Why there may be yellow whites of the eyes: possible reasons. Yellow complexion: causes, what to do Yellow eyes disease

Yellowing of the eye membranes can be diagnosed using different methods:

  1. Clinical analysis of blood and urine.
  2. Performing an ultrasound of the suspected diseased organ.
  3. Conducting a CT scan of the abdominal organs.
  4. Carrying out immunological and genetic tests.

Depending on the form of the pathology, as well as on the body system that provoked the appearance of yellow eyes, individual research methods are prescribed.

Treatment

Treatment of yellows involves treating the organ or body system that caused the unpleasant symptom. Doctors recommend first getting rid of bad habits and change your diet. It is important to exclude flour, too salty/sweet, spicy and fried foods. Drinking alcohol is prohibited.

Diagnosis and treatment of yellow eyes

The treatment method is determined as follows:

  1. The patient comes to the clinic with a problem of yellow membranes of the eye.
  2. The doctor examines the eyes and gives instructions to go comprehensive study, refers to a specialist.
  3. Further, the treatment of yellow eyes depends on the disease, which will be confirmed through diagnostic measures.

Liver diseases– carry out conservative treatment. Also, if necessary, surgical intervention may be required. Pharmacotherapy often includes a number of groups of drugs that will help to have a comprehensive effect on a particular disease of the hepatobiliary system.

Blood diseases– often treated with conservative comprehensive treatment, however, some forms of pathologies cannot be completely cured.

Surgical treatment of most pathologies that cause yellow sclera

For blood diseases it is recommended to use:

  • etiotropic therapy (malaria, babesiosis, poisoning with hemolytic poisons);
  • antimalarials (malaria);
  • splenectomy (erythrocyte membranopathy);
  • transfusion of red blood cells (erythrocyte enzymopathy, erythrocyte hemoglobinopathy);
  • immunosuppressants and cytostatics (autoimmune hemolytic anemia);
  • antibiotics (babesiol).

Biliary tract diseases– symptomatic treatment is indicated to remove congestion in the biliary tract.

How to get rid of yellow eyes?

It is impossible to clear yellowness from your eyes on your own. To do this, it is necessary to identify exact reason symptom, and then undergo a course of treatment.

Why is the urine dark when the sclera is yellow?

This is due to the fact that direct bilirubin, which is also released into the blood when liver function is impaired, can not only accumulate in the mucous membranes and skin, but also penetrate into the urine. There it reacts and turns the urine dark.

Why do the whites of the eyes turn yellow after a high dose of alcohol?

Yellowing of the sclera after large doses of alcohol causes toxic hepatitis, in which the liver is able to repair itself over time. But its functionality is temporarily impaired, so all the bilirubin that circulates in the blood accumulates in the skin and sclera, turning them yellow.

What do high temperatures and yellow eyes mean?

As a rule, if a person has an elevated body temperature, they speak of inflammatory processes in the patient’s body. An increase in temperature is a signal of the beginning of the immune system’s fight against harmful microorganisms. Therefore, if a patient has yellow eyes and fever, they speak of infectious pathologies of the liver. Sometimes this happens due to gallstone disease or cancer.

Are there any eye drops for yellow sclera?

No, they don't exist. In order to get rid of the problem, you need to cure the underlying disease. Since yellow eyes are a sign of internal disease.

The color of your face has become unnatural, somehow yellow. You worry, you understand that something wrong is happening with your health. But what exactly could be the reason for such unpleasant metamorphoses with your appearance? Let's try to find the answer to this question together.

Perhaps your face has a yellowish tint because you have problems with your liver, which makes it difficult for you to remove the pigment bilirubin from your body. What liver diseases are we talking about specifically? About quite serious ones, namely:

    Various forms of hepatitis.

    Cholecystitis.

  1. Helminths (or simply worms).

In the presence of these diseases it is also common:

    The urine becomes very dark and the stool turns pale.

    Appetite is almost completely absent, weight decreases sharply.

    Often feels hot and cold (or, in other words, has a fever).

    Severe pain in the abdominal area.

If this is about you, don’t hide under the covers (you’re already an adult) and urgently run to take a blood test to check your bilirubin levels.

Bilirubin causes yellowing of the skin color and the white of the eye.

arrow_left Bilirubin causes yellowing of the skin color and the white of the eye.

Gallbladder and stones

Your face may also turn yellow because stones cause bile to “get stuck” in the gallbladder.

In addition to yellow skin color, with similar problem(called gallstones) often:

    Pain in the area of ​​the right hypochondrium.

    There is a strong heaviness in the stomach.

    I often feel nauseous (even when my stomach seems to be empty).

    Pronounced, noticeable bruises appear under the eyes, the color of which cannot be hidden by any foundation.

The thyroid gland helps break down the pigment beta-carotene. If for some reason she does not do this, beta-carotene begins to accumulate in the body (or rather, in subcutaneous fat), and the skin color on the face becomes yellowish-orange. Most often this happens when a person has hypothyroidism (deficiency of thyroid hormones).

Your face may turn yellow due to:

    Diseases of the pancreas (primarily pancreatitis).

    Heart and blood pressure problems.

    Diseases of the spleen.

    Various ailments of the gastrointestinal tract.

    Various oncological diseases. With such ailments, the face becomes “waxy” and acquires a cold yellow tint.




Thyroid hormone deficiency is the cause of an “orange” face

arrow_left Thyroid hormone deficiency is the cause of an “orange” face

Are you already panicking, are you going to the doctor? Calm down - maybe everything is not so dramatic, and your skin turned yellow simply because you:

    Big fan of freshly squeezed carrot juice, Korean salads and other carrot dishes.

    Every day you load up on carotene-rich fruits and vegetables (and this includes not only tangerines, oranges and other citrus fruits, but also broccoli, pumpkin and rose hips).

    You put too much vinegar and cumin in your food.

    You smoke too much.

    She has a big sweet tooth and can’t go a day without sweets, cakes and pastries.

    A confirmed night owl and coffee lover. Yes, yes - your skin may have turned yellow due to lack of sleep and caffeine addiction.

    Do you like to pump iron and go on starvation diets at the same time? The combination is not the most advantageous - it sometimes makes your face turn yellow.

    A fan of solariums and sunbathing. Don’t forget - everything should be in moderation, even the source of life - the sun.




Smoking is one of the common reasons yellowing of the skin

arrow_left Smoking is one of the common causes of yellowing of the skin

Removing yellowness with folk remedies

Has the yellowness of your face begun to negatively affect your mood, drive you into deep depression, and deprive you of your vitality? Then you definitely need to “whiten.” This can be done quite inexpensively using simple homemade masks.

Curd option

The mask is prepared literally instantly:

    Take one tablespoon of sour cream and 2 tablespoons of cottage cheese. You mix them.

    You apply the mask to your face for half an hour, and then wash it off with lukewarm water.

Apply the curd mask 2-3 times a week for a month, and the yellowness will be removed.

