What does it mean if the eyeball is yellow. Causes of yellowing of the whites of the eyes

Indicates that the person is developing jaundice. This term is understood as a pathological condition that accompanies diseases of the liver, blood, pancreas, bile ducts. All these disorders lead to blockage of the bile ducts and an increase in the level of bilirubin in the blood.

With jaundice, not only the sclera of the eyes turn yellow, the patient's skin begins to itch, the body temperature rises, pains occur in the right hypochondrium, and a bitter taste appears in the mouth. Additional symptoms of jaundice are nausea and an enlarged liver.

What is eye white?

The white of the eye is its sclera. This is the largest part of the organ of vision. The sclera should normally be white. Actually for this reason it is called protein. The sclera consists mainly of connective tissue, thanks to which it has exactly white color.

The eyes turn yellow because the level of bilirubin in the blood rises. is a bile pigment that is yellow in color. It appears in the blood as a result of the breakdown of hemoglobin, myoglobin and cytochromes. However, this bilirubin is called indirect because it is toxic to the body. The faster it is possible to neutralize it, the less harm it will cause to health.

Indirect bilirubin in the liver is neutralized. It is this organ that binds its molecules with glucuronic acid, due to which they are transformed into direct bilirubin molecules. He, through the hepatic ducts, enters the bile and is excreted from the body. Some of it can be absorbed back into the bloodstream. Therefore, the total bilirubin level consists of direct and indirect bilirubin. The share of the latter should not exceed 25%.

Normally, the level of total bilirubin in the blood is 8.5-20.5 μmol / L. If these values \u200b\u200bgo beyond the mark of 30-35 μmol / l, then the patient develops jaundice, in which the whites of the eyes and skin turn yellow. Excess bilirubin penetrates into their structure and gives them the appropriate color.

The reasons for yellowing of the sclera of the eyes are the following:

Liver disease.

Diseases of the blood.

Violations metabolic processes in the body.

Acute or chronic pancreatitis.

Each of these reasons should be considered in more detail.

Video: Live Healthy! Liver health "bilirubin test":

It is the liver that neutralizes indirect bilirubin. If, due to one or another disease, she cannot cope with her duties, then the concentration of this substance in the blood increases. A person can visually assess this by the yellowed sclera of the eyes.

Liver diseases in which the eyes turn yellow:

Violation of its metabolism, or rather an excess in the blood, is associated with many pathologies:

• hepatitis;

Pathological yellowness of the skin can be a consequence of oncology, and yellow irises of the eyes and eyelids - a defect in fat metabolism and excess cholesterol.

Causes of yellowing of the skin

The main and obvious causes of yellowing of the skin are disorders in the liver and gallbladder, as a result of which the concentration of bilirubin increases. Damage to the work of hepatic filter cells, cessation of the removal of excess red enzyme from the tissues occur as a result of:

• hepatitis;

With pathologies of the gallbladder, when the correct outflow of bile into the gastrointestinal tract is disturbed, stones appear, yellowing of the sclera and skin... You should immediately consult a doctor if not only yellowness of the skin appears, but also fever, itching, digestive disorders, bad smell from the mouth, urine became dark, painful sensations appeared in the side.

Unreasonable jaundice - how not to turn yellow? (video)

Why does yellowness of the skin and eyes appear? How to cure such a pathology and eliminate its causes? We learn from the video.

Physiological jaundice in infants

After birth in the first days, the skin of 50% of babies turns yellow, sometimes the whites of the eyes. In this case, the color of urine, feces does not change. Ultrasound does not show an increase in the spleen or liver. This is not a disease, but a physiological process associated with restructuring child's body after birth. Usually, the yellowness goes away on its own after 5-7 days. Babies born ahead of time, with jaundice should be under medical supervision.

In order for the process of gradual withdrawal of excess bilirubin to pass as safely as possible for the baby, it should be applied more often to the breast so that the milk flushes out pigment cells. With a child, it is necessary to walk more often in the air with diffused sunlight. Sunbathing is shown to infants so that vitamin D produced in the skin helps to remove the coloring pigment from the skin.

How to eliminate a symptom

To normalize the liver, hepatoprotectors, antispasmodics, antiviral, choleretic, anti-inflammatory drugs and homeopathy are prescribed:

• "Essentiale forte"

With a yellow complexion, you cannot eat fatty fish, smoked meat, eggs, smoked meats, canned food, cocoa, radishes, legumes, mushrooms. It is better to refuse white bread, alcohol, muffins, black tea and pastries, salads with mayonnaise and carbohydrate products. It is better to replace them with low-fat varieties of poultry, fish, mild cheese, steamed dishes with meat, low-fat dairy products, fresh non-acidic fruits.

• lemons and other citrus fruits;

For the prevention of jaundice, vaccinations are carried out, it is forbidden to use common manicure objects, visit questionable dentists, use someone else's razor, combs and other objects on which someone else's blood or saliva may remain. Hands should be washed after outside, especially for children.

Why the whites of the eyes turn yellow and what to do

Yellow whites of the eyes is a symptom that indicates serious problems with the internal organs. A change in the color of proteins should alert you and prompt you to take immediate action, as it can be caused by liver dysfunction (serious pathology), viral hepatitis, and other dangerous infections that require treatment. Jaundice of the sclera often occurs in diseases of the gallbladder and biliary tract, it can also appear as a result of the presence of malignant formations of different localization. Who to seek help and how to treat yellow squirrels - below.

Symptom definition

In the central part of the eye, you can see a dark point - this is the pupil. At the periphery of the pupil is the iris (or iris), which gives the eyes a specific color. If you move from the inner edge of this shell to the outer one, you can see a white structure - this is a protein (another name is sclera), which occupies five-sixths of the entire surface of the outer shell. Normally, the protein part has white color, and if it turns yellow, then we are talking about eye jaundice.

Causes of occurrence

The yellowing of proteins in most cases is associated with an increase in the concentration of bilirubin in the blood. Bilirubin is a bile pigment formed during the breakdown of hemoglobin, myoglobin and cytochromes, the color is yellow. Immediately after the breakdown of the listed types of proteins, a compound toxic to the body is formed, which must be rendered harmless. If everything is in order with the liver, then there are no problems, but the organ may not cope.

The main reason for the yellowing of the protein is the increased concentration of bilirubin in the blood. And it can rise for various reasons.

Jaundice (yellowing of the sclera of the eyes and skin of the body) begins when the bilirubin concentration is higher than mmol / l. This is because, at such concentrations, bilirubin begins to diffuse (i.e., penetrate) into peripheral tissues and stain them. There are three degrees of severity of the disease - mild, moderate and severe. With mild, the concentration of bilirubin is up to 86 μmol / L, and with severe - 159 μmol / L or more.

Possible diseases

Let's consider the main diseases that can cause yellowing of the white part of the eye.

Liver disease

In the first group - various diseases liver. They lead to disruption of the processes of binding of indirect bilirubin. As a result, the concentration of total bilirubin reaches critical levels, the element leaves the vessels and enters the whites of the eyes, being deposited on them.

Blood diseases

With blood diseases, marked hemolysis (or destruction) of erythrocytes is noted. As a result, the hemoglobin content increases, which then breaks down to form indirect bilirubin. The concentration of this element becomes too high, and the liver cannot detoxify it.

Biliary tract problems

Jaundice of the sclera in diseases of the biliary tract occurs as a result of the accumulation of large amounts of direct bilirubin in the blood. The outflow of bile is disrupted, the intrahepatic ducts rupture, and toxic components penetrate into the blood.

Disruption of metabolic processes

Three types of metabolic disorders lead to yellowing of the sclera. These are exchange disorders:

If there are problems with the exchange of copper or iron, these elements begin to accumulate in the liver and damage its tissues, causing cirrhosis. With amyloidosis (a violation of protein metabolism), an abnormal amyloid protein begins to be deposited in the liver, which destroys the structure of the organ. As a result, the liver begins to work incorrectly, ceasing to remove indirect bilirubin.

Features of the selection of color contact lenses green are described in this article.

Pancreatitis (acute and chronic)

In acute or chronic form of pancreatitis (pancreatitis - inflammation of the pancreas), edema occurs and, accordingly, an increase in the pancreas. She begins to press on the bile duct (common bile duct), as a result of which the work of the latter is disrupted. Bile stagnates in the biliary tract, intrahepatic capillaries break, and bile components enter the blood.

Jaundice of newborns

Separately, it is necessary to consider such a disease as jaundice of newborns. The yellowing of the sclera in this case is usually caused by liver failure and often goes away on its own. Also, the yellow whites of the eyes in babies can indicate problems with the liver, intestines or blood, a lack of certain enzymes. Types of neonatal jaundice - Crigler-Nayyar syndrome, Dabin-Johnson syndrome, physiological and nuclear jaundice, infectious hepatitis. The baby must be supervised by a pediatrician.

Jaundice occurs in most newborns and usually goes away on its own. But it can also be a symptom of serious pathologies of internal organs, therefore, medical supervision is mandatory.

Other reasons

Yellow proteins can be a symptom of malignant conjunctivitis. Such diseases are rare, but cannot be ruled out. Pinguecula, pterygium and others can also cause yellowing of the sclera. eye diseases... At risk are people working at a computer and suffering from bad habits (especially a love of alcohol).

Diagnostic methods

To diagnose the causes of jaundice, the sclera of the eyes are used different types research - laboratory, clinical, radiation. Basic:

• collection of anamnesis;
• inspection;
• analyzes of blood parameters - biochemical, general, toxicological, genetic, immunological;
• analyzes of urine and feces.

Thorough diagnostics is a guarantee of an accurate diagnosis and correct treatment.

The doctor prescribes diagnostic methods individually after taking an anamnesis and examining the patient.

Treatment

There is only one way to remove the yellowness of the sclera - by curing the pathology that caused the yellowing. There are no other ways to solve the problem, since yellowness appears as a result of the deposition of bilirubin in the white part of the eye with the bloodstream. To prescribe therapy, contact two specialists - an ophthalmologist and a therapist.

Treatment of demodicosis of the eyelids in humans is described in this article.

Prevention

To minimize the risks of jaundice:

• eat a balanced diet;
• give up junk food (salted, smoked, flour);
• try to drink alcohol as little as possible;
• walk regularly in the fresh air;
• get enough sleep;
• take regular breaks when working at a computer;
• take vitamins (in courses, preferably twice a year).

Since the sclera can turn yellow due to overwork, do compresses and use special drops to relieve tension.

