Normal count for liver. 12 Health Risks of Chronic Heavy Drinking

19.05.197218.08.2021 by alexxlab

What are the health risks of chronic heavy drinking? Learn about the consequences of excessive alcohol consumption, including risks of anemia, cancer, heart disease, cirrhosis, dementia, and more.

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Alcohol and Health Risks

Alcohol consumption can cause numerous diseases. Many people know that heavy drinking can lead to cirrhosis of the liver and is a leading cause of automobile accidents. But did you know chronic drinking can also lead to cancer and heart attack? Read on to find out consequences of heavy drinking.

Anemia

Excessive alcohol use can affect the hematologic system, which is made up of the blood, spleen, bone marrow, and the liver. It can cause your red blood cell count to be abnormally low, which is a condition called anemia. Symptoms of anemia include fatigue, shortness of breath, and lightheadedness.

Cancer

Chronic alcohol drinking can increase your risk for developing cancer. The body converts the alcohol you drink into acetaldehyde, which is a known carcinogen (substance that causes cancer). Cancers often found in heavy drinkers include those of the mouth, pharynx (throat), larynx (voice box), esophagus, liver, breast, and colorectal region. Many heavy drinkers also smoke, which further increases cancer risk.

Cardiovascular Disease

Heavy drinking and binge drinking can cause heart disease or stroke. It can raise the levels of fats in the blood (triglycerides), lead to high blood pressure, and stroke. It can also cause cardiomyopathy (weakening of the heart muscle), and the heart-rhythm abnormalities atrial and ventricular fibrillation.

Cirrhosis

Alcohol causes inflammation of the liver, and chronic drinking can cause scarring of liver tissue that leads to cirrhosis, a potentially fatal condition in which the liver is so scarred it can no longer function. The risk increases the longer you have been drinking. Not all heavy drinkers will develop cirrhosis, though it seems to run in families, and women get it more often than men.

Dementia

Heavy drinking can affect the brain and can lead to memory loss and some symptoms of dementia. Alcohol-related brain damage can mirror some symptoms of dementia, like poor judgment and difficulty in decision-making. Heavy alcohol drinking over a long period of time may result in Korsakoff’s syndrome, a condition in which people may suffer short-term memory loss. In addition, heavy drinking may result in nutritional deficiencies that can also lead to symptoms of dementia.

Depression

Alcohol abuse and depression are often associated. In some cases, people are depressed and turn to alcohol to self-medicate. However, studies show that many people who drink heavily develop depression.

Seizures

Heavy or binge drinking, or alcohol withdrawal, can lead to a form of epilepsy called status epilepticus, or an acute, prolonged epileptic seizure, which is a life-threatening condition. Excessive alcohol use can also trigger epilepsy in some people who did not have the condition before they started drinking. Some epilepsy medications may make you more sensitive to the effects of alcohol, and alcohol may interfere with some medications used to treat epilepsy.

Gout

Gout is a type of arthritis caused by the formation of uric acid crystals in the joints. It can be very painful. Alcohol intake may increase the risk of developing gout, particularly in men, and beer seems to cause the condition more than other types of alcohol. If you already have gout, drinking alcohol may worsen your symptoms.

High Blood Pressure

Alcohol can cause high blood pressure (hypertension). The more alcohol a person drinks, the greater their risk for developing high blood pressure. Hypertension can become chronic, and can lead to other medical conditions including heart disease, stroke, and kidney disease.

Infectious Diseases

Excessive alcohol use can weaken the immune system, and make it easier for you to get infections. Chronic drinkers are more likely to contract diseases such as tuberculosis, pneumonia, HIV/AIDS, and sexually transmitted diseases (STDs). STDs are a concern because heavy drinkers are also more likely to engage in risky sexual behaviors. Even binge drinking on one day can affect your body’s ability to fight off infection for up to 24 hours.

Nerve Damage

Alcoholic neuropathy is a form of nerve damage caused by heavy drinking. The combination of alcohol being toxic to nerve cells, combined with the poor nutrition that often accompanies alcohol abuse is believed to cause this condition. Symptoms include numbness, tingling and pain, muscle weakness usually in the extremities, loss of bladder or bowel control, impotence, diarrhea, nausea and vomiting, or difficulties with balance and coordination.

12 Health Risks of Chronic Heavy Drinking

Alcohol and Health Risks

1. Anemia

2. Cancer

3. Cardiovascular Disease

4. Cirrhosis

5. Dementia

6. Depression

7. Seizures

8. Gout

9. High Blood Pressure

10. Infectious Diseases

11. Nerve Damage

12. Pancreatitis

Heavy drinking can lead to pancreatitis, which is a dangerous condition involving inflammation of the pancreas. Symptoms may include acute abdominal pain, nausea, and vomiting. Chronic pancreatitis from chronic drinking may lead to malabsorption of nutrients and diabetes.

Summary

Chronic heavy alcohol use can have many damaging effects on the body. Talk to your doctor about ways to cut down on your drinking or stop drinking entirely to reduce your chances of developing health complications from drinking.

Liver function tests (LFT) | Health Navigator NZ

A liver function test (LFT) is a blood test that measures the levels of several substances (enzymes and proteins) excreted by your liver. Levels that are higher or lower than normal can indicate liver problems.

Key points

The liver function test (LFT) is also called a hepatic function panel (hepatic refers to the liver).

The liver function test is not done routinely, but is requested to establish the presence of damage or inflammation in your liver.

To perform a liver function test, a blood sample is drawn from a vein in your arm and collected in a tube. This tube is sent to the laboratory for analysis.

What is a liver function test (LFT)?

The liver function test measures the levels of different substances (enzymes and proteins) excreted by your liver, such as:

alanine aminotransferase (ALT)

alkaline phosphatase (ALP)

aspartate aminotransferase (AST)

gamma-glutamyl transferase (GGT)

bilirubin

albumin

total protein.

When is a liver function test done?

A liver function test is not done routinely but is requested in certain situations, to establish the presence of damage or inflammation in the liver. Your doctor may ask for this test to be done to:

screen for potential liver problems or infections affecting your liver, such as hepatitis A, hepatitis B and hepatitis C

help in the diagnosis of other conditions such as gallstones

monitor the progression and severity of liver disease and to determine how well a treatment is working

monitor side effects if you are taking prescription or non-prescription medicines that can affect liver functioning.

How do I prepare for a liver function test?

For the most part, you don’t need to do anything before having this test. It can be done at any time of the day. Some medicines may affect the test so tell your doctor about all prescription and non-prescription medicines (such as herbal products) you take.

How is the sample collected for testing?

A blood sample is taken by a needle placed in a vein in your arm. An elastic band is wrapped around your upper arm. It may feel tight for a few seconds. You may feel nothing at all from the needle, or you may feel a small brief sting or pinch. The blood sample is collected in a tube, which is sent to the laboratory for analysis.

What do my results mean?

Interpreting liver function test results is not always easy and is best done in consultation with your healthcare team. They will know what is normal for you and how these results relate to your clinical picture. Often, if there is a mild abnormality, all that may be needed is to repeat the test in a month or two’s time as many changes can be temporary and return to normal.

On its own, a liver function test cannot usually provide a definitive diagnosis of a condition, but it can provide important clues about possible problems with your liver

Alanine aminotransferase (ALT) – when your liver is damaged, ALT is released into your bloodstream and levels increase.

Alkaline phosphatase (ALP) – higher than normal levels may indicate liver damage or disease, such as a blocked bile duct, or certain bone diseases.

