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Liver chart levels: Normal, High, and Low Ranges, Chart & Results


Middle-aged Woman With Abnormal Liver Enzyme Levels

This case is typical of non-alcoholic fatty liver disease (NAFLD), formerly called non-alcoholic steatohepatitis. This condition is now the most common cause of elevated liver enzyme levels in the United States; thus, choice A is true.

Epidemiology. The epidemiology of this condition parallels that of the increasingly prevalent metabolic syndrome. NAFLD becomes more common with increasing body weight: it affects roughly two-thirds of persons with a BMI of greater than 30 kg/m2 and more than 90% of those with a BMI of greater than 39 kg/m2.1,2 Other epidemiologic risk factors include diabetes/glucose intolerance and hypertriglyceridemia, which were present in this case.

Clinical features. The typical presentation is the asymptomatic elevation of transaminase levels in an obese patient. Frequently, a battery of studies to exclude other causes of hepatitis are performed, including serologic testing for hepatitis B and C; serum iron studies for hemochromatosis; and immunologic assays, such as antinuclear antibody/antimitochondrial antibody for the autoimmune hepatitis syndromes.

A careful history taking is required to exclude toxic causes—medications and particularly alcohol. In fact, the diagnosis of NAFLD requires that daily alcohol intake be less than 20 g/d for women and 30 g/d for men (less than 1.5 and less than 2 standard drinks, respectively).3

The pattern of laboratory results yields clues to the likelihood or not of NAFLD. In alcoholic liver disease, the AST/ALT ratio is typically greater than 2, while in NAFLD the ratio is less than 1, as in this case. As a rule, elevations are moderate, 1 to 4 times normal; higher elevations suggest other diagnoses or, less typically, more severe liver damage from NAFLD.

Further workup. Additional diagnostic studies include a liver ultrasound examination, which identifies fat in the liver with a specificity of about 85% and a sensitivity of greater than 90%.3 Liver biopsy is “controversial” in a majority of studies. Biopsy is the only reliable method to definitively diagnose NAFLD and to ascertain extent of pathology, presence of cirrhosis, and prognosis. 2,3 However, on the negative ledger are the benign course of NAFLD in most patients, the lack of proven therapies in any event, and the small but not inconsequential risk associated with biopsy.2,3 The consensus is that most patients do not require biopsy, particularly early in the workup, making choice C the correct one here. Exceptions may include patients who have risk factors for cirrhosis, such as morbid obesity (BMI of greater than 39 kg/m2), AST/ALT ratios greater than 1,2,3 and persistent enzyme elevations despite appropriate lifestyle. None of these risk factors is present here.

Management. To date, there is no specific, effective therapy for NAFLD. Appropriate lifestyle changes are the first step. Thus, exercise and slow, controlled weight loss to achieve a BMI of 25 kg/m2 and avoidance of concordant risk factors such as alcohol consumption are indicated not only to ameliorate NAFLD but also to lessen general cardiovascular risk as well.

Metformin, the glitazones, and various statins have been shown to lower liver enzyme levels. Vitamins and antioxidants can also reduce transaminase levels and even improve liver biopsy histologic findings. However, to date no intervention has demonstrated improvement in morbidity or mortality in controlled trials.

With regard to statins (choice B), the hepatic metabolism of these agents and the occasional liver toxicity they cause have given some investigators and clinicians pause about their use in patients with NAFLD. Experience and at least one good trial4 have shown that statins can be safely used in patients with NAFLD when indicated; moreover, the American College of Cardiology guidelines advise that statins should be used when indicated in patients with mild to moderate NAFLD (liver enzyme levels of less than 3 times normal) with careful clinical and laborator y monitoring.5

Outcome of this case. The patient was counseled to cease alcohol intake and to continue her statin therapy. Weight loss was advised, but at 6-month follow-up her BMI has not changed. Her liver enzyme levels remain elevated but stable. No biopsy is planned at present, but she will be closely monitored.

NAFLD is the most common cause of elevated transaminases in the United States. Obesity, diabetes, and elevated triglycerides are risk factors. Prognosis overall is good, although a minority of patients progress to cirrhosis. Liver biopsy is not required in most patients. 

Liver function test – Normal range chart

Proper functioning of your liver is essential to keep proteins and enzymes at their optimal levels. As liver helps clean your system and also enables storage of needful energies, health of liver gains an added significance. Liver function test can tell if your liver is in good shape. Most of the symptoms associated with liver problems are very common. It may be required to have a watchful eye over changes in appetite, anomalies in the color of your eyes or skin – as these signs may indicate a likely risk to the normal functioning of your liver.

Your liver is one great filter. Its main function is to filter out impurities from your blood. Before the blood from your gastrointestinal tract goes to other parts of your body, your liver cleans it. This organ thus ensures your body gains access to a pure form of blood – i.e., devoid of toxins or any waste materials. Liver also provides your body with proteins necessary to clot blood and also helps store nutrients, sugars, etc. Not stopping with these, your liver produces juices to help your body to digest foods you eat.

The most common disorders affecting liver are cirrhosis, cancers, hepatitis, formation of gallstones, failure of liver, etc. Cirrhosis is not an overnight occurrence; instead, it takes a fairly long time for it to show up. This condition can occur due to an excessive consumption of alcohol, an untreated infection of your liver (such as hepatitis B or C) and being overweight or obese. Commonly observed cancerous growth in liver – known as hepatocellular carcinoma – is linked to the incidence of cirrhosis. Hepatitis denotes an inflammation or swelling of your liver. This is triggered by viral attacks – most common among such viruses are hepatitis A, B or C. Apart from viral attacks, it can show up due to non-contagious reasons as well, especially being addicted to alcohol or obesity. In some cases, consumption of drugs causing allergies can lead to a swollen liver.

Gallbladder – this organ is seen below your liver – helps in digestion by secreting a fluid called as bile. When there is a build-up of cholesterol in the bile, the undissolved fats can turn into stones. Your gallbladder may also contain stones if your bile has a higher concentration of bilirubin. These stones can be as big as a ping pong ball or as small as grains of sand.

Liver function test

Tests done to understand how your liver functions focus on the level of proteins and enzymes in your blood. As your liver assumes a multi-functional role, a dysfunction can lead to serious implications. The liver function test is done by drawing a small sample of blood. This is drawn from a site – in the arm – especially, near the elbow. Your doctor may advise taking these tests across a few weeks. Such tests may help understand how the levels of proteins or enzymes vary with time. Key enzymes and proteins whose levels the liver function test helps to understand include-Aspartate aminotransferase (AST)

The most widely utilized enzyme in your liver is aspartate aminotransferase (AST, also labelled as SGOT). It may also be found in the cells of your muscles, brain, heart, lungs, pancreas, etc. When your blood contains excessive amounts of AST or SGOT, it signifies a likely liver dysfunction. Why? A liver disorder is a possible reason for its inability to contain this enzyme within it, and thus making it to blend with blood in copious quantities. However, as AST is also found in other sites, it is not a direct indicator of a possible liver condition. So, as compared to AST, medical experts lay more emphasis on the levels of a fellow-enzyme called ALT. Hence, ALT is considered a better diagnostic-marker to understand the health of liver.

Normal reference range for SGOT is 5 to 35 units per liter. Per liter here refers to a liter of serum. Level of SGOT reflects the condition of your liver’s efficiency levels. A higher value indicates a likely injury or damage of the liver. But, you need to remember that this enzyme is also found in your muscular cells. Hence, an increased count can represent a possible damage of your muscles. So, your doctor may conduct a careful examination of your muscles and liver to ascertain your present medical condition. Often, an escalated level is linked to the possibility of liver cirrhosis.

Alanine aminotransferase (ALT, also labelled as SGPT)

This enzyme is found in greater proportion in your liver. But, it is also found in your muscles and kidneys to a limited extent. A likely injury or damage to your liver may increase its concentration level in your blood. The normal range of reference for concentration of SGPT is 7 to 56 units per liter of serum. When this level reaches 250 units per liter, a liver injury may not necessarily be a reason. Your doctor may have to diagnose the condition of your kidneys, muscles or heart. However, when the level of ALT crosses 490 units per liter, it is generally due to a liver condition. The likely causes of such an escalated level include presence of excessive toxins in liver, ischemic liver condition or due to an inflammation (hepatitis).

It has been observed that hepatitis C is very likely to escalate the levels of ALT much more than hepatitis A or B. If your liver tests indicate a constant hike in ALT level for more than 25 weeks, it is considered as a chronic condition. Apart from hepatitis, obesity among children and fatty liver conditions (either as a congenital or an overweight condition) can also cause changes to ALT levels.


This is secreted from your bile as well as through urine. It is observed in two distinct variants namely, conjugated and unconjugated bilirubin. Conjugated bilirubin is soluble in water while its unconjugated variant is soluble in fats. A damage of your liver or hepatitis caused by a viral infection is a likely reason for an increase in conjugated bilirubin. Its normal range is 0.05 to 0.35 mg / dL. On the other hand, unconjugated bilirubin is a catabolic outcome of red cells of your blood. Your liver conjugates this variant with the help of an enzyme. The normal range of unconjugated bilirubin in is 0.1 to 0.65 mg / dL. Also, the normal range of total bilirubin is 0.1 to 1.0 mg / dL. When the share of total bilirubin crosses 1.5x the normal upper limit, this condition is diagnosed as a possible liver injury or damage. When the range crosses 2x, it is treated as jaundice.

A few other conditions like say, an acute spell of appendicitis can increase the total bilirubin level by more than five to six times its normal upper limit.