If the skin on your face has become not only yellow, but also oily, it is better to use yogurt rather than sour cream. Also, in this case, it won’t hurt to add one tablespoon of fresh cucumber (chopped, of course) to the mask.

Cucumber option

The mask recipe is elementary. Just cut the cucumber into small circles and apply it to your face.

But here is an alternative, more sophisticated option:

    Grind the cucumber using a grater.

    Squeeze out its juice and then mix it with olive oil.

    Add lemon pulp and apply the resulting mixture to your face for half an hour.

Carrot mask

Everything is very simple here:

    Mix 3 tablespoons of carrots (chopped, of course) with one tablespoon of sour cream.

    Add one teaspoon of vegetable oil to this mixture.

    Apply the mask and leave it on for 20-30 minutes.




Berry facial brighteners

Berries are not only an excellent whitener, they also cleanse the skin well and act as a kind of natural “peeling.”

Red berries (raspberries, viburnum, strawberries) will help you best:

    Moisten a piece of gauze in the juice of some red berry.

    You apply it to your yellowed face for a couple of minutes.

Here's an alternative recipe:

    Grind the red berries and squeeze the juice out of them.

    Apply the resulting puree to yellowed skin.

    Keep it on for 15-20 minutes and then rinse with warm running water.

    After this, apply some nourishing cream to your face.

Well, watch the video “How to lighten your skin and protect yourself from the sun”:

Eyes are a mirror of a person’s soul and at the same time his health. Yellowed whites usually do not cause discomfort, so they are often ignored. However, this condition indicates problems in the body, and sometimes serious diseases.

Only a doctor can determine exactly why the whites of the eyes turn yellow.

Why do the whites of the eyes turn yellow?

This phenomenon may be associated with a disease of the eyes themselves or internal organs.

2. Eye diseases and malignant formations are accompanied not only by changes in the color of the proteins, but also by redness and discomfort.

3. Excessive eye strain caused by lack of sleep, working at a computer, prolonged exposure to rooms with poor lighting and other factors is often accompanied by yellowing of the whites.

To find out the causes of the phenomenon, one examination by an ophthalmologist is not always enough - tests and additional examinations. It is almost impossible to independently determine what is causing this phenomenon.

What to do if the whites of your eyes turn yellow?

If a symptom appears, you should immediately consult a doctor for advice. It will help determine whether the yellowing of the eyes is due to increased bilirubin (therefore, health problems) or due to fatigue. Sometimes a change in the color of the whites of the eyes is caused by excessive consumption of foods that have a coloring effect (carrots, for example).

Until the true cause of yellowing eyes is determined, it is worth taking care of your body. First of all, you need to reduce the load to which the liver is exposed. To do this you will have to:

· stop drinking alcohol;

· limit flour products in the diet;

· exclude salty and spicy dishes from the menu.

It is important to provide your eyes with proper rest:

· take walks in the fresh air more often;

· Take constant breaks when working with a computer;

· get enough sleep.

The human eye is an organ whose proper functioning is important for health and happy life. Ignored alarming symptoms and advanced diseases lead to vision deterioration or loss, which is why it is so important to begin eliminating them in a timely manner.

Diagnosis is required even when yellowing of the eyes does not cause discomfort: the causes may be dangerous or not, but in any case they signal a problem and require attention.

Yellowing of the skin of the face and sclera of the eyes is an indicator of organic problems. Negative color changes in most cases are a sign that pathologies have appeared in the body associated with impaired absorption of nutrients, cardiovascular activity or liver disease.

The causes of yellowing of the skin and eye sclera may not depend on the state of health. Change in body color is caused by orange or carrot diet, taking certain medications, and impaired removal of bilirubin from the body.

Bilirubin is an organic pigment formed during the breakdown of the protein substance in hemoglobin; it is contained in red blood cells - blood particles that perform a transport function. As bilirubin accumulates, a gradual yellowing of the skin and whites of the eyes begins to be noticed. Accumulation of bilirubin is associated with liver disease.

Yellow skin - what are the reasons?

If we consider the reasons explaining why the skin and whites of the eyes have turned yellow, then liver diseases are in first place among the factors causing negative changes.

This condition occurs when the liver parenchyma is damaged or when there is increased hemolysis of red blood cells - erythrocytes. The consequence of organic disorders is a decrease or blocking of bile secretion.

The causes of liver dysfunction are:

  • infectious diseases - hepatitis of various etiologies, malaria, hemolytic anemia;
  • alcoholism;
  • drug use;
  • gallbladder disease.

Negative changes are not limited to yellowing of the whites of the eyes and body color.

Symptoms of diseases:

  • rapid fatigue after physical activity;
  • low-grade fever;
  • darkening of urine and the appearance of whitish stools;
  • nausea;
  • dizziness;

The second reason explaining why the skin turns yellow and the sclera of the eyes darken is disruption of the thyroid gland. It is she who produces substances that are responsible for the digestibility of beta-carotene. In this case, the whites of the eyes first turn yellow, and only then other symptoms associated with the general condition appear.

General change appearance It begins with the eyes - the whites and irises, then the eyelids and face darken, and only then the pigmentation spreads throughout the body.

There is no need to look for diseases in your own body if you adhere to a mono-diet - carrot, pumpkin or orange. When suddenly switching to foods containing beta-carotene in excess, the body does not have time to adapt. The result is a change in pigmentation and a chicken-like skin tone.

Causes yellowness:

  • smoking - in this case, the change in pigmentation begins from the fingertips, and then the whites of the eyes are involved;
  • frequent depression and increased physical activity - the liver reacts with functional disorders, digestive and metabolic processes in the intestines are upset, and intoxication of the body begins;
  • eating disorders - problems with the gallbladder appear;
  • skin care using masks made from turmeric, cumin, carrots and sea buckthorn oil.

The latter cause does not cause changes in the pigmentation of the eyelids and whites of the eyes.

A person rarely notices yellowing of the skin himself - if the condition is not accompanied by painful symptoms - mainly those around him point out negative changes in appearance.

You should not try to solve the problem on your own - you should definitely consult a doctor. Diagnosis and treatment are prescribed only after full examination body - you will have to donate blood and urine for general and specific tests, undergo special examinations.

Even if the skin turns yellow and the whites of the eyes change color due to malnutrition, this indicates temporary liver dysfunction. Without medical recommendations eliminate cosmetic defect It will be difficult even if you switch to a regular diet.

Infant jaundice

Newborns often have yellow skin in the first days after birth. The eye sclera in this case is also not bluish, as usual in infants, but has a sandy tint. Jaundice in newborns in most cases is physiological in nature and dangerous disease– such as adult hepatitis – is not. It is explained by the newborn’s adaptation to extrauterine life.

The liver does not yet produce a sufficient amount of enzymes to remove bilirubin, or the simultaneous breakdown of a large number of red blood cells has occurred, without which the fetus would not survive in the mother’s body.