Aspartate aminotransferase (AST) – an increase in AST levels may indicate liver damage or disease.

Bilirubin – bilirubin is produced during the normal breakdown of red blood cells. Raised levels of bilirubin (called jaundice) may indicate liver damage or disease.

Albumin and total protein – lower than normal levels of albumin and total protein may indicate liver damage or disease.

Gamma-glutamyl transferase (GGT) – higher than normal levels may indicate liver or bile duct damage.

Learn more

The following is further reading that gives you more information on the full blood count test. Be aware that websites from other countries may contain information that differs from New Zealand recommendations.

Blood test safety information Labtests, NZ
Liver function tests Patient Info, UK
Lab tests online Australasian Association of Clinical Biochemists

Higher Level of SGPT Risks | Causes | Symptoms

What is Higher Level of SGPT?

SGPT exists predominantly in the liver and leaks into the bloodstream when produced in excess. The SGPT normal range is about 7 to 56 units per liter of blood serum. Thus, very high level of SGPT in the blood can be an indication of damage or problems related to the liver. Certain diseases like cirrhosis and hepatitis raise the blood serum SGPT levels, so do specific medications including statin used to lower cholesterol.

What Causes High SGPT?

There are many conditions and diseases, which can result in increased SGPT level.

Drinking Alcohol

Acute viral hepatitis A and B

Celiac disease

Diabetes

Heart attack

Obesity

Hepatitis C

Epstein-Barr virus

Gallbladder inflammation (cholecystitis)

Dermatomyositis

Symptoms of High SGPT Level:

The high SGPT level symptoms include –

Vomiting and nausea

Weakness

Fatigue

Leg swelling

Shortness of breath

Excessive bleeding or bruising

Jaundice

If you find these warning signs, you need to immediately consult your doctor and undergo SGPT blood test which will help you know whether your SGPT level is normal.

To reduce the SGPT level, diet modifications are needed. Your daily diet should consist of at least one fruit containing vitamin D. Alternatively, you can simply stand out in the sunlight for at least 20 minutes per day to get vitamin D. Couple it with some exercises that will help you stay healthy.

It is always recommended to have a regular whole body checkup with your doctor. The signs and symptoms of high SGPT level may not be noticeable immediately and hence, it is always better to have a preventive approach rather than taking action after the high-level findings. You can get the SGPT blood test done in a renowned hospital where it is a part of preventive health checkups.

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LFT results are not diagnostic of a specific condition; they indicate that there may be a problem with the liver. In a person who does not have symptoms or identifiable risk factors, abnormal liver test results may indicate a temporary liver injury or reflect something that is happening elsewhere in the body – such as in the skeletal muscles, pancreas, or heart. It may also indicate early liver disease and the need for further testing and/or periodic monitoring.

Results of LFTs are usually evaluated together. Several sets of results from tests performed over a few days or weeks are often assessed together to determine if a pattern is present. Each person will have a unique set of test results that will typically change over time. A doctor evaluates the combination of liver test results to gain clues about the underlying condition. Often, further testing is necessary to determine what is causing the liver damage and/or disease.

Type of liver condition or disease	Bilirubin	ALT and AST	ALP and GGT	Albumin	PT
liver damage (due, for example, to infection, toxins or drugs, etc. )	Normal or increased usually after ALT and AST are already increased	Usually greatly increased; ALT is usually higher than AST	Normal or only moderately increased	Normal	Usually normal
forms of various liver disorders	Normal or increased	Moderately increased	Normal to slightly increased	Normal	Normal
Alcoholic Hepatitis	Normal or increased	AST is usually higher than the level of ALT	Normal or moderately increased, GGT markedly increased	Normal	Normal
	May be increased but this usually occurs later in the disease	AST is usually higher than ALT but levels are usually lower than in alcoholic disease	Normal or increased	Usually decreased	Usually prolonged
Bile duct obstruction, cholestasis	Normal or increased; increased in complete obstruction	Normal to moderately increased	Increased; often greater than 4 times what is normal	Usually normal but if the disease is chronic, levels may decrease	Usually normal
Cancer that has spread to the liver (metastasized)	Usually normal	Normal or slightly increased	Usually greatly increased	Normal	Normal
Cancer originating in the liver (hepatocellular carcinoma, HCC)	May be increased, especially if the disease has progressed	AST higher than ALT but levels lower than that seen in alcoholic disease	Normal or increased	Usually decreased	Usually prolonged
Autoimmune	Normal or increased	Moderately increased	Normal or slightly increased	Normal or decreased	Normal

Type of liver condition or disease

Bilirubin

ALT and AST

ALP and GGT

Albumin

liver damage (due, for example, to infection, toxins or drugs, etc. )

Normal or increased usually after ALT and AST are already increased

Usually greatly increased; ALT is usually higher than AST

Normal or only moderately increased

Normal

Usually normal

forms of various liver disorders

Normal or increased

Moderately increased

Normal to slightly increased

Normal

Alcoholic Hepatitis

Normal or increased

AST is usually higher than the level of ALT

Normal or moderately increased, GGT markedly increased

Normal

May be increased but this usually occurs later in the disease

AST is usually higher than ALT but levels are usually lower than in alcoholic disease

Normal or increased

Usually decreased

Usually prolonged

Bile duct obstruction, cholestasis

Normal or increased; increased in complete obstruction

Normal to moderately increased

Increased; often greater than 4 times what is normal

Usually normal but if the disease is chronic, levels may decrease

Usually normal

Cancer that has spread to the liver (metastasized)

Usually normal

Normal or slightly increased

Usually greatly increased

Normal

Cancer originating in the liver (hepatocellular carcinoma, HCC)

May be increased, especially if the disease has progressed

AST higher than ALT but levels lower than that seen in alcoholic disease

Normal or increased

Usually decreased

Usually prolonged

Autoimmune

Normal or increased

Moderately increased

Normal or slightly increased

Normal or decreased

Normal

If a person is taking drugs that may affect their liver, then abnormal test results may indicate a need to re-evaluate the dosage or choice of medication. When a person with liver disease is being monitored, then the doctor will evaluate the results of the liver panel together to determine if liver function in worsening or improving. For example, increasingly abnormal bilirubin, albumin, and/or PT may indicate a deterioration in liver function, while stable or improving results of these tests may indicate liver function preservation or improvement.

Aspartate aminotransferase (AST)

A very high level of AST is frequently seen with acute hepatitis. AST may be normal to moderately increased with chronic hepatitis. In people with blocked bile ducts, cirrhosis, and liver cancer, AST concentrations may be moderately increased or close to normal. When liver damage is due to alcohol, AST often increases much more than ALT (this is a pattern seen with few other liver diseases). AST is also increased after heart attacks and with muscle injury.

Unfortunately only about half of all tumours will give a raised reading of AFP. So a normal AFP test does not exclude the presence of HCC. This is further complicated by the fact that AFP is also produced by proliferating liver cells so somebody with cirrhosis and liver regeneration is likely to have raised AFP levels already. As a consequence doctors will probably want to monitor whether the AFP levels are stable or not. Rising levels of AFP are more likely to indicate HCC.

Ultrasound is usually the first screening test carried out if HCC is suspected. The accuracy of an ultrasound depends very much on the technician or radiologist who performs the scan. Some experienced operators may be able to detect lesions (areas of abnormal tissue) as small as 0.5cm. Others may only be able to identify much larger lesions. An ultrasound has the advantages of not involving ionizing radiation and intravenous contrast material (injecting a chemical into the body to improve the contrast of the imaging). The cost of ultrasound is also lower than other types of scans.

