bilirubin is released into the reticuloendothelial system. As unconjugated bilirubin is water insoluble, it binds with albumin and is transported to the liver. Unconjugated bilirubin exists in majority as a component of total bilirubin when compared to direct bilirubin. In the liver, the unconjugated bilirubin enters the hepatocyte and is conjugated with glucuronic acid by the enzyme UDP-glucuronyltransferase (UGT), rendering it water soluble.1 This conversion process, from the unconjugated form to “direct”, or conjugated, form allows bilirubin to be transported through the canalicular membrane, mix with other components of bile within the biliary tree, and flow into the duodenum.2,3,4 In the duodenum, part of the direct bilirubin is reabsorbed while the rest is converted to urobilinogen by intestinal flora and excreted in the urine and stool. In addition, there is also a delta bilirubin, which can also be referred to as biliprotein, which is produced by reaction of conjugated bilirubin with albumin.5 It is important to note that the half-life of this product is about 17-20 days (the same as albumin) accounting for prolonged jaundice in patients recovering from hepatitis or obstruction.6 The total bilirubin, which is a measure of both direct and indirect forms, has a normal reference range of 0.1-1.0 mg/dL.

Historically, in order to determine the serum levels of the two types of bilirubin, laboratories utilized the technique developed through the van den Bergh diazo reaction,7 which was able to separate water soluble conjugated bilirubin from unconjugated bilirubin for individual measurement. The accuracy of the direct bilirubin levels increased as the total bilirubin rose. The direct, or conjugated, bilirubin reference range is 0.0-0.3 mg/dL in a normal individual and should be no more than 20% of the total bilirubin when the total bilirubin is elevated due to non-hepatic causes, such as hemolysis or congestive heart failure. The indirect or unconjugated bilirubin is obtained by subtracting the direct bilirubin level from the total bilirubin.

Identifying the subtype of bilirubin, which is elevated, allows for accurate diagnosis when analyzing bilirubin levels. Isolated elevation of unconjugated bilirubin occurs mainly secondary to increased bilirubin production, decreased hepatic uptake and decreased bilirubin conjugation. Elevated levels of unsuccessful erythrocyte production, hemolysis, or reabsorption of large hematomas may lead to increased unconjugated bilirubin levels. Fulminant Wilson’s disease can cause isolated elevation in unconjugated bilirubin secondary to the release of copper in the blood resulting in cellular lysis 8 Unsuccessful erythrocyte production exists in the setting of rapid heme and hemoglobin turnover in the bone marrow due to premature destruction of red blood cells. There exists evidence that in these conditions there is also presence of erythroid hyperplasia of bone marrow, reticulocytosis, increased iron turnover with diminished red blood cell incorporation, and hemosiderosis of hepatic parenchymal cells and Kupffer cells. However, why this occurs in the bone marrow is not known.8

Isolated elevation of unconjugated bilirubin also may be due to genetically inadequate UGT production preventing conjugation in disease processes such as Gilbert’s syndrome and Crigler-Najjar disease.9 Gilbert’s syndrome is a commonly seen disorder, which is relatively benign. The hyperbilirubinemia in Gilbert’s syndrome is exacerbated with fasting.10 Elevated conjugated bilirubin can be caused secondary to inherited or acquired conditions. Genetic disease processes such as Dubin-Johnson and Rotor syndrome cause an impaired hepatocellular secretion of bilirubin into the bile canaliculus causing elevated conjugated bilirubin.11,12 As the anatomy suggests, elevations in conjugated bilirubin can occur secondary to hepatocellular dysfunction and cholestatic processes, which impair bile, flow. It has been found that despite the loss of liver function in hepatocellular disease processes, such as cirrhosis, UGT is produced at an increased rate in the remaining functioning hepatocytes forming conjugated bilirubin, such that increase in total bilirubin may not occur until late in the course of disease.13,14 Cholestasis can occur either because of impaired secretion into a bile canaliculus or impaired transit through the biliary tree and into the duodenum. Some of the causes of intra hepatic cholestasis are drug toxicity, primary biliary cirrhosis, primary sclerosing cholangitis, viral hepatitis, cholestasis of pregnancy, benign postoperative cholestasis, infiltrative liver diseases, sepsis and total parenteral nutrition. Certain causes of extra hepatic cholestasis are choledolithiasis, malignant obstruction secondary to a mass in the pancreas, bile duct, gall bladder or ampulla, primary sclerosing cholangitis with an extra hepatic bile duct stricture, chronic pancreatitis and AIDS cholangiopathy.

Alkaline Phosphatase and gamma-glutamyltansferase

Alkaline phosphatase (ALP) is a zinc metalloenzyme and can be found in many different tissues, with most clinical relevance due to production in the bone, intestine, kidney or liver, and with more than 80% of serum ALP originating from bone or liver.15 The average serum level of ALP in a normal adult male is 45 to 115 U/L. There are certain physiological causes that lead to increased alkaline phosphatase, examples being the during the third trimester of pregnancy secondary to the influx of alkaline phosphatate from the placenta, in adolescents secondary to increase in bone turnover, or some individuals with an increased production of intestinal alkaline phosphatase which is familial and benign.10 Although it is generally ordered as part of routine liver chemistry, ALP abnormalities should be evaluated within the framework of hepatobiliary vs non-hepatobiliary diseases. In the liver, ALP is present in the hepatocytes on the cannalicular membrane, but is localized to the microvilli of the bile canaliculus, and elevated levels typically reflect a cholestatic disease process. The half life of ALP is one week and, as a result, even after the cholestatic process has resolved, the normalization of the ALP level may lag. In order to distinguish whether an isolated elevation of ALP is of hepatic origin, one could order ALP isozymes, which fractionate the total ALP into its tissues of origin. Alternatively, confirmation via a gamma-glutamyltransferase (GGT) level can be performed since GGT is more concentrated in hepatic tissue1 and is not present in bone. A concurrent elevation of ALP and GGT excludes a boney origin of the enzyme. It is important to note that initially the only notable abnormality that may be seen in infiltrative diseases such as primary biliary cirrhosis, sarcoidosis, primary sclerosing cholangitis, etc. is isolated elevations in ALP.1 Elevation in ALP is typically seen for duration of more than six months in these conditions. These cases normally require follow up with imaging or liver biopsy. ALP can also interestingly be raised in various neoplasms, which do not involve the bone or liver directly. This occurs secondary to an isozyme of ALP called the ‘Regan isoenzyme’.17

GGT is an enzyme primarily located in hepatocytes, epithelial lining of biliary ducts, pancreas, renal tubules and the intestine. The normal GGT level in adult male ranges from 9 to 48 U/L. GGT levels may be elevated in a large variety of common diseases such as diabetes, hyperthyroidism, pancreatitis, alcoholism, COPD and rheumatoid arthritis and also as a result of various medications like coumadin, carbamazepine, phenytoin, and barbiturates. Hence the specificity for liver disease is poor. Isolated GGT elevation may be seen in alcohol abuse. Note, however, the degree of GGT elevation does not directly correlate with the amount of alcohol consumed.11

Aminotransferases – Alanine aminotransferase (ALT) & Aspartate aminotransferase (AST)

In 1955, serum AST and ALT elevations were first noted in patients with known viral hepatitis and other hepatic specific diseases.18 Aminotransferases are so named as their enzymatic function is to transfer amino groups to form pyruvate via AST and form oxaloacetate via ALT. While present in several tissues including skeletal and cardiac muscle and erythrocytes, clinically relevant elevations are usually reflective of liver disease, especially with respect to ALT elevations, isolated elevations of which should be assumed to reflect liver disease until proven otherwise. Their location within the hepatocyte is imperative to understanding the elevation patterns seen in various liver diseases. AST has two isoenzyme forms, with 80% operating as a mitochondrial isoenzyme; however, most of the circulating serum AST is derived from the cytoplasmic isoenzyme.19 Conversely, ALT is found only in the cytosol and is more specific to liver tissue. This makes an elevated ALT more specific for hepatocellular injury than AST. Elevated ALT levels however have also been noted in myopathic diseases.20

When determining a laboratory range for aminotransferases, important characteristics must be considered. Interestingly, as body mass index (BMI) increases, so does ALT; ALT is also higher in males relative to females. It is worth noting as well that AST levels may be 215% higher in African-American males.21 As ALT has more specificity for hepatocellular injury, cutoff values are important to ensure proper inclusion of patients with liver disease and elevated aminotransferases without unnecessary evaluation of patients with potentially normal levels.22 For the purposes of this article, we use a reference range for ALT as 7 to 55 U/L and AST as 8 to 48 U/L, with an understanding that a wide upper limit variability exists across different laboratories likely related to different reference standards.23 The magnitude of transaminase elevation relative to the upper limit of normal may help to narrow down the differential diagnosis for the cause of hepatocellular injury. Specifically, aminotransferase levels that are 15x or more the upper limit of normal deserve to be considered separately from mild or moderate elevations.13 Also to further classify pathologies, it is important to consider the ratio of ALT to AST.


Albumin is a plasma protein produced solely in the liver, with a half-life of three weeks.24 As a result, a decrease in the albumin level compared to normal (<3.5 g/L) signifies a liver disease which has been occurring for greater than three weeks. Albumin level can be influenced by other factors such as the nutritional status, catabolism, hormonal factors, and urinary and gastrointestinal losses. As a result, these factors should be taken into consideration when interpreting albumin levels. In conclusion albumin is useful to interpret chronic and progressive liver disease and is also used to predict the prognosis of liver disease.

Prothrombin Time (PT)

All coagulation factors are produced in the liver. Factor VIII is produced in endothelial cells outside the liver in addition to being produced by the sinusoidal cells in the liver. The rate of conversion of prothrombin to thrombin requiring factors II, V, VII, X and fibrinogen is the measurement of prothrombin time (PT), thus a function of the liver. Prothrombin time can be prolonged even in a severe liver disease of < 24 hours secondary to the half life of most factors being equal to or less than 24 hours.2 It should also be noted that vitamin K is required in the production of factors II, VII IX and X. As a result, vitamin K deficiency can also cause prolonged prothrombin time. Some other factors that should be considered in cases of prolonged prothrombin time are warfarin therapy, disseminated intravascular coagulation (DIC), hypothermia and steatorrhea.

International Normalized Ratio (INR)

In order to avoid variability in laboratory values, international normalized ratio (INR) is more commonly tested instead of or in place of PT. The results are interpreted in the same way as PT would be interpreted. It is calculated according to a formula as follows:
International normalized ratio = [patient PT/mean control PT] ISI
(ISI = international sensitivity index).

Patterns Of The Liver Function Tests

Once a general understanding of each individual liver enzyme has been achieved, clinicians can then use the liver enzyme panel to begin recognizing patterns. Each test is important to understand; however the elevation of each in relation to the other parts of the panel is what is most useful in interpreting disease processes. In this section we will describe the different liver enzyme patterns and their associated disease processes.

The liver enzyme panel abnormalities can be broken down into two main subgroups, which will be discussed individually. These subgroups are a cholestatic pattern and a hepatocellular pattern. These subgroups will then be broken down further into respective categories. The R ratio has been described to assess whether the pattern of liver injury is hepatocellular, cholestatic, or mixed and may be applied in drug-induced liver injury.26 The R ratio is calculated by the formula R = (ALT value ÷ ALT ULN) ÷ (alkaline phosphatase value ÷ alkaline phosphatase ULN). An R ratio of >5 is defined as hepatocellular, <2 is cholestatic, and 2-5 is a mixed pattern. This paper will describe hepatocellar and cholestatic patterns.