Prevention of the appearance of jaundice of the sclera of the eyes is reduced to the normalization of the daily routine and lifestyle. Give up bad habits, get enough sleep, eat a balanced diet, do not drink alcohol - and everything will be fine.

Video

findings

Yellowing of proteins - alarming symptom... If you find appropriate changes, immediately seek help from a physician or ophthalmologist. The doctor will conduct an examination, ask you about your well-being and, most likely, prescribe additional tests to make an accurate diagnosis. The method of treatment depends on the cause of the jaundice.

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The information on the site is presented for informational purposes only, be sure to contact your optometrist.

Yellow skin color

The yellow color of the skin and the whites of the eyes is a condition that is a consequence of an excess of bilirubin in the body. Bilirubin is a yellow pigment that results from the breakdown of dead red blood cells in the liver. As a rule, the liver gets rid of bilirubin due to its excretory function.

Jaundice can indicate serious problems with the function of the liver, gallbladder, or pancreas. A yellow tint to the skin and eyes characterizes jaundice. In more severe cases, the whites of the eyes may turn brown. Other symptoms may include dark urine and pale stools.

If an underlying medical condition such as hepatitis is the culprit for yellowing of the skin, other symptoms such as excessive fatigue and vomiting may be present.

Sometimes yellow skin color has no good reason. This condition may be the result of high levels of beta-carotene in the body. Beta-carotene is an antioxidant found in carrots and pumpkin. A large amount of these foods in the diet can cause temporary yellowing of the skin.

But most often, yellowness of the skin, especially the whites of the eyes, indicates problems with the liver.

The type of treatment depends on the underlying cause. In mild cases, yellowness of the skin can go away without treatment. However, severe cases require treatment. Treatment is directed at the cause, not the symptomatology. Once treatment is started, the yellowing of the skin is likely to diminish.

Jaundice usually resolves when the underlying cause has been eliminated. Moderate cases of jaundice in newborns usually go away on their own, without treatment and do not raise questions about liver diagnostics.

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Disease Symptoms - Yellow skin color

Alphabet search

Yellow skin color

Under what diseases does Yellow skin color appear:

Acute and chronic hepatitis,

Concrements of the gallbladder and biliary tract.

Which doctor should i contact if yellow skin color occurs

Are you worried about Yellow skin color? Do you want to know more detailed information or do you need an inspection? You can make an appointment with a doctor - the Eurolab clinic is always at your service! Top Doctors will examine you, study external signs and help identify the disease by symptoms, advise you and provide help needed... You can also call a doctor at home. The Eurolab clinic is open for you around the clock.

The phone number of our clinic in Kiev: (+3 (multichannel). The secretary of the clinic will select a convenient day and hour for you to visit the doctor. Our coordinates and directions are indicated here. Look in more detail about all the services of the clinic on its personal page.

If you have previously performed any research, be sure to take their results for a consultation with a doctor. If the research has not been performed, we will do everything necessary in our clinic or with our colleagues in other clinics.

Do you have Yellow skin? You need to be very careful about your health in general. People do not pay enough attention to the symptoms of diseases and do not realize that these diseases can be life-threatening. There are many diseases that at first do not manifest themselves in our body, but in the end it turns out that, unfortunately, it is too late to treat them. Each disease has its own specific signs, characteristic external manifestations - the so-called symptoms of the disease. Identifying symptoms is the first step in diagnosing diseases in general. To do this, you just need to be examined by a doctor several times a year in order not only to prevent a terrible disease, but also to maintain healthy mind in the body and the body as a whole.

If you want to ask a question to the doctor, use the section online consultation, perhaps you will find there answers to your questions and read tips on personal care. If you are interested in reviews of clinics and doctors - try to find the information you need on the forum. Also register on medical portal Eurolab to be constantly updated latest news and updates of information on the site, which will be automatically sent to your mail.

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Yellow eye symptom: diagnosis, symptoms, treatment

If the whites of the eyes become yellow, you should consult a doctor, you cannot leave this symptom unattended - the yellow tint will not disappear on its own.

Yellowing can indicate a number of pathologies that can occur in the body.

For example, after examination and analysis, the patient is diagnosed with: viral hepatitis, liver disease, infection, conjunctival disease or even malignant tumors.

Problems with the gallbladder and biliary tract can also provoke yellowing of the whites of the eyes.

Causes of yellow eye symptom

There are a number of reasons why the whites of the eyes can turn yellow:

IN medical practice many diseases of various localization are known, in which patients have yellow white of the eyes. Let's consider the most common ones.

Liver disease

The most common cause of yellow eye whites is various diseases liver.

These include hepatitis, cancer, fatty liver, cholecystitis, cirrhosis, etc. There are three factors that cause hepatitis:

For example, common acetylsalicylic acid can cause a hepatoxic reaction, so if your eyes turn yellow, you can look for the cause in the lists of medications you take.

Drugs that cause liver toxicity:

• cytostatics,
• antibiotics,
• antiviral medications,
• anti-tuberculosis drugs.

Consider another cause of yellow eye syndrome. Red blood cells - erythrocytes - contain a substance called bilirubin, an enzyme that, when broken down, may yellow the sclera and whites of the eyes.

When elevated level bilirubin in the blood, you can be sure that the cause of yellowing of the eyes is hepatitis (more often hepatitis A, a characteristic feature of which is the yellowness of the skin and eyes).

There are three types of jaundice, depending on the level of excretion of bilirubin:

1. Hemolytic jaundice. It can occur with an accelerated breakdown of hemoglobin - bilirubin is formed in such an amount that the liver does not have time to process indirect bilirubin in a straight line.
2. Hepatic jaundice. It is caused by liver damage under the influence of the following reasons: drug, viral, toxic effects, alcohol poisoning, cirrhosis of the liver, pseudotuberculosis, leptospirosis, etc. In such cases, the level of indirect bilirubin in the blood increases significantly (the liver is not able to process it and bilirubin is absorbed back into the blood) ...
3. Cholestatic jaundice. Yellowing of the whites of the eyes may be due to blockage of the bile ducts by a tumor or stones.

In the news (here) a list of eye drops for allergies.

Jaundice of newborns

In the first days of a baby's birth, the whites of his eyes, as well as his skin, may turn yellow. Doctors call this condition of the baby jaundice and this is due to the fact that the baby's blood during intrauterine development is saturated with a large number of red blood cells.

With the birth of a person, his body no longer requires so many red blood cells and they begin to rapidly disintegrate and go out, thereby causing jaundice. After 1-2 weeks, the yellowness disappears, otherwise the baby is hospitalized for a more thorough examination.

Malignant formations

With the development of such a not simple disease as melanoma (neoplasms of the conjunctiva), the whites of the eyes also take on a yellow color. The disease is difficult to diagnose and treat, so you should not take independent actions.

Eye diseases

The symptom of yellow eyes can occur with diseases of the visual system, for example, they include:

• pterygium - this disease is characterized by an extensive proliferation of the conjunctiva, as a result of which it is possible to irrevocably lose sight,
• pinguecula - in connection with the disturbed process of lipid metabolism, a yellow wen appears.

Gilbert's disease

This disease is constitutional jaundice, the frequency of which is assessed in different ways: if we take into account clinical signs, then such a syndrome is rare, and if we take into account bilirubinemia, then we can say that Gilbert's disease occurs quite often.

Boys suffer from this ailment 3-5 times more often than girls. It should be noted that the diagnosis of this disease is difficult due to the moderate increase in the level of bilirubin in the blood.

The yellowness of the sclera of the eyes appears only with increased hemolysis or with a long delay in feeding. Fasting causes an increase in the activity of bilirubin production, which affects the whites of the eyes.

There is no cure for Gilbert's disease, but there is a way to reduce the yellowness of the eyes - an emulsion from soy eliminates hyperbilirubinemia. Sparing diet number 5, choleretic substances and vitamins also help.

Other cases that result in yellow eye symptom

1. Alcohol abuse, unhealthy diet. To normalize the patient's condition, it is necessary to adhere to a diet, refuse spicy, salty and fried foods, alcohol, flour. Eat more foods that contain vitamin C, and also eat more fruits.
2. The defeat of the internal organs. Jaundice of the sclera is also observed with some problems with the gallbladder and biliary tract.

Prevention of eye jaundice

Preventive action against any disease significantly reduces the percentage of its occurrence and possible complications. This also applies to vision.

To prevent the appearance of the yellow eye symptom, you must:

• food should be as balanced as possible, including a large amount of vegetables, protein, fruits, excluding salty, flour, alcoholic beverages, fried, smoked,
• daily long walks in the fresh air,
• full sleep (recommended daily at least 8 hours),
• you definitely need rest when working at a computer monitor,
• taking multivitamin preparations (especially those that have a positive effect on vision are recommended),
• in the event of eye fatigue and the appearance of jaundice, you can use special eye drops or lotions with drugs.

Output

Yellow eye syndrome cannot appear just like that, it is always preceded by some reason, therefore it is very important to consult a specialist doctor in time for qualified help.

But which doctor should you make an appointment with? It can be an ophthalmologist, a therapist. Having made additional analyzes of urine and blood, the doctor will make the correct diagnosis and, of course, prescribe the necessary treatment, and the sooner this is done, the less undesirable consequences and all kinds of complications can be avoided.

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Yellow eyes. Causes of yellowness of the whites of the eyes, diagnosis of causes, treatment of pathologies

Frequently asked Questions

The site provides background information. Adequate diagnosis and treatment of the disease is possible under the supervision of a conscientious doctor.

What is the white part of the eye?

The structure of the mucous membrane of the eye and the membranes of the eye

• outer (fibrous) shell of the eyeball;
• middle (vascular) shell of the eyeball;
• inner (sensitive) shell of the eyeball.

Outer shell of the eyeball

• anterior stratified squamous epithelium;
• anterior border membrane;
• intrinsic corneal substance (consists of homogeneous connective tissue plates and flat cells, which are a type of fibroblasts);
• the posterior border membrane (Descemet's membrane), which mainly consists of collagen fibers;
• posterior epithelium, which is represented by the endothelium.

Due to its transparency, the cornea easily transmits light rays. It also has the ability to refraction, as a result of which this structure is still referred to as the refractive apparatus of the eye (together with the lens, vitreous body, fluids of the eye chambers). In addition, the cornea performs a protective function and protects the eye from various traumatic effects.