When performed with an enhancing contrast agent CT scans can be just as sensitive as ultrasound. This is because the agent improves the imaging of the arterial and venous systems. CT scans are much less operator-dependent than ultrasound. They also have the advantage of being able to provide images of more areas of the body. CT scans are considerably more expensive than ultrasound and expose people to ionising radiation.

In this procedure a catheter is inserted into the hepatic artery and intravenous contrast material is injected into the liver. It may be useful for evaluating difficult lesions but it also involves ionizing radiation risks, arterial puncture and the administration of contrast agent. Hepatic angiography is usually carried out on people who are considered to be at high risk but who have failed to show any signs of HCC with other imaging studies. At the time of angiography, if a tumour is detected, it may be decided to block the artery feeding the tumour and before injecting anticancer drugs into it (chemoembolisation).

MRI is becoming increasingly popular for the diagnosis of hepatic tumours. Like a CT scan it can examine large areas of the chest and abdomen in a single session. But because no ionizing radiation is involved the imaging can be repeated many times with little risk. The technology has evolved to the point that the newer MRIs can reconstruct images of the bile ducts, the gallbladder and of the arteries and veins of the liver. The use of intravenous contrast agents significantly increases the sensitivity of the procedure, but also increases the costs. MRI is currently expensive and availability of MRI machines is limited.

What is fatty liver?
Fatty liver is not a disease, but a pathological finding. A more appropriate term is fatty filtration of the liver.

What causes fatty liver?
Fatty liver can be caused by certain chemical compounds, nutritional or endocrine disorders, and by genetic factors. Drugs and chemical compounds
that can cause fatty liver include alcohol, tetracycline, methotrexate, valproic acid, cortisone and cortisone-like medications, carbon
tetrachloride, and other solvents. Of these, alcohol is by far the most common cause. Liver inflammation may accompany exposure to these toxins and
is responsible for the associated symptoms of fever, fatigue and jaundice.

Nutritional causes of fat in the liver include starvation, malnutrition, or obesity. Fat in the liver can also occur with rapid or extreme weight
reduction such as might occur following an intestinal or gastric bypass operation for obesity. In some patients with fatty liver the fat is
accompanied by inflammation (steatohepatitis), and occasionally the fat and inflammation may lead to scarring of the liver (fibrosis).

How can fatty liver easily be identified?
Fat in the liver usually does not produce any specific signs or symptoms. Occasionally patients will experience a dull pain in the right upper abdomen.
Blood tests may reveal an elevation of the liver chemistries (SGOT or AST, SGPT or ALT, GGT, Alkaline phosphatase). A fatty liver may be detected on an
ultrasound, CT, or magnetic resonance (MRI), examination of the liver. Confirmation of the diagnosis requires a liver biopsy. In mild cases, where
the patient has no symptoms and the liver chemistries are normal or minimally elevated, a biopsy may not be required.

Fatty liver due to obesity is best managed with a program of weight reduction, consisting of a nutritious, low fat diet, and exercise. In
patients with diabetes, fatty liver is managed with diet and better control of blood sugar. In individuals with elevated cholesterol or
triglycerides, diet therapy is prescribed first. Patients not responding to diet, and in
those with severe elevations of cholesterol and triglycerides, specific medications to reduce the these levels may be prescribed (e. g., Questran,
Colestid, Lopid, Lipitor, Pravachol, Lescol, Zocor, Mevacor). Niacin is generally avoided because of its tendency to cause liver test elevations by
itself. Some patients may be treated with dietary supplements. (e.g., lecithin,
L-carnitine). L-carnitine may enhance fat metabolism by the liver, whereas lecithin may prevent some of the tissue damage caused when oxygen
reacts with fat during routine chemical reactions in the liver (lipid
peroxidation).

The liver is considered one of the most important organs in humans, since it works almost for wear and tear, performing a huge number of functions at the same time every day. Exposure to viruses, malnutrition, obesity, the influence of negative environmental factors and internal pathological changes have a detrimental effect on the state of this important organ.The most common method of examining the liver for signs of pathology is the method of ultrasound diagnostics. Ultrasound makes it possible to determine the volume of the liver, to assess the contours of the organ and its tissue structure. With the help of ultrasound dopplerometry, the vessels supplying the liver are additionally evaluated – these are the portal and hepatic veins, the hepatic artery.

Liver elastometry is a modern method of obtaining and evaluating an ultrasound image. Elastometry is now considered the third ultrasound technology after ultrasound and Doppler imaging.Thanks to her, there has been a significant qualitative leap in the differential diagnosis of focal pathology of the liver and superficially located organs. This method opened up new and very promising possibilities of imaging – determination and comparison of the elasticity of body tissues.

The GE Logiq E9 expert ultrasound system used at the Medical Diagnostic Center is designed for a wide range of examinations, including shear wave elastometry and compression elastography.These methods expand the capabilities of the ultrasound system and increase the reliability of ultrasound diagnostics, including when examining patients with chronic liver diseases. The choice of a place for measuring tissue elasticity indicators is made using a test volume on a two-dimensional ultrasound image, and the numerical values of the elasticity indicator are given in kilopascals, therefore the method is called quantitative ultrasound elastography or elastometry.

Results F1 – F3 mean an active decrease in the elasticity of the liver due to the replacement of the parenchyma with connective tissue, which occurs with hepatitis B and C. At this stage, it is necessary to start treatment as soon as possible. The main danger in patients with hepatitis is the progression of fibrosis. In just a couple of years, the F1 stage can go to F3. Therefore, patients with the result of elastometry in the F1 stage must be re-examined once a year. This will allow you to identify changes in time and begin treatment.

The term fibrosis is applied not only to the liver disease of the same name, it is a general medical concept that denotes an abnormal formation of connective tissue, accompanied by scarring.Thus, the tissue of the organ can react to an acute inflammatory process, trying to isolate the focus of inflammation from neighboring, while healthy tissues. It is important to understand that liver fibrosis and cirrhosis are not identical concepts. Fibrous changes can be stopped, and the affected organ can actually be restored. But without proper and timely treatment, the process of tissue change becomes irreversible.

Ultrasound examination is a diagnostic procedure during which pathological changes in organs can be detected. This manipulation is absolutely painless, which allows even small children to be diagnosed. In order for the ultrasound of the abdominal organs to become as informative as possible, you need to properly prepare for the procedure.What the research includes and what the preparation consists of, we will consider further.

This manipulation is extremely simple. The patient is required to lie motionless on his back. The person is laid on a flat horizontal couch, first asked to undress to the waist. The area to be examined is lubricated with a special gel, which will facilitate the movement of the ultrasonic transducer. At the request of the doctor, you may need to hold your breath for a few seconds, turn on your side or on your stomach.

Test organ	Standard
Liver	Echogenicity of the liver is normal.The length of the right lobe does not exceed 5 cm. The thickness is not more than 14 cm. The thickness of the left lobe should not exceed 7 cm, length up to 10 cm.
Spleen	The structure and surface of the organ without obvious changes. Length about 11-13 cm. Width and thickness up to 5 cm.
Kidneys	The width, depending on age, varies 4-6 cm. The length is not more than 11 cm. The thickness is 4-5 cm. Pathological changes in the structure of the parenchyma or pelvis were not identified.There are no foreign bodies.
Gallbladder	No foreign bodies. The shape is oblong. Wall thickness up to 0.5 cm. Volume does not exceed 70 cubic cm.
Pancreas	The contour is smooth, without pathologies. The tail is up to 3 cm, the head is up to 3.5 cm, the body is up to 2.5 cm. The Wirsung duct is not widened.

