Yellow eyes. Are yellow whites of the eyes bad? What makes the whites of the eyes and skin yellow

Yellow skin of the face, hands, and other parts of the human body can be observed in various diseases associated with the activity of the internal organs of a person.

How does yellow skin appear?

Yellow skin color related to products - a pigment that is part of the blood. Bilirubin is a breakdown product of proteins contained in red blood cells and performs a transport function in the body (moving carbon dioxide and oxygen). Bilirubin is excreted from the human body with the stool. If, due to certain reasons, a lot of it accumulates in the human body, then yellow spots on the skin may be the result.

Due to the increase in the content of bilirubin in the body, the skin turns yellow in the first place. A person may have yellow skin on the legs, yellow skin under the eyes, yellow skin around the nails, etc. The whites of the eyes, palms, and the lower surface of the tongue may also turn yellow. At the same time, urine darkens in a person, it acquires the color of beer.

If the skin on the body or on the hands is yellow, then this may be due to a high level carotene in blood. Most often, yellow skin around the mouth or yellow skin around the eyes is observed in people who have been on an orange or diet for a long time, use certain medicines.

If yellowing of the skin is still associated with impaired excretion of bilirubin from the body, then in this case three types of jaundice are determined.

Hemolytic jaundice diagnosed with too rapid breakdown of hemoglobin. In this case, a very large amount of bilirubin is formed, and the liver cannot effectively process indirect bilirubin into direct one. As a result, the level of indirect bilirubin increases.

Development hepatic jaundice associated with liver damage viral hepatitis , the effects of alcohol, etc. In this case, the amount of direct bilirubin in the blood increases.

cholestatic jaundice develops due to violations of the movement of bile, since the bile ducts are clogged in the human body. In the blood, there is an increase in the amount of direct bilirubin.

Why does yellow skin appear?

The causes of yellowness of the skin should sometimes be sought in the condition and functioning of the human biliary tract. In this case, a comprehensive examination will help answer the question of why the skin color is yellow. In addition, yellowing of the skin can occur with alcohol intoxication, poisoning with medicines or toxic substances, with serious hemorrhages and burns. However, if even after the examination the question of why the skin is yellow remains open, then a person should definitely pay attention to the general lifestyle. After all, sometimes yellowing of the skin occurs with malicious smoking, with a person’s almost constant stay indoors. It is imperative to reconsider the diet, as an excess of sweet and dry foods in the diet can lead to yellowness of the skin.

The skin can also turn yellow due to eating a large amount of carrots and dishes from it, as well as with the constant addition of cumin and vinegar to food, the effect of which provokes the accumulation of bile vapor in the blood.

If a pale yellow skin color is noted, and at the same time there are yellow spots on the iris of the eye and on the eyelid, then it can be suspected that lipid metabolism is disturbed in the body, as a result of which the content increases.

Sometimes the yellowness of the skin may indicate the progression of an oncological disease in the human body. Yellowness of the skin with cancer is noticeable on the face, while there is a "waxy" bloodless skin tone.

If the shade of the skin becomes orange, then this may be a symptom. With this disease, the functioning of the thyroid gland is disrupted. With such a pathology in the body, there may be an insufficient amount of those substances that process beta-carotene. As a result, carotene accumulates in subcutaneous fat, which leads to. In this case, the endocrinologist will tell you how to get rid of the yellowness of the skin after establishing an accurate diagnosis.

If a yellow skin color is observed in a newborn baby, then this phenomenon may be associated with the reaction of his body to serious changes, that is, a change in the environment. In this case, we are talking about the so-called physiological jaundice. In a baby, bilirubin is produced in very large quantities. Around the third week of life, skin color gradually becomes normal. However, you still need to consult a doctor in order not to miss the development of pathological jaundice.

How to get rid of yellow skin?

Before practicing any methods of treating this condition, it is necessary to determine the cause of the yellowing of the skin. With severe yellowness of the skin, you should contact an infectious disease specialist, endocrinologist, gastroenterologist, hematologist.