Hepatocellular Disease Pattern

Hepatocellular pattern is diagnosed with a disproportionate elevation in AST and ALT relative to alkaline phosphatase. For the purpose of this paper we will use the following definitions to describe the magnitude of elevations of AST and ALT (Table 1).

It is important to identify acute liver failure or fulminant liver failure as diagnosed by hepatic encephalopathy and coagulopathy in a patient with no prior history of liver disease. For acute liver failure, it is not imperative to describe the magnitude of rise in ALT or AST. Rapid involvement of the consultancy groups and evaluation of liver transplant should be begun early on.

Causes of Aminotransferase Elevation Massive Elevation

(More than 10,000 times the upper limit)
There is an overlap for the causes of elevation in AST and ALT between the groups of severe and massive elevation in AST and ALT. Ischemic liver disease, toxin and viruses related injuries can cause a massive elevation in AST and ALT. They are described further in the section below. It is also important to note that massive AST elevations can be seen in heat stroke and rhabdomyolysis.

Severe (15 times or greater than the upper limit of normal)

The severe elevations of serum aminotransferase levels are mainly found in the setting of excessive hepatocellular injury or necrosis in an acute setting. Although highly elevated aminotransferases can suggest an acute injury, the actual quantification of hepatocyte necrosis cannot be inferred. Furthermore, extremely elevated aminotransferases do not indicate prognosis.10 The differential is limited and generally includes a drug or toxin induced hepatotoxicity, acute viral hepatitis, or ischemic hepatitis. Toxin-related hepatitis and acute viral hepatitis can increase the AST and ALT levels to >25 times the upper limit of normal, while ischemic hepatopathy can increase the levels to >50 times.

Many medications and toxins can cause liver injury. Some of the commonly seen medications are non-steroidal anti-inflammatory drugs, antibiotics, statins, antiepileptic drugs, and antituberculous drugs. It is also pertinent to note that certain herbal remedies and illicit drugs can cause liver injury.10 In the United States (USA), the leading cause of acute liver failure is acetaminophen poisoning, accounting for 46% of cases.27 Hepatotoxicity occurs when sulfate and glucuronide metabolic pathways become saturated, pushing more acetaminophen metabolism towards the cytochrome P450 pathway that results in the formation of the toxic metabolite N-acetyl-p-benzoquinoneimine (NAPQ1). Chronic alcohol abusers can be more prone to acute liver failure in the setting of acetaminophen use and caution should be taken when treating these patients.28 Cytochrome P-450, principally cytochrome CYP2E1, metabolizes acetaminophen into a toxic metabolite, which is detoxified by glutathione under normal circumstances. CYP2E1 also detoxifies ethanol. Thus in chronic alcohol abusers, there is increase in CYP2E1 which increases the metabolism of acetaminophen into its toxic metabolites.29 Careful attention to occupational history should be given to patients with excessive aminotransferase elevation. Occupations that could lead to aminotransferase elevation include mushroom picking (Amanita phalloides) and those involved in the chemical industry (vinyl chloride).30

Acute hepatitis can also be caused by infection with any of the primary hepatitis viruses (A-E). Hepatitis B and hepatitis C are most prevalent in the USA, with hepatitis B being the leading cause of acute viral hepatitis in the USA. Viral serological tests are important to differentiate acute from chronic hepatitis.
Hepatitis A is transmitted by the fecal oral route. It is a RNA virus, which has an

incubation period of a few weeks. The IgM antibodies to hepatitis A remain in the body for a period of three to six months after the infection.31

Hepatitis B is mainly spread through unsafe sexual practice, parental drug use or vertical transmission. Hepatitis B surface antigen (HBSAg) is positive in either acute or chronic hepatitis B infection, while HBV core IgM antibody generally specifies the acute state. Checking for HBVsAg and HBVDNA would indicate whether there is an active infection and infectivity of the virus. In addition, checking for hepatitis B surface antibody would indicate immunity to hepatitis B either secondary to resolution of a prior infection or vaccination.

Hepatitis C is transmitted through parental drug use, cocaine inhalation, blood transfusion prior to 1992, tattoos or body piercings, needle stick injury and unsafe sexual practices. Hepatitis C antibody testing is sensitive. Presence of HCV viremia should be confirmed in the setting of a positive antibody with the HCV RNA PCR assay, which has high sensitivity and specificity. Hepatology should be consulted for patients positive for hepatitis C for evaluation of treatment, education on hepatitis C, and screening for cirrhosis and hepatocellular carcinoma.

Hepatitis D is an RNA virus that is only seen in the presence of hepatitis B surface antigen positivity. Suspicion for hepatitis D should arise when hepatitis B presents with fulminant hepatitis. Acute co-infection with hepatitis D is diagnosed when HBSAg, IgM anti-HBc, and total anti- HDV are present.

Another cause of acute hepatitis is hepatitis E virus. It is an enterically transmitted RNA virus. Another method of transmission of hepatitis E is through vertical transmission. Anti-HEV immunoglobulin IgM and IgG are used to detect hepatitis E. HEV RNA is used to confirm the presence of hepatitis E.

Occasionally, in the setting of acute hepatitis with excessively elevated AST and ALT levels, history and serology may not uncover a toxic or viral cause, and in these cases ischemic hepatitis should be considered. In ischemic hepatitis, the AST and ALT levels have the potential to increase to >50x the upper limit of normal. Several mechanisms can result in massive AST and ALT elevation, including decreased blood flow in instances such as hypotension, sepsis, hemorrhage, and myocardial infarctions.13 Concurrent elevation of lactate dehydrogenase (LDH) may suggest the diagnosis of ischemic hepatitis.32 These examples highlight the importance of a thorough history and physical examination to help stratify differential diagnoses in the setting of severe aminotransferase elevation.

Mild to Moderate (5-15 times the upper limit of normal)

Borderline and mild elevation in AST and ALT are seen in a variety of diseases. Moderate increase in AST and ALT often coincides with causes of mild and severe elevations.
The two most commonly identified non-viral entities, alcoholic liver disease and non-alcoholic fatty liver disease, will be briefly described below.

Alcoholic Liver Disease

Alcohol ingestion can cause elevation in liver chemistries. Alcohol ingestion can be an independendant cause or can attenuate transaminitis concurrent with other chronic liver diseases. Alcohol can cause a wide spectrum of liver disease from fatty liver to alcoholic hepatitis to alcoholic cirrhosis. These conditions can also be present all at once in an individual. Liver biopsy is useful to identify the stage and severity of liver disease since the liver chemistries do not always correlate with these.33,34 The definition of significant alcohol consumption has been suggested as >210 g of alcohol per week in men and >140 g per week in women.35 In practice, an AST:ALT ratio of 2-3:1 raises the suspicion for alcoholic liver disease. It has been demonstrated that alcohol consumption leads to decrease in plasma pyridoxal 5′-phosphate.36 This decrease in levels results in a decrease in ALT activity. The decrease in plasma pyridoxal 5′-phosphate does not have an effect on AST leading to the ratio of AST:ALT being 3:1. Once alcohol abstinence is observed with appropriate nutritional uptake, plasma pyridoxal 5′-phosphate normalizes causing a normal ALT level.36,37,38 When alcohol use is felt to cause liver disease, it is strongly recommended to quit alcohol use, and appropriate counseling should be given.

Non-Alcoholic Fatty Liver Disease and Nonalcoholic Steato-Hepatitis

Nonalcoholic fatty liver disease (NAFLD) is defined as (a) there is evidence of hepatic steatosis, either by imaging or by histology and (b) absence of causes for secondary hepatic fat accumulation such as significant alcohol consumption, use of medication that could cause fatty liver injury, or hereditary disorders. NAFLD is commonly seen in individuals with the metabolic syndrome, characterized by obesity, diabetes mellitus, and dyslipidemia. Histologically, NAFLD can be characterized as non-alcoholic liver (NAFL) or non alcoholic steato-hepatitis (NASH). Differentiation of NAFL from NASH is characterized by the presence of inflammation and hepatocellular injury, in the form of ballooning of the hepatocytes, with or without fibrosis, in the setting of NASH. It is concluded that patients with NAFL have a rather benign, slow progression (if any) histologically, while NASH can rapidly progress to the cirrhotic stage.39,40 Steatohepatitis and fibrosis as seen in NAFLD cannot be assessed accurately with serum transaminases, emphasizing the importance of further evaluation with imaging studies such as ultrasound, computed tomography (CT) or magnetic resonance imaging (MRI) and magnetic resonance elastrography (MRE) or with liver biopsy. MRE has proven to be a non-invasive, feasible and accurate modality to identify hepatic steatosis and fibrosis. MRE quantifies the extent of hepatic fibrosis with great accuracy. As compared to ultrasound, MRE is beneficial secondary to being non-technician dependant and being able to identify small amount of fibrosis. However liver biopsy continues to be the preferred modality to differentiate NAFL and NASH. The procedure related morbidity and mortality, cost and sampling error of liver biopsy has lead to interest is identifying non invasive biomarkers to identify steatohepatitis and fibrosis in NAFLD. The NAFLD fibrosis score, enhanced liver fibrosis (ELF) panel and transient elastography are identified as non-invasive methods to identify the spectrum and stage of NAFLD. The NAFLD fibrosis score is comprised of six variables (age, BMI, hyperglycemia, platelet count, albumin, AST/ALT ratio) and it is calculated using the published formula (http://nafldscore.com). Cytokeratin-18 (CK18) fragments have been investigated extensively as novel biomarkers for the presence of steatohepatitis in patients with NAFLD.41,42 Weight loss in the form of decreased caloric intake and exercise is recommended as the primary treatment. Vitamin E (a-tocopherol) administered at daily doses of 800 IU/day improves liver histology in many non-diabetic adults with biopsy-proven NASH and therefore it should be considered as a first-line pharmacotherapy for this patient population.43,44


AST/ALT ratios are of great diagnostic aid. An AST:ALT ratio of 2-3:1 raises the suspicion for alcoholic liver disease as discussed previously under the section of alcoholic liver disease. ALT has a longer half life compared to AST. The half life of ALT is 47 +/- 10 hours and that of AST is 17+/- 5 hours. In cholecystitis secondary to gallstone impaction in the distal cystic duct or choledocholithiasis, there is as increase in the AST:ALT ratio initially. However once disimpaction of the stone either spontaneously or iatrogenically is achieved, there is a reversal of this ratio secondary to ALT having a longer half life as compared to AST. It is also important to note that in chronic hepatitis the AST:ALT ratio may be increased up to 1. In advanced hepatic fibrosis, there is a reversal in the AST:ALT ratio in chronic as compared to acute hepatitis. Studies have shown that this is mainly caused by to the increased catabolism of ALT. Earlier it was thought to be secondary to increased production of AST and decreased production of ALT, which has now proven to not be the cause of the ratio reversal.45,46

Cholestatic Liver Disease Pattern

Cholestatic injury is defined as disproportionate elevation in alkaline phosphatase level as compared with AST and ALT levels. Anatomic obstructions to bile flow (extrahepatic cholestasis) or inability to form bile by the hepatocytes (intra-hepatic cholestasis) can cause a cholestatic injury pattern.