Middle shell of the eyeball

Inner shell of the eyeball

Causes of yellow eyes

Liver disease as a cause of yellowing of the whites of the eyes

Hepatitis

Qiwe syndrome

Cirrhosis of the liver

Liver cancer

Echinococcosis of the liver

Liver sarcoidosis

Liver amebiasis

Diseases of the blood as a cause of yellowing of the whites of the eyes

Malaria

Erythrocyte membranopathies

Erythrocyte enzymopathies

Erythrocytic hemoglobinopathies

Autoimmune hemolytic anemias

Babesiosis

Poisoning with hemolytic poisons

Diseases of the biliary tract as a cause of yellowing of the whites of the eyes

Primary sclerosing cholangitis

Cholelithiasis

Tumors of the organs of the biliopancreatoduodenal zone

Opisthorchiasis

Disruption of metabolic processes in the body as a cause of yellowing of the whites of the eyes

Hemochromatosis

Wilson-Konovalov disease

Gilbert's disease

Crigler-Nayyar syndrome

Dabin-Johnson syndrome

Amyloidosis

Acute or chronic pancreatitis as a cause of yellowing of the whites of the eyes

Diagnostics of the causes of yellow eyes

Diagnosis of liver diseases

For certain indications (for example, an enlarged liver and spleen of unknown etiology, conflicting results laboratory research and others), patients with liver diseases undergo a percutaneous liver biopsy (inserting a needle through the skin into the liver under local anesthesia), which allows them to take a piece of liver tissue from them for histological examination (examination of the tissue under a microscope in a laboratory). Most often, liver biopsy is performed in order to confirm the presence of a malignant tumor in the liver, liver sarcoidosis in the patient, to establish the cause of hepatitis (or cirrhosis of the liver), its stage, and severity.

Diagnosis of blood diseases

Diagnosis of diseases of the biliary tract

Diagnosis of pathologies associated with metabolic disorders in the body

Diagnostics of the acute or chronic pancreatitis

Treatment of pathologies leading to yellow eyes

Treatment of liver diseases

Complete abstinence from alcohol is considered the main treatment for Ziwe syndrome. Also, with this syndrome, hepatoprotective agents are prescribed that strengthen the wall of hepatocytes (liver cells).

If cirrhosis of the liver occurs against the background of alcoholism, then ursodeoxycholic acid is prescribed to such patients (it accelerates the outflow of bile from the liver and protects its cells from damage). With viral cirrhosis of the liver, patients are prescribed antiviral agents... In autoimmune cirrhosis, immunosuppressants are prescribed, that is, drugs that reduce the activity of immune responses in the body. If cirrhosis appears against the background of Wilson-Konovalov disease (a pathology associated with the accumulation of copper in tissues) or hemochromatosis (a disease in which iron accumulates in tissues), then such patients are prescribed a special diet and detoxifying agents that form complexes with copper (or iron) and remove it from the body through the kidneys with urine.

Liver cancer is a rather serious disease that is more effectively treated only in the most early stages... At later stages, this pathology is practically incurable. For the treatment of liver cancer, a variety of methods are used, which may include surgical (mechanical removal of the tumor, liver transplantation, cryodestruction, etc.), radiation (irradiation of the tumor with ionizing radiation, radioembolization, etc.) and chemical methods (introduction of acetic acid, ethanol and etc.).

Liver sarcoidosis is treated with immunosuppressants and cytostatics. These drugs suppress immune responses in the body, reduce the formation of inflammatory granulomatous infiltrates, inhibit the multiplication of immunocytes (cells immune system) and the release of inflammatory cytokines (substances that regulate the cells of the immune system). In severe cases, with liver failure, a new liver is transplanted.

With amoebiasis of the liver, amoebicides are prescribed (drugs that destroy harmful amoeba). Most often they are metronidazole, emetine, tinidazole, ornidazole, etofamide, chloroquine. These drugs also have anti-inflammatory and antibacterial effects. When abscesses form inside the liver, surgical treatment is also sometimes performed, which consists in draining its cavity and removing necrotic masses (dead liver tissue).

Treatment of blood diseases

Malaria is treated with antimalarial drugs (chloroquine, quinine, artemether, halofantrine, mefloquine, fancidar, etc.). These drugs are prescribed according to special therapeutic regimens, which are selected depending on the type of malaria, its severity and the presence of complications. In severe cases, in the presence of complications, detoxifying, rehydrating (normalizing the total volume of fluid in the body), antibacterial, anticonvulsant, anti-inflammatory drugs, infusion of erythrocyte mass (drugs containing donor red blood cells) or whole blood, hemodialysis, oxygen therapy are prescribed.

Patients with erythrocyte membranopathies are prescribed symptomatic treatment, which most often consists of splenectomy (removal of the spleen), injections of erythrocyte mass (a drug containing donor red blood cells), prescription of vitamins B12 and B9. In some cases, transfusion whole blood, and also prescribe steroid anti-inflammatory drugs and cholekinetics (drugs that accelerate the excretion of bile from the liver).

Currently, there is no therapeutic method that would allow the patient to get rid of any kind of erythrocyte enzymopathy, therefore, these pathologies are treated only symptomatically. With them, transfusions of red blood cells (a drug containing donor red blood cells) or whole blood are usually prescribed for severe hemolytic crises (that is, periods characterized by massive destruction of the patient's red blood cells). In severe cases, bone marrow transplantation is performed.

Treatment of erythrocytic hemoglobinopathies should be aimed at correcting the deficiency of hemoglobin, erythrocytes in the blood, iron deficiency in the body, therapy of oxygen deficiency and avoiding factors provoking hemolytic crises (periods of breakdown of red blood cells in the blood) factors (smoking, alcohol consumption, some drugs, ionizing radiation, heavy physical activity, drugs, etc.). To replenish the deficiency of erythrocytes and hemoglobin in the blood, all patients are prescribed infusions of whole blood or erythrocyte mass (a preparation containing donor erythrocytes), as well as vitamins B9 and B12. Iron supplements are prescribed to correct iron deficiency. In some cases, according to certain clinical indications, patients with erythrocytic hemoglobinopathies can be surgically transplanted bone marrow or removed the spleen.

Autoimmune hemolytic anemias are treated with immunosuppressants and cytostatics, which suppress the immune system and interfere with the production and secretion of autoimmune red blood cell autoantibodies. To compensate for the deficiency of destroyed erythrocytes, erythrocyte mass (a drug containing donor erythrocytes) or whole blood is injected into patients. To neutralize harmful products released from hemolyzed erythrocytes, detoxification therapy is performed (prescribe hemodez, albumin, rheopolyglucin, plasmapheresis). To prevent thrombosis, which is common in these patients, anticoagulants (anticoagulants) are prescribed.

Hemolytic poisoning is treated with various antidotes (antidotes), which are selected depending on the type of substance that caused the intoxication. Also, such patients are prescribed detoxifying substances and hemodialysis (blood purification using a special device), which are designed to remove from the blood both the poisons themselves and the decay products of their own erythrocytes. Lavage of the gastrointestinal tract is carried out only if the poisoning happened after eating the poison.

Treatment of diseases of the biliary tract

Primary sclerosing cholangitis is a rapidly progressive disease that usually leads to the development of biliary cirrhosis. An etiotropic treatment for this disease has not yet been developed, since no one knows its cause. Therefore, these patients are treated symptomatically. Therapy is mainly aimed at preventing bile stagnation inside the liver. For this purpose, anticholestatics are used (cholestyramine, ursodeoxycholic acid, bilignin, etc.). The same drugs have hepatoprotective properties, that is, they protect liver cells from damage.

Gallstone disease is treated with various methods. First of all, such patients are prescribed a diet with the exclusion of very fatty and high-calorie foods from the use. Secondly, they are prescribed medications (chenodeoxycholic and ursodeoxycholic acids), which can dissolve stones right in the gallbladder. However, these drugs are usually not prescribed for all patients. Drug therapy indicated only in cases where the function of the gallbladder and the patency of the bile ducts are preserved (that is, the stones do not block the bile ducts). For the same indications, lithotripsy is performed - the destruction of stones under the action of specially created shock waves. In case of blockage of the bile ducts with stones, jaundice and cholecystitis (inflammation of the mucous membrane of the gallbladder), surgery is often performed to remove the gallbladder.

The main method of treatment of tumors of the organs of the biliopancreatoduodenal zone is surgical intervention. Radiation therapy and chemotherapy are less effective in such cases.

In the presence of hemochromatosis, the patient is prescribed detoxifying drugs (deferoxamine), which are able to bind iron in the blood well and remove it through the kidneys. Besides medicines such patients are often prescribed a diet that excludes the intake of foods containing large quantities of iron, as well as bloodletting, through which it is possible to quickly remove a certain amount of iron from the body. It is believed that when 500 ml of blood is bleed, about 250 mg of iron is instantly excreted from the human body.

With Wilson-Konovalov disease, a diet is prescribed that minimizes the intake of large amounts of copper into the body with food, as well as detoxifying drugs (penicillamine, unitiol) that remove free copper from the body. In addition, such patients are prescribed hepatoprotectors (increase the resistance of liver cells to damage), B vitamins, zinc preparations (slow down the absorption of copper in the intestine), anti-inflammatory drugs, immunosuppressants (suppress immune reactions in the body), choleretic drugs (improve the excretion of bile from the liver) ...

During exacerbations of Gilbert's disease, hepatoprotectors are prescribed (protect liver cells from damage), choleretic agents (improve the excretion of bile from the liver), barbiturates (reduce the level of bilirubin in the blood), B vitamins. An important means of preventing exacerbations of this pathology is the strict maintenance of a certain lifestyle and the maximum avoidance of provoking factors (stress, starvation, heavy physical exertion, alcohol consumption, smoking, etc.), which can contribute to an increase in the level of indirect bilirubin in the blood.

With Crigler-Nayyar syndrome, various methods of detoxification of the body are used (prescription of barbiturates, drinking plenty of fluids, plasmapheresis, hemosorption, administration of albumin). In some cases, phototherapy is prescribed (irradiation of the skin with special lamps, as a result of which the destruction of bilirubin in the body occurs), blood transfusions, liver transplantation.

Patients with Dabin-Johnson syndrome are prescribed B vitamins and choleretic agents (they promote the excretion of bile from the liver). They are contraindicated in insolation (prolonged exposure to sunlight). As far as possible, such patients are advised to avoid provoking factors (heavy physical exertion, stress, alcohol consumption, hepatotoxic drugs, fasting, trauma, viral or bacterial infections and etc.).

Drug treatment for liver amyloidosis is always selected individually. The drugs of choice are immunosuppressants (suppress immune reactions in the body), cytostatics (slow down the processes of cell pressure in tissues), hepatoprotectors (protect liver cells from damage). For some forms of amyloidosis, a liver transplant is performed.