The baby’s body usually copes with adaptation on its own - pigmentation is restored 3-10 days after birth.

Physiological jaundice negative symptoms not accompanied by:

  • the child is not capricious;
  • eats well;
  • physiological development is not impaired.

If parents notice a deterioration in health and the yellowness of the body does not go away by the 10th day of life, pathological jaundice can be suspected. In this case, you need to consult a doctor - pathological jaundice can be caused by congenital pathologies or genetic factors, acquired diseases... Pathological jaundice is treated using medications– in some cases, surgical intervention is necessary.

Yellowness of the skin and its treatment in adults

If changes in the pigmentation of the eye sclera and body color are associated with a health condition, self-medication is dangerous. In this case, you need to put yourself in your hands official medicine and strictly follow the instructions received.

Hepatitis of all types, thyroid diseases, oncological processes, diseases associated with the excretion of bilirubin and the absorption of nutrients are a direct threat to health, and sometimes life. If the doctor insists on giving up bad habits, the recommendations should be followed immediately.

When the yellowness is mild, organic reasons for changes in pigmentation have not been identified - they are associated with disruption of the usual lifestyle, accumulated stress and fatigue, unfavorable environmental situation– you should pay attention to your daily routine.

To return a healthy skin color in a short time, it is advisable to get rid of bad habits, balance rest and physical activity, try to avoid stress factors, and pay more attention to facial and body care.

Homemade masks made from the following products effectively whiten your skin:

  • cucumber;
  • parsley;
  • lemon;
  • cottage cheese;
  • sour cream;
  • chamomile oil.

If possible, it is advisable to visit a cosmetology salon - salon treatments will help you cope with pigmentation changes faster.

At the first symptom of ailments against the background of yellowing of the sclera of the eyes, it is necessary to consult a doctor without waiting for changes in body pigmentation to appear. This sign indicates serious organic disorders.

In the very central part of the eye you can see a dark point - the pupil ( through it light penetrates into the eyeball), on 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 edge, you will notice that it sharply 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 layer of the eye. The white layer of the eye is also called the sclera. This membrane occupies five-sixths of the entire surface area of ​​the outer membrane of the eye. The sclera of the eye has White color (in fact, that’s why it’s 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 membranes of the eye

The human visual organ consists of the eyeball, extraocular muscles, eyelids, lacrimal apparatus, blood vessels and nerves. This organ is a peripheral part visual analyzer and is necessary for visual perception of external objects. The main structure in the organ of vision is the eyeball. It is located in the orbit and has an irregular spherical shape. Visually, on a person’s face, you can only see anterior section 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 depths of the orbit.

There are three main membranes in the eyeball:

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

Outer lining 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 ​​the eye. The cornea of ​​the eye is located in the front central part of the eyeball. Due to the absence of blood vessels and the homogeneity of its tissue, the cornea is transparent, so the pupil and iris of the eye can be seen through it.

The cornea consists of the following layers:

  • anterior stratified squamous epithelium;
  • anterior limiting membrane;
  • own substance of the cornea ( consists of homogeneous connective tissue plates and flat cells, which are a type of fibroblasts);
  • posterior limiting membrane ( Descemet's membrane), which mainly consists of collagen fibers;
  • posterior epithelium, which is represented by endothelium.
Due to its transparency, the cornea easily transmits light rays. It also has the ability to refract light, as a result of which this structure is also referred to as the light refractive apparatus of the eye ( along with the lens, vitreous, fluids of the chambers of the eye). In addition, the cornea performs a protective function and protects the eye from various traumatic effects.

The cornea of ​​the eye is the most convex part of the eyeball. Along the periphery, the cornea of ​​the eye smoothly passes into the sclera of the eyeball, which is the second important department outer shell of the eye. This section occupies most of the area of ​​the outer shell of the eye. The sclera of the eye is represented by dense fibrous 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 endothelium. Conjunctiva ( conjunctiva) is a relatively thin membrane that consists of columnar stratified epithelium. This membrane covers the eyelids from the inside ( secular part of the conjunctiva) and the eyeball outside ( ocular part of the conjunctiva). Moreover, the cornea this structure does not cover.

The outer layer of the eyeball performs a number of important functions. Firstly, it is the strongest compared to the other two membranes of the eyeball, as a result of which its presence helps protect the organ of vision from traumatic damage. Secondly, the outer shell of the eye, due to its strength, helps maintain the eyeball a certain anatomical shape. Thirdly, the extraocular muscles are attached to this membrane, as a result of which the eyeball can make various movements in the orbit.

Middle layer of the eyeball

The middle layer of the eyeball is located inside the eye. It consists of three parts of unequal size ( back, middle and front). Of all the parts of the middle shell, only the iris can be visually seen ( 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) is not adjacent 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 separates the lens from each other ( a transparent structure located directly opposite the pupil inside the eyeball and is a biological lens) and iris. This chamber is also filled with intraocular fluid.

The posterior part of the middle layer of the eyeball is called the uvea propria. It is located directly under the white membrane of the eye in the back part. It consists of 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 lining of the eyeball) eyes. The posterior part of the tunica media covers almost two-thirds of the entire area of ​​the sclera, and is therefore the largest of all three parts of the tunica media.

A little in front of her ( posterior part of the middle shell), in the form of a ring, the ciliary body ( middle part middle layer of the eyeball), represented by the ciliary muscle, which plays important role in accommodation of the eye ( it regulates the curvature of the lens and fixes it in a certain position). Also included in the ciliary ( ciliary) bodies are included special epithelial cells, which are involved in the production of intraocular fluid that fills the anterior and posterior chambers of the eye.

Inner lining of the eyeball

The inner lining of the eyeball ( or retina) envelops the iris, ciliary body and the choroid of the eyeball from the inside. The set of places where the retina is adjacent to the iris and the ciliary body is called non-visual ( blind) part of the retina. The remaining, posterior, larger part of the retina is called visual. This part of the retina perceives light entering the eyeball. 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 ( protein that carries oxygen in the blood), myoglobin ( protein that carries oxygen in muscles) and cytochromes ( enzymes of the cell respiratory chain). 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 neutralized as quickly as possible. Neutralization of indirect bilirubin occurs only in the liver. This type of bilirubin is not excreted through the kidneys.

In liver cells, indirect bilirubin binds to glucuronic acid ( chemical needed to neutralize bilirubin), and it is converted into direct bilirubin ( neutralized bilirubin). Next, direct bilirubin is transported by liver cells into bile, through which it is excreted from the body. In some cases, some of it may be absorbed back into the blood. Therefore, two main fractions of bilirubin are always present in the blood - direct bilirubin and indirect bilirubin. These two fractions together make up the total bilirubin in the blood. Indirect bilirubin accounts for about 75% of 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) into peripheral tissues and stains them yellow. There are three degrees of severity of jaundice ( that is, the severity of jaundice). At mild degree the concentration of total bilirubin in the blood reaches 86 µmol/l. With an average degree, the patient’s blood level of bilirubin ranges from 87 to 159 µmol/l. With severe severity, its concentration in the blood plasma is above 159 µmol/l.