The treatment of a person who has yellow skin of the hands, face or other areas of the body is carried out depending on the diagnosis that was established by the specialist. Sometimes, in the absence of serious diseases, the yellowness of the skin may disappear on its own after a while, without treatment.

As a rule, for diseases of the liver, biliary tract, complex treatment is prescribed. Already in the first days of therapy, the yellowing of the skin, as a rule, decreases. Comprehensive treatment may include medication, physiotherapy, surgery.

In newborns, signs of physiological yellowing of the skin disappear a few weeks after birth. However, the doctor must monitor the child's health in order not to miss the development of liver pathology. Sometimes newborns are given phototherapy: for a while, the baby is exposed to the glow of a fluorescent lamp. Under its action, bilirubin is destroyed and excreted from the body.

To prevent yellowing of the skin, one should be attentive to the state of health and consult a doctor at the first symptoms of diseases. Measures should be taken to prevent infection with viral hepatitis (protected sex, good hygiene).

A change in the color of the whites of the eyes is always a serious signal of a health disorder. In almost all cases, people try to see a doctor and undergo a thorough diagnosis. In most cases, this pathology is associated with disorders of the liver or eye diseases.

Why do eyes change color

The substance bilirubin is responsible for the yellow tint of the eyeballs and skin. Even with its slight increase, the white and pink hue changes to icteric or icteric gray, depending on the causes of the disorder.

Bilirubin is a substance, which appears during metabolic processes of the most important blood element hemoglobin. It is thanks to him that oxygen is supplied to other organs through the blood. In some pathological conditions and diseases, erythrocytes, which contain a large amount of hemoglobin, begin to disintegrate. This provokes the "release" of a huge amount of the substance bilirubin. Therefore, if yellow whites of the eyes appear, the causes and treatment are associated primarily with a high level of bilirubin.

If the bilirubin level is normal, then, most likely, liver diseases that lead to yellow sclera of the eyes of the reason are that the enzymes of the organ cannot process even the normal amount of this bilirubin and the level of the substance rises pathologically.

Varieties of jaundice for reasons of violation

Liver dysfunction

Liver dysfunction is the main cause of yellowing of the eyeballs. In contrast to trauma and lesions of the conjunctiva and sclera, in liver pathology, the sclera is modified in both eyes and is symmetrical. Additional symptoms are: discoloration of urine and feces, pain in the lower hypochondrium. Liver treatment should be started immediately to prevent serious complications.

Causes of the yellow protein of the eye in violation of the liver

Diagnosis of liver disease is based on a biochemical blood test., in which attention is paid to bilirubin. This substance is the primary cause of yellow whites of the eyes. It is important to measure the level of both direct and indirect bilirubin. Usually, the appointment of treatment occurs immediately after the study of the liver using ultrasound diagnostics.

A general practitioner, surgeon or infectious disease specialist can treat yellowing of the sclera of the eye and skin. In most cases, drug therapy and observation is enough for a person. Serious liver damage requires an organ transplant.

Newborn jaundice

Newborn jaundice is a common syndrome that occurs in many children in the first hours after birth. Most often, it occurs in children who were born prematurely or had pathologies of intrauterine development. Such children are distinguished by yellow whites of the eyes.

The cause of neonatal jaundice is primarily associated with a large number of red blood cells. They appear in the baby's body while still in the womb, and after birth they begin to actively disintegrate and the liver ceases to cope with its task.

With jaundice in newborns, the baby's eye sclera, like the skin, become bright yellow. This pathology can have different degrees of severity, but in most cases it is successfully treated in the first weeks of life with the help of exposure to ultraviolet rays. In severe lesions, the child may be prescribed medication. Typically, yellowing of the eye sclera in the first days of life does not affect the further health of the child and his development.

Eye diseases that lead to yellowing of the sclera

There are a number of diseases that have a vivid symptom - yellowing of the sclera of the eyeball. This can occur with severe conjunctivitis or eye injuries.

Other diseases that lead to yellowing of the whites of the eyes:

Other causes of yellow eyes

Eyes are not only a mirror of the soul, but also a reflection of the state of the body. The sclera of the eye often signals processes that can harm health.