Treatment of acute or chronic pancreatitis

What pathologies are the most common yellow sclera of the eyes in newborns?

• Crigler-Nayar Syndrome. Crigler-Nayyar syndrome is a pathology in which the liver cells lack an enzyme (glucuronyl transferase) that converts indirect bilirubin into direct bilirubin, as a result of which the former accumulates in the blood, penetrates into the sclera of the eyes and stains them yellow.
• Dabin-Johnson syndrome. Dabin-Johnson syndrome is a congenital disease in which the excretion of direct bilirubin from the liver cells is impaired, due to which there is a violation of the removal of bilirubin from the liver and the whole organism as a whole.
• Physiological jaundice of newborns. During intrauterine development, the fetus has a large amount of fetal hemoglobin in its erythrocytes. When a child is born, this type of hemoglobin is replaced with normal hemoglobin (HbA-hemoglobin), which is the dominant (predominant) form in all children and adults. This change is accompanied by yellowing of the skin and sclera of the eyes of the newborn and lasts the first 7 to 8 days of his life.
• Kernicterus. Kernicterus is a pathological condition in which the level of indirect bilirubin (more than 300 μmol / L) in the blood of newborns increases sharply. The reason for this increase may be the incompatibility of the mother and the fetus in blood groups, hereditary erythrocytic membranopathies, Hirschsprung's disease, congenital pyloric stenosis (obstruction of the pylorus of the stomach), etc.
• Infectious hepatitis. Infectious hepatitis in newborns most often occurs when their mothers are not seen by doctors during pregnancy and do not undergo various laboratory tests for the presence of infections (toxoplasmosis, herpes, cytomegalovirus, hepatitis B, etc.).

In the very central part of the eye, you can see a dark point - the pupil ( through it, light penetrates into the eyeball), along the periphery of it there is a colored structure - the iris, which gives the eyes a certain color ( green, blue, brown, etc.). If you move from the inner edge of the iris to its outer, you can see that it abruptly turns into a whitish structure - the tunica albuginea ( part) eyes. The white part of the eye is one of the two main sections of the outer shell of the eye. The white membrane of the eye is also called the sclera of the eye. This membrane occupies five-sixths of the entire surface area of \u200b\u200bthe outer membrane of the eye. The sclera of the eye is white ( in fact, that's why it is called protein) due to the fact that it consists of a large amount of connective tissue.

The structure of the mucous membrane of the eye and the membranes of the eye

The human organ of vision consists of the eyeball, oculomotor muscles, eyelids, lacrimal apparatus, blood vessels and nerves. This organ is a peripheral part of the visual analyzer and is necessary for the visual perception of external objects. The main structure in the organ of vision is the eyeball. It is located in the eye socket and has an irregular spherical shape. Visually, on a person's face, you can see only the anterior part of the eyeball, which is only a small part of it and is covered in front by the eyelids. Most of this anatomical structure ( eyeball) is hidden in the depth of the eye socket.

IN eyeball there are three main shells:

• outdoor ( fibrous) the shell of the eyeball;
• average ( vascular) the shell of the eyeball;
• internal ( sensitive) the shell of the eyeball.

Outer shell of the eyeball

The outer shell of the eyeball consists of two important sections, which differ from each other in their anatomical structure and functions. The first section is called the cornea of \u200b\u200bthe eye. The cornea of \u200b\u200bthe eye is located in the anterior central part of the eyeball. Due to the lack of blood vessels and the homogeneity of its tissue, the cornea is transparent, so through it you can see the pupil and iris of the eye.

The cornea is composed of the following layers:

• anterior stratified squamous epithelium;
• anterior border membrane;
• intrinsic corneal substance ( consists of homogeneous connective tissue plates and flat cells, which are a type of fibroblasts);
• posterior boundary membrane ( descemet shell), which mainly consists of collagen fibers;
• posterior epithelium, which is represented by the endothelium.

Due to its transparency, the cornea easily transmits light rays. It also has the ability to refraction, as a result of which this structure is still referred to as the refractive apparatus of the eye ( together with the lens, vitreous humor, eye chamber fluids). In addition, the cornea performs a protective function and protects the eye from various traumatic effects.

The cornea of \u200b\u200bthe eye is the most prominent part of the eyeball. Along the periphery, the cornea of \u200b\u200bthe eye smoothly passes into the sclera of the eyeball, which is the second important part of the outer shell of the eye. This section occupies most of the area of \u200b\u200bthe outer shell of the eye. The sclera of the eye is represented by a dense fibrous formed connective tissue, consisting of bundles of collagen fibers with an admixture of elastic fibers and fibroblasts ( connective tissue cells). The outer surface of the sclera is covered in front by the conjunctiva, and the back by the endothelium. Conjunctiva ( conjunctiva) Is a relatively thin shell, which consists of a cylindrical stratified epithelium. This shell covers the inside of the eyelids ( secular part of the conjunctiva) and the eyeball outside ( ocular conjunctiva). Moreover, this structure does not cover the cornea.

The outer shell of the eyeball has a number of important functions. Firstly, it is the most durable in comparison with the other two membranes of the eyeball, as a result of which its presence allows you to protect the organ of vision from traumatic damage. Secondly, due to its strength, the outer shell of the eye helps to maintain a certain anatomical shape of the eyeball. Thirdly, the oculomotor muscles are attached to this membrane, as a result of which the eyeball can make various movements in the orbit.

Middle shell of the eyeball

The middle shell of the eyeball is located inside the eye. It consists of three parts of unequal size ( back, middle and front). Of all parts of the middle shell, only the iris can be visually discerned ( anterior part of the middle shell of the eyeball), which is located between the pupil and the sclera of the eyes. It is the iris that gives the eyes a certain color. It consists of loose connective tissue, blood vessels, smooth muscles, nerves and pigment cells. Iris of the eye ( unlike the other two parts of the middle shell) does not adhere to the outer shell of the eyeball and is separated from the cornea by the anterior chamber of the eye, which contains intraocular fluid. Behind the iris is the posterior chamber of the eye, which delimits the lens ( a transparent structure that sits directly opposite the pupil inside the eyeball and is a biological lens) and the iris. This chamber is also filled with intraocular fluid.

The back of the middle membrane of the eyeball is called the own choroid of the eyeball. It is located directly under the white of the eye at the back of the eye. It includes a large number of vessels, connective tissue fibers, pigment and endothelial cells. The main function of this anatomical structure is to provide nutrients to the retinal cells ( inner shell of the eyeball) eyes. The posterior part of the middle shell lines almost two-thirds of the entire area of \u200b\u200bthe sclera, and therefore is the largest of all three parts of the middle shell.

Slightly in front of her ( the back of the middle shell), in the form of a ring, the ciliary body is located ( middle part of the middle shell of the eyeball), represented by the ciliary muscle, which plays an important role in the accommodation of the eye ( it regulates the curvature of the lens and fixes it in a certain position). Also in the composition of the ciliary ( ciliary) the body includes special epithelial cells that are engaged in the production of intraocular fluid that fills the anterior and rear camera eyes.

Inner shell of the eyeball

The inner shell of the eyeball ( or retina) envelops the iris, the ciliary body and its own choroid from the inside. The collection of those places where the retina is adjacent to the iris and to ciliary body called blind ( blind) part of the retina. The rest, the posterior, more extensive part of the retina is called the visual retina. In this part of the retina, the perception of light entering the eyeball occurs. This perception is possible due to the presence of special photoreceptor cells inside the retina. The retina itself consists of ten layers, which differ from each other in different anatomical structures.

Causes of yellow eyes

Yellowing of the whites of the eyes is most often associated with an increase in the concentration of bilirubin in the blood. Bilirubin is a yellow bile pigment that is formed in the body during the breakdown of hemoglobin ( blood oxygen carrying protein), myoglobin ( muscle oxygen carrying protein) and cytochromes ( respiratory chain enzymes). Formed immediately after the breakdown of these three types of proteins ( hemoglobin, cytochromes and myoglobin) bilirubin is called indirect bilirubin. This compound is very toxic to the body, so it must be rendered harmless as soon as possible. Indirect bilirubin is neutralized only in the liver. This type of bilirubin is not excreted through the kidneys.

In liver cells, indirect bilirubin binds to glucuronic acid ( chemical required to neutralize bilirubin), and it turns into direct bilirubin ( neutralized bilirubin). Further, direct bilirubin is transported by liver cells into bile, through which it is excreted from the body. In some cases, some of it can be sucked back into the blood. Therefore, there are always two main fractions of bilirubin in the blood - direct bilirubin and indirect bilirubin. These two fractions together make up the total bilirubin in the blood. The indirect bilirubin accounts for about 75% of the total bilirubin. Reference ( limit) the concentration of total bilirubin in the blood is 8.5 - 20.5 μmol / l.

An increase in the concentration of total bilirubin above 30 - 35 μmol / l leads to the appearance of jaundice in the patient ( yellowing of the skin and sclera of the eyes). This happens because at such concentrations it ( bilirubin) diffuses ( penetrates) in peripheral tissues and stains them yellow. There are three degrees of severity of jaundice ( that is, the severity of jaundice). With a mild degree, the concentration of total bilirubin in the blood reaches 86 μmol / l. With an average degree in the patient's blood, the bilirubin level is in the range from 87 to 159 μmol / l. With a pronounced degree of severity, its concentration in blood plasma is higher than 159 μmol / L.

Causes of yellowing of the sclera of the eyes

All these listed factors ( viruses, bacteria, etc.) cause damage to liver cells, as a result of which their gradual destruction occurs, which is accompanied by the appearance of inflammation in the liver. This is accompanied by a violation of its full function and the loss of the ability to neutralize indirect bilirubin coming from the blood to the liver for processing. In addition, with hepatitis, direct bilirubin ( as liver cells are destroyed, and he is thrown out of them into the surrounding space). The accumulation of direct and indirect bilirubin in the blood contributes to their deposition in various tissues and, in particular, in the skin and mucous membranes. Therefore, with lesions of the liver, yellowing of the skin and white membrane occurs ( sclera) eyes.

Qiwe syndrome

Zive syndrome is a rare syndrome ( set of pathological signs), which is characterized by the appearance of jaundice in the patient ( yellowing of the sclera and skin), enlarged liver, hemolytic anemia ( a decrease in the content of hemoglobin and erythrocytes in the blood as a result of the destruction of the latter), hyperbilirubinemia ( increased blood levels of bilirubin) and hyperlipidemia ( increased content blood fat). This syndrome is observed in people who abuse alcohol. The yellowing of the white membrane of the eyes in Qive syndrome is caused by an increase in the level of bilirubin ( mainly due to indirect) in the blood, due to the destruction of red blood cells and liver dysfunction. In most cases, these patients develop fatty hepatosis ( dystrophy) liver, that is, pathological deposits inside the parenchyma ( fabrics) liver fat.