Once the origin of alkaline phosphatase has been identified as the liver, it is recommended to evaluate with an ultrasound or other form of liver imaging to identify whether the source is intra-hepatic or extra-hepatic. An MRI/MRCP (magnetic resonance cholangiopancreatography), endoscopic retrograde cholangiopancreatography and/or endoscopic ultrasound can be ordered to better examine the bile duct morphology. In the presence of biliary dilation, the source of a cholestatic pattern is most likely extra hepatic, while the absence would indicate an intra hepatic source. Causes of cholestatic liver disease as outlined in Figure 1.

For intrahepatic cholestasis, autoimmune markers including antimitochondrial antibody, antinuclear antibody, and smooth muscle antibody should be checked to assess for PBC or auto- immune cholangiopathy. Finally, pregnancy testing in women of childbearing age should be done to assess for intrahepatic cholestasis of pregnancy. Other infiltrative disorders may raise the alkaline phosphatase and cause intrahepatic cholestasis, including sarcoidosis, atypical fungal infection, or malignancies. In these instances of infiltrative diseases, a liver biopsy may be considered to assess for primary biliary cirrhosis or other infiltrative diseases.

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High liver enzymes in untreated hyperthyroidism can improve after treatment

The authors evaluated combined results from 25 studies, each of which looked at liver function tests in at least 10 patients with newly diagnosed and untreated hyperthyroidism. They did not include any patients who had underlying liver disease or very severe hyperthyroidism. Patients in the study had hyperthyroidism from Graves’ disease, toxic multinodular goiter, and toxic adenoma. Liver function tests measured in each study included alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), total bilirubin (BIL), glutamyl transferase (GGT), prothrombin time, lactate dehydrogenase, and albumin.

A total of 6345 patients (age 19-77 years; 3061 females and 898 males) were included. Overall, 55% of patients had at least one abnormal liver function test at diagnosis. In patients with Graves’ disease, 60% of patients had at least one liver function test at diagnosis. Frequency of abnormal levels of each liver function tests were 33% for ALT, 23% for AST, 44% for ALP, 12% for BIL, and 24% for GGT. Liver function tests improved in many patients after treatment of hyperthyroidism with antithyroid drugs and the return of thyroid hormone levels to normal. Frequency of normalization of each of abnormal liver function tests after treatment were 83% for ALT, 87% for AST, 53% for ALP, 50% for BIL, and 70% for GGT.

This systematic review showed that high blood liver function tests are common in patients with newly diagnosed and untreated hyperthyroidism. Frequency of having at least one abnormal liver function test in patients was 55%, much higher than 32% as reported in previous studies. In most cases, liver function tests were only mildly elevated, up to 5 times the normal range. However, high liver function tests became normal in most of these patients after they were treated with antithyroid drugs and thyroid hormone levels became normal.

The American Thyroid Association currently recommends checking baseline liver function tests in patients with newly diagnosed hyperthyroidism. These studies show that antithyroid drugs can be safely used in patients with mild liver function test increases and will usually result in resolution of the liver abnormalities. However, these patients should be monitored carefully to make sure liver function tests improve with improvement of hyperthyroidism.

— Sun Y. Lee, MD

Additional Hepatitis B Blood Tests

Additional Hepatitis B Blood Tests

Hepatitis B can be a complicated liver infection to understand, so additional blood tests may be ordered so your health provider has a better understanding of what kind of care and follow-up is needed.

Anti-HBc IgM or anti-HBc IgG (anti-hepatitis B core IgM or IgG)

Sometimes an anti-HBc IgM or anti-HBc IgG blood test may be ordered to clarify if a person has a new “acute” hepatitis B infection or “chronic” infection.

  • A positive/reactive anti-HBc IgM test result usually indicates a new acute infection.
  • A positive/reactive anti-HBc IgG test usually indicates a chronic infection.

These test results must be explained by your health care provider because they can be confusing. For example, sometimes the liver of a person who is chronically infected with hepatitis B may become more inflamed than usual (this is called a “liver flare”). So a chronically infected person could also test positive for the anti-HBc IgM blood test, although this usually indicates a new infection

Thus, it is important to be seen by a health care provider who understands hepatitis B so you get the right diagnosis and the right care and follow-up.  

HBeAg (Hepatitis B e-Antigen) – This is a viral protein made by the hepatitis B virus and is released from the infected liver cells into the blood. This test detects how much virus is in the blood as a result of very active viral replication. A negative test result indicates the virus may not be actively reproducing in the liver. In general, a person is considered very infectious when the test is positive, and less infectious when the test is negative. The loss of e-Antigen can occur naturally or as a result of drug treatment. Sometimes a negative test result can indicate a mutant hepatitis B virus is present. So, the absence of e-Antigen does not always mean there is little or no active viral replication. The doctor can confirm with additional tests.

  • A positive HBeAg indicates high levels of virus in the blood and a person is considered infectious.
  • A negative HBeAg indicates very low to no virus in the blood and a person is usually considered less infectious; sometimes this can indicate a person has a mutant hepatitis B virus (see below).

The hepatitis B e-antigen test result is often used to monitor the effectiveness of many hepatitis B drug therapies that aim to change a chronically infected person’s e-antigen status from “positive” to “negative.” By achieving a “negative” e-antigen result, this means that the hepatitis B drug successfully stopped or slowed down the virus replication. Although this is not a cure, stopping or slowing down the virus will result in less damage to the liver, which decreases the risk of developing serious liver disease in the future.

Some people with chronic hepatitis B naturally lose e-antigen and develop e-antibody, even without treatment. To make things a bit more confusing, however, there are some chronically infected patients with a high viral load who are untreated and still test “negative” for the hepatitis B e-antigen. So, the absence of e-antigen does not always mean there is no active viral replication. Instead, these persons have a mutant hepatitis B virus that does not produce the e-antigen. As a result, treating someone who is e-antigen negative (but with a high viral load) is difficult because the mutant hepatitis B virus is more resistant to the current drugs. In addition, the absence of e-antigen makes it harder to evaluate whether a drug is working or not.

anti-HBe or HBeAb (Hepatitis B e-Antibody) – This is not a protective antibody. It is made in response to the hepatitis B e-antigen. Chronically infected individuals who stop producing e-antigen sometimes produce e-antibodies. The clinical significance of this result is not fully understood, but it is generally considered to be a good thing. For those with e-antigen negative chronic hepatitis B infections (meaning they have a mutant virus), the presence of anti-HBe may still be associated with active viral replication.

Hepatitis B Virus DNA Quantification (“viral load”) – This blood test measures the amount of hepatitis B virus DNA (or viral load) in the blood of chronically infected patients. The blood is tested using a Polymerase Chain Reaction (PCR) technique that is highly sophisticated and accurate. The hepatitis B “viral load” provides important information, but should only be considered in relation to other information such as your e-antigen status and liver enzymes test results (see below). The viral load is usually measured in “international units per milliliter” (IU/mL), but may also be measured in “copies per milliliter”(cp/ml). There are approximately 5 copies in one international unit.

HBsAg Quantitative (quantitative hepatitis B surface antigen / qHBsAg) – This blood test measures the actual amount of hepatitis B surface antigen in the blood. When used in combination with the HBV DNA test, qHBsAg can provide a liver specialist with additional insights to an individual’s HBV infection. It can also be used in predicting and monitoring treatment response.

Hepatitis B Drug Resistance, Genotype, and BCP/PreCore Mutation – This blood test is not commonly ordered. A liver specialist may order the test to determine a patient’s hepatitis B virus genotype (A-H) for research purposes and to detect a viral mutation that may be associated with resistance to current treatments. This is a Polymerase Chain Reaction test, which again, is not readily available or used  outside large teaching hospitals.


Liver Related Blood Tests

The hepatitis B virus specifically attacks the liver, so health care providers will order blood tests to monitor the health of your liver. Some of the most common liver related blood tests are described below.

These blood tests measure potential liver damage (or liver inflammation). If a person is infected with the hepatitis B virus, the liver cells can be injured by the virus and then the liver enzymes can leak into the bloodstream. The higher the number, the greater the risk of potential liver damage.

ALT (alanine aminotransferase) is found almost exclusively in the liver and is monitored most closely in a chronic hepatitis B infection. This test is useful in deciding whether a patient would benefit from treatment or for evaluating how well a person is responding to therapy. The upper limits of normal for ALT in healthy adults is 35 U/L for men and 25 U/L for women.

AST (aspartate aminotransferase) is found in the liver, heart and muscle so is less accurate than the ALT in measuring liver damage. But this enzyme is often ordered to help monitor potential liver damage from the hepatitis B virus.

AFP (Alpha-FetoProtein) – This is a normal protein produced in the developing fetus, thus, pregnant women will have elevated AFP. Other adults, however, should not have elevated AFP in their blood. This test is used to screen for primary liver cancer patients with chronic hepatitis B. Patients should have their AFP levels monitored at every visit since hepatitis B is the leading cause of liver cancer. If the AFP level is high, the health care provider will order more blood tests and imaging studies.

Ferritin – Iron is stored in the liver in the form of ferritin. Increased levels of ferritin indicate that a high level of iron is being stored. This could result from an increased iron intake in the diet (vitamin supplements, food cooked in iron pots, etc.). For people living with chronic hepatitis B, a high level can indicate liver damage since ferritin is leaked into the bloodstream as liver cells are injured by the virus.


Additional Blood Tests Your Doctor May Order

If you have been diagnosed with chronic hepatitis B, your doctor may order a Hepatic Function Panel (Liver Function Tests, (LFTs), liver profile) and a Complete Blood Count (CBC).  A number of the blood test results included in these panels are useful in evaluating liver disease, in general, and are not necessarily specific to hepatitis B. Your doctor will be able to explain your personal results in detail, but the chart below provides a quick reference for interpreting your test results.


Normal Range

Abnormal Range

Abnormal Range

 Liver Enzymes   
Aspartate aminotransferase (AST) 30 IU/mL for men and 19 IU/mL for women 40-200 IU/L >200 IU/lL
Alanine aminotransferase
35 IU/mL for men and 25 IU/mL for women 40-200 IU/L >200 IU/L
Gamma-glutamyl transferase (GGT) <60 IU/L 60-200 IU/L >200 IU/L
Alkaline phosphatase <112 IU/L 112-300 IU/L >300 IU/L
 Liver Function Tests   
Total Bilirubin <1.2 mg/dL
(<20.5 umol/L)

1.2-2.5 mg/dL
(20.5-43 umol/L)

>2.5 mg/dL
(42.8 umol/L)
Albumin 3.5-4.5 g/dL 3.0-3.5 g/dL <3.0 g/dL
Prothrombin time <14 seconds 14-17 seconds >17 seconds
 Blood Count   

White blood count

>6000 3000-6000 <3000
Hematocrit (HCT) >40 35-40 <35
Platelets >150,000 100,000-150,000 <100,000
IU= International Unit L=liter dL=deciliter mg=milligrams




90,000 The liver is at risk. How to Watch Out for Liver Disease? What tests should be taken regularly?

It is believed that there are safe doses of alcohol and on the Internet you can find norms that seem to be recommended by the world health organization. In fact, WHO warns that there is no safe dose of alcohol .

We know that there is a level of alcohol consumption at which the risk of various ailments is low, but the WHO does not establish clear values ​​for such doses, medical evidence suggests that it is safer for health not to drink.The more a person drinks, the higher the risk of getting sick. Alcoholic liver disease, which leads to cirrhosis, can become one of the serious, but imperceptibly developing diseases of the liver.

Often, a person simply does not know about problems with the liver, because this organ is very patient – and until it suffers thoroughly, it tries not to betray the existing problems in any way. Therefore, it is better to periodically check the condition of the liver.

Will the liver hurt if you exceed the safe alcohol intake?