Alkaline phosphatase (ALP)

This enzyme is seen in cells found on the walls of ducts carrying bile. However, the same enzyme is also present in your kidneys, bones and on the walls or linings of small intestine. The normal range of ALP is noted as 40 to 133 units per liter. An escalation from this range is often observed during a spell of hepatitis. Also, a moderate increase beyond the range is seen during cirrhosis of liver as well as myocardial infraction or a congestion of your cardiac muscles. As this enzyme is also seen in the placenta, pregnant women have higher levels of ALP (in the range of 200 units per liter or even more) can be observed in the 3rd trimester of pregnancy.


This is a type of protein your liver makes. Albumin makes for a significant portion of proteins made in liver. The normal range of albumin is 3.5 to 5.3 g / dL. Hence, a diminished presence of albumin indicates a possible damage – especially, cirrhosis of the liver. You may need to note that a kidney disorder may also drain away albumin through urine.


Like albumin, it is another protein that your liver makes. Its normal range is 2.3 to 3.5 gm / dL. When globulin levels fall below its normal range, it can signify a liver dysfunction or a renal disorder. On the other hand, a higher level of globulin indicates autoimmune conditions such as arthritis, cancers, etc.

In essence, liver function test is performed if you are experiencing various signs of a likely liver damage. The test can help assess damage of your liver due to infections or regular intake of a few medicines. The liver function test can also help track the progress of a treatment plan and check improvements in the health of your liver. Of the many parameters, albumin level is an indication of your liver’s ability to make albumin while bilirubin level shows the efficiency at which it is disposed. ALP is an indicator of the health of your bile ducts while AST and ALT related tests are done to check damages or injuries in your liver.

Your doctor may provide needful medical attention even for a slight escalation of the above levels. This is because such increases can be due to an underlying liver condition. In general, you are advised to take your liver health with topmost priority as some disorders can be near-fatal in nature.

AST & ALT in the Liver | Levels & Significance – Video & Lesson Transcript

Human liver location

Liver Enzymes: What are AST & ALT?

The liver produces a large number of catalytic and metabolic enzymes that aid in the breakdown of foods, the removal of toxins, and the synthesis of molecules such as glycogen (a storage version of the energy-rich glucose). Two key liver enzymes are AST (asparatate aminotranferase) and ALT (alanine aminotransferase). As transaminase enzymes, they catalyze the reversible conversion of amino acids by the transference of amino groups. This reaction is a key step to breaking down proteins into amino acid building blocks, readying them for further metabolism. Alkaline phosphatase (ALP) is another key liver enzyme that can be used to indicate liver damage as it specifically increases due to blockages of bile ducts. These enzymes are easy to detect in routine blood samples and as such can be used in health diagnostics. When levels change from normal, to either high or low, information can be inferred about possible liver damage, improper function, or viral infections.

Significance of ALT & AST

AST and ALT hold great clinical significance as their increase (or rapid decrease) in blood serum can indicate problems within the liver. These enzymes are used as an indicator of the level of liver damage, as they are released into the bloodstream as liver cells (hepatocytes) and die and break apart due to a variety of damage. A mixture of clinical information can be obtained through the levels of these enzymes, ranging from the individual levels, the correlations between their levels, and the direct ratios between them.

Within a healthy adult, Columbia University Medical Center (a large transplant center in New York, NY) defines normality as AST within a range of 12-38 International Units (IU) per milliliter (ml) of serum and ALT between 7-41 IU/ml. Often used in diagnosis, a level limit is set as the Upper Limit of Normal (ULN), though there seems to be no consensus on what that limit is as it varies up to twofold from lab to lab and center to center. This ULN indicates to a doctor that an issue may be present if the levels of AST or ALT are beyond (either too high or too low) this limit. A mild increase of ALT and AST is described as less than 5 times the ULN and can be an indication of chronic Hepatitis C or B, acute viral or autoimmune hepatitis, non-alcoholic fatty liver disease, alcohol-related liver disease, or from a variety of medications. A moderate increase in AST and ALT levels (at 5-15 times the ULN) indicates a progressive liver disease from a variety of sources. At 15 times the ULN, severe liver injury has or is occurring, stemming again from acute liver disorders.

Taken individually, the serum levels of these two enzymes can indicate specific issues, but their direct ratio is also an important indication of specific issues. As ALT is at its highest concentration in the liver, it is used predominately as an indication for a variety of liver issues. AST, on the other hand, is present in other organs including the heart, muscles, kidneys, brain, pancreas, and lungs. Therefore, the relationship between these two enzymes can reveal more information about the state of disease of the patient. For example, if the ALT level is greater than the AST level, this could indicate that the damage that is causing the elevated levels in the bloodstream is coming from the liver and not other parts of the body. Whereas if the AST level is greater than the ALT blood serum levels, the damage is coming from other sources, such as the heart or pancreas. These values help doctors narrow down the possible causes towards a full diagnosis.

Medications That Can Increase AST ALT Levels

Specific medications often used to treat pain or inflammation (such as non-steroidal anti-inflammatory drugs like ibuprofen, naproxen, and acetaminophen), if taken at high doses, at the wrong intervals, or in conjunction with alcohol, can cause elevated liver enzymes that can be confused with severe liver damage or even liver failure. A variety of other medications can elevate liver enzymes, but to a lesser degree and can easily be ruled out as cause as they tend to be prescription medications. These include (but are not limited to) statins, antibiotics, certain cardiovascular drugs, antidepressants, or pain management medicines such as oxycontin.


As part of a clinical evaluation, doctors can also use the ratio of AST to ALT to help determine the source of the elevations (or drops) in these enzymes. This ratio is created by simply dividing the units of AST by the units of ALT. In healthy adults, this ratio should be around 1.15, whereas in unhealthy or liver-damaged individuals, this ratio can be as high as 6.0. Even levels ranging to 2.0 can indicate serious problems including alcoholic liver disease or cirrhosis (or scarring) of the liver. At lower than normal levels, this ratio may indicate an acute viral hepatitis infection.

Test to Detect Liver Function

The determination of the levels of both AST and ALT and other proteins and liver enzymes are done during a routine liver function blood panel. The procedure is relatively simple and includes taking a small vial of blood, removal of the red blood cells through concentration, and subsequent analysis. These panels may include many different evaluations including the presence of total proteins, amounts of bilirubin (a waste product that can build up in a poorly functioning liver), and albumin (a stabilizing fluid that ensures healthy cell function).

Multiple blood draw tubes awaiting processing for a liver functional panel

When Are Tests Required?

These tests are usually ordered by a doctor after specific indication that a liver problem may be present. Some indications to warrant the use of a liver function test could include jaundice (a yellowing of the skin or eyes), exposure or possible exposure to viral hepatitis, experiencing unexpected weight loss or fatigue, abdominal swelling or pain, darkened urine and light stools or persistent diarrhea.

Lesson Summary

The liver is a key internal organ, involved in the breakdown of food and storage of energy-rich metabolites like glycogen. It acts as a global filter to remove toxins and build enzymes and proteins involved in metabolism to provide energy to the rest of the body. AST (asparatate aminotranferase) and ALT (alanine aminotransferase) are important liver enzymes involved in amino acid metabolism. Their level within the body is a key indicator of liver function and potentially problematic issues. Any deviation from normal levels can indicate to a doctor a variety of liver or internal organs issues, ranging from damage, viral infection, to overall poor or loss of function. The testing of these enzymes is rapid, requiring only a simple blood draw and a routine set of abundance tests. These numbers can quickly lead a doctor to what may be causing the symptoms. Enzymatic levels on either side of the upper limit of normal can reveal the severity of the issue and allow a doctor to infer the root cause. Lower than normal levels can indicate a viral hepatitis infection; higher than normal levels, depending on the ranges, can indicate a variety of issues ranging from non-alcoholic fatty liver disease to a severe loss of liver function.

Symptoms of unexpected weight loss, fatigue, swelling or abdominal pain, persistent diarrhea, or darkened urine might indicate problems with a liver or with other internal organs. A doctor given these symptoms would order a liver function blood panel. From the data obtained from this series of tests, a doctor will be able to make a more informed diagnosis as to what may be causing these symptoms. AST and ALT are both very important enzymes in the function of the liver; they can reveal large amounts of information about the health and function of internal organs.

Liver Function Tests | CS Mott Children’s Hospital

Test Overview

Some blood tests are used to determine whether your liver is damaged or inflamed. Although these tests help your doctor evaluate how well your liver is working, they cannot tell if you have hepatitis C.

Tests that assess liver function

Your doctor may do tests to measure certain chemicals produced by the liver. These tests can help your doctor check how well your liver is working.

Tests may measure:

  • Bilirubin.
  • Albumin.
  • Total serum protein.

Tests that check for inflammation of the liver (liver enzyme studies)

Your liver may be damaged if you have increased levels of:

  • Alanine aminotransferase (ALT or SGPT).
  • Aspartate aminotransferase (AST or SGOT).

An increased level of alkaline phosphatase (AP) may indicate blockage of bile ducts.

Why It Is Done

Liver tests are done when a medical history or physical exam suggests that something may be wrong with your liver.

These tests can also help diagnose long-term (chronic) infection. If liver enzymes are high, a test for hepatitis C antibodies may be done to see if you have hepatitis C.

If you are being treated with antiviral therapy, you may have liver tests from time to time to see whether treatment is working.

How To Prepare

In general, there’s nothing you have to do before this test, unless your doctor tells you to.

How It Is Done

A health professional uses a needle to take a blood sample, usually from the arm.