What are the key symptoms or syndromes in these patients? First, as a rule, this is liver failure of at least moderate severity, and, as a rule, severe liver failure. Also in such patients, hypoxemia is noted: when breathing with ordinary air, the partial oxygen tension is no more than 70 millimeters in these patients without attempts to increase this oxygen tension by giving a gas mixture with a high oxygen content.The next criterion is the dilatation of the vessels of the lungs, which can be determined by X-ray and computed tomography. Also, in such patients with special studies, an increased alveolar-arterial oxygen gradient, more than 15 millimeters, is found. This indicates that in these patients a kind of block is formed at the level of the alveolar-capillary membrane, which leads to the fact that the diffusion of oxygen from the alveoli into the arterial blood is significantly hampered.Another key criterion is the presence of an intrapulmonary shunt in these patients, and an intrapulmonary shunt can be both functional and anatomical. Finally, these patients have arterial hypocapnia. This is primarily due to the fact that shortness of breath is always recorded in these patients, and hypocapnia is recorded due to hyperventilation.

In the clinic, hepatopulmonary syndrome is divided into two types: hepatopulmonary syndrome of the first type and the second type. In hepatopulmonary syndrome of the first type, dilatation of the precapillaries and capillaries of the lungs is observed, that is, dilatation of the microvascular bed of the pulmonary artery. There is a decrease in the time of contact of blood with the alveoli due to the acceleration of blood flow. As a rule, such patients have a hyperdynamic type of heart functioning, insufficient blood oxygenation, as we have already said, and an increase in blood oxygenation against the background of breathing with a mixture with an increased oxygen tension.

The slide shows a diagram of the normal interaction of the alveoli and capillaries of the lungs (non-oxygenated blood is shown in blue): blue erythrocytes through the pulmonary artery system through the precapillaries, capillaries reach the respiratory units of the lungs, alveoli, and due to the diffusion of oxygen from the alveoli through the alveolar-capillary membrane, this diffusion is carried out easily, the blood erythrocytes are saturated with oxygen, and the blood leaving the respiratory unit is saturated with oxygen. You see, red erythrocytes indicate that the process of blood oxygenation is carried out in full.

What happens in patients with hepatopulmonary syndrome? This front, dilated vessel, you see here a large number of blue-stained red blood cells – therefore, non-oxygenated red blood cells carrying reduced hemoglobin, and to a much lesser extent red blood cells saturated with oxygen. Why is this happening? We see that the vessel is dilated and, therefore, diffusion of oxygen to the center of the vessel and to the far periphery of the vessel is impeded.From this it already follows that from the total volume of flowing blood and flowing erythrocytes, only a certain, smaller part of erythrocytes is oxygenated. The blood is only partially oxygenated. And this is typical for hepatopulmonary syndrome of the first type. If such a patient is provided with breathing with a gas mixture with a high oxygen content, then due to the partial pressure of oxygen in the alveoli, oxygenation will occur to a greater extent, and this increased oxygenation will lead to the elimination of hypoxemia.

The inferior vessel is the vessel that essentially represents the pathogenesis of what occurs in type II hepatopulmonary syndrome.There is no vascular dilatation, but a shunt is formed between the pulmonary artery system and the pulmonary vein system. And, therefore, blood as a whole does not come into contact with the alveoli, and in a non-oxygenated state is transported from the pulmonary artery system to the pulmonary vein system. Therefore, it makes no sense to prescribe an oxygen mixture to such a patient, since oxygen will not reach the vessels that bypass the pulmonary artery and pulmonary veins. This is type II hepatopulmonary syndrome. So, in the first case we are talking about a functional shunt from right to left, in the second case we are talking about a real anatomical shunt from right to left.

Without dwelling on the pathogenesis of the formation of hepatopulmonary syndrome, I will only point out some mediators of pulmonary vasodilation in hepatopulmonary syndrome. These include nitric oxide and products of endotoxemia and tumor necrotizing factor. Due to hypoxemia, pulmonary angiogenesis is activated. Taken together, all this leads to hyperdynamic blood circulation due to an increase in cardiac output, due to a decrease in systemic vascular resistance, due to a decrease in pulmonary vascular resistance.The result is a decrease in the arterial-venous oxygen gradient.

The next slide shows, in a slightly different version, the lumen of the vessel as a result of the stress effects of the mediators I mentioned. Stimulation of the vascular endothelium with endothelin occurs, which leads to the activation of NO-synthase in the vascular endothelium. Under the influence of NO synthase, a large amount of nitric oxide is formed. Nitric oxide acts on the smooth muscles of the pulmonary vessels and leads to their dilatation, to expansion and to the formation of a functional shunt or anatomical shunt.

What are the main clinical symptoms? First of all, the appearance of shortness of breath. Shortness of breath in a patient with cirrhosis of the liver – at first glance, it seems like an inexplicable and difficult to understand event, but when a doctor in a severe patient with cirrhosis of the liver, in a patient with liver failure suddenly discovers the appearance, an increase in shortness of breath, then of course, the doctor should think about respiratory syndromes, one of which can complicate the course of cirrhosis in such patients.

A very important distinguishing symptom of hepatopulmonary syndrome is the appearance of shortness of breath in an upright position, this symptom is called platypnea. Why does platypnea appear? Due to the redistribution of blood in the lungs, due to a decrease in ventilation of a significant respiratory area of the lungs. Unlike, for example, shortness of breath in heart failure, which appears and intensifies in a horizontal position, with hepatopulmonary syndrome, we register platipnea – shortness of breath in an upright position.

At the same time, when measuring the oxygen tension in the blood in such patients, we find a decrease in saturation in the upright position, this symptom is called orthodeoxia. Its reason is the same as platypnea – an increase in poorly ventilated areas of the lung, an increase in the manifestations of a pulmonary-cardiac bypass from right to left. On X-ray examination, we find intrapulmonary dilatation. Contrast-enhanced echocardiography is also very important.

This slide shows hepatopulmonary syndrome in a 69-year-old patient with cirrhosis.A high-resolution computed tomography scan was performed, and we see dilated pulmonary vessels (white pulmonary vessels) diverging by the corolla. And what attracts attention is seen as a crown, dilatation of the distal pulmonary arteries with subpleural telangiectasias. That is, in addition to expanding the root of the lung on the left and on the right, dilatation of the pulmonary vessels, especially on the right they are visible, we see along the periphery, like the crown, indeed, dilatation of the distal pulmonary arteries with subpleural telangiectasias (shown by arrows on the slide).

The next slide shows hepatopulmonary syndrome in a 36-year-old female patient. The right picture shows a large liver, a large spleen, all signs of portal hypertension, varicose veins in the central part of the esophagus. On the lung image, we see nodular dilatation of the peripheral pulmonary vessels. As in the previous patient, the expansion of the roots of the lungs, diverging dilated pulmonary vessels are visible. And along the periphery, we see dilatation of the pulmonary vessels (arrows shown), connected to the feeding arteries and draining veins.Thus, on the face of the dilatation not only of the central, but also of the peripheral pulmonary vessels.