Cirrhosis of the liver

Liver cirrhosis is a pathology in which the liver is damaged and its normal tissue is replaced by pathological connective tissue. With this disease, connective tissue begins to grow in the liver, which gradually replaces the usual liver tissue, as a result of which the liver begins to function poorly. It loses the ability to neutralize various compounds harmful to the body ( ammonia, bilirubin, acetone, phenol, etc.). Violation of the detoxifying ability of the liver leads to the fact that these toxic metabolic products begin to accumulate in the blood and have an adverse effect on the organs and tissues of the body. Bilirubin ( indirect), circulating in large quantities in the bloodstream, is gradually deposited in the skin, the white membrane of the eyes, the brain and other organs. The deposition of bilirubin in the tissues gives them a yellow color, therefore, with cirrhosis of the liver, icterus is noted ( yellowing) sclera and skin.

If the disease is not treated for a long time, then the echinococcal cyst begins to gradually increase in size and squeeze the surrounding liver tissues, which is why they die off ( atrophy of the liver parenchyma). As a result of this, a mechanical replacement of normal liver tissue occurs, in the place of which a cyst occurs. At some point, when the cyst reaches a large size, the liver loses its ability to bind and neutralize indirect blood bilirubin, as a result of which it accumulates first in it, and then in the skin and in the white membrane of the eyes, giving them a characteristic yellow color.

Liver sarcoidosis

Sarcoidosis is chronic illness, in which in various tissues and organs ( lungs, liver, kidneys, intestines, etc.) granulomas appear. Granuloma is a focus of accumulation of lymphocytes, macrophages and epithelioid cells. Granulomas in sarcoidosis appear as a result of an inadequate immune response of the body to certain antigens ( foreign particles). This is facilitated by various infectious ( viruses, bacteria) and non-infectious factors (genetic predisposition, human contact with toxic substances, etc.).

As a result of the impact of such factors on human tissue, the functioning of the immune system is disrupted. If it detects some antigens in the tissues, then hyperimmune ( excessive immune) response, and in the places of localization of such antigens, cells of the immune system begin to accumulate, resulting in small foci of inflammation. These lesions visually look like nodules ( or granulomas) other than normal tissue. Granulomas can vary in size and location. Inside such foci, the cells of the immune system, as a rule, act ineffectively, so these granulomas persist for a long time, and in some cases they can increase in size. In addition, with sarcoidosis, new granulomas constantly appear ( especially if the disease is not treated).

The constant growth of already existing granulomas and the appearance of new pathological foci in various organs disrupts their normal architectonics ( structure) and work. Organs gradually lose their functions, due to the fact that granulomatous infiltrates replace their normal parenchyma ( the cloth). If, for example, sarcoidosis affects the lungs ( and they are most often damaged by this disease), then the patient has a cough, shortness of breath, chest pain, excessive fatigue due to lack of air. If the liver is damaged, then, first of all, its detoxifying and protein-synthetic ( the synthesis of blood proteins is disrupted in the liver) functions.

The main manifestation of extraintestinal amebiasis is liver damage. When pathogenic amoebas enter the liver, they cause tissue damage there. First, hepatitis occurs ( inflammation of the liver tissue). After some time, in the absence of a proper immune response, the patient at the site of injury ( and inflammation) abscesses ( pus-filled cavities). There can be a large number of such abscesses. In the absence of treatment for liver amebiasis, its various functions are impaired, including the neutralization of bilirubin in the blood ( indirect bilirubin).

These merozoites then enter the bloodstream and penetrate into erythrocytes and begin to divide there again ( erythrocytic schizogony). At the end of erythrocyte schizogony, the infected erythrocytes are completely destroyed and release a large amount of multiplied merozoites, which again penetrate into new erythrocytes for reproduction. Thus, this process is cyclical. Each new destruction of erythrocytes is accompanied by the release into the blood of not only new populations of malaria merozoites, but also the rest of the contents of erythrocytes and, in particular, a protein - hemoglobin. When this protein breaks down, bilirubin is formed ( indirect), which must be rendered harmless in the liver.

The problem is that in malaria, a very significant number of red blood cells are destroyed and a huge amount of indirect bilirubin is formed in the blood, which the liver does not have time to process. Therefore, with malaria, patients develop hyperbilirubinemia ( an increase in the level of bilirubin in the blood) and jaundice ( yellowing of the skin and sclera of the eyes), which occurs due to the partial deposition of bilirubin in the tissues.

Erythrocyte membranopathies

Erythrocyte membranopathies are a set of hereditary pathologies, which are based on congenital defects in genes encoding proteins ( glycophorin C, alpha-spectrin, etc.), which are part of the membranes of erythrocytes. Such defects lead to a disruption in the production of membrane proteins during the formation of red blood cells in the bone marrow, as a result of which the membranes of the older red blood cells circulating in the blood change their shape. In addition, with these pathologies, their membranes become defective, they have an incorrect permeability to various substances and a low resistance to damaging factors, and therefore such erythrocytes are quickly destroyed and do not live long.

The most famous erythrocytic membranopathies are Minkowski-Shoffard disease, hereditary elliptocytosis, hereditary stomatocytosis, hereditary acanthocytosis, and hereditary pyropoikilocytosis. All these pathologies are characterized by a triad of clinical signs - jaundice, hemolytic anemia ( decrease in the number of red blood cells as a result of their destruction) and splenomegaly ( ). The appearance of jaundice in such patients is explained by the fact that with erythrocytic membranopathies there is frequent destruction of defective red blood cells in the blood, which is accompanied by the release of a large amount of hemoglobin, which is then converted into indirect bilirubin. The liver cannot immediately process huge amounts of indirect bilirubin and remove it from the blood. Therefore, this metabolite ( exchange product) accumulates in the blood and subsequently settles in the tissues, causing yellowing of the white membrane of the eyes and skin.

Erythrocyte enzymopathies

Erythrocyte enzymopathies - group hereditary diseases, in which the production of enzymes is disrupted in erythrocytes ( proteins that accelerate biochemical reactions) that control the course of metabolic reactions ( metabolic reactions). This leads to an inferiority of energy metabolism, the accumulation of intermediate reaction products and a deficiency of energy in the erythrocytes themselves. Under conditions of energy deficiency in erythrocytes, the transport of various substances through their membrane slows down, which contributes to their shrinkage and destruction. There are also certain erythrocyte membranopathies, in which there may be a deficiency of enzymes of the antioxidant systems of erythrocytes ( e.g. pentose phosphate cycle, glutathione system), which often leads to a decrease in their resistance to the effects of free oxygen radicals and rapid destruction.

In any case, a deficiency of enzymes in erythrocyte enzymopathies leads to a decrease in the life span of erythrocytes and their rapid death, which is accompanied by the release of a large amount of hemoglobin into the blood and the appearance of hemolytic anemia ( pathology in which there is a deficiency of erythrocytes and hemoglobin in the blood, resulting from the destruction of erythrocytes) and jaundice. The appearance of the latter is due to the fact that the liver does not have time to quickly process and remove from the blood indirect bilirubin, formed in huge quantities during the breakdown of hemoglobin. Therefore, indirect bilirubin is deposited in the skin and white of the eyes and causes them to turn yellow.

Erythrocytic hemoglobinopathies

Erythrocytic hemoglobinopathies are a group of congenital diseases, the origin of which is based on genetically mediated defects in the formation of hemoglobin in erythrocytes. Some of the most common hemoglobinopathies are sickle cell anemia, alpha thalassemia, and beta thalassemia. With these pathologies, erythrocytes contain abnormal hemoglobin, which performs its function poorly ( oxygen transport), and the erythrocytes themselves lose strength and shape, as a result of which they quickly undergo lysis ( destruction) and have a short life span in the blood.

Therefore, patients with one of these diseases often have hemolytic anemia ( a decrease in the level of erythrocytes in the blood, due to their destruction), jaundice and oxygen deficiency ( due to impaired oxygen transport by hemoglobin). The onset of jaundice can be explained by the fact that with erythrocytic hemoglobinopathies there is a significant release of pathological hemoglobin into the blood from decaying erythrocytes. This hemoglobin is subsequently degraded and converted into indirect bilirubin. Since with these pathologies the destruction of a large number of erythrocytes takes place, then, accordingly, there will be a lot of indirect bilirubin in the blood, which the liver is not able to quickly neutralize. This leads to its accumulation in the blood and other tissues and organs. If this bilirubin penetrates the skin and the white membrane of the eyes, then they turn yellow. Yellowing of the white of the eyes and skin is called jaundice.

Autoimmune hemolytic anemias

Autoimmune hemolytic anemias are a group of pathologies in which erythrocytes in the blood are damaged due to their binding to autoimmune ( pathological) antibodies ( protective protein molecules circulating in the blood and directed against the body's own cells). These antibodies begin to be synthesized by the cells of the immune system when its proper functioning is disrupted, which can be caused by genetic defects in immunocytes ( cells of the immune system). Impaired immune system function can also be triggered external factors environment ( for example, viruses, bacteria, toxins, ionizing radiation, etc.).

When normal erythrocytes bind to autoimmune ( pathological) antibodies destroy them ( hemolysis). The destruction of a large number of red blood cells leads to the appearance of hemolytic anemia ( that is, a decrease in red blood cells, due to their sudden intravascular destruction). Such anemia is completely called autoimmune hemolytic anemia ( AIGA). Depending on the type of autoimmune antibodies that cause destruction of erythrocytes in the blood, all autoimmune hemolytic anemias are divided into types ( for example, AIHA with warm hemolysins, AIHA with incomplete cold agglutinins, Fisher-Evans syndrome, etc.). All autoimmune hemolytic anemias are accompanied by an increase in the concentration of indirect bilirubin in the blood ( due to the increased yield of hemoglobin from damaged erythrocytes). When deposited in tissues, this chemical metabolite causes them to yellow, therefore, with these pathologies, patients often have yellow skin and sclera.

Babesiosis

Babesiosis is an infectious disease resulting from human infection with protozoa of the genus Babesia ( Babesia). The mechanism of transmission of infection is transmissible, that is, a person acquires this disease through tick bites ( genera Dermacentor, Hyalomma, Rhipicephalus). Mostly people who are constantly in contact with pets and have a fairly pronounced immunodeficiency get sick ( for example, patients with HIV infection, infections, etc.). A person with normal immunity can also become infected with babesiosis, but the disease will be asymptomatic.