All levels are within the normal range.


One or more levels are outside the normal range. Abnormal liver function tests may mean that your liver is inflamed or is not working normally. This can be a sign that you have a viral infection.


Current as of:
September 23, 2020

Author: Healthwise Staff
Medical Review:
E. Gregory Thompson MD – Internal Medicine
Adam Husney MD – Family Medicine
Martin J. Gabica MD – Family Medicine
W. Thomas London MD – Hepatology

Current as of: September 23, 2020

Healthwise Staff

Medical Review:E. Gregory Thompson MD – Internal Medicine & Adam Husney MD – Family Medicine & Martin J. Gabica MD – Family Medicine & W. Thomas London MD – Hepatology

Understanding MELD Score for Liver Transplant

Anyone with a serious liver disease should understand what a MELD score is and how doctors arrive at this important number. If you are a candidate for a liver transplant, a MELD score helps determine how urgently you need a transplant.

The MELD score ranges from six to 40 and is based on results from several lab tests. The higher the number, the more likely you are to receive a liver from a deceased donor when an organ becomes available.

What Does MELD Score Mean?

The MELD score estimates a patient’s chances of surviving their disease during the next three months. Organ allocation is determined by the Organ Procurement and Transplantation Network (OPTN). Livers from deceased donors are allocated to the sickest patients first.

Liver Transplant Waiting List: Additional Considerations

Your MELD score is a prime indicator in determining how urgently you need a transplant. But, it isn’t the only factor. Other considerations include:

  • Your blood type
  • Your body size relative to the donor’s
  • Geographical considerations (i.e. how close you are to the donor liver)
  • Current supply of, and demand for, deceased donor livers

Living-Donor Liver Transplant for Patients with a Low MELD Score

While patients with a MELD score less than 15 are often not listed for a liver transplant because their chance of receiving a liver through traditional allocation is so low, a living-donor liver transplant offers a life-saving option and the opportunity to receive a transplant sooner. By exploring a living donor transplant, patients with a low MELD score can still be considered for a liver transplant.

How Is Your MELD Score Calculated?

Your MELD score is based on results from four blood tests that, together, show how well your body is functioning. You will be tested for:

  • INR (internal normalized ratio): Indicates whether your liver is making the proteins necessary for blood to clot
  • Creatinine: Indicates how well your kidneys are working
  • Bilirubin: Indicates how well your liver is clearing a substance called bile
  • Serum sodium: Indicates how well your body is regulating fluid balance

How Often Is Your MELD Score Updated?

Your MELD score changes as your condition changes. If you get sicker, your score goes up.

Depending on how critical your disease is, your MELD score may be recalculated as often as once a week.

Doctors look at your last MELD score to determine when to order new lab tests.

Here are typical MELD scores and how often they’re recalculated:

  • 25 or higher: Every week
  • 19-24: Every 30 days
  • 11-18: Every three months
  • 10 or less: Once a year

Updating Your MELD Score

Since your MELD score is calculated by your doctor, you’re not responsible for updating it. It’s up to your doctor to decide when you need new tests.

Make sure you attend all follow-up appointments and complete all necessary lab tests — and check in with your doctor anytime your condition worsens. You should call your transplant coordinator if you have questions about your MELD score.

Additional Questions? Contact Us

To learn more about the liver transplant process and for answers to your MELD score questions, visit UPMC Transplant Services or call 833-514-5999.



The term “liver function tests” (often abbreviated to “LFTs” by your doctor) is a commonly used term applied to a variety of blood tests that reflect the general state of the liver and biliary system. Routine blood tests can be either tests that are simply markers of liver or biliary tract injury (the liver enzymes tests), or true LFTs, such as serum albumin or prothrombin time. In addition, your doctor may order specific liver tests that if positive, can determine the specific cause of liver disease.

What do liver enzyme tests show?

There are two general categories of “liver enzymes” used in liver function tests. The first group includes alanine aminotransferase (ALT) and aspartate aminotransferase (AST), formerly referred to as the SGPT and SGOT respectively. These enzymes are indicators of liver cell damage.

The other frequently used liver enzymes are alkaline phosphatase (ALP) and gammaglutamyltranspeptidase (GGT) – these indicate obstruction to the biliary system, either within the liver or in the larger bile channels outside the liver. However, both liver and biliary disease often cause a simultaneous disturbance of the liver enzymes indicating liver cell damage and obstruction of the biliary system.

ALT (alanine aminotransferase) and AST (aspartate aminotransferase) :

These enzymes are located in liver cells and ‘leak out’ when liver cells are injured, making their way into general circulatory system. The term hepatitis is used to describe a liver disease where ALT and AST are the predominantly elevated liver enzymes. ALT is thought to be a more specific indicator of liver inflammation, since AST elevation may be associated with diseases of other organs such as the heart or muscle. In acute liver injury such as acute viral hepatitis, ALT and AST may be elevated to the high 100s or over 1,000 U/L. In chronic hepatitis or cirrhosis, the elevation of these enzymes may be minimal (less than 2-3 times normal) or moderate (100-300 U/L). Mild or moderate elevations of ALT or AST are nonspecific and may be caused by a wide range of liver diseases. ALT and AST are often used to monitor the course of chronic hepatitis and the response to treatments, such as interferon and prednisone.

(ALP) alkaline phosphatase and (GGT) gammaglutamyltranspeptidase

ALP and the GGT are elevated in a large number of disorders affecting the drainage of bile from the liver to the small intestine. The term cholestasis is used when ALP and GGT are the predominantly elevated liver enzymes. Common examples of cholestatic liver disease include a gallstone or tumour blocking the common bile duct just outside the liver; or alcoholic liver disease or drug-induced hepatitis blocking the flow of bile in smaller bile channels within the liver.

ALP is also found in other organs such as bone, placenta and intestine. For this reason, GGT is used as a supplementary test to be sure the elevation of ALP is actually coming from the liver or the biliary tract.

GGT is not elevated in diseases of bone, placenta or intestine. Mild or moderate elevation of GGT in the presence of a normal alkaline phosphatase is difficult to interpret and is often caused by changes in the liver cell enzymes induced by alcohol or medications, but without causing injury to the liver.


Bilirubin is the main bile pigment in humans formed primarily from the breakdown of “heme” in red blood cells. Heme is taken up from blood processed through the liver, and then secreted into the bile by the liver. Normal individuals have only a small amount of bilirubin circulating in blood (less than 20mmol/L).

Some conditions, including liver and biliary disease or the excessive destruction of red blood cells, cause increased levels of bilirubin in the blood stream. Levels greater than 50-60mmol/L are usually noticeable as jaundice, a yellow discolouration of the skin and eyes. The bilirubin may be elevated in many forms of liver or biliary tract disease, so it is a nonspecific marker of liver disease. However, serum bilirubin is generally considered a true test of liver function (LFT), since it reflects the liver’s ability to take up, process, and secrete bilirubin into the bile.

True LFTs – Albumin and prothrombin time

Two other commonly used indicators of liver function are the serum albumin and prothrombin time.

Albumin is one of the major proteins made by the liver. In chronic liver disease, less albumin is produced so in more advanced liver disease, the level of the serum albumin is reduced (less than 35 g/dL).

The prothrombin time (PT) is a test used to assess blood clotting, or coagulation. Blood clotting factors are proteins also made by the liver. When the liver is significantly damaged there is reduced production of coagulation factors resulting in longer prothrombin time.

Prothrombin time is a useful test of liver function – there is a good correlation between abnormalities in coagulation measured by the prothrombin time and the severity of liver dysfunction. Prothrombin time is usually expressed in seconds and is compared to a normal, or control patient’s blood. This comparison gives the prothrombin ratio (PR), referred to as the international normalised ratio (INR).

What do LFT results show?

Altered liver function tests only indicate liver or biliary dysfunction – they do not identify the cause. To make a precise diagnosis of the cause of liver disease or elevated liver enzyme tests, additional specific and specialised tests must be used.

Further tests:

Your doctor will be guided by which of these may be needed in the light of your particular illness;

1-There are specific blood tests that allow the precise diagnosis of hepatitis A, B, C, D and E as well as other viruses that affect the liver.

2-Elevations in serum iron – the percent of iron saturated in blood – or the iron storage protein ferritin, may indicate the presence of haemochromatosis, a liver disease associated with excess iron storage.

3-Wilson’s disease involves abnormal metabolism of copper. There is an accumulation of copper in the liver, a deficiency of serum ceruloplasmin and excessive excretion of copper into the urine.

4-Low levels of serum alpha-1-antitrypsin may indicate the presence of lung and/or liver disease in children or adults with alpha-1-antitrypsin deficiency.

5-A positive anti-mitochondrial antibody indicates the underlying condition of primary biliary cirrhosis.

6-The presence of antinuclear antibodies or anti-smooth muscle antibodies are clues to the diagnosis of autoimmune hepatitis.

7-An elevated alpha-fetoprotein test is often elevated in primary liver cancer.


Radiology, such as ultrasound or CT scan, is a complimentary tool to blood tests and may also be useful in making a precise diagnosis particularly when biliary disease or a liver tumour is suspected.

Lastly, a liver biopsy may also be required both to determine the cause (where blood and radiology have been unhelpful) and to assess the severity of the liver disease.


Once a liver or biliary disorder is suspected, your doctor, having first undertaken a full medical history and physical examination, will arrange for you to undergo liver enzyme and liver function tests (LFTs), through blood tests. The pattern of liver enzyme test results will hopefully guide subsequent investigations, if necessary.