What happens if we inject a suspension of air into such patients. What is air suspension? A saline solution is taken and very vigorously shaken to the smallest air bubbles – this is approximately what we see when we open the faucet in the kitchen or bathroom, we pour and see that the water is whitish.This whiteness is due to the huge amount of small suspended air bubbles. We inject approximately the same suspension intravenously into the decubital vein, and we immediately get an image of these bubbles in the right chambers of the heart: in the right atrium and right ventricle. But unlike healthy people, in whom these bubbles dissolve in the vessels of the pulmonary artery, in people with dilated pulmonary vessels, in patients with hepatopulmonary syndrome, these tiny bubbles penetrate into the right chambers of the heart. Moreover, the filling of the right chambers of the heart with these microvesicles of air is observed very quickly: after two or three heartbeats. And the presence of these bubbles in the right chambers of the heart definitely speaks of the dilatation of the pulmonary artery, of the dilatation of the vascular bed of the pulmonary artery.

Inhibition of NO-stimulated guanylate cyclase is carried out by regular intravenous administration of methylene blue. Somatostatin analogs are prescribed. These are anecdotal observations, literally isolated clinical representations, in which the authors have shown certain positive effects when prescribing analogs of somatostatin, cyclophosphamide, indomethacin, and so on. There is practically no systemic therapy for hepatopulmonary syndrome. The method of choice is liver transplantation.

How can the development of portopulmonary hypertension be suspected? Again, the most important symptom is the appearance of shortness of breath in patients with liver cirrhosis.Shortness of breath is often severe. A rather rapidly developing dilatation of the jugular veins is observed. There is an emphasis of the II tone on the pulmonary artery, systolic murmur of tricuspid regurgitation and symptoms of right-heart decompensation. In fact, these are symptoms of a rapidly growing cor pulmonale.

In all likelihood, recurrent pulmonary embolism contributes to the development of portopulmonary hypertension. Moreover, pulmonary embolism in patients with liver cirrhosis has a somewhat unusual path. In particular, thromboembolism of the pulmonary artery can be carried out from the dilated veins of the esophagus. All this together leads to the overproduction of serotonin, interleukin-1, thromboxane, vasoactive intestinal peptide and severe spasm of the pulmonary arteries.

An example of portopulmonary hypertension in a 57-year-old male with cirrhosis. In the left picture we see cardiomegaly – a large heart is quite distinct, and pulmonary arteries are dilated. The roots of the lungs are largely expanded, and the vascular pattern can be traced relatively evenly strengthened both in the upper and lower parts of the lung.And on the right, we see a cardinal sign – this is a large, dilated pulmonary trunk, from which the right and left pulmonary arteries depart, and the diameter of this pulmonary trunk is larger than the adjacent ascending aorta. In the same patient, a pronounced dilatation of the right ventricle is noted on the right. The interventricular septum, due to the high pressure in the right ventricle, bends towards the left ventricle, and you see significant hypertrophy of the wall of the right ventricle (indicated by the arrow). And on perfusion lung scintigraphy, we see with you multiple focal perfusion defects in both anterior and posterior projections.Of course, in such patients it is very difficult to differentiate what causes these perfusion defects: a really pronounced spasm, only a spasm, or a spasm in combination, for example, with recurrent pulmonary embolism.

Treatment includes the appointment of vasodilators, in particular Prostacyclin (Epoprostenol) and Sildenafil. The treatment is currently not developed, that is, the treatment is essentially the same as we use in patients with pulmonary hypertension due to recurrent pulmonary embolism.The method of choice is liver transplantation, and with an average pressure of less than 35 millimeters, we expect a good prognosis, and with a pressure of more than 35-40 millimeters, the prognosis becomes largely dubious.

The clinic of this complication includes, of course, severe shortness of breath and all manifestations of hypoxemia. On the roentgenogram, we see typical focal shadows at an early stage, at the stage of interstitial edema. Further, we observe diffuse bilateral consolidation in the exudative and proliferative stages, and then the stage of developing bronchioloalveolar fibrosis. On computed topography, we see with you diffuse bilateral changes in the shape of “ground glass”, confirming the presence of bronchioloalveolitis and fibrosis, and extensive bilateral consolidation as a final in patients who managed to arrest acute respiratory distress syndrome.And running ahead, I will say that the treatment is prostaglandin E and artificial ventilation of the lungs – we have no other approaches.

The next slide on the right shows a section of the alveoli seen in patients with respiratory distress syndrome. Pay attention, the lower part of the alveolus, here is the basement membrane, the alveolar wall is practically devoid of epithelial coating, because in such patients necrosis and apoptosis of the cellular elements of the alveolar lining occur. And as a compensatory mechanism, as a compensatory reaction in such patients, the inner surface of the alveoli is filled with hyaline membranes.Essentially, for pathologists, the detection of the hyaline membrane serves as a key criterion for the diagnosis of acute respiratory distress syndrome. The presence of a hyaline membrane replacing the epithelial lining, a significant expansion of the alveolar-capillary space due to edema and due to the emerging fibrosis, of course, explains the severe shortness of breath and hypoxemia that is observed in such patients.

The next slide shows the clinical presentation of acute respiratory distress syndrome in a 49-year-old woman with fulminant hepatitis. On the chest radiograph, we see bilateral diffuse shadows, which indicate the transition of the interstitial phase of edema to the alveolar phase of edema, and with computer topographic resolution – diffuse bilateral changes of both the “ground glass” type and the type of cellular lung. The air bronchogram is clearly visible, and against the background of this air bronchogram and dilated pulmonary vessels, we see these edematous-fibrotic changes in both pulmonary fields.

Morphology.In the left image, the arrow shows the famous hyaline membranes, which for pathologists are the main diagnostic key for recognizing acute respiratory distress syndrome. In the center, you see granular deposits around the alveoli, which indicate the formation of perialveolar inflammation and the formation of perialveolar fibrosis. In the right image, you see the blue deposits – these are large deposits of collagen in the alveoli that lead to consolidation of the lung in surviving patients and the development of diffuse pulmonary fibrosis.

Thus, we talked with you about three severe variants of respiratory complications in liver diseases, in particular in liver failure. This is hepatopulmonary syndrome – it is based on dilatation of the precapillary and capillary beds and the formation of functional, with hepatopulmonary syndrome of the first type, and anatomical arteriovenous shunts. The clinical picture of its development occurs against the background of liver failure, dilatation of intrapulmonary vessels. The key symptoms are the appearance of platypnea and orthodeoxia.The treatment is liver transplantation.

The fundamental role of the liver in metabolic processes and its close connection with the organs of the endocrine system determine its defeat in the pathology of the thyroid gland. In most cases, liver damage in hyperthyroidism is limited to asymptomatic changes in laboratory parameters and much less often acquires a clinical embodiment. The incidence of biochemical abnormalities in patients with newly diagnosed hyperthyroidism reaches 45–90% [1], and the clarification of the thyroid status is recognized as justified with an increase in liver enzymes of unknown etiology [2, 3].Clinically significant cases of liver damage associated with hyperthyroidism are rare and are represented by single descriptions. One of the most substantial “collections” belongs to D. Mazo et al. [4], who summarized information about 8 cases, 2 of which were fatal, and one required liver transplantation.

Liver diseases in patients with hyperthyroidism can appear in three forms: drug hepatitis developing in response to thyreostatics, concomitant autoimmune liver diseases and, finally, hepatopathy as a direct manifestation of thyrotoxicosis [4-6].Hepatotoxicity of thyreostatics is manifested in less than 0.5% of cases [4] and is more often associated with the use of propylthiouracil than methimazole, which is mainly metabolized by the kidneys. Cases of toxic hepatitis have also been reported during treatment with radioactive iodine [7]. The universal autoimmune nature of the pathological process explains the cases of the combination of Graves’ disease with autoimmune hepatitis [4, 5, 8] and primary biliary cirrhosis [6].