Usually the eyeballs turn very yellow in people who abuse alcohol and especially cigarettes. Heavy smokers are distinguished by "unhealthy" shades of the sclera, which become only noticeable over the years.

If the liver does not cope with its task, the eyes can give out such a condition. The reason may lie not only in the disease, but also in the abuse of a large amount of fried, fatty and smoked foods. Poor quality foods, vegetables, fruits, berries and mushrooms with a lot of toxins can lead to a gradual yellowing of the eyeballs.

Chronic eye fatigue also signals itself by a change in the color of the white of the eye.. This is due to a long stay at the computer or other work that greatly strains the eyesight. Special treatment for chronic eye fatigue is not required. A person can be prescribed drops with vitamins, remedies for dry eyes. It is recommended to refrain from excessive eye strain and constantly get enough sleep.

Do I need to immediately call an ambulance if the whites of the eyes turn yellow, and tune in to the treatment of jaundice? No. Even the diagnosis of hepatitis - more commonly called "jaundice" - has other symptoms, and the presence of the disease must be confirmed by a doctor. In addition, yellow eyes are not necessarily hepatitis A. There are many diseases that have the same symptom, and not all require hospitalization.

If a person has yellow eyeballs, the reasons may be as follows:

There are also absolutely “harmless” causes of this condition that do not require urgent treatment, but gradually undermine the body from the inside - chronic lack of sleep, constant sitting at a computer monitor, bad habits - in particular, smoking.

Yellowness in the eyes is a mandatory reason to see a doctor, even if there is no temperature and nausea. It is always necessary to find out why the eyeballs have changed their color. The chance to eliminate ophthalmic diseases at the first sign of a change in the color of the eye proteins is almost 100% - if the symptom is neglected, you can lose your eyesight.

Red blood cells in the human body contain bilirubin, which is produced by the liver. Why is bilirubin needed? This enzyme has an important role in the process of digestion - it emulsifies fats and prepares them for splitting, which occurs in the duodenum. If there were no bilirubin, fat particles would not be absorbed. If the synthesis of bilirubin is increased, or the body does not perceive it, the whites of the eyes immediately turn yellow.

Violation of the production of bilirubin indicates a pathology of the liver of a different nature.

Allocate the following types of hepatitis.

1. Hemolytic. It develops with the accelerated breakdown of hemoglobin - the liver does not have time to process the amount of indirect hemoglobin that is formed during the breakdown of red blood cells into direct hemoglobin.
2. Hepatic.

It is called:

• Viral lesions. Symptoms of the disease with various strains of viruses: chills, headache, fever, fever, abdominal pain, nausea, loss of appetite, enlargement of the liver, discoloration of stools and urine - the stool becomes light, and the urine becomes dark.
• Leptospirosis. The onset is sudden, the temperature rises sharply, hemorrhagic syndrome, myalgia (muscle pain) appear, ESR rises, hemoglobin levels decrease, and thrombocytopenia occurs. The liver increases from the first days of the disease.
• Toxic hepatitis develops acutely, and the symptoms resemble viral hepatitis. The kidneys can be simultaneously affected - renal failure occurs. Hepatic function is impaired.
• Symptoms of acute alcoholic lesions resemble the development of viral hepatitis.

Additional symptoms are diarrhea, ascites.

1. Cholestatic jaundice. The bile ducts are clogged with stones or stagnation of bile, which causes nausea, dizziness, pain in the right hypochondrium.
2. enzymopathic jaundice. Due to a hereditary defect in the enzyme system of the body, the synthesis of bilirubin is insufficient.

Newborn jaundice rarely leads to pathological changes in the liver. It occurs in the first days after birth due to adaptation to the extrauterine period. Before childbirth, a huge amount of red blood cells enters the blood of the fetus, and the liver cannot cope with the processing of bilirubin, which was released during their decay. Newborn jaundice usually goes away on its own on the 10-12th day of life.

Newborn jaundice is dangerous when the parents' Rh factor is incompatible. In this case, babies need treatment.

Chronic liver disease may have the following symptoms: pain in the hypochondrium on the right, nausea, enlarged spleen, subfebrile temperature, esophageal varicose veins, ascites, anemia, and others.