If the liver enzymes suggest liver cell injury then additional blood tests will often be needed. Conversely if biliary disease is suspected then radiology might be a more appropriate first test. However, in many instances both additional blood tests and radiology are required to make a diagnosis and to plan management.

Liver Cancer Stages

After someone is diagnosed with liver cancer, doctors will try to figure out if it has spread, and if so, how far. This process is called staging. The stage of a cancer describes how much cancer is in the body. It helps determine how serious the cancer is and how best to treat it. Doctors also use a cancer’s stage when talking about survival statistics.

Liver cancer stages range from stage I (1) through IV (4). As a rule, the lower the number, the less the cancer has spread. A higher number, such as stage IV, means cancer has spread more. Although each person’s cancer experience is unique, cancers with similar stages tend to have a similar outlook and are often treated in much the same way.

How is the stage determined?

There are several staging systems for liver cancer, and not all doctors use the same system. The staging system most often used in the United States for liver cancer is the AJCC (American Joint Committee on Cancer) TNM system, which is based on 3 key pieces of information:

  • The extent (size) of the tumor (T): How large has the cancer grown? Is there more than one tumor in the liver? Has the cancer reached nearby structures like the veins in the liver?
  • The spread to nearby lymph nodes (N): Has the cancer spread to nearby lymph nodes?
  • The spread (metastasis) to distant sites (M): Has the cancer spread to distant lymph nodes or distant organs such as the bones or lungs?

The system described below is the most recent AJCC system, effective January 2018.

Numbers or letters after T, N, and M provide more details about each of these factors. Higher numbers mean the cancer is more advanced. Once a person’s T, N, and M categories have been determined, this information is combined in a process called stage grouping to assign an overall stage. For more information see Cancer Staging.

Liver cancer is usually staged based on the results of the physical exam, biopsies, and imaging tests (ultrasound, CT or MRI scan, etc.), also called a clinical stage. If surgery is done, the pathologic stage (also called the surgical stage) is determined by examining tissue removed during an operation.

Cancer staging can be complex, so ask your doctor to explain it to you in a way you understand.

AJCC Stage

Stage grouping

Stage description*





A single tumor 2 cm (4/5 inch) or smaller that hasn’t grown into blood vessels (T1a).

It has not spread to nearby lymph nodes (N0) or to distant sites (M0).





A single tumor larger than 2cm (4/5 inch) that hasn’t grown into blood vessels (T1b).

The cancer has not spread to nearby lymph nodes (N0) or to distant sites (M0).





Either a single tumor larger than 2 cm (4/5 inch) that has grown into blood vessels, OR more than one tumor but none larger than 5 cm (about 2 inches) across (T2).

It has not spread to nearby lymph nodes (N0) or to distant sites (M0).








More than one tumor, with at least one tumor larger than 5 cm across (T3).

It has not spread to nearby lymph nodes (N0) or to distant sites (M0).





At least one tumor (any size) that has grown into a major branch of a large vein of the liver (the portal or hepatic vein) (T4).

It has not spread to nearby lymph nodes (N0) or to distant sites (M0).


Any T



A single tumor or multiple tumors of any size (Any T) that has spread to nearby lymph nodes (N1) but not to distant sites (M0).


Any T

Any N


A single tumor or multiple tumors of any size (any T).

It might or might not have spread to nearby lymph nodes (any N).

It has spread to distant organs such as the bones or lungs (M1).



* The following additional categories are not listed on the table above: 

  • TX: Main tumor cannot be assessed due to lack of information.
  • T0: No evidence of a primary tumor.
  • NX: Regional lymph nodes cannot be assessed due to lack of information. 

Other liver cancer staging systems

The staging systems for most types of cancer depend only on the extent of the cancer, but liver cancer is complicated by the fact that most patients have damage to the rest of their liver along with the cancer. This also affects treatment options and survival outlook.

Although the TNM system defines the extent of liver cancer in some detail, it does not take liver function into account. Several other staging systems have been developed that include both of these factors:

  • The Barcelona Clinic Liver Cancer (BCLC) system
  • The Cancer of the Liver Italian Program (CLIP) system
  • The Okuda system

These staging systems have not been compared against each other. Some are used more than others in different parts of the world, but at this time there is no single staging system that all doctors use. If you have questions about the stage of your cancer or which system your doctor uses, be sure to ask.

Child-Pugh score (cirrhosis staging system)

The Child-Pugh score measures liver function, especially in people with cirrhosis. Many people with liver cancer also have cirrhosis, and in order to treat the cancer, doctors need to know how well the liver is working. This system looks at 5 factors, the first 3 of which are results of blood tests:

  • Blood levels of bilirubin (the substance that can cause yellowing of the skin and eyes)
  • Blood levels of albumin (a major protein normally made by the liver)
  • The prothrombin time (measures how well the liver is making blood clotting factors)
  • Whether there is fluid (ascites) in the abdomen
  • Whether the liver disease is affecting brain function

Based on these factors, there are 3 classes of liver function. If all these factors are normal, then liver function is called class A. Mild abnormalities are class B, and severe abnormalities are class C. People with liver cancer and class C cirrhosis are often too sick for surgery or other major cancer treatments.

The Child-Pugh score is actually part of the BCLC and CLIP staging systems mentioned previously.

Liver cancer classification

Formal staging systems (such as those described before) can often help doctors determine a patient’s prognosis (outlook). But for treatment purposes, doctors often classify liver cancers more simply, based on whether or not they can be cut out (resected) completely. Resectable means able to be removed by surgery.

Potentially resectable or transplantable cancers

If the patient is healthy enough for surgery, these cancers can be completely removed by surgery or treated with a liver transplant. . This would include most stage I and some stage II cancers in the TNM system, in patients who do not have cirrhosis or other serious medical problems. Only a small number of patients with liver cancer have this type of tumor.

Unresectable cancers

Cancers that have not spread to the lymph nodes or distant organs but cannot be completely removed by surgery are classified as unresectable. This includes cancers that have spread throughout the liver or can’t be removed safely because they are close to the area where the liver meets the main arteries, veins, and bile ducts.

Inoperable cancer with only local disease

The cancer is small enough and in the right place to be removed but you aren’t healthy enough for surgery. Often this is because the non-cancerous part of your liver is not healthy (because of cirrhosis, for example), and if the cancer is removed, there might not be enough healthy liver tissue left for it to function properly. It could also mean that you have serious medical problems that make surgery unsafe.

Advanced (metastatic) cancers

Cancers that have spread to lymph nodes or other organs are classified as advanced. These would include stages IVA and IVB cancers in the TNM system. Most advanced liver cancers cannot be treated with surgery.

90,000 Full transcriptomic profiling of the liver of C57BLACK / 6J mice fed diets with excess fat, fructose and cholesterol

GENETICS Vol. 55 No. 4 2019

TOTAL CRYPTOMAL PROFILING OF THE LIVER with 9000 differential intake induced by 372 express 3,000 rations 9000

significance level p ≤ 0.05 for groups of mice 2–6 (in comparison with group 1, which received a balanced

lusynthetic diet)

* Each column selectively presents no more than 10 genes with the highest differential expression in modulus for

each groups of animals in the specified range of log2FC values.


Genes with positive differential expression (enhancement) *

differential expression, log2FC

> 1> 0.7−1.0 ≥0.5−0.7

2Dcx, Slc39a3, Setd3 Prickle1, Limd2, 1700018F24Rik, Myl100018F24Rik, Myl100018F24Rik , Zfp949, Agtpbp1

Srsf10, Adss, Fam53a, 4

4933402N03Rik, Gnpat, Rps18,

Gzme, L1td1, Cpa5, Olfr1012

3Nxnl1, Glelf, Opp30003

3Nxnl1, Glelf, Oda3000 , Rpp38, P2ry12

Cldn20, Adal, Atf1, LOC102640328,

Ythdc1, C130060K24Rik, Tifab,

Dcun1d1, Tia1, Adgrv1

Gm21992, Spata5l1, Sec24d,

Tbkbp1, Znhit2, Polr2k,

2810433D01Rik, 2010106E10Rik ,

Casr, Defb5

4Nepn, Slc35f5, Pgm3, Stam,

LOC102632594, 2310057M21Rik,

Arl6ip4, Bcl2l11, Rdm1

4933408 Cbd14, Hlfik378 , Rad50, Ccdc162,

Fbxw11, Slc25a18, Ikzf1, App

Adamtsl4, Brox, Smc1b, Gli3,

Adgrb2, Ostm1, Qars, Mfsd2b,

9000R8 4930474h , Tuba1a,

Csf2rb, Adss, Gm3448, Phf23,

Myh21, Thoc3

Gm17115, Mthfd2l, Vmn2r62,

Ankrd23, Bcl2l11, Otud2 Tme

9000 , Pabpc4,

Timp2, Arhgef19, Map3k6,

Serpine2, Rabggta, Sdr9c7, Anks3

6Pum2, Vmn2r12, Bcs1l, Kcnc4,


Rpg16rip1l, Olf30007, Ghang3

Rpg16rip1l, Olf3000r7, Ghara

Rpg16rip1l, Olf3000r7, Ghara

Rpg16rip1l, Olf300027 , Net1, Mtmr2,

Peg3os, Mrm1, Nxnl1, Slc37a3,

Dapk3, Commd8, Gm6109,


Adam33, Smr3a, Lpcat3, Snx25k Nrch2 Arge2 9000 Adgrv1


Genes with negatives total differential expression (suppression) *

differential expression, log2FC

<–1 (–1.0) - <(- 0.7) (–0.7) −≤ (–0.5)