Most of hemolytic poisons are represented by artificially synthesized chemicals ( benzene, phenol, aniline, nitrites, chloroform, trinitrotoluene, phenylhydrazine, sulfapyridine, hydroquinone, potassium bromate, arsenic, lead, copper, etc.), which are used in various industries ( chemical, medical, fuel, etc.). therefore most of hemolytic poisoning occurs in industrial workers who are constantly in contact with these toxic substances.

Under the influence of hemolytic poisons, erythrocyte membranes are deformed, as a result of which they are destroyed. There are also some hemolytic poisons that block the course of enzymatic processes inside erythrocytes, due to which their energy metabolism or their antioxidant capacity is disrupted ( resistance to free oxygen radicals), as a result of which they are destroyed. Certain chemical substances are able to change the structure of erythrocyte membranes in such a way that it becomes unrecognizable and alien to the cells of the immune system. This is how acquired autoimmune hemolytic anemias arise. With them, the immune system destroys the patient's own erythrocytes, so their number in the blood is significantly reduced.

Thus, in case of poisoning with hemolytic poisons due to various mechanisms, a massive destruction of erythrocytes inside the vessels occurs. This is accompanied by the release into the blood of a large amount of hemoglobin, which is subsequently converted into bilirubin ( indirect). High concentrations of this bilirubin in the blood lead to its deposition in the skin and sclera of the eyes, which is accompanied by their yellowing.

Diseases of the biliary tract as a cause of yellowing of the whites of the eyes

Bile is a yellow-brown biological fluid that is produced in the liver and secreted into the duodenum. Bile plays an important role in the digestive processes in the intestines. Also, together with bile, various harmful substances are excreted that are unnecessary for the body ( direct bilirubin, cholesterol, bile acids, steroids, metals, etc.). Before reaching the intestines, bile passes through the biliary tract ( intrahepatic and extrahepatic). In diseases of these pathways, it becomes difficult to transport bile into the duodenum, due to their partial or complete blockage. This is accompanied by an increase in pressure in the bile ducts located above the blockage. In those places where the wall of these ducts is thinnest, it breaks, and part of the bile enters the bloodstream. Therefore, in diseases of the biliary tract ( primary sclerosing cholangitis, cholelithiasis, tumors of the organs of the biliopancreatoduodenal zone, opisthorchiasis) in the blood, the level of direct bilirubin rises and jaundice is observed.

Primary sclerosing cholangitis

Primary sclerosing cholangitis is a disease of unknown nature in which chronic inflammatory processes in the walls of the intrahepatic and extrahepatic bile ducts. Due to constant inflammation, the walls of these ducts undergo pathological changes, they thicken, narrow, coarse and deform. As the disease progresses, the lumen of the affected biliary tract is completely obliterated ( closes). Such paths become completely non-functional, bile does not move along them from the liver to duodenum... The more such ducts are affected, the more difficult it is to transport bile to the intestines. If a large number of bile ducts are damaged inside the liver, bile stagnation occurs ( cholestasis), which is accompanied by its partial penetration into the blood. Since direct bilirubin is part of the bile, it gradually accumulates in the skin and sclera of the eyes, which is why they turn yellow.

Cholelithiasis

Gallstone disease is a pathology in which stones appear in the gallbladder or in the biliary tract. The cause of its occurrence is a violation of the ratio of substances ( cholesterol, bilirubin, bile acids) in bile. In such cases, some substances ( such as cholesterol) becomes larger than all the others. Bile is oversaturated with them, and they precipitate. Sediment particles gradually stick together and overlap, resulting in the formation of stones.

The development of this disease can be facilitated by stagnation of bile ( congenital anomalies gallbladder, biliary dyskinesia, scars and adhesions in the bile ducts), inflammatory processes in the biliary tract ( inflammation of the mucous membrane of the gallbladder or bile ducts), diseases of the endocrine system ( diabetes mellitus, hypothyroidism), obesity, unhealthy diet ( excessive consumption of fatty foods), pregnancy, certain medications ( estrogens, clofibrate, etc.), liver disease ( hepatitis, liver cirrhosis, liver cancer), hemolytic anemias ( pathology associated with a decrease in the number of red blood cells in the blood, due to their destruction).

Stones formed with gallstone disease can be located in the so-called blind spots in the biliary system ( for example, in the body or the fundus of the gallbladder). In such cases, this disease does not manifest itself clinically, since the stones do not block the bile ducts, and the outflow of bile through the biliary system is preserved. If these stones suddenly fall from the gallbladder into the bile ducts, then the movement of bile through them slows down sharply. Bile accumulates in large volumes in the sections of the biliary system located above the obstacle. This leads to an increase in pressure in the bile ducts. Under such conditions, the intrahepatic bile ducts are destroyed inside the liver, and bile goes directly into the blood.

Due to the fact that bile contains a large amount of bilirubin ( direct), then its concentration in the blood increases. Moreover, such an increase is always proportional to the duration of the blockage of the bile ducts with a stone. At a certain concentration of direct bilirubin in the blood, it penetrates the skin and white membranes of the eyes and stains them yellow.

Tumors of the organs of the biliopancreatoduodenal zone

The organs of the biliopancreatoduodenal zone include the extrahepatic bile ducts, gallbladder, pancreas and duodenum. These organs are very close to each other on the top floor. abdominal... In addition, they are functionally interconnected, so tumors of all these organs have similar symptoms. With tumors of the organs of the biliopancreatoduodenal zone, yellowing of the skin and sclera of the eyes is very often noted. This is explained by the fact that, if they are present, there is a mechanical blockage of the extrahepatic bile ducts ( or gallbladder) and bile entering them ( into the ducts) from the liver stagnates. Such stagnation is observed not only in the extrahepatic ducts, but also in the intrahepatic ducts, which are very thin and fragile. Intrahepatic ducts, when stagnant in them, bile can rupture, as a result of which it enters the blood. Bilirubin ( straight), which is part of its composition, gradually accumulates in the skin and white membrane of the eyes and stains them yellow.

Crigler-Nayyar syndrome

Crigler-Najjar syndrome is an inherited liver disease in which there is a defect in the gene that encodes the amino acid sequence of an enzyme ( uridine-5-diphosphate glucuronyl transferase) liver cells involved in the detoxification and binding of indirect bilirubin with glucuronic acid inside hepatocytes ( liver cells). As a result of this defect, the elimination of indirect bilirubin from the blood is impaired. It accumulates in the blood, and then in the skin and sclera of the eyes, as a result of which they turn yellow.

There are two types of Crigler-Nayyar syndrome. The first type is characterized by severe clinical symptoms and severe jaundice. With it, the enzyme is completely absent in the liver cells ( uridine-5-diphosphate glucuronyltransferase), which binds indirect bilirubin. This type of Crigler-Nayyar syndrome usually leads to death of patients at a very early age.

In the second type, which is also called Arias syndrome, this enzyme is present in hepatocytes, but its amount, compared to the norm, is much lower. With this type, the clinical symptoms are also quite pronounced, but the survival rate in such patients is much higher. Clinical symptoms appear in patients with the second type of Crigler-Nayyar syndrome a little later ( during the first years of life). The clinical course of this type is chronic, with periods of exacerbations and remissions ( asymptomatic course). Exacerbations in patients with Crigler-Nayyard syndrome are observed much more often than in patients with Gilbert's disease.

Dabin-Johnson syndrome

Dabin-Johnson syndrome is also a hereditary liver disease. With this pathology, the release process is disrupted ( into the bile ducts) from the liver cells of detoxified bilirubin ( direct), as a result of which it first accumulates in them ( in liver cells), and then enters the bloodstream. The cause of this disorder is a hereditary defect in the gene that is responsible for the synthesis of direct bilirubin carrier proteins localized on the membrane of hepatocytes ( liver cells). The accumulation of direct bilirubin in the blood gradually leads to its retention in the skin and white membrane of the eyes, which is why they turn yellow.

The first signs of Dabin-Johnson syndrome in patients usually appear at a young age ( mostly in men). Jaundice is almost always persistent and is often associated with various dyspeptic ( nausea, vomiting, abdominal pain, poor appetite, diarrhea, etc.) and asthenovegetative ( headache, dizziness, weakness, depression, etc.) symptoms. This syndrome does not affect life expectancy, however, in such patients, its quality is significantly reduced ( due to persistent symptoms of the disease). If the disease goes into remission ( asymptomatic course), then it can quickly escalate if the patient is exposed to various provoking factors ( heavy physical exertion, stress, alcohol consumption, starvation, trauma, viral or bacterial infections, etc.), which are recommended to be avoided whenever possible.

Amyloidosis

Amyloidosis is a systemic disease, as a result of which in various organs ( kidneys, heart, esophagus, liver, intestines, spleen, etc.) accumulates an abnormal protein - amyloid. The cause of the appearance of amyloid is a violation of protein metabolism in the body. There are purchased ( for example, ASC1-amyloidosis, AA-amyloidosis, AH-amyloidosis, etc.) and hereditary ( AL amyloidosis) forms of this pathology. The chemical structure of amyloid and its origin depend on the form of amyloidosis. For example, in AL-amyloidosis, amyloid consists of clusters of light chains ( fragments) immunoglobulins ( protective molecules that circulate in the blood). In AH amyloidosis, amyloid deposits are composed of beta-2 microglobulin ( one of the blood plasma proteins).

Since one of the main components of bile is bilirubin ( straight), then its level in the blood increases sharply. A large amount of bilirubin in the blood plasma contributes to its penetration and retention in peripheral tissues ( especially in the skin and sclera of the eyes), which leads to their yellowing. Jaundice ( yellowing of the skin and white of the eyes) can be observed in both acute and chronic pancreatitis.

Diagnostics of the causes of yellow eyes

To diagnose the causes of yellow eyes, various types of research can be used ( clinical, radiation, laboratory). The main clinical methods diagnostics are the collection of anamnesis ( clarification of the entire history of the development of the disease) at the patient and his examination. Of the radiation methods of research, doctors most often give preference to ultrasound and computed tomography of the abdominal organs ( in case of suspicion of any pathology of the liver, pancreas or biliary tract). In the diagnosis of yellow eyes, various types of blood tests are also used ( complete blood count, biochemical blood test, immunological and genetic tests, toxicological blood test), feces and urine tests.