Causes of yellowing of the sclera of the eyes

All of these factors ( viruses, bacteria, etc.) cause damage to liver cells, resulting in their gradual destruction, which is accompanied by the appearance of inflammation in the liver. This is accompanied by a violation of its full function and loss of the ability to neutralize indirect bilirubin coming from the blood to the liver for processing. In addition, with hepatitis, direct bilirubin also accumulates in the blood ( since the liver cells are destroyed, and it is released from 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 liver damage, yellowing of the skin and tunica albuginea occurs ( sclera) eye.

Ziewe syndrome

Ziewe 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 ( decrease in the content of hemoglobin and red blood cells in the blood as a result of the destruction of the latter), hyperbilirubinemia ( increase in bilirubin levels in the blood) and hyperlipidemia ( increased content blood fats). This syndrome is observed in people who abuse alcohol. The yellowing of the white of the eyes in Zieve syndrome is caused by an increase in bilirubin levels ( mainly due to indirect) in the blood, due to the destruction of red blood cells and liver dysfunction. In most cases, such patients develop fatty liver disease ( dystrophy) liver, that is, pathological deposition 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 normal liver tissue, as a result of which the liver begins to function poorly. It loses its 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, white membrane of the eyes, 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, the hydatid cyst begins to gradually increase in size and put pressure on the surrounding liver tissue, causing them to die ( atrophy of the liver parenchyma). As a result, mechanical replacement of normal liver tissue occurs, in place of which a cyst appears. At a certain point, when the cyst reaches a large size, the liver loses the ability to bind and neutralize indirect bilirubin in the blood, as a result of which it accumulates first in it, and then in the skin and in the white of the eyes, giving them a characteristic yellow color.

Sarcoidosis of the liver

Sarcoidosis is a chronic disease in which 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 diseases ( 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 where such antigens are localized, cells of the immune system begin to accumulate, resulting in small foci of inflammation. These lesions visually look like nodules ( or granulomas), different from normal tissues. Granulomas can have different sizes and locations. Inside such lesions, immune system cells tend to 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 existing granulomas and the emergence of new pathological foci in various organs disrupts their normal architecture ( structure) and work. Organs gradually lose their functions due to the fact that granulomatous infiltrates replace their normal parenchyma ( textile). If, for example, sarcoidosis affects the lungs ( and they are most often damaged by this disease), then the patient experiences a cough, shortness of breath, chest pain, and excessive fatigue due to lack of air. If the liver is damaged, then, first of all, its detoxifying and protein-synthetic functions are disrupted ( 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. Hepatitis occurs first 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 can form inside the liver ( cavities filled with pus). There can be a large number of such abscesses. In the absence of treatment, liver amebiasis disrupts its various functions, including the neutralization of bilirubin in the blood ( indirect bilirubin).

These merozoites then enter the bloodstream and invade red blood cells and begin to divide there again ( erythrocyte schizogony). At the end of erythrocyte schizogony, the infected erythrocytes are completely destroyed and release large numbers of multiplied merozoites, which re-enter new erythrocytes to reproduce. Thus, this process occurs cyclically. Each new destruction of erythrocytes is accompanied by the release into the blood of not only new populations of malarial merozoites, but also the rest of the erythrocyte contents and, in particular, the protein - hemoglobin. The breakdown of this protein produces bilirubin ( indirect), which must be neutralized in the liver.

The problem is that with 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 ( increase in blood bilirubin levels) and jaundice ( yellowing of the skin and sclera of the eyes), which occurs due to partial precipitation of bilirubin in tissues.

Erythrocyte membranopathies

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

The most well-known erythrocyte membranopathies are Minkowski-Choffard disease, hereditary elliptocytosis, hereditary stomatocytosis, hereditary acanthocytosis, and hereditary pyropoikilocytosis. All these pathologies are characterized by a triad 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 erythrocyte membranopathies, frequent destruction of defective red blood cells occurs in the blood, which is accompanied by the release of large amounts of hemoglobin, which is then converted into indirect bilirubin. The liver cannot immediately process large amounts of indirect bilirubin and remove it from the blood. Therefore, this metabolite ( product of exchange) 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 in red blood cells is disrupted ( proteins that accelerate biochemical reactions), controlling the course of metabolic reactions ( exchange reactions). This leads to inferior energy metabolism, accumulation of intermediate reaction products and energy deficiency in the red blood cells themselves. Under conditions of energy deficiency in red blood cells, the transport of various substances through their membrane slows down, which contributes to their wrinkling and destruction. There are also certain erythrocyte membranopathies in which there may be a deficiency of red blood cell antioxidant enzymes ( for example, pentose phosphate cycle, glutathione system), which often leads to a decrease in their resistance to oxygen free radicals and rapid destruction.

In any case, enzyme deficiency in erythrocyte enzymopathies leads to a decrease in the life expectancy of erythrocytes and their rapid death, which is accompanied by the release of large amounts of hemoglobin into the blood and the appearance of hemolytic anemia ( a pathology in which there is a deficiency of red blood cells and hemoglobin in the blood resulting from the destruction of red blood cells) 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.

Erythrocyte hemoglobinopathies

Erythrocyte 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, red blood cells contain abnormal hemoglobin, which does not perform its function well ( oxygen transfer), and the red blood cells themselves lose strength and shape, as a result of which they quickly undergo lysis ( destruction) and have a short lifespan in the blood.

Therefore, patients with one of these diseases often have hemolytic anemia ( decrease in the level of red blood cells in the blood due to their destruction), jaundice and oxygen deficiency ( due to disruption of oxygen transport by hemoglobin). The occurrence of jaundice can be explained by the fact that with erythrocyte hemoglobinopathies there is a significant release of pathological hemoglobin into the blood from decaying red blood cells. This hemoglobin subsequently undergoes breakdown and turns into indirect bilirubin. Since in these pathologies a large number of red blood cells are destroyed, 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 white of the eyes, they turn yellow. Yellowing of the whites of the eyes and skin is called jaundice.

Autoimmune hemolytic anemias

Autoimmune hemolytic anemia is a group of pathologies in which red blood cells are damaged due to their binding to autoimmune ( pathological) antibodies ( protective protein molecules that circulate in the blood and are directed against the body's own cells). These antibodies begin to be synthesized by cells of the immune system when it is disrupted. proper operation, which may be caused by genetic defects in immunocytes ( cells of the immune system). Immune system dysfunction can also be caused by external factors environment (for example, viruses, bacteria, toxins, ionizing radiation and etc.).