Treatment of all liver diseases is the prerogative of the doctor. In this case, folk methods can only have an additional effect.

The yellowness of the eyeball and iris can be caused by malignant formations of the tissues of the organ of vision - more often the conjunctiva. Yellowness is one of the symptoms of melanoma in the eye area. So do not delay a visit to the ophthalmologist if there are discomfort in the eye socket and yellow spots on the surface of the eye, which can be seen when looking at yourself in the mirror.

Proteins turn yellow in diseases such as pinguecula and pterygium.

A pinguecula is a small formation similar to a wen, which is localized due to a violation of lipid metabolism in the body on the eyeball.

Pterygium is an overgrowth of the conjunctiva of the eye (popularly called the disease "wild meat"). It begins to enter the sclera and reduces the field of view.

Surgical treatment of pinguecula and pterygium. Pterygium can be eliminated only at the initial stage. If the conjunctiva grows so large that it closes the pupil, then reverse recovery is impossible.

All eye diseases are a reason to consult an ophthalmologist.

This disease has a second name - constitutional jaundice. Boys get sick 5 times more often than girls. If we consider only clinical signs - yellowing of the eyelids and eyeballs, then we can say that Gilbert's disease is rare. However, if you pay attention to the blood formula regarding the emerging bilirubinemia, then the frequency of manifestations increases.

Yellowness of the sclera does not always appear, but only with a delay in feeding, due to which hemolysis increases. That is, in the absence of starvation, symptoms of the disease do not occur.

It is impossible to cure Gilbert's disease, but there are ways to eliminate the symptoms. This is a sparing diet, the use of choleretic drugs and soy emulsions.

Smoking itself does not affect the color of the sclera, but it must be taken into account that the constant supply of nicotine to the body increases the load on the liver.

In addition to nicotine, when smoking, other combustion products, tars and toxins enter the body. The liver is involved in cleansing the body, and overloads negatively affect its function.

That is why long-term smokers have yellowish whites of the eyes and skin. In medicine, this is called "signs of subacute toxic hepatitis."

If the unhealthy appearance and yellowness of the eyeballs are caused by eye fatigue, it is necessary to balance the work and rest regimen, walk more, increase the amount of healthy food in the diet - vegetables, fruits, seafood and nuts - which includes vitamins for the eyes: A, C, E , nicotinic and folic acid, saturated fatty acids.

Sometimes the eyeballs turn yellow if there is a lot of carotene in the body. This happens, for example, if you "abuse" carrots. In this case, the treatment is a variety of diet.

In all other situations - when the color of the sclera changes - you need to see a doctor. This state is a signal: not everything is in order in the body.

are a sign that the patient has

jaundice. Jaundice is a pathological condition that occurs when

diseases of the liver, diseases of the blood

Pancreas, bile ducts and associated with an increase in the concentration in the blood of total

bilirubin

Jaundice is not only accompanied by yellowing of the eyes. With it, the skin often turns yellow, skin

Fever, pain in the right hypochondrium, sensation

bitterness in the mouth decreased appetite

Appears

nausea, vomiting, headache

weakness insomnia

Enlargement of the liver and

spleen

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, vessels and nerves. This organ is the 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 only see 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.

There are three main membranes in the eyeball:

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

The 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 ​​​​the eye. The cornea of ​​the eye is located in the anterior 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);
• the posterior limiting 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 also 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.

The cornea 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 section of the outer shell of the eye. This department occupies most of the area of ​​the 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 anteriorly by the conjunctiva, and the posterior by the endothelium. conjunctiva (

conjunctiva

) is a relatively thin shell, which consists of a cylindrical stratified epithelium. This sheath covers the inside of the eyelids (

secular part of the conjunctiva

) and the eyeball outside (

ocular part of the conjunctiva

). Moreover, this structure does not cover the cornea.

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

Middle shell of the eyeball

The middle layer of the eyeball is located inside the eye. It consists of three unequal parts (

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 (

a transparent structure that is located directly opposite the pupil inside the eyeball and is a biological lens

) and rainbow. This chamber is also filled with intraocular fluid.