2Gm19583, Kif1a, Sugp2, Gm8096 C130060K24Rik, Mbtd1, Capzb,

Moxd2, Dpy19l3, Gm35405,

p, UOC1026


Zfp750, Rad54l2, Gm32639, Mpdz,

Ndnf, Gm14486, Zbbx, Ppfibp1,

2300002M23Rik, Prdm14

3Rbm7ka, Nfx1 ,


Gm36561, Asb1, Hs3st2, Tmem14a,

Ggta1, Trpm1, Pigo, Agbl3, Ccz1,


Tmem194b, Lcn1, Olf30002 Tmem194b, Lcn2, Olfr8000, Dcn2, Olf3000r,

Tmem194b, Lcn1, Olfr8h14

Gm28729, Gm35973

4Timp2, Lrp2bp, Nxnl1, Znhit2,

Rundc3a, 5730559C18Rik,

Gm15413, Mtap7d3,

LOC105246305, Adgrv1

Chka, Ovol3, Cd209a, Cd79b,

Ndufb7, Gm14285, Cd36, Ipo13 ,

Ptrf, Tekt5, Gtf2h3

Gm14902, Olfr1195, Zp3, Sh4d21,

Cfa p20, 9230102K24Rik, Rab2b,

Mapre3, Gm4793, Rbfa

5Il7, Tpm2, Olfr1261, Ildr1, Phb,

Chm, 9630013A20Rik, Asb3, Myo9b, 9000b3

Lin30 Ccz1, Tmem260,

C030013G03Rik, Adgrv1, Gm17762,


Pigo, Gm9936, Hnrnpu, Pdgfa,

Prkacb, Radkacb, Rad50, Rnf30


Prkacb, Radi50, Rnf304000, Cybb3000,

Prkacb, Radi50, Rnf304000,

Prkacb, Radioplast A630019I02Rik, Rpl34, Fam181b,

Myo9b, Rp1, Jmjd7, Gm3646

6430562O15Rik, Insig2,

4930407I19Rik, Ctage5, Zbtb42,

LOC102636590, Qars, Iqch, Olfr10,

Gm7562, Cd209a

Gm6377, Supv3l1, Mypn, Rpl24,

Smco4, Gm15672, Dgkb, Gm11529,

Arl6ip4, 9130409I23Rik, Wdr27

Cancer spread in the world in 10 schemes

  • Valeria Perasso
  • Bi World Service
  • 2

    February 4 is World Cancer Day.The goal is to popularize information and combat prejudices associated with this terrible disease.

    Cancers are the leading cause of death worldwide. Billions of dollars are spent on cancer treatments.

    It is known about cancer that it is not one disease, but at least 200 – and each of them has its own symptoms, methods of diagnosis and treatment.

    The World Health Organization estimates that the number of cancer cases will increase by 70% in the next 20 years.

    What does this mean for humanity? Below are 10 graphical diagrams to help you assess the extent of the disease.

    According to British oncologists, the list of the most common types of cancer has changed little over the past 40 years.

    The four most common cancers – lung, breast, bowel and prostate – account for 42% of all cancers worldwide, according to the Globoscan project, a database maintained by the International Cancer Registry Association.

    Lung cancer is the most common cancer in men worldwide, while breast cancer is most common in women.

    • 32.6 million people – this is the number of cancer patients worldwide (these are people who were diagnosed with cancer five years before the end of 2012)


    The most recent World Health Organization report indicates that more than 60% of new cases are reported in Africa, Asia, Central and South America.

    70% of all cancer deaths in the world occur in countries in these regions.

    However, cancer incidence does not necessarily correlate with overall mortality in specific countries. In some regions, more resources are available to treat cancer patients and improve their chances of survival.

    For example, Europe and North America have lower cancer deaths than total cases, while Asia and Africa have higher cancer deaths.



    90,224 If we consider the number of cancer cases by country, the highest incidence of diseases for men and women is observed in Denmark, where in 2012 an indicator of 338 diseases was recorded per 100 thousand people.

    These five countries are followed by the USA, Ireland, Korea, the Netherlands and New Caledonia.

    The Middle East has the worst readings in Israel, which is ranked 19th in the list of 50 countries.



    The main risk factors differ little from country to country.

    Smoking remains the most significant risk factor, accounting for about 20% of lung cancer deaths.

    Alcohol consumption is the most common cause of death in Europe and America, and unhealthy diets and obesity are increasingly common risk factors in low- and middle-income countries.

    In addition, infections are responsible for 18% of cancer cases globally, and this percentage is much higher in poorer regions.

    Treatment of viral hepatitis and other liver diseases. Use of sodium hypochlorite in the treatment of alcoholic liver disease (report).

    Myazin R.G.

    XVI Russian Congress: “Hepatology Today”, Moscow, March 21-23, 2011


    In the Russian Federation, over the past decades, a consistently high level of toxic liver damage has been recorded due to the use of alcohol and its substitutes.In this regard, the application of new effective methods of drug treatment of alcoholic liver disease (ABD) is relevant. One of the promising areas for the treatment of this large group of patients is the use of sodium hypochlorite (HCN).

    It is known that under natural conditions in the human body, sodium hypochlorite (NaClOˉ) is produced by macrophages in the process of bacterial phagocytosis and is a substance with almost universal detoxifying properties. Being a donor of active oxygen and a powerful oxidizing agent, sodium hypochlorite in the body breaks down into hypochlorite anion (ClOˉ) and sodium ion (Na +).Hypochlorite anion reacts with a huge amount of substrates found in biological fluids, on cell membranes and inside them. As a result of oxidation or chlorination of these substrates, the multidirectional effect of sodium hypochlorite on the body is manifested, in particular, on the correction of metabolic processes in the liver.

    Purpose of the study:

    To substantiate the expediency of using sodium hypochlorite solutions as an effective detoxification agent in patients with alcoholic liver disease.

    Materials and methods:

    We studied a group of patients from 76 patients in whom, according to the anamnesis, the relationship of the disease with regular and long-term alcohol abuse and its surrogates was clearly traced. The duration of the disease in the group was 5.1 ± 0.8 years.

    Initially, before the course of therapy with sodium hypochlorite, a moderate increase in lipid peroxidation (LPO) parameters was observed in the group. The concentrations of malondialdehyde (MDA) and diene conjugates (DC) in blood plasma exceeded the control values ​​by 116.4% (p <0.05) and 52.2% (p <0.05), respectively.This was accompanied by an insignificant increase in the activity of liver antioxidant defense enzymes (AOD) - catalase (Cat) by 8.5% (p> 0.05), superoxide dismutase (SOD) – by 9.4% (p> 0.05), and a significant a compensatory increase in the activity of glutathione peroxidase (GP) by 148.9% (p <0.05), aimed at inactivating lipid hydroperoxides.

    To assess the severity of the cytolysis syndrome, we studied the levels of liver-specific liver enzymes – serum urocaninase (SU), serum histidase (SG), N-acetyl-b-D-glucosaminidase (NAG), serine dehydrogenase (SDH), threonine dehydrogenase (TDH) as well as serum transaminases.A significant increase in all these samples was noted. In particular, the activity of ALT and AST exceeded the control values ​​for these enzymes (ALT – 0.59 μkat / L, p <0.05; AST - 0.48 μkat / L, p <0.05). A significant increase in the activity of other liver-specific enzymes was also noted: SU up to 1.26 ± 0.3 units, SG up to 1.06 ± 0.28 units, NAG by 42.3%, SDH and TDH by 75% and 72%, respectively. (p <0.05).

    Indicators of mesenchymal-inflammatory syndrome in patients before the course of therapy with sodium hypochlorite also exceeded the control values.The level of ceruloplasmin in them by 38%, and the value of the thymol test – by 115% were higher than the control values ​​(p <0.05).

    The level of total bilirubin in the group as an indicator of cholestasis syndrome initially exceeded the control values, amounting to 33.4 μmol / L (p <0.05).

    In 5 patients with chronic alcoholic disease, the diagnosis was confirmed by liver puncture biopsy data.

    After a complete clinical and laboratory study of patients, we carried out a course treatment with sodium hypochlorite.During treatment with sodium hypochlorite, none of the patients in this group received additional therapy with hepatoprotectors. In a number of patients, only symptomatic therapy was prescribed according to indications (β-blockers, diuretics).

    A sodium hypochlorite solution was prepared from a pharmacopoeial physiological solution by electrolysis on an electrochemical detoxification apparatus: “DEO-01MEDEK” with selective control of the concentration of the resulting solution by titration. Then the drug was injected into the peripheral (ulnar) vein of patients at a concentration of 200 mg / l (0.02%) at a rate of 30 drops per minute with a volume of 400 ml per infusion.During the course of treatment, from 3 to 7 daily intravenous drip procedures were carried out.

    We then re-examined the entire laboratory data set in all patients in the group. The dynamics obtained before and after treatment is shown in the table. Data are presented as M ± m, where M is the arithmetic mean and m is the standard error.