When tying normal red blood cells with autoimmune ( pathological) antibodies destroy them ( hemolysis). Destruction large number red blood cells leads to hemolytic anemia ( that is, a decrease in red blood cells due to their sudden intravascular destruction). This anemia is completely called autoimmune hemolytic anemia ( AIGA). Depending on the type of autoimmune antibodies that cause destruction of red blood cells 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 increased release of hemoglobin from damaged red blood cells). Precipitated in the tissues, this chemical metabolite causes them to turn yellow, so with these pathologies, patients often have yellow skin and sclera.

Babesiosis

Babesiosis is an infectious disease that occurs as a result of 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). The disease mainly affects people who are constantly in contact with pets and have a fairly pronounced immunodeficiency ( 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 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.). That's why most of Poisoning with hemolytic poisons occurs among workers of industrial enterprises who are constantly in contact with these toxic substances.

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

Thus, during poisoning with hemolytic poisons, massive destruction of red blood cells inside the vessels occurs due to various mechanisms. This is accompanied by the release of a large amount of hemoglobin into the blood, 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 yellowing of the eyes.

Biliary tract diseases as a cause of yellowing of the whites of the eyes

Bile is biological fluid yellow-brown in color, which is produced in the liver and secreted into the duodenum. Bile plays an important role in digestive processes, occurring in the intestines. Also, along with bile, various harmful substances are excreted, 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). With diseases of these pathways, it becomes difficult to transport bile to 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 ruptures, and part of the bile enters the blood. Therefore, for diseases of the biliary tract ( primary sclerosing cholangitis, cholelithiasis, tumors of the organs of the biliopancreatoduodenal zone, opisthorchiasis) the level of direct bilirubin in the blood increases and jaundice is observed.

Primary sclerosing cholangitis

Primary sclerosing cholangitis is a disease of unknown origin 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, become rough and deformed. As the disease progresses, the lumen of the affected biliary tract is completely obliterated ( closes). Such pathways become completely non-functional; bile does not move through them from the liver to the duodenum. The more such ducts are affected, the more difficult it is for bile to be transported 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 bile contains direct bilirubin, it gradually accumulates in the skin and sclera of the eyes, causing them to turn yellow.

Cholelithiasis

Gallstone disease is a pathology in which stones appear in the gallbladder or bile ducts. The reason for its occurrence is a violation of the ratio of substances ( cholesterol, bilirubin, bile acids) in bile. In such cases, some substances ( for example cholesterol) becomes larger than all the others. The bile becomes oversaturated with them, and they precipitate. The sediment particles gradually stick together and overlap each other, 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 endocrine system (diabetes mellitus, hypothyroidism), obesity, poor nutrition (excessive consumption of fatty foods), pregnancy, certain medications ( estrogens, clofibrate, etc.), liver diseases ( hepatitis, liver cirrhosis, liver cancer), hemolytic anemia ( pathology associated with a decrease in the number of red blood cells in the blood due to their destruction).

Stones formed during cholelithiasis may be located in the so-called blind spots in the biliary system ( for example, in the body or bottom 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 parts of the biliary system located above the obstruction. This leads to increased pressure in the bile ducts. Under such conditions, the intrahepatic bile ducts inside the liver are destroyed, and bile goes directly into the blood.

Due to the fact that bile contains a large amount of bilirubin ( direct), then its concentration increases in the blood. Moreover, such an increase is always proportional to the duration of 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 colors them yellow.

Tumors of organs of the biliopancreatoduodenal zone

The organs of the biliopancreaticoduodenal zone include the extrahepatic bile ducts, gallbladder, pancreas and duodenum. These organs are located very close to each other in the upper floor of the abdominal cavity. In addition, they are functionally interconnected, so tumors of all these organs have similar symptoms. With tumors of the organs of the biliopancreaticoduodenal zone, yellowing of the skin and sclera of the eyes is very often observed. 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 bile stagnates in them, can rupture, as a result of which it penetrates into the blood. Bilirubin ( straight), which is part of it, gradually accumulates in the skin and white of the eyes and colors them yellow.


Crigler-Najjar syndrome

Crigler-Najjar syndrome is a hereditary liver disease in which there is a defect in the gene encoding the amino acid sequence of the enzyme ( uridine 5-diphosphate glucuronyl transferase) liver cells involved in the neutralization and binding of indirect bilirubin with glucuronic acid inside hepatocytes ( liver cells). As a result of this defect, the removal of indirect bilirubin from the blood is impaired. It accumulates in the blood, and then in the skin and sclera of the eyes, causing them to turn yellow.

There are two types of Crigler-Najjar syndrome. The first type is characterized by severe clinical symptoms and severe jaundice. With it, the liver cells completely lack the enzyme ( uridine 5-diphosphate glucuronyltransferase), binding indirect bilirubin. This type of Crigler-Nayjar syndrome usually causes death in 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 significantly lower. With this type clinical symptoms is also quite pronounced, but the survival rate in such patients is much higher. Clinical symptoms appear in patients with the second type of Crigler-Nayjar 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). Exacerbations in patients with Crigler-Najjar syndrome are observed much more often than in patients with Gilbert's disease.

Dubin-Johnson syndrome

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

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

Amyloidosis

Amyloidosis – systemic disease, as a result of which in various organs ( kidneys, heart, esophagus, liver, intestines, spleen, etc.) an abnormal protein – amyloid – accumulates. The cause of amyloid is a disorder of protein metabolism in the body. There are acquired ( for example, ASC1 amyloidosis, AA amyloidosis, AH amyloidosis, etc.) and hereditary ( AL amyloidosis) forms of this pathology. Chemical structure amyloid and its origin depend on the form of amyloidosis. For example, in AL amyloidosis, the amyloid consists of accumulations 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 promotes 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 whites of the eyes) can be observed in both acute and chronic pancreatitis.

Diagnosis of the causes of yellow eyes

To diagnose the causes of yellow eyes can be used different kinds research ( clinical, radiation, laboratory). The main clinical diagnostic methods are taking anamnesis ( clarification of the entire history of the development of the disease) in the patient and his examination. Of the radiological research methods, 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 diagnosing yellowness of the eyes, various types of blood tests are also used ( complete blood count, biochemical blood test, immunological and genetic tests, toxicological blood test), stool tests 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, loss of 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 experience additional signs. For example, with liver echinococcosis, various allergic reactions on the skin are often observed ( skin rashes, itching, redness of the skin, etc.). With liver sarcoidosis, pain may occur in the chest, joints, muscles, shortness of breath, cough, hoarseness, increase in the size of peripheral lymph nodes (inguinal, occipital, elbow, cervical, axillary, etc.), arthritis ( joint inflammation), deterioration of visual acuity, etc.

In patients with liver amoebiasis pain syndrome often begins in the central part of the abdomen, which is associated with the preliminary entry of harmful microorganisms into the intestines. In addition, they experience diarrhea with blood and mucus, false urges, dehydration of the body, and hypovitaminosis. Patients with liver cirrhosis often experience nosebleeds, bleeding gums, skin itching, palmar erythema ( small red rash on the palms of the hands), gynecomastia ( increase in the size of the mammary glands in men), spider veins on the skin, swelling.