Since there are no nerve endings in the liver, it is “silent” for a long time.Unpleasant sensations of heaviness in the right hypochondrium, pain and discomfort may appear due to stretching of the liver capsule when its size increases. As for jaundice, pruritus, dark urine and light stool, these symptoms can be signs of hepatitis – damage and inflammation of liver cells of infectious or toxic origin. A more frequent symptom of liver disease is a lack of energy and increased fatigue, but since this symptom can be found in many other diseases. If painful symptoms bother, then you need to be examined.It is especially important to do this for those who do not adhere to the principles of a healthy lifestyle or have to take medications for a long time.

How to avoid liver disease? What tests should be taken regularly?

The best thing we can do for our liver is, without expecting symptoms, regularly once a year to take a biochemical blood test from a vein, checking the level of bilirubin (direct and total) and 4 liver enzymes (AST, ALT, thyroid thyroid hormone and GGT ). This test – Examination of the liver, basic – will assess the toxic effect of harmful substances on the cells of the organ.This examination is necessary if you suspect a current liver disease or in conditions associated with damage to the liver cells themselves, and with impaired outflow of bile.

Advanced complex Liver examination is most appropriate for patients with pre-existing liver diseases, both to assess the current state and to assess the effectiveness of the treatment. In addition to the above-mentioned analyzes, this complex includes a test for prothrombin, the level of total protein and protein fractions is determined, and the ability of the liver to synthesize the substances necessary for the body – cholinesterase and cholesterol is assessed.

There are many different tests for liver disease. What is the most accurate analysis?

Blood tests for total, direct and indirect bilirubin are an important marker for assessing liver function. They are usually prescribed when jaundice occurs or if liver disease (such as hepatitis) is suspected.

Alanine aminotransferase (ALT) is an enzyme of the liver cells. When liver cells are damaged, the level of ALT in the blood rises. Moreover, this happens long before the onset of jaundice.A significant (more than 10-fold) increase in ALT levels is usually associated with either acute viral hepatitis or acute toxic liver damage. A moderate increase in ALT (several times) is characteristic of chronic viral hepatitis, impaired outflow of bile and chronic diseases of the hepato-biliary zone, as well as alcohol abuse and liver damage in infectious diseases.

The second enzyme, aspartate aminotransferase (AST), is less indicative, but important in the complex diagnosis of liver function.It is usually given along with an ALT test.

An increase in alkaline phosphatase (ALP) can be observed in violation of the outflow of bile and other liver diseases, as well as in any form of cholestasis (difficulty in bile secretion).

GGT (gamma glutamyl transferase) is an enzyme involved in the metabolism of amino acids. Its increased concentration in the blood serum is most often a marker of the obstruction of the outflow of bile, as well as intoxication caused by alcohol or drugs.A blood test for GGT is important for the diagnosis of many liver diseases.

Why is there no one test, to assess the liver function is always offered to pass a set of tests?

In fact, it is very important to pass all tests in combination, because it is important to change each of the indicators in combination with each other. For example, high AST levels may indicate not only liver problems, but also damage to the heart muscle. Or, say, a simultaneous increase in GGT and ALP suggests cholestasis, but if GGT rises in isolation from ALP, then one can suspect that the whole point is in the long-term use of alcohol.An increase in alkaline phosphatase at normal GGT values ​​rather speaks not of liver disease, but of the presence of bone tissue diseases.

indicators, norm, decoding. Preparation for a blood test for biochemistry


Tavolzhanskaya Tatiana Vasilievna

Leading physician

Family doctor

Biochemical blood test is a laboratory research method that allows, based on the measurement of certain parameters, to get an idea of ​​the state of metabolism (proteins, carbohydrates, fats), as well as the work of various internal organs.This analysis is informative and quite reliable. Based on the results of the analysis, specialists can get an idea of ​​the functioning of the kidneys, liver, gallbladder, pancreas and some other organs, as well as identify the lack of trace elements and vitamins. A biochemical blood test is used in gastroenterology, therapy, urology, cardiology, gynecology and other areas of medicine.

When is a biochemical blood test prescribed?

The doctor may prescribe a biochemical blood test in the following cases:

  • in order to identify pathology.A biochemical blood test can help establish abnormalities in the work of an organ, even if there are no symptoms shown. That is why doctors recommend donating blood for biochemistry analysis twice a year as a screening examination. This will allow the detection of diseases at an early stage, which will greatly facilitate their subsequent treatment. The revealed changes in the chemical composition indicate an unfavorable situation and mean the need for medical intervention.
  • To clarify the diagnosis.The results of a biochemical blood test make it possible to clarify the picture of the disease and are a necessary addition to the examination data and patient complaints.
  • In order to monitor the course of treatment and the course of the disease. For this purpose, the analysis of biochemistry is prescribed for diseases of the internal organs (kidneys, liver, pancreas), vitamin deficiencies, and intoxication of the body.

Indicators of biochemical blood analysis: norm and deviations. Decoding of biochemical blood test

The required indicators for biochemical analysis are determined by the attending physician.The set of indicators may depend on the nature of the disease and the patient’s condition. Standard biochemical analysis includes the following main indicators:

  • total protein – total protein concentration. The norm is 65-85 g / l. An increased value of this indicator may indicate an infectious disease, arthritis, rheumatism or cancer. A lower value may indicate liver disease, intestinal disease, kidney disease, or cancer;
  • glucose .The norm is 3.5-6.5 mmol / l. The increased value of this indicator indicates the threat of diabetes mellitus;
  • urea – protein breakdown product. The norm is -1.7-8.3 mmol / l. An increased level of urea indicates a malfunction in the kidneys, urinary tract, may indicate heart failure, bleeding or tumors. A short-term increase in urea levels may be due to intense physical activity
  • cholesterol – a component of fat metabolism.The norm for total cholesterol is 3.5-5.7 mmol / l. An increased value of the indicator indicates the risk of diseases of the cardiovascular system, atherosclerosis or liver disease. Total cholesterol consists of three indicators – VLDL (very low density lipoprotein), LDL (low density lipoprotein) and HDL (high density lipoprotein). Lipoproteins of very low density and low density are deposited in plaques on the walls of blood vessels and contribute to the development of atherosclerosis. High-density lipoproteins, on the contrary, help to inhibit atherosclerosis, “pulling” cholesterol from the plaques.Normal values: for LDL – <0.9 mmol / L; for HDL -> 0.09 mmol / L.
  • bilirubin is a pigment resulting from the breakdown of hemoglobin. Norm: total bilirubin – 3.4-20.5 μmol / l. An increased value of the indicator can be caused by hepatitis, liver cirrhosis, poisoning and gallstone disease. Direct bilirubin (normal): 0-8.6 μmol / L.

Also, the indicators include: ASAT, ALAT (enzymes produced by the liver), creatinine, triglycerides, phosphorus, sodium, uric acid, magnesium, lipase, sodium, calcium, potassium and many others.

Preparation for biochemical blood test

In order for the results of the analysis to be accurate, blood should be donated for biochemistry on an empty stomach. This is best done in the morning. If it does not work out in the morning, then you should plan so that before donating blood for analysis, do not eat or drink anything other than water for at least 6 hours.

On the eve of the analysis, you do not need to eat fatty foods and take alcohol. It is advisable not to smoke for an hour before taking the test.

If you are taking any medications, you should inform your doctor. If medication cannot be interrupted, the study may have to be postponed.

Immediately before taking the analysis, it is advisable to sit down and be at rest for 10-15 minutes in order to exclude the influence of physical and emotional stress on the research results.

Where to take a biochemical blood test in Moscow?

You can take a biochemical blood test quickly and without queuing at the Family Doctor JSC.You can take a biochemical analysis at any of our clinics, choosing the one that is located in the district of Moscow you need. If you need the test results urgently, do a biochemical blood test in CITO mode. Tests in CITO mode can be taken in polyclinic # 15. Here you can take a biochemical blood test on weekends and holidays.

For analysis for biochemistry, about 5 ml is taken from the patient. blood from the cubital vein. The analysis is carried out on an automatic analyzer that allows measurements of more than 100 different parameters.The research results are entered into an electronic form – a research form.

The results of the analysis are interpreted by the doctor individually, depending on the results of the examination, other studies, the characteristics of the patient’s body and his condition.

Do not self-medicate. Contact our specialists who will correctly diagnose and prescribe treatment.

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90,000 What analyzes can tell about heart.

What are analyzes? Analyzes are confirmation or exclusion of a particular disease, which was an opinion after a clinical examination of a patient. With their help, the doctor will find out what exactly prevents your body from living and working normally, what is the state of its individual organs and systems.

So, what do these analyzes say if there are pains in the region of the heart? Determination of enzymes contained within cells is of great importance in the diagnosis of diseases associated with myocardial damage.And depending on which and how many cells die, their values ​​will also change.

Indicators of biochemical blood test:

ALT (alanine aminotransferase): to 68E / L, when assessing the level of this enzyme, it should be borne in mind that it is contained not only in the myocardium, but to a greater extent in the liver, therefore AST and ALT are always determined together, which helps in differentiating damage to the heart and liver. The timing of the increase in ALT is similar to that of AST.

AST (aspartate aminotransferase) : up to 45E / L, this enzyme is found in large quantities in the myocardium, and its increase, in most cases, indicates damage to cardiomyocytes – muscle cells of the heart; an increase in AST in the blood serum is observed in myocardial infarction (95-98%) cases within 6-12 hours from the onset of the disease.The maximum increase is noted on days 2-4, and on days 5-7, the enzyme level returns to normal. There is a clear relationship between the AST numbers and the size of the heart muscle necrosis focus. Therefore, if the amount of necrosis is less than 5 mm in diameter, it is possible to maintain the level of this enzyme within the normal range, which must also be taken into account.

LDH (lactate dehydrogenase) and the fractions that make up this indicator: up to 250 U / L, is considered a specific marker in AMI, an increase in the activity of the isoenzyme LDH1 and LDH2, even with normal indicators of total LDH activity, indicates the presence of small necrosis in the heart muscle.With AMI, its level rises rapidly by 2-4 days, and returns to normal only at 2-3 weeks. The LDH level provides valuable information about MI throughout the course of the disease. Other fractions LDH3 and LDH4 are enzymes of the lung tissue, LDH5 – liver.

CPK (creatine phosphokinase) and the fractions that make up this enzyme: up to 190 U / L, creatine phosphokinase – is considered a specific marker (especially an increase of more than 10 times) in acute myocardial infarction. It increases in the acute period (in the first 4-8 hours from the onset of the disease), much ahead of the activity of the above enzymes and is a marker of early diagnosis of AMI, especially the CPK-MB isoenzyme.After 8-14 hours, the CPK value can reach its maximum value, and normalization can occur in 3-4 days. Also, the value of CPK can increase with myocarditis;

troponin test: to 0.4 μg / l. Troponin is a specific contractile protein that is part of the structure of the heart muscle and skeletal muscles. This test is a diagnostic marker for suspected acute myocardial cell damage, is one of the key results in the diagnosis of acute myocardial infarction;

myoglobin: 12-92 μg / l.A muscle tissue protein that is involved in cell respiration. If it appears in the blood, it is regarded as a decay product of the muscle tissue of the heart or skeleton, with the appropriate clinic, it may indicate necrosis (necrosis) of the focus of the muscle tissue of the heart, therefore it is also considered a specific marker of this pathology.

Indicators of ALT, AST, CPK, CPK-MB, LDH, myoglobin and troponin test closely correlate with the size of the necrosis focus in the heart muscle, and therefore have not only diagnostic, but also prognostic value.