    Indicators of LPO, AOD, cytolysis syndromes, mesenchymal inflammation

    and cholestasis in patients with alcoholic liver disease

    before and after a course of sodium hypochlorite therapy


    Data of healthy persons

    (n = 30)

    Group of patients with ABP (n = 76)

    Indicator dynamics

    Student’s coefficient

    before HCN therapy

    after HCN therapy

    M ± m

    M ± m

    M ± m



    MDA, μmol / L

    5.98 ± 1.71

    12.94 ± 0.57

    8.85 ± 0.36

    ↓ 31.6 *

    p <0.01

    DC, units / ml

    0.9 ± 0.1

    1.37 ± 0.08

    0.89 ± 0.04

    ↓ 35.3 *

    p <0.01

    Cat, μmol / ml / min

    16.8 ± 6.16

    18.23 ± 0.97

    22.00 ± 0.8

    ↑ 20.7 *

    p <0.01

    SOD, u.f / ml

    2.13 ± 0.26

    2.33 ± 0.33

    2.85 ± 0.24

    ↑ 22.3 *

    p <0.01

    GP, μmol / ml / min

    1.84 ± 0.18

    4.58 ± 0.48

    5.92 ± 0.39

    ↑ 29.4 *

    p <0.01

    SU, unit


    1.26 ± 0.3

    0.27 ± 0.05

    ↓ 78.7 *

    p <0.01

    SG, unit


    1.06 ± 0.28

    0.15 ± 0.03

    ↓ 86.3 *

    p <0.01

    NAG, nmol / ml / min

    10.05 ± 1.5

    14.3 ± 0.86

    9.68 ± 0.21

    ↓ 32.3 *

    p <0.01

    SDH, μmol / L / h

    to 54

    75.48 ± 5.41

    55.86 ± 4.0

    ↓ 26.0 *

    p <0.01

    TDG, μmol / L / h

    to 54

    72.23 ± 6.79

    58.73 ± 5.2

    ↓ 18.7 *

    p <0.01

    ALT, μkat / L

    0.09 ± 0.02

    0.59 ± 0.06

    0.2 ± 0.03

    ↓ 65.4 *

    p <0.01

    AST, μkat / l

    0.11 ± 0.02

    0.48 ± 0.03

    0.15 ± 0.02

    ↓ 69.0 *

    p <0.01

    Ceruloplasmin, mg%

    34.0 ± 9.0

    47.07 ± 2.16

    38.03 ± 1.55

    ↓ 19.2 *

    p <0.01

    Thymol sample, units

    2.5 ± 1.5

    5.37 ± 0.81

    3.09 ± 0.27

    ↓ 42.5 *

    p <0.01

    Total bilirubin, μmol / L

    12.8 ± 9.4

    33.4 ± 5.6

    11.7 + 2.2

    ↓ 65.0 *

    p <0.01

    * p <0.01.

    It was noted that sodium hypochlorite therapy caused positive laboratory dynamics in 70 patients, which amounted to 92.1% of the entire group of patients with alcoholic liver disease.

    There were no side effects of sodium hypochlorite therapy in any of the patients in the group with alcoholic liver disease.

    According to the data obtained, after a course of treatment with sodium hypochlorite in patients in the study group, there is a significant decrease in the levels of MDA – by 31.6% (p <0.05) and DC - by 35.3% (p <0.05).In this case, the activity of AOD enzymes significantly increases. The levels of Cat, SOD, and HP increased by 20.7% (p <0.05), 22.3% (p <0.05), and 29.4% (p <0.05), respectively.

    Thus, the use of sodium hypochlorite therapy in patients with ABD leads to a significant decrease in the level of both primary and intermediate lipid peroxidation products. At the same time, there is a significant stimulation of the activity of the antioxidant system, which indicates the activation of reserve mechanisms of the liver antioxidant defense aimed at reducing the excessive accumulation of lipid hydroperoxides.

    After a course of sodium hypochlorite therapy, patients in the group showed a decrease in the severity of cytolysis syndrome. They have a significant decrease in the activity of ALT by 65.4% (p <0.05) and AST by 69.0%, leading to the normalization of the level of transaminases (ALT - 0.20 μkat / l, AST - 0.15 μkat / l). All indicators of liver-specific enzymes are also significantly reduced. SU and SG decrease by 78.7% and 86.3%, respectively (p <0.05). The levels of SDH and TDH decrease by 26% and 18.7% (p <0.05), practically reaching the normal values ​​of the control group (SDH - 55.9 μmol / L / h, TDH - 58.7 μmol / L / h) ...There is also a normalization of NAG (9.68 nmol / ml / min) with a decrease of 32.3% (p <0.05).

    Thus, in patients with ABD under the influence of sodium hypochlorite therapy, the cytolytic syndrome significantly decreases, which was manifested in the normalization of the activity of transaminases, NAG and a pronounced decrease in the activity of SU, SG, SDH and TDH.

    After sodium hypochlorite therapy, patients in the study group showed a significant decrease in the manifestations of mesenchymal-inflammatory syndrome – stabilization of the level of ceruloplasmin (38 mg%) with a decrease in it by 19.2% (p <0.05), as well as normalization of the thymol test level with reducing it by 42.5% (p <0.05).

    Thus, in patients with ABD, sodium hypochlorite therapy leads to a significant decrease in the manifestations of mesenchymal-inflammatory syndrome, accompanied by a significant decrease in sediment samples.

    After a course of sodium hypochlorite therapy, patients in the group showed a significant decrease in the level of total bilirubin by 65.0% (p <0.05) to the norm (11.7 μmol / l).

    Thus, in the group of patients with ALD under the influence of sodium hypochlorite therapy, correction of the cholestasis syndrome is observed.

    When comparing with laboratory parameters of patients with ALD who were treated with basic hepatoprotectors, in the group of patients with ALD after therapy with sodium hypochlorite, a more pronounced and reliable positive dynamics of laboratory data was noted.

    Diagrams 1 and 2 clearly show the comparative dynamics before and after treatment of the most striking indicators of LPO and AOD (MDA and Cat), as well as indicators of cytolysis (AST and SU) in patients with alcoholic liver disease treated with sodium hypochlorite and basic hepatoprotectors.

    Diagram 1:

    Dynamics of LPO and AOD (MDA and Cat) indicators in patients with alcoholic liver disease before and after treatment with sodium hypochlorite and hepatoprotectors

    * p <0.05.

    Diagram 2:

    Dynamics of cytolysis indices (AST and SU) in patients with alcoholic liver disease before and after treatment with sodium hypochlorite and hepatoprotectors

    * p <0.05.

    We also carried out a prospective observation of the long-term results of sodium hypochlorite therapy in this group of patients for 3 months. It was found that sodium hypochlorite has a significant long-term positive effect in patients in the ABP group, which is expressed in stabilization after 3 months in the majority of patients with LPO, AOD, cytolysis, cholestasis and mesenchymal inflammation. During 3 months of follow-up, the subjective state of most patients with ABD remained satisfactory, they did not notice pain and heaviness in the right hypochondrium, as well as itching.Nevertheless, in some patients (11 people, which amounted to 14.5% of the group), after 3 months, negative dynamics of laboratory data was noted, which, nevertheless, did not reach the figures that had taken place before the start of treatment. In all these patients, according to the anamnesis, there were repeated alcoholic excesses after the end of the course of therapy with sodium hypochlorite.


    In the studied group of patients with alcoholic liver disease, a pronounced increase in LPO processes was initially noted, manifested by the accumulation of both its primary and intermediate products, which was accompanied by a slight unreliable stimulation of the liver antioxidant system.Also, in this group of patients, pronounced signs of cytolysis, mesenchymal inflammation and cholestasis are found.

    The use of sodium hypochlorite therapy in these patients leads to a significant decrease in lipid peroxidation, restoration of the antioxidant system, a decrease in the manifestations of cytolysis, cholestasis and mesenchymal inflammation.

    Sodium hypochlorite has a significant long-term positive effect in patients with alcoholic liver disease, expressed in stabilization after 3 months in most of them LPO, AOD, cytolysis, cholestasis, mesenchymal inflammation indicators and improves the subjective state of patients.

    The method of treating ABD using intravenous drip infusion of sodium hypochlorite does not cause side effects and is pharmacoeconomically beneficial.

    Thus, sodium hypochlorite therapy is an effective and promising method of treating patients with alcoholic liver disease, which dictates the widespread introduction of this method in specialized medical centers.

    Presentation of the report in MS PowerPoint format – download.

    Also published in this section:

    Experience with sodium hypochlorite in non-alcoholic steatohepatitis
    Emelyanov D.N., Myazin R.G., Statsenko I.Yu., Sviridenko O.Yu., Leshina O.A.
    Published in the quarterly scientific and practical journal: “Bulletin of the Volgograd State Medical University”, 2016, No. 2 (58). Pp. 136-139 (published by the Higher Attestation Commission). UDC 616.36-002: 615.244
    Sodium hypochlorite in the treatment of alcoholic liver disease
    Myazin R.G., Emelyanov D.N., Statsenko I.Yu.
    Proceedings of the scientific-practical conference of the teaching staff dedicated to the 80th anniversary of the Volgograd State Medical University.Section IX: Internal Medicine and Clinical Diagnostics. 2015.S. 285-288.
    Evaluation of the effect of sodium hypochlorite therapy on lipid peroxidation, antioxidant protection, cytolysis and cholestasis syndromes in patients with toxic hepatitis
    Emelyanov D.N., Myazin R.G.
    Bulletin of AGIUV, No. 4, 2013, pp. 79-81.
    Detoxifying and antioxidant effects of sodium hypochlorite in the treatment of alcoholic liver disease
    Myazin R.G.
    Published in the collection of abstracts of the 15th Jubilee International Slavic-Baltic Scientific Forum: “St. Petersburg – Gastro-2013”, 13-15.05.2013, and in the journal: “Gastroenterology of St. Petersburg”, St. Petersburg, 2013, No. 2, theses No. 68, pp. M21-M22.
    Experience of using sodium hypochlorite in the treatment of Wilson-Konovalov’s disease
    Myazin R.G., Emelyanov D.N., Statsenko I.Yu., Sviridenko O.Yu.
    Materials of the XVII Russian Congress: “Hepatology Today”, Moscow, 19-21.03.2012, and “Russian Journal of Gastroenterology, Hepatology, Coloproctology”, v. XXII, 2012, No. 2, Appendix No. 39, section: “Metabolic disorders of the liver.” P. 35.
    Effect of sodium hypochlorite therapy on lipid peroxidation, antioxidant protection, cytolytic and mesenchymal-inflammatory syndromes in patients with toxic hepatitis
    Emelyanov D.N., Myazin R.G.
    Journal: “Bulletin of the Volgograd State Medical University”, 2011, No. 2, p.100-102 (VAK list). UDC 616.36-002: 615.244.
    Use of sodium hypochlorite in the treatment of alcoholic liver disease
    Emelyanov D.N., Myazin R.G., Statsenko I.Yu.
    Collection of abstracts of the XVI Russian Congress: “Hepatology Today”, Moscow, March 21-23, 2011, and “Russian Journal of Gastroenterology, Hepatology, Coloproctology”, vol. XXI, 2011, No. 1, Appendix No. 37, p. . 208.
    Changes in the level of the enzyme ceruloplasmin in patients with alcoholic liver disease treated with sodium hypochlorite
    Emelyanov D.N., Statsenko I.Yu., Sviridenko O.Yu., Myazin R.G., Leshina O.A.
    Collection of abstracts of the XV Russian conference: “Hepatology Today”, Moscow, 15-17.03.2010, and “Russian Journal of Gastroenterology, Hepatology, Coloproctology”, vol. XX, 2010, No. 1, Appendix No. 35, abstracts No. 273, p. 75.
    Sodium hypochlorite in the treatment of non-alcoholic steatohepatitis
    Myazin R.G., Emelyanov D.N., Statsenko I.Yu.
    Collection of abstracts of the XIV Russian conference: “Hepatology today”, Moscow, 16-18.03.2009, and “Russian Journal of Gastroenterology, Hepatology, Coloproctology”, v. XIX, 2009, No. 1, Appendix No. 33, Abstracts No. 292, p. 78.
    Sodium hypochlorite in the treatment of primary biliary cirrhosis
    Myazin R.G., Emelyanov D.N., Statsenko I.Yu., Sviridenko O.Yu., Al-Tamimi D.Kh.
    Collection of abstracts of the XIII Russian conference: “Hepatology Today”, Moscow, 17-19.03.2008, and “Russian Journal of Gastroenterology, Hepatology, Coloproctology”, vol.XVIII, 2008, No. 1, Appendix No. 31, Abstracts No. 34, p. 13.
    Combination of sodium hypochlorite and metadoxil in the treatment of patients with chronic toxic hepatitis
    Myazin R.G., Emelyanov D.N., Statsenko I.Yu., Davidyan V.S.
    Collection of materials of the jubilee Russian scientific conference with international participation dedicated to the 175th anniversary of the birth of S.P. Botkin, May 29-31, 2007, St. Petersburg, 2007, pp. 56-57.
    Use of sodium hypochlorite in the treatment of alcoholic hepatitis
    Myazin R.G., Emelyanov D.N., Statsenko I.Yu., Popova T.N., Kirina M.A.
    Collection of abstracts of the 9th International Slavic-Baltic Scientific Forum: “St. Petersburg – Gastro-2007”, 16-18.05.2007, and the journal: “Gastroenterology of St. Petersburg”, 2007, No. 1-2 , Abstracts No. 281, p. M 78-M 79.
    The state of lipid peroxidation and the antioxidant defense system in patients with toxic hepatitis
    Emelyanov D.N., Sviridenko O.Yu., Statsenko I.Yu., Myazin R.G., Godovalova L.A.
    Collection of abstracts of the XII Russian conference: “Hepatology Today”, Moscow, 19-21.03.2007, and “Russian Journal of Gastroenterology, Hepatology, Coloproctology”, v. XVII, 2007, No. 1, Appendix No. 29, abstracts No. 231, p. 64.
    The effectiveness of sodium hypochlorite therapy in patients with chronic alcoholic and toxic hepatitis
    Myazin R.G.
    Collection of abstracts of the XI Regional conference of young researchers of the Volgograd region.Volgograd State Medical University, 08-10.11.2006, Volgograd, direction 18: “Clinical aspects of medicine”, p. 50.
    Effect of sodium hypochlorite treatment in patients with liver cirrhosis
    Myazin R.G., Emelyanov D.N., Statsenko I.Yu.
    Collection of materials of the XII Russian Gastroenterological Week, Moscow, October 16-18, 2006, and “Russian Journal of Gastroenterology, Hepatology, Coloproctology”, No. 5, vol.XVI, 2006, Appendix No. 28, Abstracts No. 310, p. 84.
    The use of sodium hypochlorite for the treatment of patients with chronic diffuse liver diseases
    Myazin R.G., Skvortsov V.V., Emelyanov D.N.
    Scientific and practical journal: “Clinical Nutrition”, St. Petersburg, 2005, No. 4, pp. 35-36.
    Dynamics of the total activity of ceruloplasmin in patients with chronic diffuse liver diseases treated with sodium hypochlorite
    Myazin R.G.
    Collection of materials of the final scientific conference: “Actual problems of experimental and clinical medicine”, VolGMU, April 21-25, 2003, Volgograd, direction 7: “Internal diseases”, pp. 105-106.
    Hypochlorite therapy – a new method of treatment in hepatology
    Myazin R.G.
    Collection of materials of the 6th Regional Conference of Young Researchers of the Volgograd Region, 13-16.11.2001, pp. 64-65.
    Hepatolenticular degeneration
    Emelyanov D.N., Statsenko I.Yu., Skvortsov V.V., Leshina O.A., Myazin R.G.
    Magazine: “Medline Express”, St. Petersburg, No. 8-9 (174), August-September 2004, pp. 18-19.
    Long-term results of treatment of patients with chronic diffuse liver diseases with sodium hypochlorite
    Myazin R.G.
    Collection of abstracts of the 8th Regional Conference of Young Researchers of the Volgograd Region, Volgograd State Medical University, November 11-14, 2003, direction 18: “Clinical aspects of medicine”, theses No. 19, p.114-115.
    Effect of sodium hypochlorite therapy in patients with chronic hepatitis of non-viral etiology
    Myazin R.G., Emelyanov D.N., Statsenko I.Yu., Sviridenko O.Yu., Godovalova L.A.
    Collection of abstracts of the XI Russian conference: “Hepatology Today”, Moscow, 27-29.03.2006, and “Russian Journal of Gastroenterology, Hepatology, Coloproctology”, vol. XVI, 2006, No. 1, theses No. 253, p. . 72.
    Sodium hypochlorite is a promising method for the treatment of patients with chronic diffuse liver diseases (report)
    V.V., Skvortsova Z.S., Sviridenko O.Yu., Skvortsov V.V., Myazin R.G.
    Collection of abstracts of the 4th Russian Scientific Forum with international participation: “Gastro-2002”, St. Petersburg, 17-21.09.2002, and scientific and practical journal: “Gastroenterology of St. Petersburg”, 2002, no. 2-3, theses No. 284, p. 88.
    The use of sodium hypochlorite in hepatology (report)
    Myazin R.G.
    Collection of abstracts of the 60th anniversary conference of students and young scientists: “Medicine at the beginning of the new century: Achievements and prospects”,
    April 23-26, 2002, Volgograd, p.265-266.

    What is Opioid Potency?

    Opioid potency measures how much pain medication is needed for pain relief. Morphine is often used as a reference for this measurement. Charts are available to show healthcare providers how much of a given pain reliever, such as tramadol, will be required to achieve the effect of a standardized dose of morphine, such as 10 mg taken orally.When deciding what to recommend to a patient, available medications and pain levels are considered to decide which medication is appropriate.

    These compounds have been used in the treatment of pain for centuries, and a variety of them are produced, including very powerful synthetic ones. Effects can vary depending on the drug and how it is delivered. Oral drugs need higher doses to be effective than those given directly into the bloodstream.In addition, patients with liver dysfunction may process the drug differently and thus achieve different levels of pain control. The development of opioid potency equivalence charts allows healthcare providers to determine which drug to use, when, and at what dosage.

    Some examples of lower opioid drugs ranked below morphine in potency include codeine and aspirin. Stronger medications such as fentanyl and methadone are also available.Healthcare professionals deciding what to recommend should consider effective pain control to maintain reasonable patient baseline levels and may also consider the risk of pain breakthrough. Patients with this type of pain may experience sudden outbursts that require a fast-acting analgesic with higher opioid activity.

    Health care providers may want to keep patients on low-strength opioids for as long as possible. This can reduce the risk of side effects and help the patient maintain mental clarity while gaining pain control.In some cases, switching may be required due to increased pain levels, the development of tolerance, or a change in the patient’s condition; for example, someone may no longer be able to take oral medications and need to switch to a patch or intravenous delivery method.

    When switching between pain medications, opioid potency is an important factor. A patient who took codeine for pain could not, for example, switch to fentanyl, a much more potent drug, without careful monitoring.Dosage may require several careful adjustments to find the effective level for the patient. Analgesics can also be combined to control both chronic and breakthrough pain; cancer patients, for example, may need fast-acting opioids in addition to ongoing pain management.