In addition to the symptoms in patients with liver diseases, it is important to qualitatively collect anamnestic data that the doctor receives during the questioning of 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), Zieve syndrome, liver amoebiasis, liver echinococcosis. So, for example, if a patient, in a conversation with a doctor, mentions that before the symptoms of the disease appeared, he had been using certain types of drugs for a long time ( paracetamol, tetracycline, aminazine, methotrexate, diclofenac, ibuprofen, nimesulide, etc.), which may adversely affect liver function, the doctor concludes that possible pathology The reason the patient came to him was drug-induced hepatitis.

The most common changes in general analysis blood in patients with liver disease are anemia ( ), leukocytosis ( increase in the number of leukocytes in the blood), increase in ESR ( ), thrombocytopenia ( decrease in the number of platelets in the blood), sometimes leukopenia ( ) and lymphopenia ( ). With echinococcosis and sarcoidosis of the liver, eosinophilia is possible ( increase in the number of eosinophils in the blood). It is worth noting that based on the results of a general blood test, a definitive diagnosis of any specific liver disease cannot be made.

IN biochemical analysis In the blood of patients with liver diseases, an increase in the content of total bilirubin, cholesterol, bile acids, globulins, and 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. Hypercalcemia may occur in sarcoidosis ( increase in blood calcium levels) and increase in ACE ( angiotensin converting enzyme).

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

In some cases, patients with infectious diseases liver ( for example, with viral hepatitis, amoebiasis, cytomegalovirus infection, etc.) PCR is prescribed ( polymerase chain reaction) is one of the laboratory diagnostic methods that allows you to identify DNA particles ( genetic material) harmful pathogens in the blood. Some of the most important methods for diagnosing liver diseases are radiation methods research – ultrasound examination ( Ultrasound) And CT scan (CT).

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

Name of pathology Characteristic pathological changes for this pathology
Hepatitis Increased liver size, heterogeneity of the internal structure of the liver, decreased echogenicity ( density) its parenchyma, depletion of the vascular pattern.
Ziewe syndrome The same as for hepatitis.
Cirrhosis of the liver Enlarged liver and spleen, possible presence of ascites ( ). The liver has an uneven, nodular surface. Directly inside the liver, a significant disruption 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. The presence inside the liver of one or more large, focal formations that have irregular shape and areas with increased and decreased echogenicity ( density).
Liver echinococcosis An increase in the size of the liver, deformation of its structure, the presence inside it of one or more spherical pathological formations that have clear boundaries, smooth contours, an anechoic structure inside and different sizes. Along the periphery of these formations, fibrosis of the adjacent liver tissue is possible.
Sarcoidosis of the liver Enlargement of the liver, significant deformation of its internal architecture ( structures), diffuse fibrosis of its parenchyma, depletion of the vascular pattern, expansion of the portal vein. Ascites is also sometimes present ( accumulation of fluid in the abdominal cavity) and splenomegaly ( enlargement of the spleen).
Amebiasis of the liver Enlargement of the liver. In its parenchyma ( liver tissue) one or more pathological round formations can be identified ( abscesses) with unclear contours and different sizes which contain liquid with gas bubbles.

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

Diagnosis of blood diseases

In addition to yellowing of the tunica albuginea ( sclera) eyes and skin in case of blood diseases, enlargement of the liver and spleen, fever, chills, general weakness, increased fatigue, shortness of breath, rapid heartbeat, dizziness, possible development of thrombosis, nausea, vomiting, drowsiness, darkening of urine and feces, convulsions may also be observed. In case of poisoning with hemolytic poisons, the clinical picture depends entirely on the type of hemolytic poison, the route of its entry into the body and its concentration. Therefore, it is quite difficult to predict exactly what symptoms the patient will have in such cases.

Important information for diagnosing blood diseases is provided by taking an anamnesis, in which doctors quite often establish them possible reasons development. Anamnestic data are especially important when diagnosing malaria or babesiosis ( for example, the patient’s stay in endemic areas of these infections), poisoning with hemolytic poisons ( working with toxic substances, constant use of certain medications, etc.). At hereditary pathologies (erythrocyte membranopathies, erythrocyte enzymopathies, erythrocyte hemoglobinopathies, congenital autoimmune hemolytic anemias) yellowness of the sclera of the eyes appears periodically in patients, often from birth and is often associated with various provoking factors ( for example, physical activity, taking medications, stress, drinking alcohol, hypothermia, etc.).

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

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

Immunological blood testing for blood diseases is also equally important. It helps to detect antibodies against pathogens of malaria and babesiosis, to identify autoantibodies to red blood cells in autoimmune hemolytic anemia ( AIHA with warm hemolysins, AIHA with incomplete cold agglutinins, Fisher-Evans syndrome, etc.). Genetic research methods are mainly used in diagnostics congenital pathologies blood ( erythrocyte membranopathies, erythrocyte enzymopathies, erythrocyte hemoglobinopathies), which cause yellowing of the eyes. These methods help determine the presence of defects in various genes encoding membrane proteins or red blood cell enzymes. As additional research for erythrocyte hemoglobinopathies, hemoglobin electrophoresis is performed ( protein that carries oxygen 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 diseases is confirmed using ultrasound or computed tomography. In some cases, they are prescribed a puncture of the ilium or sternum to collect bone marrow. The formation of all red blood cells that circulate in the blood occurs in the bone marrow, so this study allows us to assess the state of the hematopoietic system and identify various disorders in the production of red blood cells.

Diagnosis of biliary tract diseases

Diseases of the biliary tract are characterized by yellowing of the sclera of the eyes and 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 ( liver enlargement), splenomegaly ( enlarged spleen), headache.

A general blood test often reveals anemia in such patients ( decrease in the number of red blood cells and hemoglobin in the blood), leukocytosis ( ), increase in ESR ( erythrocyte sedimentation rate), eosinophilia ( increase in the number of eosinophils in the blood). The most common pathological changes in biochemical blood tests in patients with biliary tract diseases 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, evaluate functional state Vater's papilla ( space in the wall duodenum where the common bile duct opens into it). This test can also be used to perform a biopsy ( select a piece of pathological tissue for cytological examination) tumors of the duodenum. To assess the condition of the bile ducts and pancreas, 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 cholelithiasis are cholecystography ( x-ray method gallbladder studies) 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 allow you to evaluate the correct functioning of the gallbladder and biliary tract, their shape, structure, size, and identify the presence of a tumor in them, foreign bodies. Ultrasound examination is also often prescribed to patients with suspected pancreatic tumors or opisthorchiasis.