The back part of the middle shell of the eyeball is called the own choroid of the eyeball. It is located directly under the white of the eye in the back of it. 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 cells of the retina (

inner lining of the eyeball

) eyes. The posterior part of the middle shell lines almost two-thirds of the entire area of ​​the sclera, and therefore is the largest of all three parts of the middle shell.

A little ahead of her

back of 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

) of the body includes special epithelial cells that are engaged in the production of intraocular fluid that fills the anterior and posterior chambers of the eye.

The inner lining of the eyeball

or retina

) envelops the inside of the iris, the ciliary body and the own choroid of the eyeball. The totality of those places where the retina is adjacent to the iris and to the ciliary body is called non-visual (

) part of the retina. The rest, posterior, more extensive part of the retina is called visual. In this part of the retina, light is perceived as it enters 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.

In the liver cells, indirect bilirubin binds to glucuronic acid (a chemical substance necessary to neutralize bilirubin), and it turns into direct bilirubin (detoxified bilirubin). Further, direct bilirubin is transported by liver cells to bile, through which it is excreted from the body. In some cases, some of it can be reabsorbed 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 blood bilirubin. Indirect bilirubin accounts for about 75% of total bilirubin. The reference (limiting) values ​​​​of the concentration in the blood of total bilirubin are 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

). With a mild degree, the concentration in the blood of total bilirubin reaches 86 µmol / l. With an average degree in the blood of a patient, the level of bilirubin 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

In the liver, indirect bilirubin, which circulates in the blood, is detoxified and direct bilirubin is formed. Therefore, when it is damaged in the blood, the concentration of total bilirubin immediately increases and yellowing of the whites of the eyes occurs. Yellowing of the eyes can be triggered by various liver pathologies that are of infectious and non-infectious origin. Infectious diseases of the liver include viral, bacterial

hepatitis

inflammation of the liver tissue

amebiazechinococcosis

liver. Non-communicable diseases of the liver can be toxic hepatitis, cirrhosis,

liver cancersarcoidosis

liver, Ziwe syndrome.

Hepatitis is a disease of the gastrointestinal system in which there is inflammation of the liver parenchyma (

). Hepatitis can appear as a result of penetration into the liver of various

hepatitis A, B, C virus, cytomegalovirus, Epstein-Barr virus, yellow fever virus, etc.

bacteria

leptospirosis, syphilis, tuberculosis, etc.

amoebiasis, echinococcosis, ascariasis, schistosomiasis, etc.

toxins

ethyl alcohol, chlorpromazine, tetracycline, methyldopa, methotrexate, dichloroethane, phenol, benzene, etc.

). Therefore, depending on the etiology (

origin reasons

) all hepatitis are divided into viral, bacterial, toxic (

or medicinal

All of these listed 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 a 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 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

and mucous membranes. Therefore, with liver damage, yellowing of the skin and albuginea occurs (

Ziwe syndrome is a rare syndrome (

set of pathological features

), which is characterized by the appearance of jaundice in the patient (

yellowing of the sclera and skin

), enlarged liver, hemolytic anemia (

), hyperbilirubinemia (

increase in blood bilirubin

) and hyperlipidemia (

increased levels of fat in the blood

). This syndrome is observed in people who abuse alcohol. Yellowing of the whites of the eyes in Zieve syndrome is caused by an increase in the level of bilirubin (

mainly through indirect

) in the blood, due to the destruction of red blood cells and impaired liver function. In most cases, these patients develop fatty liver (

dystrophy

) of the liver, i.e. pathological deposition within the parenchyma (

) liver fat.

Cirrhosis of the liver is a pathology in which liver damage occurs 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 hepatic 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 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.

Cirrhosis of the liver is usually the most unfavorable complication of various hepatitis (

inflammation of the liver

). The most common causes that lead to the development of cirrhosis of the liver are

alcoholism

Hepatitis B, C and D viruses, congestive venous insufficiency (

for example, heart disease, Budd-Chiari disease, etc.

), primary sclerosing

cholangitis

inflammation of the lining of the bile ducts

), drug-induced hepatitis (

against the background of long-term use of antibiotics, cytostatics, immunosuppressants, etc.