    90,000 Changes in the activity of inflammation and the severity of fibrosis in patients with alcoholic cirrhosis of the liver after transplantation of autogenous hematopoietic stem cells

    & nbsp


    Burganova G.R., Abdulkhakov S.R., Gumerova A.A., Gazizov I.M., Yilmaz T.S., Titova M.A., Odintsova A.Kh., Kiyasov A.P.

    The most informative method for assessing the results of treatment of chronic liver diseases is morphological analysis of biopsies. The aim of the study was to study the effectiveness of transplantation of autogenous hematopoietic stem cells in the treatment of alcoholic liver cirrhosis. The studies were carried out on liver biopsies of 11 patients with alcoholic liver cirrhosis.Biopsies were obtained before the introduction of autogenous hematopoietic stem cells into the celiac trunk, as well as after 3 and 12 months. after transplantation and stained with hematoxylin-eosin and according to Van Gieson’s method. The results of the study showed that after 3 and 12 months. after transplantation, there is an improvement in the structure of the liver and a decrease in the index of histological activity. When analyzing the fibrosis index, no significant dynamics of indicators was noted. Our data indicate that the transplantation of autogenous hematopoietic stem cells into patients with alcoholic cirrhosis of the liver is a fairly effective method to reduce the activity of inflammation in the liver and improve its morphological structure.

    A characteristic feature of liver diseases, which in many respects complicates their diagnosis, is the discrepancy between clinical and laboratory manifestations of the severity of morphological changes in the liver. The level of aminotransferases in serum depends little on the pathological changes in the liver and can remain within the normal range, including in liver cirrhosis, and can also change spontaneously or in response to various factors not related to the course of the disease [1-3] …Instrumental studies also do not provide reliable information about the severity of the pathological process [4] . Thus, morphological examination still remains the “gold standard” for the diagnosis of inflammatory changes and liver fibrosis. According to the existing classification of chronic hepatitis [5] , the final and complete diagnosis should reflect the etiology, degree of activity and stage of the disease. Morphological analysis of liver biopsies is the only way to determine the activity and stage of chronic hepatitis, predict the course of the disease, identify the mechanisms of damage and monitor the effectiveness of treatment, in this case, stem cell therapy.The aim of the study was to determine the effect of transplantation of autogenous hematopoietic stem cells (HSC) on the activity of inflammation and the severity of fibrosis in patients with alcoholic liver cirrhosis.

    Material and methods

    Clinical and morphological studies were performed with the written informed consent of patients and in accordance with the ethical standards of the Declaration of Helsinki (2000), approved by the Academic Council of Kazan State Medical University and the Ethics Committee of the Ministry of Health of the Republic of Tatarstan.

    The clinical study included 11 patients with alcoholic cirrhosis of the liver (Child-Pugh class A and B) who had undergone liver biopsy prior to treatment. Then, for 5 days, patients were injected with a preparation of granulocyte colony-stimulating factor at a dose of 480 μg, after which they received autogenous HSCs (as part of the leukocyte mass with a high content of nucleated mononuclear cells). Isolated HSCs were injected into the celiac trunk. After 3 and 12 months. after transplantation, repeated liver biopsies were performed.Paraffin sections of biopsy specimens were stained with hematoxylin-eosin and hematoxylin-microfuchsin according to the Van Gieson method. The resulting histological preparations were examined according to the protocol, which is a unified scoring system, including the assessment of the histological activity of the inflammatory process and the severity of fibrosis [6, 7] by three independent morphologists to increase the reliability of the assessment results.


    Before transplantation of autogenous HSCs, the histological activity index (IHA) ranged from 10 to 15 points (on average, 11.7 points), which corresponds to moderate and severe chronic hepatitis.In a comparative analysis after 3 months. after transplantation, almost all patients showed a decrease in IHA (Fig. 1): in numerical terms, IHA was in the range of 8-14 points (on average 10.6 points, which corresponds to mild and moderate chronic hepatitis).

    After 12 months. after autotransplantation of the fraction of peripheral blood mononuclear cells in the analysis of liver biopsies, we observed an increase in the range of IHA values ​​from 8 to 15 points (on average – 10.2 points, Fig. 2).These diagrams clearly illustrate the decrease in IHA in patients with alcoholic liver cirrhosis after 3 months. after transplantation of peripheral blood mononuclear cells with a tendency to a continuing slower decrease in IHA within 12 months.

    When analyzing the fibrosis index (IF), we observed a similar picture: before transplantation, 4 out of 11 patients in the study group were diagnosed with cirrhosis, and 7 other patients had liver fibrosis of varying severity (Fig. 3). After 3 months. after transplantation, the morphological diagnosis of cirrhosis was made in 2 patients, 12 months later.- 3 patients (Fig. 4). In contrast to IHA, when analyzing the average index of IF, there was a slight decrease in IF after 3 months. after transplantation and return to the initial level after 12 months.


    In a significant number of works devoted to the study of the possibility of using stem cells of various origins in the treatment of patients with chronic liver diseases, the authors assessed the effectiveness of cell transplantation by changing the parameters of the Child-Pugh scale, MELD index and biochemical parameters [8, 9] .However, the latter, in particular, the level of aminotransferases, do not reflect changes in the histological structure in the liver and have no prognostic value [10] .

    In 2006, work [11] was published, in which for the first time the effectiveness of stem cell therapy for chronic hepatitis and liver cirrhosis was assessed using immunohistochemical analysis of liver biopsies. Biopsies were performed before cell injection and after 4 weeks. after bone marrow cell transplantation.A significant increase in cell proliferation and expression of a-fetoprotein was found after 4 weeks. after transplantation, which, together with an improvement in serum albumin and total protein levels, a decrease in Child-Pugh scores and the absence of side effects, allowed the authors to conclude that this method is promising in the treatment of decompensated liver cirrhosis.

    Taking into account the need for a morphological assessment of the effectiveness of transplantation at a later date after the introduction of cells, on the one hand, and the invasiveness of the manipulation, on the other hand, we analyzed liver biopsies and assessed the morphological picture at three periods: before the introduction of autogenous HSCs, after 3 months.and 12 months. after transplantation. For the first time during these periods of observation, we were able to demonstrate the effect of transplantation of peripheral blood mononuclear cells in terms of reducing the activity of the inflammatory process. The absence of significant dynamics of IF indices may be due to the fact that picrofuchsin reveals already formed connective tissue, which does not disappear after the introduction of stem cells into the liver vessel. However, given the decrease in inflammatory activity, it can be assumed that the administration of autogenous HSCs can slow down the further progression of fibrosis and the accumulation of connective tissue in the liver.

    Our data indicate that transplantation of autogenous HSCs into the celiac trunk in patients with alcoholic cirrhosis of the liver is a safe and rather effective method allowing to reduce the activity of inflammation in the liver, improve its morphological structure, and, as a consequence, delay the progression of fibrosis.

    High position of the diaphragm domes. Glossary of terms of radiation diagnostics

    High position of the domes of the diaphragm

    High standing of the domes of the diaphragm – pathological displacement of the diaphragmatic muscle into the chest cavity, which leads to disruption of the functioning of internal organs, in particular to problems with breathing, gastrointestinal tract, etc.

    The diaphragm is a buffer between the thoracic and abdominal cavities just below the lungs and is a muscle, acting as a barrier between the chest and abdominal organs. The liver, spleen, and heart are also located in the immediate vicinity of the diaphragm. If the diaphragm, consisting of a rather rigid muscle plate, is displaced higher with its apex and wings, this somehow affects the location of adjacent organs.

    The high position of the dome of the diaphragm significantly reduces the patient’s quality of life.The most common manifestations of a displacement of the diaphragm are choking, lack of air, pressure in the upper abdomen.

    Reasons for the high standing of the dome of the diaphragm

    There are three types of pathological changes of this kind, indicating the cause of the displacement of the diaphragm:

    • Left-sided displacement of the dome of the diaphragm occurs due to bursting diseases of the digestive system and spleen. Such diseases include hepatomegaly, flatulence, splenomegaly.
    • Right-side high standing of the dome of the diaphragm is usually caused by diseases of the liver, which is located on the right.
    • Displacement of the dome of the diaphragm on both sides may indicate all of the above causes, or the problem is related to pathological changes in the diaphragm itself.

    Diseases of the diaphragm affecting its location and shape include:

    Diaphragmatitis – inflammation of the diaphragm, causing swelling and enlargement of the dome of the muscle.Chronic cough, mechanical damage, parasitic infections lead to inflammation.

    Diaphragm paralysis – occurs due to impaired transmission of impulses in the phrenic nerve.

    Diaphragmatic hernia (under certain conditions).

    Also among the reasons for the high standing of the diaphragm should be mentioned degenerative diseases of the spine, trauma, hyperplasia of the tissues of some organs, diseases of the vessels feeding the internal organs closest to the diaphragm.

    The high standing of the dome of the diaphragm amenable to successful treatment – after the cause of the displacement is clarified and corrected, the problem is solved.

    Diagnostics of the high standing of the dome of the diaphragm is carried out on CT. Sometimes the patient is recommended to undergo additional examinations, for example, to pass laboratory tests if the displacement is caused by infectious diseases.

    90,000% d1% 83% d0% b3% d0% bb% d0% b5% d1% 80% d0% be% d0% b4 +% d1% 87% d0% b5% d1% 82% d1% 8b% d1% 80% d0% b5% d1% 85% d1% 85% d0% bb% d0% be% d1% 80% d0% b8% d1% 81% d1% 82% d1% 8b% d0% b9 – from Russian into all languages ​​

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