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

Diagnosis of pathologies associated with metabolic disorders in the body

The main symptoms of pathologies associated with the disorder metabolic processes in the body are jaundice ( yellowing of eyes and skin), pain in the right hypochondrium, 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, tremors of the limbs , peripheral edema, mental retardation, psychosis. It is important to note the fact that in most of these pathologies ( amyloidosis, Wilson-Konovalov disease, hemochromatosis, Crigler-Najjar syndrome, Dabin-Johnson syndrome) affects not only the liver, but also other organs ( brain, heart, kidneys, eyes, intestines, etc.). Therefore, the list of the above symptoms can expand significantly ( 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 ( except for some forms of amyloidosis), their first symptoms appear in early childhood or adolescence. Yellowing of the eyes is more often the first sign of Crigler-Nayjar syndrome, Dubin-Johnson syndrome or Gilbert's disease than amyloidosis, hemochromatosis and Wilson-Konovalov disease. Jaundice in these last three pathologies appears later. For pathologies associated with impaired bilirubin metabolism ( Crigler-Najjar syndrome, Dubin-Johnson syndrome, Gilbert's disease), the eyes usually begin to turn yellow due to various provoking factors - fasting, stress, severe physical activity, drinking excessive amounts of alcohol, mechanical injuries, taking medications ( antibiotics, glucocorticoids, cytostatics, hormones, anticonvulsants, etc.), smoking. With hemochromatosis, Wilson-Konovalov disease and amyloidosis, the yellowness of the sclera of the eyes is most often constant. Transmission of all hereditary diseases ( Crigler-Nayjar syndrome, Dubin-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 sign. The doctor takes these features into account when collecting anamnesis ( questioning the patient).

In a general blood test in patients with pathologies associated with metabolic disorders in the body, leukocytosis is the most common ( increase in the number of leukocytes in the blood), anemia ( decrease in the number of red blood cells and hemoglobin in the blood), increase in ESR ( erythrocyte sedimentation rate), lymphopenia ( decrease in the number of lymphocytes in the blood), thrombocytopenia ( decrease in the number of platelets in the blood), sometimes leukopenia ( 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, and an increase in the activity of aspartate aminotransferase ( AST), alanine aminotransferase ( ALT), alkaline phosphatase, gamma-glutamyl transpeptidase, decrease in the amount of albumin, prothrombin index.

Based on the results of an ultrasound 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 ( taking a piece of tissue for histological examination). In parallel with histological examination carry out genetic research, which is mainly used in the diagnosis of Crigler-Nayjar syndrome, Dubin-Johnson syndrome, Gilbert's disease and hemochromatosis. This study identifies mutations characteristic of these pathologies ( defects) in genes.

Diagnosis of 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 girdling nature, nausea, vomiting, loss of appetite, belching, heartburn, diarrhea with steatorrhea ( feces are foul-smelling, mushy, sticky, with a greasy sheen), weight loss. A general blood test can reveal leukocytosis ( increase in the number of leukocytes in the blood) and increase in ESR ( erythrocyte sedimentation rate), in severe clinical cases anemia is possible ( decrease in the number of red blood cells and hemoglobin).

In a biochemical blood test in such patients, an increase in the activity of certain enzymes can be detected ( 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 research methods ( ultrasound, computed tomography) make it possible to identify certain pathological changes in the pancreas ( proliferation of connective tissue, presence of cysts, increase in size, etc.), their localization and various complications ( including compression of the extrahepatic bile ducts), which causes jaundice in these patients.

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 of the digestive system ( liver, pancreas, biliary tract). Therefore, if this symptom appears, it is better to seek help from a gastroenterologist. In some cases, yellowing of the eyes can be caused 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 see your family doctor or general practitioner. 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 depending on different groups pathologies ( liver diseases, biliary tract diseases, blood diseases, pancreatitis, metabolic disorders).

Treatment of liver diseases

Treatment of liver diseases includes the use of conservative and surgical methods. Patients with hepatitis, liver cirrhosis, Zieve syndrome, amebiasis, and liver sarcoidosis are most often treated with conservative methods. Surgical intervention is often prescribed for patients with cancer and liver echinococcosis.

Ziewe syndrome
The main treatment method for Zieve syndrome is complete abstinence from drinking alcohol. Also, for this syndrome, hepatoprotective agents are prescribed that strengthen the hepatocyte wall ( liver cells).

Cirrhosis of the liver
If cirrhosis of the liver occurs due to alcoholism, then such patients are prescribed ursodeoxycholic acid ( accelerates the flow of bile from the liver and protects its cells from damage). For viral cirrhosis of the liver, patients are prescribed antivirals. For autoimmune cirrhosis, immunosuppressants are prescribed, that is, drugs that reduce the activity of immune reactions 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.

For primary sclerosing cholangitis, bile acid sequestrants are prescribed - drugs that bind bile acids. In case of liver cirrhosis caused by taking medications, stop treatment with these drugs. For Budd-Chiari disease ( pathology in which blockage of the hepatic veins occurs) 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, which is more effectively treated only in the most early stages. At later stages, this pathology is practically incurable. A variety of techniques are used to treat liver cancer, which may include surgery ( mechanical tumor removal, liver transplantation, cryodestruction, etc.), radial ( irradiation of the tumor with ionizing radiation, radioembolization, etc.) and chemical methods ( injection of acetic acid, ethanol, etc. into the tumor.).

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

Amebiasis of the liver
For liver amebiasis, amoebicides are prescribed ( medicines that destroy harmful amoebas). Most often they are metronidazole, emetine, tinidazole, ornidazole, etofamide, chloroquine. These drugs also have anti-inflammatory and antibacterial effect. When abscesses form inside the liver, it is also sometimes carried out surgery, which consists in draining its cavity and removing necrotic masses ( dead liver tissue).

Treatment of blood diseases

Blood diseases that cause yellowing of the eyes are most often treated conservatively. Some of them ( malaria, babesiosis, poisoning with hemolytic poisons) can be cured by prescribing etiotropic drugs to the patient that can eliminate the cause of the disease. Other pathologies ( erythrocyte membranopathies, erythrocyte enzymopathies, erythrocyte hemoglobinopathies, autoimmune hemolytic anemias) cannot be completely cured, so such patients are prescribed symptomatic treatment.

Malaria
Malaria is treated with antimalarial drugs ( chloroquine, quinine, artemether, halofantrine, mefloquine, fansidar, etc.). These drugs are prescribed according to special therapeutic treatment 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 ( normalize the total volume of fluid in the body), antibacterial, anticonvulsant, anti-inflammatory drugs, red blood cell infusions ( preparations containing donor red blood cells) or whole blood, hemodialysis, oxygen therapy.

Erythrocyte membranopathies
Patients with erythrocyte membranopathies are prescribed symptomatic treatment, which most often consists of splenectomy ( removal of the spleen), red blood cell infusions ( ), prescription of vitamins B12 and B9. In some cases, whole blood is transfused, and steroidal anti-inflammatory drugs and cholekinetics are also prescribed ( drugs that accelerate the excretion of bile from the liver).

Erythrocyte enzymopathies
Currently, there is no treatment method that would allow the patient to get rid of any type of erythrocyte enzymopathy, therefore these pathologies are treated only symptomatically. For them, red blood cell transfusions are usually prescribed ( preparation containing donor red blood cells) or whole blood in severe hemolytic crises ( that is, periods characterized by massive destruction of red blood cells in the patient). In severe cases, bone marrow transplantation is performed.