Diagnosis of liver diseases

The main symptoms of liver disease are pain in the right hypochondrium, fever, a feeling of bitterness in the mouth, decreased appetite, jaundice ( yellowing of the sclera of the eyes and skin), headache, general weakness, decreased performance, insomnia, nausea, vomiting, enlarged liver, flatulence. Also, depending on the disease, such patients may have additional symptoms. For example, with echinococcosis of the liver, various allergic reactions on the skin ( rashes on the skin, itching, redness of the skin, etc.). With sarcoidosis of the liver, pain in the chest, joints, muscles, shortness of breath, cough, hoarseness, increase in the size of the peripheral lymph nodes (inguinal, occipital, elbow, cervical, axillary, etc.), arthritis ( joint inflammation), deterioration of visual acuity, etc.

In patients with liver amebiasis, pain syndrome often begins in the central part of the abdomen, which is associated with the preliminary ingress of harmful microorganisms into the intestines. In addition, they have diarrhea with blood and mucus, false desires, dehydration of the body, hypovitaminosis. In patients with cirrhosis of the liver, nosebleeds, bleeding gums, pruritus, palmar erythema ( red, small-spotted rash on the palms), gynecomastia ( enlargement of the mammary glands in men), spider veins on the skin, edema.

In addition to symptoms in patients with liver disease, it is important to collect high-quality anamnestic data, which the doctor receives in the process of questioning the patient. These data will allow the attending physician to suspect a certain liver pathology. This is especially true for medicinal, alcoholic, infectious, toxic hepatitis (liver inflammation), Tsive's syndrome, liver amebiasis, liver echinococcosis. So, for example, if a patient in a conversation with a doctor mentions that before the onset of symptoms of the disease, he used certain types of drugs for a long time ( paracetamol, tetracycline, chlorpromazine, methotrexate, diclofenac, ibuprofen, nimesulide, etc.), which can adversely affect the liver, the doctor concludes that a possible pathology due to which the patient turned to him is drug hepatitis.

The most common CBC changes in patients with liver disease are anemia ( ), leukocytosis ( an increase in the number of leukocytes in the blood), increased ESR ( ), thrombocytopenia ( a decrease in the number of platelets in the blood), sometimes leukopenia ( ) and lymphopenia ( ). With echinococcosis and sarcoidosis of the liver, eosinophilia is possible ( an increase in the number of eosinophils in the blood). It should be noted that based on the results of a general blood test, it is impossible to make a definitive diagnosis of any specific liver disease.

In a biochemical blood test in patients with liver diseases, an increase in the content of total bilirubin, cholesterol, bile acids, globulins, an increase in the activity of alanine aminotransferase ( ALT), aspartate aminotransferase ( AST), gamma glutamyl transpeptidase, alkaline phosphatase, decrease in the amount of albumin, prothrombin index. With sarcoidosis, hypercalcemia ( increased blood calcium) and an increase in ACE ( angiotensin converting enzyme).

An immunological blood test is most often prescribed for patients with suspected viral hepatitis ( conduct a study for markers of hepatitis - HbsAg, anti-Hbs, HBeAg, anti-Hbc IgG, etc.), liver echinococcosis ( prescribe a study for antibodies to echinococcus), liver amebiasis ( prescribe a test for anti-amebic antibodies), autoimmune hepatitis ( a study for the presence of circulating immune complexes, antinuclear, antimitochondrial autoantibodies, antibodies to smooth muscles, to deoxyribonucleoprotein, etc.), liver cancer ( study for alpha-fetoprotein - one of the tumor markers), Infectious mononucleosis ( test for antibodies to the Epstein-Barr virus), cytomegalovirus infection ( test for antibodies to cytomegalovirus virus).

In some cases, patients with infectious liver diseases ( for example, with viral hepatitis, amebiasis, cytomegalovirus infection and etc.) appoint PCR ( polymerase chain reaction) Is one of the methods of laboratory diagnostics that allows to identify DNA particles ( genetic material) harmful pathogens in the blood. Some of the most important methods for diagnosing liver diseases are beam methods research - ultrasound procedure (Ultrasound) and computed tomography ( CT scan).

The main pathological changes that are detected by radiation methods of research in liver diseases

Pathology name	Typical pathological changes for this pathology
Hepatitis	Enlargement of the liver in size, heterogeneity of the internal structure of the liver, decreased echogenicity ( density) of her parenchyma, depletion of the vascular pattern.
Qiwe syndrome	The same as with hepatitis.
Cirrhosis of the liver	Enlargement of the liver and spleen in size, possibly the presence of ascites ( ). The liver has an uneven, knobby surface. Directly inside the liver, a significant violation of its structure can be detected ( architectonics), focal sclerosis ( replacement of normal connective tissue), depletion of the vascular pattern, expansion of the portal vein.
Liver cancer	Enlargement of the liver in size. The presence inside the liver of one or more large, focal formations that have an irregular shape and areas with increased and decreased echogenicity ( density).
Echinococcosis of the liver	Enlargement of the liver in size, deformation of its structure, the presence inside it of one or more spherical pathological formations with clear boundaries, smooth contours, anechoic structure inside and different sizes. On the periphery of these formations, fibrosis of the hepatic tissue adjacent to them is possible.
Liver sarcoidosis	Enlargement of the liver in size, significant deformation of its internal architectonics ( structures), diffuse fibrosis of her parenchyma, depletion of the vascular pattern, expansion of the portal vein. Also sometimes ascites is present ( accumulation of fluid in the abdomen) and splenomegaly ( enlargement of the spleen in size).
Liver amebiasis	Enlargement of the liver in size. In its parenchyma ( liver tissue), one or more pathological rounded formations ( abscesses) with fuzzy contours and different sizes that contain a liquid with gas bubbles.

For certain indications ( for example, enlargement of the liver and spleen of unclear etiology, conflicting laboratory results, etc.) patients with liver disease undergo a percutaneous liver biopsy ( insertion of a needle through the skin into the liver under local anesthesia), which allows you to take a piece of liver tissue from them for histological examination ( examining tissue under a microscope in a laboratory). Most often, liver biopsy is performed in order to confirm the presence of a malignant tumor in the liver, liver sarcoidosis in the patient, to establish the cause of hepatitis ( or cirrhosis), its stage, severity.

Diagnosis of blood diseases

In addition to yellowing of the tunica albuginea ( sclera) of the eyes and skin with blood diseases, an increase in the liver and spleen, fever, chills, general weakness, increased fatigue, shortness of breath, heart palpitations, dizziness, thrombosis may develop, nausea, vomiting, drowsiness, darkening of urine and feces, convulsions. In case of poisoning with hemolytic poisons, the clinical picture completely depends on the type of hemolytic poison, on the way it enters the body and concentration. Therefore, it is rather difficult to predict which symptoms the patient will have in such cases.

Anamnesis, in which doctors quite often establish them, provides important information for the diagnosis of blood diseases. possible reasons development. Anamnestic data are especially important in the diagnosis of malaria or babesiosis ( for example, the patient's stay in endemic foci of these infections), poisoning with hemolytic poisons ( work with toxic substances, the constant use of certain medical supplies and etc.). With hereditary pathologies ( erythrocyte membranopathies, erythrocyte enzymopathies, erythrocyte hemoglobinopathies, congenital autoimmune hemolytic anemias) jaundice of the sclera of the eyes in patients appears periodically, often from birth and is often associated with various provoking factors ( for example, exercise, medication, stress, alcohol consumption, hypothermia, etc.).

In a general blood test for blood diseases that cause yellowing of the eyes, a decrease in the number of erythrocytes and hemoglobin, an increase in ESR ( erythrocyte sedimentation rate), reticulocytosis ( an increase in the content of reticulocytes in the blood - young erythrocytes), thrombocytopenia ( decreased blood platelet count). Microscopy of blood products can reveal poikilocytosis ( change in the shape of red blood cells) and anisocytosis ( change in the size of red blood cells). For the diagnosis of malaria and babesiosis, a thick drop and thin smear method is used to identify the causative agents of these diseases inside the red blood cells.

In the biochemical analysis of blood in patients with blood diseases, an increase in the content of total bilirubin ( due to the fraction of indirect bilirubin), free hemoglobin, iron, increased activity of lactate dehydrogenase ( LDH), a decrease in the content of haptoglobin. With erythrocyte enzymopathies, a decrease in the concentration or complete absence of certain enzymes ( for example, glucose-6-phosphate dehydrogenase, pyruvate kinase, etc.) inside erythrocytes. In case of poisoning with hemolytic poisons, a toxicological study of the blood is carried out to identify in its plasma toxins that can damage erythrocytes.

Immunological blood tests for blood diseases are also equally important. It helps to detect antibodies against the causative agents of malaria and babesiosis, to identify autoantibodies to erythrocytes in autoimmune hemolytic anemias ( AIHA with warm hemolysins, AIHA with incomplete cold agglutinins, Fisher-Evans syndrome, etc.). Genetic research methods are mainly used in the diagnosis of congenital blood pathologies ( erythrocyte membranopathies, erythrocyte enzymopathies, erythrocyte hemoglobinopathies) that cause yellowing of the eyes. These methods help to establish the presence of defects in various genes encoding membrane proteins or enzymes of red blood cells. As an additional study in erythrocytic hemoglobinopathies, hemoglobin electrophoresis is performed ( oxygen-carrying protein in red blood cells). This study allows you to detect the presence of pathological forms of hemoglobin.

Enlargement of the spleen and liver in patients with blood disorders is confirmed by ultrasound or computed tomography... In some cases, they are given a puncture of the ilium or sternum to collect bone marrow. In the bone marrow, all the red blood cells that circulate in the blood are formed, so this study allows you to assess the state of the hematopoietic system and identify various disorders in the production of red blood cells.

Diagnosis of diseases of the biliary tract

For diseases of the biliary tract, yellowing of the sclera of the eyes and skin, skin itching, pain in the right hypochondrium, weight loss, fever, heaviness in the abdomen, flatulence, nausea, vomiting, general malaise, myalgia ( muscle pain), arthralgia ( joint pain), hepatomegaly ( enlarged liver), splenomegaly ( enlarged spleen), headache.

In the general analysis of blood in such patients, anemia is often found ( a decrease in the number of red blood cells and hemoglobin in the blood), leukocytosis ( ), increased ESR ( erythrocyte sedimentation rate), eosinophilia ( an increase in the number of eosinophils in the blood). The most common pathological changes in the biochemical analysis of blood in patients with diseases of the biliary tract are an increase in total bilirubin ( mainly due to direct bilirubin), bile acids, cholesterol, triglycerides, increased activity of alkaline phosphatase, alanine aminotransferase ( ALT), aspartate aminotransferase ( AST), gamma glutamyl transpeptidase.