Of the three variants of liver damage in thyrotoxicosis, only the last one, obviously, can be considered in the context of the pathogenic effect of thyroid hormones.In the already mentioned article by D. Mazo et al. [4] out of 8 described cases, 2 were presented by autoimmune hepatitis, another 3 – by drug-induced hepatitis, induced by propylthiouracil, and only the remaining 3 cases were actually a reflection of thyrotoxicosis. The mechanism of development of thyrotoxic hepatitis is explained by the disproportion between blood supply and metabolic costs of the liver, which develops in conditions of increased cardiac output [6, 9]. Right ventricular heart failure caused by thyrogenic myocardial dystrophy can exacerbate liver damage [4, 9].The concept of the direct toxic effect of excess thyroid hormones on the liver has not been convincingly confirmed [9], although it is still being discussed [5].

Patient M., 56 years old, was admitted to the city clinical hospital with complaints of jaundice, dark urine, weakness, shortness of breath with little physical exertion, swelling of the legs, abdominal enlargement, weight loss. From the anamnesis it became clear that for the last 5 years the patient has had a constant form of atrial fibrillation (attempts to restore the sinus rhythm have not been made), and 6 months ago he was diagnosed with liver cirrhosis.The patient’s state of health worsened during the last 2 months, when the above complaints appeared and intensified.

On admission, the condition was assessed as severe. The patient is emaciated (after elimination of edema: height 176 cm, body weight 52 kg, body mass index 16.8 kg / m2), the skin and sclera are intensely icteric. The borders of the heart are expanded to the left, tones are arrhythmic 98 per minute, at the apex of the heart and at the base of the xiphoid process there is a systolic murmur. The abdomen is evenly enlarged due to ascites. The liver is dense, with a smooth surface, sensitive to palpation, protrudes from under the edge of the costal arch by 5 cm.

Complete blood count documented mild anemia (hemoglobin 108 g / l, erythrocytes 3.5 × 1012 / l), which was accompanied by a reduced iron level (8.6 μmol / l) and a fairly high level of ferritin (230 μg / l). Hyperbilirubinemia was noted (total bilirubin 279.2 μmol / L, direct bilirubin 224.6 μmol / L, indirect bilirubin 54.6 μmol / L), an increase in the level of transaminases (AST 101.4 U / L, ALT 58 U / L), low values of fibrinogen (1. 02 g / l) and total cholesterol (1.87 g / l), dysproteinemia (albumin 40.7%, γ-globulin 33.1%), urobilinuria.Markers of viral hepatitis B and C were negative.

ultrasound revealed increased liver echogenicity and moderate hepatomegaly – a skew-vertical size of 167 mm (the norm is up to 150 mm). An increase in the diameter of the portal vein – 13.5 mm (the norm is up to 12 mm) and the inferior vena cava – 21 mm (the norm is up to 15-16 mm). The diameters of the bile ducts, the size of the spleen is within normal limits. A significant amount of fluid in the abdominal cavity has been confirmed.

Thus, the disease was represented by jaundice, hepatomegaly, arrhythmias like atrial fibrillation, heart failure, edematous-ascitic syndrome. Deviations of laboratory parameters fit into cytolytic, mesenchymal-inflammatory and hepatodepressive (hypoalbuminemia, hypofibrinogenemia, hypocholesterolemia) syndromes. Taking into account the revealed diffuse liver damage and unchanged bile ducts, the most probable assumption was the hepatic nature of jaundice. Standard treatment of heart failure (angiotensin-converting enzyme inhibitors, diuretics, β-blockers, cardiac glycosides) in combination with ursodeoxycholic acid drug led to a rapid elimination of edema and ascites, a significant decrease in shortness of breath; jaundice nevertheless persisted.

Performed to clarify the diagnosis, magnetic resonance imaging stated the absence of changes in the shape, size, structure and density of the liver and spleen, the lumen of the intrahepatic ducts, lymph nodes of the abdominal cavity and retroperitoneal space; the diameters of the portal and inferior vena cava during the treatment acquired normal values, there was no free fluid in the abdominal cavity.

Negative markers of viral hepatitis, the absence of choledochoectasia and structural changes in the liver tissue did not give grounds to speak of primary damage to the liver and biliary system. Atrial fibrillation, total heart failure, cardiomegaly in combination with systolic murmur indicated a possible heart defect. In such circumstances, jaundice and hepatomegaly could be considered as a manifestation of cardiac fibrosis of the liver, but this version did not fit the high and persistent level of bilirubin and pronounced laboratory signs of hepatodepression.

The performed echocardiography revealed signs of pulmonary hypertension and cor pulmonale: dilatation of the atrial cavities (left 4.3 cm, right 6.9 × 5.0 cm) and right ventricle (3.0 cm), increase in the diameter of the pulmonary artery 2.8 cm, tricuspid regurgitation of the II degree. The valve cusps were intact, there were no violations of local myocardial contractility, and the ejection fraction was 65%.

With the so-called “cardiogenic liver”, the liver tissue is damaged due to an increase in central venous pressure and insufficient arterial perfusion.In the clinical picture, hepatomegaly comes to the fore, while jaundice is usually insignificant. Against the background of right ventricular failure, hyperbilirubinemic crises may develop with a significant rise in bilirubin, mainly its direct fraction. Most often, cardiac cirrhosis of the liver develops with defects of the tricuspid valve or constrictive pericarditis and in most cases proceeds latently, without pronounced exacerbations. Thus, the patient’s right ventricular failure could undoubtedly lead to congestion in the liver, but it remained unexplained that the complete elimination of edematous-ascitic syndrome (against the background of standard treatment of heart failure), the disappearance of signs of portal hypertension, normalization of liver size did not restore the functional the state of the latter.

The range of diseases with simultaneous involvement of the heart with the development of atrial and liver fibrillation includes lesions of the thyroid gland, occurring with symptoms of hyperthyroidism. A targeted examination of the patient revealed positive eye symptoms of Delrimple and Stelvag, pronounced glitter of the eyes, tremors of the body and limbs, exophthalmos. Ultrasound examination revealed reduced echogenicity and an increase in the volume of the thyroid gland up to 26.2 cm3. Signs of manifest thyrotoxicosis were documented by the level of hormones: free T4 45.0 pmol / l (normal 10.0-23.2 pmol / l), total T4 37.0 nmol / l (normal 52-155 nmol / l), T3 0 , 4 ng / ml (norm 0.8-2.8 ng / ml), TSH 0 μIU / ml (norm 0.23-3.4 μIU / ml).

Laboratory and clinical signs of thyrotoxicosis gave rise to the appointment of thiamazole, which led to a decrease in jaundice and a rapid positive dynamics of laboratory parameters. A control laboratory study showed a significant decrease in hyperbilirubinemia and normalization of the level of transaminases: total bilirubin 55.6 μmol / L, direct bilirubin 50.9 μmol / L, AST 35.4 U / L, ALT 35.1 U / L. The level of thyroid hormones was: T4 free 19.6 pmol / l; T4 total 58.0 nmol / L, T3 0.99 ng / ml, TSH 0.1 μIU / ml.

The variety of etiological factors of liver involvement in hyperthyroidism, the versatility of the clinic and the absence of specific histological markers of hepatic lesions make it difficult to establish the correct diagnosis. Liver dysfunctions in patients with hyperthyroidism include drug-induced lesions, concomitant autoimmune diseases, and thyrotoxic hepatitis itself.We have described a clinical case of thyrotoxic hepatitis, which developed against the background of Graves’ disease and complicated by edematous-ascitic syndrome and hyperbilirubinemic crisis. Concomitant thyrogenic myocardial dystrophy with cardiomegaly and atrial fibrillation complicated the diagnosis and required the exclusion of the “cardiogenic liver”.