Acid phosphatase: 67-167 nmol / (s · L), increases in activity in patients with severe, complicated MI, mainly transmural;

C-reactive protein (CRP): up to 0.5 mg / l, its detection indicates the presence of a pathological process in the body, in particular inflammatory or necrotic. It belongs to the proteins of the so-called “acute phase”. A strongly positive reaction to CRP indicates the severity of the inflammatory process.

sialic acids: 2.0-2.36 mmol / l, the content of sialic acids may increase with endocarditis, MI;

electrolytes, mainly represented by ions K + (norm 3.6 – 5.2 mmol / l), Na + (norm 135 – 145 mmol / l), Cl- (norm 100 – 106 mmol / l), Ca2 + ( norm 2.15-2.5 mmol / l). An increased amount of potassium in the serum may be accompanied by a clinically disturbed heart rhythm, which is confirmed by an ECG. Atrioventricular blockade of the cardiac conduction system may develop, a syndrome of premature excitation of the ventricles, ventricular fibrillation, and such a formidable violation as cardiac arrest may develop.Therefore, patients with cardiac arrhythmias need to control the content of K + ions in the body. On the other hand, a decrease in potassium in the blood can also lead to adverse consequences in these patients – myocardial hyporeflexia. A decrease in the level of sodium ions can be accompanied by the development of insufficiency of the cardiovascular system, since the ratio of K + and Na + ions, as regulators of processes in the cell, is in constant interaction and a decrease in one leads to an increase in the other ion.Hyperchloremia occurs in patients with kidney disease and can also lead to the development of cardiovascular failure;

lipid spectrum, is associated in a common person with the word “cholesterol”. In this case, substances (lipoproteins of various densities, triglycerides) are determined that are involved in the exchange of cholesterol (CS) (the norm in the blood is 3.1 – 5.2 mmol / l). In addition to the value of total cholesterol, an important indicator is the coefficient of atherogenicity (the norm is up to 4), which shows the ratio of “good” and bad “lipids involved in the metabolism of fats and cholesterol, and the threat of the development or progression of atherosclerosis and all the ensuing consequences.An increase in lipoprotein and triglyceride fractions can be both a physiological state (alimentary in nature) and a pathological state. An increase in lipids is characteristic of widespread atherosclerosis, obesity accompanying and causing arterial hypertension. Or it would be more accurate to say that this is a disruption in the functioning of internal organs and intermediate links of lipid and triglyceride metabolism, expressed in an increase in the atherogenic index, causes the deposition of cholesterol in vessels of various diameters, the deposition of “reserve fat”, which leads to the above diseases.Therefore, with widespread atherosclerosis, in this blood test, you can see increased values ​​of ß-lipoproteins and total cholesterol. However, a decrease in the concentration of phospholipids can be seen. But at the same time, it is necessary to take into account the fact that there are age-related fluctuations in blood fats.

coagulogram – an analysis by which you can see the “viscosity” of the blood, or in other words, whether there is a threat of blood clots, which can lead to the formation of blood clots with different localization, which in turn can be complicated by pulmonary embolism, in which there is instantaneous death.Or, on the contrary, to see how high the likelihood of bleeding is and whether it will be able to stop on its own, after an operation, for example, to replace a heart valve.

Any analysis or research gives the doctor additional information that helps to more accurately diagnose, determine the stage of the disease, and prescribe treatment. Analyzes also help to control the course of the disease, the effectiveness of the prescribed treatment, as well as to ensure the safety of therapy. But sometimes more research is required to confirm or supplement the results of past analyzes.

Fedorova Lyubov Alekseevna – doctor of the first category, therapist, cardiologist of the Tet-a-Tet Medical Center.

ALT and AST are increased in the child

01/12/2021: ALT 1010, AST 636, Bil-n total 72, straight 52, ESR 52, Platelets 248, Erythr. 3.3. Leukocytes 6.7. Eosonof. 5. Rod eater. 7. Segment. 40. Lymphocytes 37. Monocytes 11 .. Hem-n106. Glucose 4.7. Total protein 69. Creatinine 64.7. Cholesterol 3.0. Ca 2.02. P 1.48. GGT 229.9.
18.01.2021: ALT 690, AST 815, B-n total 65, straight 50, ESR 45, Gem-n 101, Thrombus 210. 3.0. Leukocytes 6.0. Eze 3. Stick-eater. 4. Segment. 55. Lymphocytes 34. Monocytes 4.
01/25/2021: ALT 365, AST 260, Bil-n total 11, straight 1.0, ESR 24, Platelets 273, Gem-n 121. Total. protein 68. 3.5. Leukocytes 11.3. Eze 2. The stick-eater. 1. Segment 51. Lymphocytes 39. Monocytes 7.
01/29/2021: ALT 370, AST 195, Bil-n total 36, straight 15, ESR 32, Platelets 254, Gem-n 123. Erythr. 3.9. Leukocytes 14.3. Ezonof 1. The stick-eater. 2. Segment. 57.Lymphocytes 32. Monocytes 8.
02/08/2021: ALT 244.9, AST 158.6, ALP 111.1. Bil-n obshch. 32.7, straight 12.7, ESR 24, Platelets 131, Gem-n 127. Eritr. 4.01. Leukocytes 19. Ezonof 1. Stick-eater. 1. Segment 46. Lymphocytes 48. Monocytes 4.
16.02.2021: ALT 192.8, AST 122.9, ALP 105.5. Bil-n obshch. 24, straight 8.3, ESR 16, Platelets 127, Gem-n 123. Eritr. 3.7. Leukocytes 14.6. Ezonof 1. The stick-eater. 1. Segment 43. Lymphocytes 51. Monocytes 4.
02.24.2021: ALT 170.3, AST 99.8, ALP 95.5. Bil-n total 18.8, straight 6.2, ESR 20, Platelets Aggregation, Gem-n 123.Eritr. 3.75. Leukocytes 15.7. Ezonof 0. Stick-eater. 1. Segment 38. Lymphocytes 51. Monocytes 9.
03.03.2021: ALT 152, AST 101.7, ALP 92.1. Bil-n total 15.1, straight 4.6, ESR 14, Platelets 159, Gem-n 118. Erythr. 3.53. Leukocytes 14.8. Ezonof 1. The stick-eater. 1. Segment 43. Lymphocytes 52. Monocytes 3. Glucose 2.9.
03/09/2021: ALT 151.8, AST 116.5, ALF 93.3. Bil-n total 17.5, straight 5, ESR 16, Platelets 127, Gem-n 121. Eritr. 3.75. Leukocytes 13.2. Ezonof 2. The stick-eater. 1. Segment 46. Lymphocytes 48. Monocytes 3. Glucose 3.1.GGT 316.8.
03/19/2021: ALT 138.8, AST 96.8, ALP 87.1. Bil-n total 13.7, straight 3.8, ESR 16, Platelets 163, Gem-n 121. Eritr. 3.73. Leukocytes 13.1. Ezonof 1. The stick-eater. 2. Segment 46. Lymphocytes 46. Monocytes 5. Glucose 2.1. GGT 244.1.
04/08/2021: ALT 88, AST 63.1, ALT 82.5. Bil-n total 14.3, straight 2.8, ESR 16, Platelets 140, Gem-n 121. Eritr. 3.8. Leukocytes 13.2. Ezonof 0. Stick-eater. 1. Segment. 44. Lymphocytes 50. Monocytes 5. GGT 163.5.
04/19/2021: ALT 73.6 AST 58.8, ALP 76.7. Bil-n total 12.5, straight 2.3, ESR 10, Platelets 144, Gem-n 128.Eritr. 4.1. Leukocytes 12.1. Ezonof 1. The stick-eater. 1. Segment. 44. Lymphocytes 49. Monocytes 5.
REDUCTION of prednisolone to 10 mg 04/22/2021. Analysis 04/29/2021: ALT 83.2 AST 65.7, ALP 80.7. Bil-n total 12.9, straight 2.7, ESR 16, platelets 120, Gem-n 119. Erythr. 3.78. Leukocytes 10.8. Ezonof 0. Stick-eater. 1. Segment. 47. Lymphocytes 48. Monocytes 4.
05/05/2021: ALT 100.9 AST 74.5, Bil-n total 12.2, straight 3.2, ESR 15, Platelets 152, Hem-n 133. Erythr. 4.21. Leukocytes 10.3. Ezonof 2. The stick-eater. 1. Segment. 47.Lymphocytes 44. Monocytes 6. GGT 115.1.
The dose of prednisolone 15mg was increased on 05/07/2021. Analysis 05/17/2021: ALT 62, AST 45, Bil-n total 12.6, straight 3.9, ESR 15, Platelets 141, Hem-n 124. Erythr. 4.01. Leukocytes 10.4. Ezonof 2. The stick-eater. 1. Segment 41. Lymphocytes 50. Monocytes 5.
20.05.2021 reduced the dose of prednisolone 12.5 mg. Analysis 05/27/2021: ALT 57.8 AST 51.7, ALP 70.5. Bil-n total 11, straight 2.6, ESR 15, Platelet aggregation, Hem-n 135. Erythr. 4.31. Leukocytes 12.6. Ezonof 1. The stick-eater. 1. Segment 41.Lymphocytes 52. Monocytes 4.
06/03/2021 reduced the dose to 10 mg. Analysis 06/07/2021: ALT 75.8 AST 59.9, ALP 66.2. Bil-n total 12.3, straight 2.8, GGT 66.8.
Please comment on the test results. And is it correct for a pediatric gastroenterologist to reduce the dosage, which again leads to an increase in transaminases?

90,000 Evaluation of liver function tests. – obstetrics and gynecology, urology, therapy, endocrinology, ultrasound diagnostics, laboratory diagnostics

Evaluation of liver tests.


Many laboratory tests can be characterized by
as “liver function tests”. These include such biochemical
indicators like alanine aminotransferase (ALT), aspartate aminotransferase
(ACT), gamma glutamyl transferase (GTT), alkaline phosphatase (ALP), bilirubin
and serum proteins (including albumin). These tests also sometimes
called functional liver function tests and liver enzymes;
however, none of the definitions is completely accurate.Only
the first four can be called actually enzymes, and only the last two
reflect the actual function of the liver. Liver tests can be used to characterize
existing violations and approximately evaluate the synthetic function
liver. These tests are not fully diagnostic, although
their various combinations are useful in the diagnosis of specific diseases.
Several other liver function tests are described below.In the end
account, some tests help to identify specific causes of diseases
liver. Neither serological (for example, the determination of antibodies to the virus
hepatitis C), nor biochemical (for example, determination of the level of alpha1-antitrypsin)
tests are usually not used for screening analysis and routine
dispensary examination.


By means of true functional liver function tests, synthetic
liver function or its ability to absorb various substances and
remove them from the bloodstream, as well as metabolize and modify
injected diagnostic drugs.Determination of albumin level
– one of the most commonly used indicators in the clinic, although
it is not highly sensitive and is influenced by
malnutrition, kidney disease and other factors. Generally
low albumin levels indicate a decrease in synthetic
liver function. Determination of prothrombin time (PT) – other
a simple test that determines the ability of the liver
synthesize blood coagulation factors.Change in prothrombin
time is associated with both a violation of the synthesizing function of the liver, and
and with a deficiency of vitamin K. Increased prothrombin time and the absence
his reactions to the introduction of vitamin K inside (5-10 mg for 3
days) indicates liver disease or vitamin malabsorption
K due to obstruction of the bile duct or intrahepatic cholestasis,
preventing the flow of bile into the duodenum.Subcutaneous
or intravenous vitamin K helps with differential
There are various tests for determining the absorption and excretory
liver function; they use substances such as bromosulfophthalein,
tricarbocyanine dye, aminopyrine, caffeine, monoacylglycinexylidide.
They are often used to assess the severity of liver damage and to predict
the outcome of the disease for research purposes, but for clinical
practice they are rarely used.