Esophagogastroduodenoscopy ( EGDS) allows you to detect a tumor in the duodenum, assess the functional state of the Vater papilla ( the place in the wall of the duodenum where the common bile duct opens into it). Also, using this study, you can conduct a biopsy ( select a piece of pathological tissue for cytological examination) tumors of the duodenum. To assess the condition of the biliary and pancreatic ducts, endoscopic retrograde cholangiopancreatography is performed. With opisthorchiasis, primary sclerosing cholangitis, tumors of the organs of the biliopancreatoduodenal zone, these ducts are often damaged.

The main methods for diagnosing gallstone disease are cholecystography ( x-ray method for examining the gallbladder) and ultrasound examination. These methods most accurately detect the presence of stones in the gallbladder and blockage of the bile ducts. In addition, these two methods make it possible to assess the correct functioning of the gallbladder and biliary tract, their shape, structure, size, reveal the presence of a tumor in them, foreign bodies... Ultrasound examination is also often prescribed for patients with suspected pancreatic tumor, opisthorchiasis.

Computed tomography and magnetic resonance imaging are usually used in the diagnosis of tumors in the organs of the biliopancreatoduodenal zone ( extrahepatic bile ducts, gallbladder, pancreas and duodenum). These methods make it possible to accurately determine the presence of a tumor, its size, localization, stage of cancer, as well as to reveal the presence of various complications.

Diagnosis of pathologies associated with metabolic disorders in the body

The main symptoms of pathologies associated with metabolic disorders in the body are jaundice ( yellowing of eyes and skin), pain in the right hypochondrium, in the joints, weakness, lethargy, decreased ability to work, enlarged liver and spleen, nausea, vomiting, poor appetite, diarrhea, headache, dizziness, bleeding gums, nosebleeds, skin sensitivity disorders, convulsions, limb tremors , peripheral edema, slowdown mental development, psychosis. It is important to note the fact that with most of these pathologies ( amyloidosis, Wilson-Konovalov disease, hemochromatosis, Crigler-Najjar syndrome, Dabin-Johnson syndrome) not only the liver is affected, but also other organs ( brain, heart, kidneys, eyes, intestines, etc.). Therefore, the list of the above symptoms can be significantly expanded ( depending on the number of affected organs and the severity of their damage).

Since almost all pathologies associated with metabolic disorders in the body are hereditary ( with the exception of some forms of amyloidosis), then their first symptoms appear in early childhood or adolescence. Yellowing of the eyes is more often the first sign of Crigler-Nayyard syndrome, Dabin-Johnson syndrome, or Gilbert's disease than amyloidosis, hemochromatosis, and Wilson-Konovalov disease. Jaundice with these last three pathologies appears later. With pathologies associated with impaired bilirubin metabolism ( crigler-Nayard syndrome, Dabin-Johnson syndrome, Gilbert's disease), the eyes usually begin to turn yellow due to various provoking factors - fasting, stress, heavy physical exertion, drinking excessive amounts of alcohol, mechanical injuries, taking medications ( antibiotics, glucocorticoids, cytostatics, hormones, anticonvulsants, etc.), smoking. In hemochromatosis, Wilson-Konovalov's disease and amyloidosis, the yellowness of the sclera of the eyes is most often constant. Transmission of all hereditary diseases ( crigler-Nayyard syndrome, Dabin-Johnson syndrome, Gilbert's disease, amyloidosis, hemochromatosis, Wilson-Konovalov disease) comes from parents, so the presence of any genetic disease in one of them can serve as an important diagnostic feature. The doctor takes these features into account when collecting anamnesis ( questioning the patient).

In the general analysis of blood in patients with pathologies associated with impaired metabolic processes in the body, leukocytosis is most common ( an increase in the number of leukocytes in the blood), anemia ( a decrease in the number of red blood cells and hemoglobin in the blood), increased ESR ( erythrocyte sedimentation rate), lymphopenia ( a decrease in the number of lymphocytes in the blood), thrombocytopenia ( a decrease in the number of platelets in the blood), sometimes leukopenia ( a decrease in the number of leukocytes in the blood). A biochemical blood test in such patients can reveal a decrease in the amount of ceruloplasmin, cholesterol, an increase in the amount of copper, total bilirubin, globulins, glucose, an increase in the activity of aspartate aminotransferase ( AST), alanine aminotransferase ( ALT), alkaline phosphatase, gamma-glutamyl transpeptidase, a decrease in the amount of albumin, prothrombin index.

Based on the results of an ultrasound scan or computed tomography, one can only suspect liver damage in a patient. Therefore, to more accurately confirm the presence of pathologies associated with metabolic disorders, patients usually undergo a biopsy of it ( taking a piece of tissue for histological examination). Parallel to histological examination conduct genetic research, which is mainly used in the diagnosis of Crigler-Nayyard syndrome, Dabin-Johnson syndrome, Gilbert's disease and hemochromatosis. This study identifies mutations characteristic of these pathologies ( defects) in genes.

Diagnostics of the acute or chronic pancreatitis

The diagnosis of pancreatitis is made on the basis of complaints, certain data from instrumental and laboratory studies. The main symptoms of acute or chronic pancreatitis are severe pain in the middle of the abdomen, often of a shingles, nausea, vomiting, impaired appetite, belching, heartburn, diarrhea with steatorrhea ( fetid feces, mushy, sticky, oily), weight loss. In a general blood test, leukocytosis can be detected ( an increase in the number of leukocytes in the blood) and an increase in ESR ( erythrocyte sedimentation rate), in severe clinical cases anemia is possible ( decrease in the number of red blood cells and hemoglobin).

In the biochemical analysis of blood in such patients, an increase in the activity of certain enzymes ( alpha-amylase, lipase, elastase, trypsin), an increase in the concentration of total bilirubin, alkaline phosphatase, gamma-glutamyl transpeptidase, glucose, a decrease in albumin, calcium and an increase in the concentration of acute phase proteins ( C-reactive protein, orosomucoid, etc.). Instrumental methods research ( ultrasound, computed tomography) allow you to identify certain pathological changes in the pancreas ( proliferation of connective tissue, the presence of cysts, an increase in size, etc.), their localization and various complications ( including compression of the extrahepatic bile ducts), due to which these patients develop jaundice.

Treatment of pathologies leading to yellow eyes

In the vast majority of cases, yellowness in the eyes occurs as a result of one or another pathology digestive system (liver, pancreas, biliary tract). Therefore, when this symptom appears, it is better to seek help from a gastroenterologist. In some cases, yellowing of the eyes can be triggered by blood diseases, which are treated and diagnosed by a hematologist. If the patient does not have the opportunity to contact these highly specialized doctors, then you can simply go to an appointment with a family doctor or therapist. It is important to understand that in order to get rid of yellowness in the eyes, you need to choose the right treatment, which differs in different groups pathologies ( liver diseases, diseases of the biliary tract, blood diseases, pancreatitis, metabolic disorders).

Treatment of liver diseases

Treatment of liver diseases includes the use of conservative and surgical methods. Most often, conservative methods are used to treat patients with hepatitis, cirrhosis of the liver, Tsive's syndrome, amebiasis, and sarcoidosis of the liver. Surgical intervention is more often prescribed for patients with cancer, liver echinococcosis.

Qiwe syndrome
Complete abstinence from alcohol is considered the main treatment for Ziwe syndrome. Also, with this syndrome, hepatoprotective agents are prescribed that strengthen the wall of hepatocytes ( liver cells).

Cirrhosis of the liver
If cirrhosis of the liver occurs against the background of alcoholism, then such patients are prescribed ursodeoxycholic acid ( accelerates the outflow of bile from the liver and protects its cells from damage). With viral cirrhosis of the liver, patients are prescribed antiviral drugs. In autoimmune cirrhosis, immunosuppressants are prescribed, that is, drugs that reduce the activity of immune responses in the body. If cirrhosis appeared against the background of Wilson-Konovalov disease ( pathology associated with the accumulation of copper in tissues) or hemochromatosis ( a disease in which iron accumulates in tissues), then such patients are prescribed a special diet and detoxifying agents that form complexes with copper ( or iron) and remove it from the body through the kidneys with urine.

In primary sclerosing cholangitis, bile acid sequestrants are prescribed - drugs that bind bile acids. With cirrhosis of the liver caused by taking medications, treatment with these drugs is stopped. With Budd-Chiari disease ( pathology in which there is a blockage of the hepatic veins) patients are prescribed anticoagulants and thrombolytic agents. These drugs accelerate the resorption of blood clots in the liver tissues and improve venous outflow from the liver.

Liver cancer
Liver cancer is a rather serious disease that can be treated more effectively only in the very early stages. At later stages, this pathology is practically incurable. A variety of techniques are used to treat liver cancer, which may include surgical ( mechanical removal of a tumor, liver transplantation, cryodestruction, etc.), ray ( irradiation of a tumor with ionizing radiation, radioembolization, etc.) and chemical methods ( introduction of acetic acid, ethanol, etc. into the tumor.).

Liver sarcoidosis
Liver sarcoidosis is treated with immunosuppressants and cytostatics. These agents suppress immune responses in the body, reduce the formation of inflammatory granulomatous infiltrates, inhibit the multiplication of immune cells ( immune system cells) and the release of inflammatory cytokines ( substances that regulate the functioning of cells of the immune system). In severe cases, with liver failure, a new liver is transplanted.

Liver amebiasis
With amebiasis of the liver, amoebicides are prescribed ( medicines that destroy harmful amoeba). Most often they are metronidazole, emetine, tinidazole, ornidazole, etofamide, chloroquine. These drugs also have anti-inflammatory and antibacterial effects. With the formation of abscesses inside the liver, surgical treatment is also sometimes performed, which consists in draining its cavity and removing necrotic masses ( dead liver tissue).

Treatment of blood diseases

Diseases of the blood that cause yellowing of the eyes are most often treated conservatively. Some of them ( malaria, babesiosis, hemolytic poisoning) can be cured by prescribing etiotropic drugs to the patient that can eliminate the cause of the disease. Other pathologies ( erythrocyte membranopathies, erythrocyte enzymopathies, erythrocytic hemoglobinopathies, autoimmune hemolytic anemias) it is impossible to completely cure, therefore, symptomatic treatment is prescribed for such patients.

Malaria
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Treatment of diseases of the biliary tract

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Treatment of acute or chronic pancreatitis

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What pathologies are the most common yellow sclera of the eyes in newborns?

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Gilbert's disease

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