Commenting on the above case, I would like to draw attention to an isolated increase in the concentration of free T4 at the initially lowered levels of total T4 and T3.Obviously, a pronounced decrease in protein-synthetic function (the fact of hepatodepression was confirmed by laboratory) led to a decrease in the synthesis of proteins-carriers of thyroid hormones, and only the level of free (not bound to proteins) T4 turned out to be informative. It is indicative that, against the background of treatment, the concentration of total T4 and T3 increased, which indirectly testified to the normalization of liver function.

The anti-rejection drugs you will take reach
effect due to interaction with the cells of your immune system.This is
can lead to a decrease in the body’s resistance to certain infections,
especially viral. After leaving the hospital, try to avoid
contact with patients with colds, cough, increased
body temperature or intestinal disorders. Feel free to wear
mask during the first year after transplantation in places of large
crowds of people. If possible, try not to use
public transport, especially during epidemics. Coming home with
streets, always wash your hands and nose thoroughly.

Mammary cancer	Identification of a node, a lump in the mammary gland, not associated with menstrual cycle or feeding, any other skin changes, nipple retraction
Cancer of the cervix or body of the uterus	Bleeding outside the menstrual cycle, pain
Colon cancer	Bleeding from the anus, blood in the stool, impaired bowel function (constipation or diarrhea)
Lymphoma	Swollen and thickened lymph nodes, unexplained fever or weight loss, nocturnal chills
Prostate cancer	Weak or intermittent urine stream when urinating, back pain, pelvic pain
Skin cancer	Permanent wound on the skin, with undermined edges, not healing, with bleeding, discoloration of the skin

Tumor	Study	Regularity
Cancer of the skin, lips	Self inspection Monthly Dermatologist examination Annually
Cancer of the cervix, body of the uterus	Examination by a gynecologist Annually Pap smear Annually
Mammary cancer	Self-palpation of the mammary glands All women once a cycle (or once a month in menopause), immediately after menstruation.Mammography Annually for women over 45
Prostate cancer	Digital rectal examination, PSA (prostate specific antigen) test	Annually for men over 50
Colon cancer	Feces for occult blood Annually for patients over 50 years of age Colonoscopy Once every 1-5 years, depending on the presence of risk factors

Try to limit carbohydrates in food – sugar and sweets,
especially if you are taking prednisone. Prednisone increases appetite and
retains fluid in tissues, leading to weight gain. remember, that
a lot of sugar is found in carbonated sugary drinks, from
the use of which is better to abstain. If you like sweet drinks,
buy sugar-free versions of them. If you like sweets, you should
buy them in the departments for patients with diabetes. Sugar in food is good
replace it with fructose, which is sold in dietary stores.
Cholesterol levels may rise after transplant. For his
You and the entire transplant team will monitor the level. For that,
to prevent cholesterol levels from increasing, you should limit it
intake in food. This applies primarily to animal fat – lard,
fatty meat, chicken skin, butter, sour cream, mayonnaise.
Egg yolk also contains a large amount of cholesterol.
Eat lean meat, cook skinless poultry, replace oil with
margarine, fry not in butter, but in olive.Try to
eat seafood, fish.

If you worked or studied before your transplant, you can return to
these activities. We usually recommend doing this after 3
months after transplantation, when repeated
hospitalization. Many patients who could not work before
transplantation, begin to work after it. If your work is related to
lifting significant weights, hypothermia, long trips to
remote places, contact with infectious patients, animals,
discuss the prospects for changing her character with your doctors.

You will need to establish contact with doctors after transplantation
primary health care – general practitioner, head
GP department, district surgeon, hepatologist, center personnel,
responsible for the dispensing of medicinal products. Write them down and keep them
phones. Let them also write down your phone number and coordinates. Do not forget
timely send copies of all extracts and all
documents related to your health.

We recommend that you visit the dentist every 6 months. Necessary
carefully follow the rules of oral hygiene after transplantation. Clean
teeth twice a day, not less than 2 minutes, if necessary
use dental floss. Change your toothbrush as often as possible,
use quality toothpaste.While taking cyclosporine
overgrowth of the mucous membrane of the gums is possible. You may need to refer to
dentist about this. Often, treatment with a dentist after
transplantation should take place while taking antibiotics.
Check with your doctor about this.

You should not self-palpate the mammary glands.
less than 1 time per month (1 growth per cycle).Self-palpation is performed immediately
after the cessation of menstruation, in front of a mirror, in lying and sitting positions.
We feel the tissues of the mammary glands between the fingers of two hands, methodically, according to
spirals, from the nipple to the periphery. Be sure to feel the fiber for
the outer edges of the pectoralis major muscles. If you have questions,
associated with self-palpation, be sure to consult a doctor
or sister.

The method of choice after transplantation is the barrier
contraception. Taking oral contraceptives after a transplant is extremely
undesirable, as it leads to an increase in pressure, increases the risk
thrombosis, affects the concentration of tacrolimus in the blood.Intrauterine
spiral after transplantation is a high risk factor in the development of infections, its
installation is also contraindicated.

Modern immunosuppressive drugs used after
transplantation, do not have a significant effect on the fetus.therefore
a woman after a transplant may well be planning a pregnancy.
It should be remembered that in this case, you need a particularly responsible
attitude towards planning and managing such a pregnancy. Decision to start
the patient accepts the child only together with the doctors of the transplant
teams. Despite the possibility of giving birth through a natural birth canal,
delivery is optimal in women after liver transplantation
by caesarean section. Since re-birth after transplant
risky, you may be offered to ligate the fallopian tubes during this
operations.Due to the fact that immunosuppressants enter the maternal
milk, breastfeeding will not be possible. Children born to mothers with
transplanted liver, according to statistics, do not have deviations from the norm
compared to other children. They are characterized by a slightly lower body weight,
they have a slightly higher risk of infectious complications, which, however, quickly
bounces back.

Do not plan any travel for at least 3 months after
transplantation, since in this period it may be necessary
unplanned hospitalization.Discuss your travel plans with
By your doctors. When traveling abroad, do not drink iced drinks. Drink
only bottled water. Use it when brushing your teeth.
Immunosuppressive drugs that you are drinking should be with
for the entire period of stay abroad in excess, in case
unexpected delays. Never check them in your luggage on the plane, and
carry only in carry-on baggage. Necessary to confirm this
you should prepare medical documents in advance. Everything you need for
the country of destination must be fully vaccinated.

The issue of vaccinations will be decided on an individual basis with
By your doctor. We often recommend getting vaccinated annually against
flu in the fall. After some vaccinations with
mucous membranes in children can release live viruses. This is normal and
safe for children, but may come with a potential risk to
patient after transplantation. If you have a child and his pediatrician
told you that he is being vaccinated with a live virus (for example, against
polio), you may need to wear a mask to avoid
contact with the virus.

If you have a pet at home, it must be well cared for. The place where he lives must be clean. The patient after organ transplantation should not be in contact with animal excrement. Do not allow the animal to lick the face or wound area.A cat or dog’s toilet should be cleaned by someone else. The toilet must be disinfected at least once a month. If an animal has bitten or scratched you, treat the wound with antiseptic solutions. Call your doctor right away. Some animals carry diseases that can be transmitted to humans. Beware of contact with exotic animals, wild animals and monkeys.