Two main mechanisms of liver damage are
damage or destruction of hepatocytes (hepatocellular mechanism)
and impaired transport of bile (cholestatic mechanism). The reasons
parenchymal liver damage are most often viral
hepatitis, autoimmune hepatitis, as well as various toxic substances
and medicines.Bile transport is impaired due to extrahepatic
obstruction of the bile ducts (for example, gallstones or when
postoperative stricture), narrowing of the intrahepatic ducts (for example
with primary sclerosing cholangitis), damage to the bile ducts
(for example, with primary biliary cirrhosis) or transport disorders
bile at the level of small bile ducts (for example, when using
chlorpromazine).In some cases, both mechanisms of damage take place.
The most specific indicator of damage to the liver parenchyma is the level
ALT. The ACT level can also be increased (although this indicator
not so specific). On the contrary, about cholestatic liver damage
an increase in the level of alkaline phosphatase is more likely to indicate. Bile
acids stimulate ALP production, but blockage or damage
bile ducts prevent it from entering the duodenum
the intestine, which leads to a significant increase in the concentration of alkaline phosphatase in the serum
blood.The ALP level is slightly increased in the early stages of the lesion
hepatic parenchyma. However, this is due to the release
enzyme from hepatocytes, rather than stimulating its synthesis. Since ALP
produced in other organs (bones, intestines), concomitant
an increase in GGT and 5′-nucleosidase levels indicates cholestatic
mechanism of defeat.


In clinical practice, the level of
two serum trans-aminases – ALT and ACT.It is used to this day,
usually the old terminology for which ALT is called serum
glutamate pyruvate transaminase, and ACT serum glutamate oxalate transaminase.
The new names more accurately reflect the function of these enzymes, which is
in the transfer of amino groups from one compound to another.
As noted above, an increase in ALT and / or ACT levels indicates
about damage to hepatocytes.It is necessary to understand how the
these tests and what factors can alter their results. Most
ALT cases are determined by the following reaction:

This reaction requires ALT and pyridoxal phosphate
(vitamin B6). It is important to understand that with the help of enzymatic reactions it is determined
not the level of the enzyme itself, but (indirectly) its catalytic activity.This analysis does not show the level of ALT, but the rate of catalyzed
reactions. The result obtained is evaluated as follows: the higher
the reaction rate, the greater the amount of ALT. The lack of response is
in the inability to determine the amount of its products when increasing
ALT level. Therefore, a reaction with a bound enzyme is used instead:

which takes place in the presence of another enzyme
– lactate dehydrogenase.During the reaction, oxidation of the reduced
nicotinamide adenine dinucleotide (N ADN), and as a by-product
its unreduced form (NAD +) is formed. OVER + absorbs light
wavelength 340 nm. Absorption is recorded using a spectrometer
and is used to determine the activity of ALT. As a result, the number
the enzyme can only be estimated indirectly. On the speed of reaction
several factors affect: temperature, concentration of substances, quantity
enzymes or cofactors, the presence of impurities inhibiting the reaction, and
See also the sensitivity of the spectrometer.For example, if the patient has
deficiency of pyridoxal phosphate, i.e. it is not enough for staging
test reaction, its speed will slow down, and ultimately there will be
received a false result of low ALT activity. This effect is often
observed in alcoholics (whose nutrition is reduced), since a deficiency
vitamin B6 leads to a limitation of the reaction rate to a greater extent,
than the ALT level.
The second controversial issue: what can be considered a normal level, and what
– a deviation from the norm? This is usually done in a local laboratory.
in an arbitrary way, for which a small group of “healthy” patients is selected
(often from a blood bank) that have their ALT levels determined and calculated
mean and standard deviation.Borders are randomly selected;
they usually correspond to the maximum and minimum values,
which were obtained from 2.5% of the selected population. However, such
the technique is unsuccessful, since the ALT level depends on many demographic
factors. In men, it is higher than in women. Obese women
have higher ALT levels than people whose weight is close to ideal.
Some racial groups have a level of
ALT is also higher.Therefore, if the examined group of patients consists of
of thin women (especially of the Caucasian race) who had
donate blood, the limits of the norm will be very low, as a result
many overweight men will have high ALT levels
even in the absence of disease. This is typical for all enzymatic
reactions described in this chapter. Therefore, the higher the level
(speed) of enzymatic reactions deviates from the norm, the more
the presence of the disease is likely.Conversely, in patients with asymptomatic
the course of liver diseases even with significant lesions of the parenchyma
ALT levels may be normal.

Therefore, the ALT level is an unreliable marker of pathological
process in the liver. With massive lesions of the hepatic parenchyma
(for example, with viral hepatitis, toxic hepatitis – poisoning
paracetamol, solvents, or fly agaric) ALT levels may be
significantly increased.In particular, with a severe overdose of paracetamol
ALT value often reaches 2000 U / L (which is about 50 times higher than
the upper limit of the norm). This indicates a significant yield
enzyme from damaged hepatocytes. In patients with chronic viral
hepatitis, ALT levels are usually higher than normal
5-10 times.


TIF – an enzyme that catalyzes the transfer of phosphate
groups.Its various isoenzymes are produced in the liver, bones and
intestines. Most hospital laboratories have equipment for
there is no separate determination of various forms of alkaline phosphatase and its source,
which leads to some difficulties in diagnosis. According to the survey
a large group of hospitalized patients, only in 65% of cases high
ALP was associated with liver disease. Increase in the level of the “hepatic” fraction
enzyme is a consequence of stimulating its synthesis with a local increase
concentration of bile acids.This occurs when cholestasis occurs,
caused by drugs, and with intra- or extrahepatic
obstruction of the biliary tract. Test reaction for determination of alkaline phosphatase:

The detection of nitrophenyl indicates the presence of
ALF. Although this reaction is not associated with an enzyme, however, problems
arising from the determination of enzyme activity and the establishment of boundaries
norms are similar to those of serum transaminases.Simultaneous
increased levels of TIF and gamma-glutamyl transpeptidase (or 5′-nucleosidase)
testifies in favor of liver disease and indicates the presence


– a decay product of erythrocytes – exists in two forms: conjugated
and unconjugated. Unconjugated bilirubin appears in plasma,
when the rate of destruction of red blood cells exceeds reserve capacity
liver by its transformation (which is often found in patients with hemolytic
anemia).A genetically determined deficiency of certain enzymes leads to
to the fact that the process of conjugation of bilirubin in the liver is wrong
or incomplete. This is most often seen in Gilbert’s syndrome.
(Gilbert), which is characterized by a relative deficiency of glucuronyl transferase
and mild hyperbilirubinemia. When fasting or
reducing the calorie intake of food (for example, in patients with viral
gastroenteritis), the level of bilirubin in the blood rises in the first place
due to its unconjugated form.If the bilirubin fractions are not tested,
a patient with abdominal pain, nausea, vomiting and hyperbilirubinemia
may be misdiagnosed as cholecystitis. Faction research
bilirubin helps to avoid unnecessary cholecystectomy
when misdiagnosed. Most often level research
bilirubin includes a biochemical reaction with the calculation of the so-called
excess time.In most laboratories, only
total bilirubin. The amount of indirect (unconjugated) bilirubin
can be calculated if the reaction is stopped at a certain time and
subtract the resulting value from the value that determines the total bilirubin.
Accurate measurement of the amount of bilirubin and its fractions is possible using
chromatography, the equipment for which is far away
not in all laboratories.Conjugated bilirubin levels rise
for many diseases: viral, toxic, medicinal and alcoholic
hepatitis, liver cirrhosis, metabolic disorders, obstruction
intra- and extrahepatic bile ducts.


In patients with liver diseases in a planned manner
specific laboratory tests are used to identify
some metabolic disorders.Hemochromatosis is a disease characterized by
excessive deposition of iron in the liver and other organs. Most likely
the cause of this disease is a violation of the regulatory mechanism
absorption of iron in the small intestine. For years, its reserves
increases in the liver, pancreas, heart and other organs.
Most often, as a screening test for hemochromatosis, they use
determination of serum ferritin levels.Its rise indicates
on the possibility of excess iron content in the body. but
ferritin levels also increase in the acute phase of inflammatory
process, so the results obtained can often be false positive.
When ferritin levels rise (usually => 400 μg / L), it is necessary to
determine the level of serum iron and iron binding capacity
(TIBC) blood. If the ratio of serum iron to TIBC exceeds
50-55%, then, most likely, the patient has hemochromatosis (and
not hemosiderosis – secondary excess iron deposition in tissues).The most reliable is the quantitative determination of iron in
biopsy of liver tissue. Then the age adjustment is calculated,
Iron Age Index:

Data has been obtained that in establishing a diagnosis can
help magnetic resonance imaging. MRI allows you to limit
range of indications for liver biopsy.

Alpha1-antitrypsin – an enzyme produced by the liver,
which helps break down trypsin and other tissue proteases.Described
many modifications (isoforms) of this enzyme, which depend on
alleles obtained from both parents, and therefore in one person
one or two forms of alpha1-antitrypsin can be found in the blood.
Z-form (so called because of its special electrophoretic activity
in gel) is a product of a genetic mutation of one of
amino acids of a widespread type of proteins – M-protein.Z-protein
is hardly released from liver cells and causes local damage,
which can lead to hepatitis or cirrhosis. To diagnose
three tests help. The first is the electrophoretic study of proteins
serum (EBS). Under the influence of an electric field, blood proteins move
in a gel and are separated; in this case, several bands are formed. One of
them, the alpha! band consists predominantly of alpha1-antitrypsin.Therefore, the deficiency of alpha! -Antitrypsin leads to its decrease. Second
the test consists in a direct assessment of the amount of enzyme using
monoclonal antibodies. The degree of binding is measured with a spectrophotometer
by the nephelometry method. The third way is to determine the phenotype of alpha1-antitrypsin.
Only a few laboratories in the United States have the ability to do this.
research aimed at recognizing the alleles of the protein contained
in serum (MM, ZZ, MZ, FZ).Patients with type ZZ protein have
homozygous alpha! -antitrypsin deficiency. This form is most often
accompanied by severe liver disease. If in hepatocytes
contains Z-protein, it can be found in liver tissue in the form
small globules stained with Schiff’s dye (PAS-positive
reaction) and resistant to the action of the enzyme diastase. In some
in hospitals, the immunofluorescence reaction is also used.

Wilson’s disease – impaired assimilation
and the accumulation of copper associated with a deficiency of the enzyme contained
in liver cells. Like iron, copper can be deposited in
many tissues of the body. Nevertheless, it accumulates mainly
in certain places. Copper deposits are found in the cornea (rings
Kayser-Fleischer) and some parts of the brain.Many
chole-static liver disease (for example, primary biliary
cirrhosis) also lead to excess copper accumulation, but copper deposits
never reach the same size as in true Wilson’s disease.
The main screening test is to determine the level of ceruloplasmin in
serum, which is reduced in 95% of individuals with Wilson’s disease. Ceruloplasmin
is a protein of the acute phase of inflammation, therefore its content increases
in patients with inflammatory processes, in whom its baseline level
was normal or low.In the process of monitoring patients regularly
the level of copper in urine and blood serum is assessed. Liver biopsy
with the subsequent quantitative assessment of the copper content in it allows
make a final diagnosis. Copper deposits in tissues are stained
special dyes (for example, rhodanine).