), hemochromatosis (

a disease in which iron accumulates in tissues

), Wilson-Konovalov disease (

pathology associated with the accumulation of copper in tissues

For liver cancer

hepatocellular carcinoma

e.g. at work

) with pesticides, heavy metals and those who eat poorly processed plant foods that may contain aflatoxins.

In liver cancer, tumor-like formations that appear in the liver are characterized by rapid, aggressive growth, due to which they quickly reach large sizes. In the process of increasing in size, the tumors crowd out the normal liver tissue, due to which the liver soon loses its normal functions, one of which is the neutralization of indirect bilirubin circulating in the blood. Therefore, in the later stages of liver cancer, hyperbilirubinemia occurs in the blood (

increased levels of bilirubin in the blood

). With a high level of bilirubin in the blood, it begins to be deposited in the skin and the white of the eyes, as a result of which the patient develops jaundice (

yellowing of the skin and sclera

Echinococcus granulosus

), which is a type of tapeworm (

). Human infection with echinococcosis occurs by eating food or water contaminated with eggs of these worms or by contact with infected animals (

dogs, horses, pigs, cows, etc.

). Therefore, this disease is observed mainly in hunters, shepherds, slaughterhouse workers and their families. When hit in

intestines

eggs of this helminth, they penetrate through its wall into the portal vein, through which these eggs reach the liver. Getting stuck in it, they transform into a cyst, which is a small volumetric formation in the form of a bubble filled with liquid with numerous echinococcus embryos.

If the disease is not treated for a long time, then the echinococcal cyst begins to gradually increase in size and compress the surrounding liver tissues, causing them to die (

atrophy of the liver parenchyma

). As a result of this, there is a mechanical replacement of normal hepatic tissue, in place of which a cyst appears. At a certain moment, 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 of the eyes, giving them a characteristic yellow color.

Sarcoidosis is a chronic disease in which various tissues and organs (

lungs, liver, kidneys, intestines, etc.

) granulomas appear. A granuloma is a collection 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 tissues, the functioning of the immune system is disrupted. If it detects some antigens in 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 foci visually look like nodules (

or granulomas

), different from normal tissues. Granulomas may vary in size and location. Inside such foci, the cells of the immune system, as a rule, act inefficiently, so these granulomas persist for a long time, and in some cases they can increase in size. In addition, new granulomas constantly appear in sarcoidosis (

especially if left untreated

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 function as granulomatous infiltrates replace their normal parenchyma (

). If, for example, sarcoidosis affects the lungs (

and they are most often damaged in this disease

), then the patient has

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 (

in the liver, the synthesis of blood proteins is disrupted

) functions.

In case of violation of the detoxifying function of the liver, various metabolites accumulate in the blood, which must be absorbed and neutralized by the liver. This explains the fact that patients with liver sarcoidosis have high levels of bilirubin in the blood. The accumulation of bilirubin in the bloodstream then leads to its deposition in various tissues. Its accumulation in the skin and sclera of the eyes leads to their yellowing.

Entamoeba histolytica

inflammation of the intestinal mucosa

). This form of amoebiasis is called intestinal amoebiasis. There is also extraintestinal amoebiasis. It appears under certain conditions (

for example, with dysbacteriosis, immunodeficiency, poor nutrition, etc.

), when amoeba can penetrate through the damaged wall of the large intestine into the blood, and then through it mix into various tissues and organs (

liver, lungs, heart, brain, etc.

The main manifestation of extraintestinal amebiasis is liver damage. When pathogenic amoebas enter the liver, they cause damage to its tissues there. Hepatitis occurs first

inflammation of the liver tissue

). Some time later, in the absence of a proper immune response, the patient at the site of injury (

and inflammation

) can form inside the liver

abscesses

cavities filled with pus

). There may be a large number of such abscesses. In the absence of treatment for liver amoebiasis, its various functions are violated, including the neutralization of bilirubin in the blood (

indirect bilirubin

In addition, due to massive damage to liver cells by amoeba, there is a significant release of bilirubin associated with glucuronic acid (

direct bilirubin

) back into the blood. Therefore, with liver amoebiasis in a patient in the blood, an increase in the concentration of total bilirubin can be observed (

due to both fractions of bilirubin

). The accumulation of bilirubin in the blood often leads to its deposition in the skin and sclera of the eyes, causing them to turn yellow.