The liver is considered the largest gland in the human body. The mass of this organ can reach 1800 grams. The liver is located under the rib and occupies a significant part of the right abdominal cavity. Among the most important functions of the liver are metabolism (glucose processing, cholesterol synthesis, etc.)protection from bacteria and toxins, production of bile necessary for digestion, production of certain hormones.

Also, the liver acts as a natural filter that protects the body from the effects of many harmful substances. But in modern conditions, this organ is heavily burdened. Often, he cannot cope with such a massive blow. The functioning is affected by an improper diet with an abundance of fast food, stress, uncontrolled intake of drugs, and a passion for alcoholic beverages.And among liver diseases, there are both functional disorders and formidable ailments – hepatitis, cirrhosis, venous thrombosis, cholangitis and oncology.

It should be understood that bilirubin is a toxic substance and very harmful to the human nervous system. Therefore, the normal functioning of the liver is aimed, among other things, at the excretion of bilirubin with bile or urine. And the excess of the indicators can indicate a variety of diseases of an important organ, blockage of the biliary tract and even about the active destruction of red blood cells in the blood.

Allowed foods on this diet include lean meats (beef, rabbit, chicken).It is recommended to boil such meat first, and then bake it a little. You can also eat lean fish. Shown to people with elevated bilirubin light soups on vegetable broths without dressing in the form of fried vegetables. Milk should be limited, but the amount of low-fat fermented milk products, on the contrary, should be increased. There are great restrictions on bread – it must necessarily be salt-free. If you cannot find one on sale, then it is better to bake it yourself. In addition, you cannot eat fresh bread, you can only eat yesterday’s.Almost any vegetables are allowed, with the exception of fresh onions, sorrel, spinach, radishes, radishes, and garlic. You also need to exclude mushrooms, sour berries and fruits. It is not recommended to eat any fried foods.

Experts say that the best prevention of liver diseases is the correct diet. It should contain a lot of fresh vegetables and fruits, vegetable oils, easily digestible proteins, low-fat dairy products.But the number of refined foods, fatty meat dishes, semi-finished products and high-calorie sweets on the menu should be limited. Regular meals, lack of overeating, and adequate physical activity are also important.

Pumpkin contains a large amount of substances that accelerate the regeneration of hepatocyte membranes. These include pectins, riboflavin, beta-carotene, and niacin. Often, pumpkin dishes are included in the menu of patients suffering from chronic liver diseases. It is also known that pumpkin has a mild choleretic effect, helps to remove harmful substances, and increases the acidity of gastric juice.

Melon is not only tasty, but also healthy fruit. It has a mild choleretic effect, inhibits the development of fatty hepatosis, prevents the formation of calculi in the gallbladder, and helps liver cells to recover.But, since there is a lot of sugar in it, you cannot abuse the melon. You also need to remember that it increases the acidity of the gastric juice. And this is not useful for gastritis and peptic ulcer disease.

Like lemon, grapefruit is high in vitamin C and many other elements. Long-term studies have shown that grapefruit can be active in cell regeneration and the detoxification process, significantly reduces cholesterol levels, helps with rheumatoid arthritis, and is a good way to prevent cancer. Red and pink varieties are high in beta-carotene and lycopene.Also in grapefruit contains a very useful flavonoid naringin. This substance is able to mitigate the adverse effects of ethanol on liver cells and helps to strengthen the antioxidant defense system of this organ.

As you know, apples are also rich in vitamin C and iron.Therefore, apples are good for the liver as well. They help prevent fatty hepatosis, accelerate the excretion of cholesterol, prevent bile stagnation, and help to cope with the adverse effects of drugs. Doctors recommend eating baked apples in the presence of various disorders in the work of the stomach and liver. So the fiber will be better absorbed, and various acids will not harm the inflamed mucous membranes.

Cranberry is a very healthy berry. It also possesses hepatoprotective properties. This berry improves the lipid profile, prevents the degeneration of liver cells into adipose and connective tissue. But you need to remember that cranberries should be limited during exacerbation of various inflammatory processes. In the “Review of natural products with a hepatoprotective effect” it was also found that the introduction of cranberries into the diet reduces the toxic effect, normalizes bilirubin levels, and prevents the accumulation of lipid oxidation products in the liver membranes.

Many spices are beneficial for liver health, but curcumin is one of the most beneficial substances that help with oxidative stress in the tissues of the organ.Iranian scientists made a systematic review of cellular mechanisms and found that curcumin induces the expression of heme oxygenase and helps to break down bilirubin, inhibits the activation and proliferation of certain enzymes, and protects the liver from fibrogenesis. According to scientists, consuming significant amounts of curcumin on a daily basis or as a dietary supplement, along with limited therapeutic options, may provide ideal prevention and treatment of liver disease.

The main benefit of meals with whole grains is that they allow overweight people to successfully lose weight. And control over body weight is one of the main factors in the prevention of various liver diseases. There are other beneficial effects on the liver when you include significant amounts of whole grains in your diet. A 2013 study found that people who eat a diet rich in whole grains tend to have a lower risk of many of the comorbidities associated with non-alcoholic fatty liver disease.These foods also help to reduce the number of fat cells in the liver and protect it from inflammation. Also, experts recommend replacing processed grain with whole grain for the preparation of most dishes.

It is known that green tea is very useful for the heart and blood vessels, but this drink can also bring many benefits to the liver. In 2016, a randomized clinical trial was conducted. Within its framework, 80 patients underwent ultrasound of fatty degeneration of the liver.Research has shown that green tea extract can be used as a therapeutic agent to increase serum liver enzymes in patients with non-alcoholic fatty liver disease. And to enhance this effect allows weight loss.

Normal count for liver. 12 Health Risks of Chronic Heavy Drinking

Alcohol and Health Risks

Anemia

Cancer

Cardiovascular Disease

Cirrhosis

Dementia

Depression

Seizures

Gout

High Blood Pressure

Infectious Diseases

Nerve Damage

12 Health Risks of Chronic Heavy Drinking

Alcohol and Health Risks

1. Anemia

2. Cancer

3. Cardiovascular Disease

4. Cirrhosis

5. Dementia

6. Depression

7. Seizures

8. Gout

9. High Blood Pressure

10. Infectious Diseases

11. Nerve Damage

12. Pancreatitis

Summary

Liver function tests (LFT) | Health Navigator NZ

Key points

What is a liver function test (LFT)?

When is a liver function test done?

How do I prepare for a liver function test?

How is the sample collected for testing?

What do my results mean?

Learn more

Higher Level of SGPT Risks | Causes | Symptoms

What is Higher Level of SGPT?

What Causes High SGPT?

Symptoms of High SGPT Level:

Liver function tests – Lab Tests Online AU

Tests for liver cancer | Hepatitis C Trust

FATTY LIVER —- What is fatty liver?

Liver elastometry – (Clinic Di Center)

Ultrasound of the abdominal organs

Which organs are checked for ultrasound of the abdominal cavity

Indications for conducting

Rules for the preparation of the patient

How the survey is conducted

Decoding

Respiratory complications in liver cirrhosis. Ivashkin V.T.

Stool color depending on the disease of the dog

Green feces

White feces

Black feces

Yellow feces

Gray feces

Interesting Topics

Thyrotoxic hepatitis | Pikulev | Endocrinology Problems

Description of a clinical case

Conclusion

Infection

The risk of developing tumors

Dangerous conditions

Exercises

Diet

Return to work or school

Primary health care

Medical records

Skincare

Dental care

Women’s health issues

Travel

Vaccinations

Eye Care

Animals

Smoking

Alcohol

Control studies

What is bilirubin and why does it rise