Diagnostic tests for the most common
metabolic disorders of the liver

Hemochromatosis Serum ferritin level> 400 μg / L TIBC> 55% Iron Age Index> 2
Alpha1-antitrypsin deficiency Serum protein electrophoresis or determination of the level of monoclonal
antibodies to alpha 1-antitrypsin
Determination of the phenotype (Pi-type) Liver biopsy with detection of PAS-positive, diastase-resistant
Wilson’s disease Ceruloplasmin level <10 mg / dL Urine / serum copper> 80 μg / 24h Liver biopsy (quantitative content of copper in tissue> 50
μg / g)

To many other hereditary
liver diseases include Gaucher disease, Niemann-Pick disease
(Niemann-Pick) and hereditary tyrosinemia.These rare diseases
usually diagnosed in children. Specific diagnostic methods
studies not covered in this chapter


– antibodies to specific cellular components that
epidemiologically associated with the development of specific diseases
liver.These include antinuclear antibodies (ANA), antibodies
to smooth muscle (ASMA, also called anti-actin antibodies),
antibodies to liver and kidney microsomes type 1 (LKM-1), antimitochondrial
antibodies (AMA), soluble hepatic antigen (SLA) and antibodies
to sialoglycoprotein receptors. Most commonly used tests
to determine ANA, ASMA and AMA; they allow you to diagnose
the most common autoimmune liver diseases.At present
time definition of SLA in the USA is not always possible. Antibodies are detected
using the following reaction: the cell culture is treated with serum
the patient, after which the formed antigen-antibody complex (AG-AT) is “labeled” bound
with fluorescein human antibodies. The resulting triple
the complex is detected by fluorescence microscopy. Separation
cells are carried out in accordance with the intensity of the luminescence and
with which part of the cell binds antibodies.Thus, the definition
the level of antibodies and the division of the results into positive and negative
very subjective. Most hepatologists make these tests in
diagnostic algorithm only if positive
results with titers greater than 1: 80 – 1: 160. ANA and ASMA
more often found in the elderly, women, and also in patients
with many other liver diseases.Therefore, the diagnosis of autoimmune
liver disease is based on the general clinical picture; at
this takes into account the age, sex of the patient, the presence of other autoimmune
processes, levels of gamma globulins and the results of liver biopsy.
It should be noted that with various autoimmune diseases, it is possible
detection of the same antibodies. The table is presented in general
features one of the classifications of autoimmune liver diseases.Was
a new scoring system is also proposed, in which the authors have tried
take into account the factors mentioned above.

Classification of autoimmune liver diseases

Type I, classic lupoid hepatitis ANA and / or ASMA
Type II, autoimmune hepatitis LKM-1
Type III, autoimmune hepatitis SLA
Primary biliary cirrhosis AMA


research methods performed with suspicion of the presence of diseases
liver, include the determination of levels of transaminases, bilirubin
and alkaline phosphatase. History, physical examination and assessment
risk factors help to decide which specific diagnostic
tests are required on a case-by-case basis.Sometimes
there are patients with latent liver diseases, the level
enzymes in which it is normal or slightly different
from such. In some patients with isolated elevation
the level of enzymes fails to diagnose any disease.
As a rule, before proceeding with a full (detailed) examination
the patient, you should double check the level of liver enzymes for
excluding laboratory error.With many diseases (for example
hepatitis B and hepatitis C) it is necessary to prove the presence of chronic
process (when pathological changes persist for more than 6
months) before starting treatment or to confirm
diagnosis or staging of the disease plan implementation
liver biopsy. Typically, the standard waiting period may vary.
depending on the severity of enzyme disorders and the likelihood
detection of a curable process.For example, a woman with increased
10 times the level of transaminases, an autoimmune thyroid disease
a history of glands and an increased globulin fraction,
apparently, exacerbation of a previously unrecognized autoimmune
hepatitis A. Determination of the autoimmune profile and early biopsy
liver will help to confirm this assumption and start on time
treatment with steroid hormones and other immunosuppressants.

marker of the rate of aging of the liver and the risk of mortality

Alanine aminotransferase (ALT) is an intracellular enzyme that is involved in the conversion of the amino acid alanine. Normally, the level of ALT in the blood is low, but with liver disease and cell destruction, it increases sharply.
ALT is often compared to the level of aspartate aminotransferase (AST), an enzyme that converts the amino acid aspartate (also called aspartic acid), also intracellular and produced mainly in the liver, heart and other muscles.When the cells of these organs are destroyed, the amount of AST in the blood also increases.

Fig. ALT / AST ratio in case of damage to the heart muscle and liver

If the elevated ALT level exceeds the elevated AST level, the liver is considered damaged (Fig.). If AST rises more than ALT, problems with the cells of the myocardium (heart muscle) or inflammation in other muscles are suggested. It should be noted that an increase in ALT levels may not always be associated with liver disease, it is observed, for example, with problems with the bile ducts.In order not to start sounding the alarm about the liver ahead of time, the level of alkaline phosphatase should be measured. Anticonvulsant, anti-inflammatory, and many other drugs, including paracetamol, antibiotics, statins, can increase ALT levels [274].

Fig. Change in the level of ALT in the blood with age [275, 276]

A decrease in the content of ALT in the blood plasma is possible with renal failure, deficiency of pyridoxine (vitamin B6), after hemodialysis and during pregnancy.

Dr. David Le Cooter from Australia with colleagues in 2010 found that over the age of 70, the ALT level decreases down to 16.8 U / L (Fig.). This increases the likelihood of sarcopenia (atrophic degeneration of skeletal muscle), wasting and low activity levels, and decreases survival. Traditionally, people with elevated ALT levels in the blood were thought to die earlier, but this study shows that people with very low ALT levels also have higher mortality, probably due to the fact that low ALT levels reflect the development of sarcopenia [275, 276].Sarcopenia is an age-related change in skeletal muscle, leading to gradual loss of muscle mass and even death. In fig. 16 shows that ALT first increases by about 50 years of age, and then tends to decrease. Perhaps this is because by the age of 50, liver damage gradually accumulates, which is reflected in an increase in ALT. Later, the age-related involution of the liver occurs, the number of its cells decreases, and at the same time the level of ALT released into the blood decreases.At the same time, after the age of 50, the level of muscle mass decreases as a result of sarcopenia, which leads to a lower production of ALT by muscle cells [275, 276, 277].
As revealed by a study of Scottish scientists in 2011, the decrease in ALT with age below 14–17 U / L is inversely related to overall mortality [278]. A population study of Danish twins has shown that in older twin pairs (73–94 years), higher ALT is not associated with mortality risk [279].
In 2014, a group of researchers from Israel also showed in 23,506 patients that ALT values ​​below 17 U / L may be a predictively unfavorable indicator of overall mortality in middle-aged people.The dependence of
survival on ALT levels (above or below 17 U / L) persisted even after adjusting for age, gender, GFR, low albumin levels, arterial hypertension, diabetes mellitus and coronary heart disease incidence [280].

Note: if the ALT level in a person’s entire life was, for example, 8 U / L, then this is probably the norm for a particular person. But if ALT was always higher than 14–17 U / L and suddenly became, for example, 8 U / L, this is a reason to consult a doctor.

The optimal ALT value is 17-30 U / L for men and 14-30 U / L for women.

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How to Optimize ALT Level

The reasons for the increase in ALT above the normal value are varied: hepatitis B, C or D, alcohol consumption, non-alcoholic fatty liver disease, and first of all, treatment should be directed to them [281]. Before taking any action, it is necessary to re-take a blood test to make sure that the ALT level is indeed elevated. It is also necessary to exclude another possible reason for the increase in ALT, for example, the use of any drugs: anti-inflammatory, antibiotics or statins [274].
In Russia, the so-called hepatoprotectors are used to protect the liver; they are presented on the market with more than 700 drugs [282, 283]. However, in the international drug classification system, there is no association of drugs under the general name “hepatoprotectors” at all. The effectiveness of most hepatoprotectors has not been confirmed by clinical trials. And some of them are potentially harmful and can have toxic effects on the liver [284].
In high-dose paracetamol (acetaminophen) treatment, the use of acetylcysteine ​​as a cover-up therapy is considered hepatoprotective [285].
Steatohepatitis is an inflammatory process in the liver against the background of its fatty degeneration. Most recently, Intercept Pharmaceuticals has successfully completed a Phase III clinical trial of obeticholic acid for the treatment of non-alcoholic steatohepatitis. It is likely that soon an effective drug for the treatment of the liver will appear in pharmacies for the first time, although at first it is very expensive [286].
Thus, it is advisable to treat the underlying disease leading to an increase in ALT, and not just a decrease in the level of the enzyme, especially since the effectiveness of almost all hepatoprotectors has not been proven.
While at a young age, too low ALT levels are not associated with an increased risk of mortality, in people over 65 years of age it is the opposite [275, 281]. But this does not mean at all that you need to increase ALT. A decrease in ALT in old age signals that sarcopenia is likely to develop – a decrease in muscle mass is one of the causes of death in older people [287].And in this case, it is advisable to prevent or slow down the development of this process with the help of regular aerobic exercise and muscle training with bodyweight exercises. Otherwise, a person may lose at least 1 year of life [288].