Erythrocytes (

red blood cells

protein that delivers oxygen to tissues

). In its chemical structure, it is a chromoprotein (

), which consists of four polypeptides (

protein

) chains and heme (

protoporphyrin IX in complex with iron

). All red blood cells that are produced in the bone marrow have a limited lifespan (

about 125 days

). When this period comes to an end, the destruction of red blood cells occurs. The hemoglobin contained in them is released into the surrounding space and then decomposes into protein and heme parts. Heme further turns into indirect bilirubin, which must be neutralized in the liver.

In blood diseases (malaria, erythrocyte membranopathies, erythrocyte enzymopathies, erythrocyte hemoglobinopathies, autoimmune hemolytic anemias, babesiosis, poisoning with hemolytic poisons), massive hemolysis (destruction) of erythrocytes is observed, resulting in a sharp increase in the amount of indirect bilirubin in the blood. Under such conditions, the liver does not have time to neutralize it. Therefore, this bilirubin penetrates tissues (for example, the whites of the eyes) and stains them yellow.

Plasmodium vivax, Plasmodium ovale, Plasmodium falciparum, Plasmodium malariae

). Infection occurs when a person is bitten by mosquitoes of the genus Anopheles (

malarial mosquitoes

), which are a kind of carriers and distributors of this infectious disease. Entering the human blood

tissue schizogony

), after which merozoites are formed (

mononuclear plasmodia

These merozoites then enter the bloodstream and invade red blood cells and begin to divide there again (

erythrocyte schizogony

). At the end of the erythrocyte schizogony, the infected erythrocytes are completely destroyed and release a large number of proliferating merozoites, which again enter new erythrocytes for reproduction. Thus, this process proceeds 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 contents of erythrocytes and, in particular, the protein - hemoglobin. When this protein breaks down, bilirubin is formed (

indirect

), which must be detoxified 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, patients with malaria develop hyperbilirubinemia (

an increase in the level of bilirubin in the blood

) and jaundice (

yellowing of the skin and eyes

), which occurs due to the partial deposition of bilirubin in the tissues.

Erythrocyte membranopathies are a set of hereditary pathologies based on congenital defects in the 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 older red blood cells circulating in the blood change their shape. In addition, with these pathologies, their membranes become defective, they have incorrect permeability for various substances and low resistance to damaging factors, and therefore such erythrocytes are quickly destroyed and do not live long.

The best-known erythrocyte membranopathies are Minkowski-Chauffard disease, hereditary elliptocytosis, hereditary stomatocytosis, hereditary acanthocytosis, and hereditary pyropoykylocytosis. All these pathologies are characterized by a triad of clinical signs - jaundice, hemolytic anemia (

a decrease in the number of red blood cells as a result of their destruction

) and splenomegaly (

enlargement of the spleen

). The appearance of jaundice in such patients is explained by the fact that with erythrocyte membranopathies there is a frequent destruction of defective erythrocytes in the blood, which is accompanied by the release of a large amount of hemoglobin, which then turns into indirect bilirubin. The liver cannot immediately process huge 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 whites of the eyes and skin.

Erythrocyte enzymopathies are a group of hereditary diseases in which the production of enzymes is impaired in red blood cells (

proteins that speed up biochemical reactions

) that control the course of metabolic reactions (

exchange reactions

). This leads to inferiority of energy metabolism, accumulation of intermediate reaction products and energy deficiency 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 wrinkling and destruction. There are also certain erythrocyte membranopathies in which there may be a deficiency in the enzymes of the antioxidant systems of erythrocytes (

e.g. pentose phosphate cycle, glutathione system

), which often leads to a decrease in their resistance to free oxygen radicals and rapid degradation.