Erythrocyte hemoglobinopathies
Treatment of erythrocyte hemoglobinopathies should be aimed at correcting hemoglobin deficiency, red blood cells in the blood, iron deficiency in the body, treating oxygen deficiency and avoiding provoking hemolytic crises ( periods of breakdown of red blood cells in the blood) factors ( smoking, drinking alcohol, certain medications, ionizing radiation, heavy physical activity, drugs, etc.). To compensate for the deficiency of red blood cells and hemoglobin in the blood, all patients are prescribed infusions of whole blood or red blood cells ( preparation containing donor red blood cells), as well as vitamins B9 and B12. Iron supplements are prescribed to correct iron deficiency. In some cases, for certain clinical indications patients with erythrocyte hemoglobinopathies can undergo surgical transplantation Bone marrow or remove the spleen.

Autoimmune hemolytic anemias
Autoimmune hemolytic anemias are treated with immunosuppressants and cytostatics, which suppress the immune system and disrupt the production and secretion of autoimmune erythrocyte autoantibodies. To compensate for the deficiency of destroyed red blood cells, patients are infused with red blood cells ( preparation containing donor red blood cells) or whole blood. For neutralization harmful products released from hemolyzed erythrocytes, detoxification therapy is carried out ( Hemodez, albumin, rheopolyglucin, plasmapheresis are prescribed). To prevent thrombosis, which often occurs in such patients, anticoagulants are prescribed ( anticoagulants).

Poisoning with hemolytic poisons
Poisoning with hemolytic poisons is treated with various antidotes ( antidotes), which are selected depending on the type of substance that caused intoxication. Also, such patients are prescribed detoxification substances and hemodialysis ( blood purification with special device ), which are designed to remove both poisons themselves and the breakdown products of their own red blood cells from the blood. Rinsing the gastrointestinal tract is carried out only if poisoning occurs after eating poison.

Treatment of biliary tract diseases

The main task of treating diseases of the biliary tract is to eliminate congestion in the biliary tract. This is achieved through etiotropic and/or symptomatic treatment. Etiotropic treatment is aimed at eliminating the very cause of blockage of the biliary tract. It is used for opisthorchiasis, tumors of the organs of the biliopancreatoduodenal zone, and cholelithiasis. For these pathologies, etiotropic treatment is often prescribed together with symptomatic treatment, which improves the flow of bile through the biliary tract, but does not neutralize the very cause of bile stagnation. Symptomatic treatment usually prescribed for primary sclerosing cholangitis.

Primary sclerosing cholangitis
Primary sclerosing cholangitis is a rapidly progressive disease that usually leads to the development of biliary cirrhosis. No etiotropic treatment against this disease has yet been developed, since no one knows its cause. Therefore, such patients are treated symptomatically. Therapy is mainly aimed at preventing stagnation of bile inside the liver. For this purpose, anticholestatics are used ( cholestyramine, ursodeoxycholic acid, bilignin, etc.). These same drugs have hepatoprotective properties, that is, they protect liver cells from damage.

Cholelithiasis
Gallstone disease treated with various methods. First of all, such patients are prescribed a diet with the exclusion of very fatty and high-calorie foods. Secondly, they are prescribed medicinal substances (chenodeoxycholic and ursodeoxycholic acids), which can dissolve stones directly in the gallbladder. However, such drugs are not usually prescribed to all patients. Drug therapy is indicated only in cases where gallbladder function and patency are preserved biliary tract (that is, stones do not block the bile ducts). For the same indications, lithotripsy is performed - the destruction of stones under the influence of specially created shock waves. If the bile ducts are blocked by stones, jaundice and cholecystitis are present ( inflammation of the gallbladder mucosa) quite often surgical intervention is performed to remove the gallbladder.

Tumors of organs of the biliopancreatoduodenal zone
The main treatment method for tumors of the biliopancreaticoduodenal zone is surgery. Radiation therapy and chemotherapy are less effective in such cases.

Hemochromatosis
If hemochromatosis is present, the patient is prescribed detoxifying drugs ( deferoxamine), which are able to bind iron well in the blood and remove it through the kidneys. In addition to medications, 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 bled, about 250 mg of iron is immediately removed from the human body.

Wilson-Konovalov disease
For Wilson-Konovalov disease, a diet is prescribed that minimizes the intake of large amounts of copper into the body from food, as well as detoxifying drugs ( penicillamine, unithiol), removing 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 intestines), anti-inflammatory drugs, immunosuppressants ( ), choleretic drugs ().

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

Crigler-Najjar syndrome
For Crigler-Najjar syndrome it is used various techniques detoxification of the body ( prescription of barbiturates, drink plenty of fluids, plasmapheresis, hemosorption, albumin administration). In some cases, phototherapy is prescribed ( irradiation of the skin with special lamps, resulting in the destruction of bilirubin in the body), blood transfusions, liver transplantation.

Dubin-Johnson syndrome
Patients with Dubin-Johnson syndrome are prescribed B vitamins and choleretic agents ( promotes the removal of bile from the liver). Sun exposure is contraindicated for them ( prolonged exposure to sun rays ). Whenever possible, such patients are advised to avoid provoking factors ( heavy physical activity, stress, alcohol consumption, hepatotoxic drugs, fasting, injuries, viral or bacterial infections, etc.).

Amyloidosis
Drug treatment for liver amyloidosis, it is always selected individually. The drugs of choice are immunosuppressants ( suppress immune reactions in the body), cytostatics ( slow down the processes of cellular 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

If acute pancreatitis occurs or recurs ( re-exacerbation) of chronic pancreatitis, fasting is prescribed in the first few days, that is, the patient should not eat during this time. He is transferred to parenteral nutrition ( that is, they inject him nutrients directly into the blood through a catheter). The next direction of treatment for pancreatitis is to reduce gastric secretion with the help of special drugs ( antacids, famotidine, pirenzepine, ranitidine, etc.), as it increases the production of enzymes in the pancreas. Because of this, in fact, fasting is prescribed on the first day, because food is an excellent stimulator of production in the stomach. gastric juice and pancreatic juice in the pancreas.
domperidone, etc.). These drugs not only have antiemetic properties, but also improve motor skills in gastrointestinal system.



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

The appearance of yellow sclera in the eyes of newborns is usually caused by functional inferiority of the liver. In newborns, the liver at birth is just beginning to get used to working independently. Therefore, they often experience certain physiological disruptions ( physiological jaundice of newborns). Yellow sclera of the eyes in newborns can also be a sign of some kind of liver or blood pathology. Some of these pathologies are predominantly congenital, that is, they involve a deficiency of certain enzymes responsible for processing and removing bilirubin from the body. Another part of these diseases is caused by certain diseases of the blood, intestines and liver.