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274. Watkins P.B., Kaplowitz N., Slattery J.T. et al. Aminotransferase elevations in healthy adults receiving 4 grams of acetaminophen daily: a randomized controlled trial.JAMA. 2006 Jul 5; 296 (1): 87-93. doi: 10.1001 / jama.296.1.87. www.ncbi.nlm.nih.gov/pubmed/16820551 (date accessed: 01/29/2021).
275. Le Couteur D.G., Blyth F.M., Creasey H.M. et al. The association of alanine transaminase with aging, frailty, and mortality. J Gerontol A Biol Sci Med Sci. 2010 Jul; 65 (7): 712-7. doi: 10.1093 / gerona / glq082. www.ncbi.nlm.nih.gov/pubmed/20498223 (date accessed: 01/29/2021).
276. Elinav E., Ben-Dov I.Z., Ackerman E. et al. Correlation between serum alanine aminotransferase activity and age: an inverted U curve pattern.Am J Gastroenterol. 2005 Oct; 100 (10): 2201-4. doi: 10.1111 / j.1572-0241.2005.41822.x. www.ncbi.nlm.nih.gov/pubmed/16181369 (date accessed: 01/29/2021).
277. Ozer J., Ratner M., Shaw M. et al. The current state of serum biomarkers of hepatotoxicity. Toxicology. 2008 Mar 20; 245 (3): 194-205. doi: 10.1016 / j.tox.2007.11.021. www.ncbi.nlm.nih.gov/pubmed/18291570 (date accessed: 01/29/2021).
278. Ford I., Mooijaart S. P., Lloyd S. et al. The inverse relationship between alanine aminotransferase in the normal range and adverse cardiovascular and non-cardiovascular outcomes.Int J Epidemiol. 2011 Dec; 40 (6): 1530-8. doi: 10.1093 / ije / dyr172. www.ncbi.nlm.nih.gov/pubmed/22158663 (date accessed: 01/29/2021).
279. Fraser A., ​​Thinggaard M., Christensen K., Lawlor D.A. Alanine aminotransferase, gamma-glutamyltransferase (GGT) and all-cause mortality: results from a population-based Danish twins study alanine aminotransferase, GGT and mortality in elderly twins. Liver Int. 2009 Nov; 29 (10): 1494-9. doi: 10.1111 / j.1478-3231.2009.02090.x. www.ncbi.nlm.nih.gov/pubmed/19686309 (date accessed: 29.01.2021).
280. Ramaty E., Maor E., Peltz-Sinvani N. et al. Low ALT blood levels predict long-term all-cause mortality among adults. A historical prospective cohort study. Eur J Intern Med. 2014 Dec; 25 (10): 919-21. doi: 10.1016 / j.ejim.2014.10.019. www.ncbi.nlm.nih.gov/pubmed/25468741 (date accessed: 01/29/2021).
281. Vento S., Nobili V. Aminotransferases as predictors of mortality. Lancet. 2008 May 31; 371 (9627): 1822-3. doi: 10.1016 / S0140-6736 (08) 60778-3. www.ncbi.nlm.nih.gov/pubmed/18514716 (date accessed: 29.01.2021).
282. Register of medicines in Russia. (RLS) Pharmacological group – Hepatoprotectors. (Electronic resource) URL: www.rlsnet.ru/fg_index_id_222.htm (date of access: 01/29/2021).
283. Register of medicines of Russia. (RLS) Pharmacological group – Hepatoprotectors. (Electronic resource) URL: www.rlsnet.ru/fg_index_id_222_sort_mnn.htm (date accessed: 01/29/2021).
284. Specialized medical portal Health-ua.com. Efficiency and safety of hepatoprotectors from the point of view of evidence-based medicine.03/27/2015. (Electronic resource) URL: http://health-ua.com/article/15676-effektivnost-i-bezopasnost-gepatoprotektorov-s-tochki-zreniya-dokazatelnoj- (date of access: 01/29/2021).
285. Barton S. Acetylcysteine ​​for Acetaminophen Overdose. Utox Apdate. 2005. Volume 7. Issue 1. (Electronic resource) URL: https://poisoncontrol.utah.edu/newsletters/pdfs/toxicology-today-archive/Vol7_No1.pdf (date accessed: 29.01.2021).
286. Von Reuss T. “Okaliva”: an important drug for the treatment of primary biliary cholangitis.Published on May 28th, 2016. Updated 12.21. (Electronic resource) URL: https://mosmedpreparaty.ru/news/16226] [https://mosmedpreparaty.ru/news/7907 (date of access: 01/29/2021).
287. Vespasiani-Gentilucci U., De Vincentis A., Ferrucci L. et al. Low Alanine Aminotransferase Levels in the Elderly Population: Frailty, Disability, Sarcopenia, and Reduced Survival. J Gerontol A Biol Sci Med Sci. 2018 Jun 14; 73 (7): 925-930. doi: 10.1093 / gerona / glx126. www.ncbi.nlm.nih.gov/pubmed/28633440 (date accessed: 29.01.2021).
288. Peltz-Sinvani N., Klempfner R., Ramaty E. et al. Low ALT Levels Independently Associated with 22-Year All-Cause Mortality Among Coronary Heart Disease Patients. J Gen Intern Med. 2016 Feb; 31 (2): 209-214. doi: 10.1007 / s11606-015-3480-6. www.ncbi.nlm.nih.gov/pubmed/26245731 (date accessed: 01/29/2021).

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Liver indices of the biochemical blood test

Liver diseases are a frequent occurrence, since this organ has a large load.This most important organ performs many functions, in particular, it is involved in metabolic processes and neutralizes toxins.

If a liver disease is suspected, the doctor first of all recommends donating blood for special biochemical tests. One of these indicators of liver function is total bilirubin, the rate of which ranges from 3.4 to 20.5 μmol / l.

It is worth considering that the level of blood counts in children and women during pregnancy has its own norms. After deciphering the analysis, an ultrasound of the liver tissue can be additionally recommended.

About the appointment of biochemical tests

The first thing that the doctor suggests to the patient in case of suspicion of a particular disease is to donate blood. Indeed, biochemical tests for liver diseases can tell a specialist a lot. We, of course, are not specialists, but it is necessary for the patient to know what features the analyzes have for liver disease. At least in order to own information.

When taking blood, which must be done on an empty stomach, liver indicators of a biochemical blood test are studied, such as hepatic cytolysis enzymes, indicators of cholestasis and protein-synthetic liver function.

Let’s consider each of these points in more detail and remember how the biochemistry of blood in liver diseases differs from the normal state of a healthy person.

Indicators of aspartate aminotransferase (AsAT)

AsAT is a cellular enzyme that takes part in the exchange of amino acids. Since it is contained in sufficient quantities in such important organs as the heart, kidneys, liver, a blood test for liver disease can reveal its increased content.This may indicate acute hepatitis, liver cancer, congestive or hemolytic jaundice.

AsAT norms:

  • for women – no more than 31 units / l
  • for men – no more than 41 units / l

Alanine aminotransferase (ALT) values ​​

This is a hepatic enzyme, also involved in the metabolism of amino acids. When the liver (and other organs) is destroyed, cells are released into the blood, therefore, blood biochemistry in liver diseases, such as chronic and acute hepatitis, tumors, congestive jaundice, will show its increased content.

AlAT norms:

  • for women – no more than 31 units / l
  • for men – no more than 41 units / l

Indicators of alkaline phosphatase

An important participant in the exchange of phosphoric acid. If a blood test for liver disease reveals an elevated level, then this may confirm malignant neoplastic liver diseases.

Alkaline phosphatase norms:

  • for women – no more than 240 units / l
  • for men – no more than 270 units / l

Indicators of gamma glutamyl transpeptidase (gamma GT)

Content of this enzyme (participates in the synthesis of amino acids) in the blood of a healthy person is negligible.Biochemical indicators of liver function, characterized by an increased content of this enzyme, may indicate some diseases of the liver, pancreas and other organs of the gastrointestinal tract.

GGT norms:

  • for women – no more than 32 units / l
  • for men – no more than 49 units / l

Indicators of bilirubin

This breakdown product of hemoglobin is part of bile and shows very well how it works liver. Elevated bilirubin is usually detected with obstruction of the biliary tract, hepatitis.The norm is no more than 20.5 mmol / l.

Indicators of albumin

Biochemical analyzes for liver diseases necessarily take into account the amount of albumin – the main protein in the blood, which is produced in the liver. When it decreases, there are grounds to talk about the death of liver cells, cirrhosis, malabsorption, etc. Normally, albumin is contained in the blood in an amount of 35-50 g / l.

Indicators of cholinesterase (ChE)

Cholinesterase is formed in the liver. Its indicators are used for a more complete assessment of liver function.If the patient has chronic liver disease, especially cirrhosis, its indicators begin to decline significantly. The rate of cholinesterase is 5300-12900 U / L.

Prothrombin index

Prothrombin is one of the main indicators of a coagulogram characterizing blood coagulation. Its synthesis takes place in the liver, and its analyzes in case of liver disease make it possible to assess the work of this organ, to identify and confirm diseases. The rates of prothrombin are 78-142%.

Blood biochemistry in liver cirrhosis

According to the results of a blood test, liver cirrhosis can be considered as deviations from the norm in a number of characteristics.But it is worth noting that this disease cannot be diagnosed without a complete, comprehensive examination of the patient. Therefore, to focus only on the indicators of a biochemical blood test in liver cirrhosis would be wrong, wrong.

The liver is the biochemical center of the whole organism. It produces proteins and breaks them down, plays an important role in carbohydrate metabolism, the metabolism of fats and cholesterol, which are broken down with the participation of bile and synthesized in the liver, bilirubin is involved in the synthesis and formation of bile, nitrogen is broken down in the liver, the liver breaks down various toxins and harmful substances, waste unnecessary steroid hormones, biogenic amines and other substances.

With cirrhosis, quite specific changes are registered in blood biochemistry. How do blood biochemistry indices change in liver cirrhosis?

  • bilirubin – an increase in total and over is observed;
  • transaminase – increase;
  • gamma glutamyl transpeptidase – increase;
  • alkaline phosphatase – increases;
  • albumin (proteins) – a decrease in the parameter is observed;
  • proteins – globulins increase;
  • prothrombin – decreases;
  • urea – reduction;
  • cholesterol – decrease;
  • haptoglobin – an increase in relation to the norm;
  • liver enzymes – increase.

Biochemical blood tests for liver cancer

When analyzing blood biochemical parameters for the diagnosis of liver cancer, it is necessary to pay attention primarily to the concentration of bilirubin. Bilirubin has two fractions: direct and indirect. An increase in any of the fractions alerts the doctor about the possible danger to the liver.

If the indirect fraction in 75% does not reflect the real picture of the liver condition, then an increase in the direct fraction or a combined increase in the direct and indirect fractions in 97% of cases indicate the disintegration of liver cells, but what caused this pathological process – cancer, cirrhosis or inflammation – this remains to be determined by other methods.Moreover, any deviation from the norm is an alarm signal.

In addition to bilirubin, one should pay attention to the so-called liver enzymes, which have the abbreviations ALT and AST. In modern analysis, they are collectively referred to as “transaminases”, which is synonymous. An increase in these indicators clearly indicates liver pathology. But the severity of the increase in concentration may fairly reflect the severity of the process – here the dependence is directly proportional.The greater the deviation from the norm, the stronger the inflammatory or other (pathological) process.

Less specific, but nevertheless significant is the increase in blood and other enzymes, such as alkaline phosphatase .

It is especially worthwhile to closely monitor the oncomarker – AFP, although it does not directly relate to blood biochemistry in liver cancer. Alpha-fetoprotein is a protein that plays a key role in the maturation of the nervous system in the fetus in the womb.At birth, its concentration drops rapidly, and eventually only traces of this protein are found in the blood of a six-month-old baby. It is important to understand that any increase in alpha-fetoprotein, even in old age, is considered a pathology – in most cases we are talking about liver cancer.

What is included in the biochemical blood test for the liver

Let’s systematize all known biochemical blood parameters that indicate liver pathology. We will try to answer the question: what indicators of blood biochemistry indicate the liver.

Enzymes (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, glutamate dehydrogenase, sorbitol dehydrogenase, gamma-glutamyltransferase, fructose monophosphate).

Let us explain what an enzyme is – a protein molecule that accelerates a certain biochemical reaction in the body at a certain temperature and other conditions of the body’s environment. Assessing the enzymes in aggregate, one can judge about metabolic disorders associated with certain liver pathologies.

Proteins, fats and electrolytes (total protein, albumin, bilirubin, cholesterol and its fractions, triglycerides, ammonia, iron, prothrombin index). Prothrombin is a protein produced in the liver and is a precursor to thrombin.

Preparation for donating blood for liver biochemistry

Preparation for donating biochemistry is quite simple, the main thing is to follow all the recommendations of your attending physician. The leading requirement is an empty stomach before examination.The time of day is not important, however, the morning hours are most convenient for both the patient and the laboratory. Nevertheless, it can be evening, the main thing is that at least six hours have passed after the last meal, or better – 8.

Snack is also undesirable. Snacks include tea, coffee, especially the sweeter dishes. The most suitable is absolutely pure plain water. You can drink it without any problems.

Nutrition before donating blood for liver biochemistry is also important.In the evening before your scheduled blood test, try not to eat tightly. This will put an increased strain on the gastrointestinal tract. Try to follow a diet that restricts fatty, fried, salty foods two to three days before taking liver biochemistry.