In any case, enzyme deficiency 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 (

a 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 indirect bilirubin from the blood, which was formed in large quantities during the breakdown of hemoglobin. Therefore, indirect bilirubin is deposited in the skin and whites of the eyes and causes them to turn yellow.

Erythrocyte hemoglobinopathies are a group of congenital diseases, the origin of which is 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 erythrocytes themselves lose their strength and shape, as a result of which they quickly undergo lysis (

destruction

) and have a short life span in the blood.

Therefore, patients suffering from one of these diseases often have hemolytic anemia (

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 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 collapsing erythrocytes. This hemoglobin is subsequently broken down and converted into indirect bilirubin. Since with these pathologies there is a destruction of a large number of red blood cells, 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 in other tissues and organs. If this bilirubin penetrates the skin and whites of the eyes, they turn yellow. Yellowing of the whites of the eyes and skin is called jaundice.

Autoimmune hemolytic anemia is 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

). Dysfunction of the immune system can also be triggered by external environmental factors (

e.g. viruses, bacteria, toxins, ionizing radiation, etc.

When normal erythrocytes bind to autoimmune (

pathological

) antibodies destroy them (

). 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

). This anemia is fully called autoimmune hemolytic anemia (

). 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 thermal 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 erythrocytes

). Being deposited in the tissues, this chemical metabolite causes them to turn yellow, therefore, with these pathologies, patients often have yellow skin and sclera of the eyes.

Babesiosis is an infectious disease resulting from human infection with protozoa of the genus Babesia (

). Transfer mechanism

infections

transmissible, that is, a person acquires this disease when bitten by ticks (

genera Dermacentor, Hyalomma, Rhipicephalus

). People who are constantly in contact with pets and have a fairly pronounced immunodeficiency (

for example, patients with HIV infection, infections, etc.

). person with normal

immunity

may also become infected with babesiosis, but the disease will be asymptomatic.

The infection enters the human blood during tick feeding (

through his saliva

destruction

) a large number of red blood cells. During their destruction, a lot of hemoglobin enters the bloodstream, which breaks down and turns into bilirubin (

indirect

). Significant concentrations of this bilirubin in the blood cause yellowing of the whites of the eyes and skin.

Hemolytic poisons are a group of chemical compounds that, when ingested, cause pronounced hemolysis (

destruction

) red blood cells, resulting in anemia (

deficiency of red blood cells and hemoglobin in the blood

) and jaundice (

yellowing of the skin and eyes

). Hemolytic poisons include various chemicals of natural or artificial origin. Poisons of natural origin include snake venoms, venoms of scorpions, spiders, bees, poisons of some mushrooms, berries, etc.

Most of the hemolytic poisons are 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 the poisoning with hemolytic poisons occurs in industrial workers who are constantly in contact with these toxic substances.

Under the influence of hemolytic poisons, the membranes of erythrocytes are deformed, as a result of which they are destroyed. There are also some hemolytic poisons that block the flow of enzymatic processes inside red blood cells, due to which they disrupt energy metabolism or their antioxidant capacity (

resistance to oxygen free radicals

), causing them to collapse. Certain chemicals are able to 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 anemia occurs. With them, the immune system destroys the patient's own red blood cells, so their number in the blood is significantly reduced.

Thus, in case of poisoning with hemolytic poisons, due to various mechanisms, massive destruction of erythrocytes inside the vessels occurs. 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 their yellowing.

Bile is a yellow-brown body 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, along with bile, various harmful substances that are unnecessary to the body are excreted (

direct bilirubin, cholesterol, bile acids, steroids, metals, etc.

). Before reaching the intestines, bile passes through the bile ducts (

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 the 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

) the level of direct bilirubin in the blood rises and jaundice is observed.

Primary sclerosing cholangitis is a disease of unknown nature, in which chronic inflammatory processes are observed 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, coarsen and deform. 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 along 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. When a large number of bile ducts are damaged, bile stasis occurs inside the liver (

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.

Gallstone disease is a pathology in which stones appear in the gallbladder or in the biliary tract. The reason for 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 each other, resulting in the formation of stones.

The development of this disease can contribute to the stagnation of bile (

congenital anomalies of the gallbladder, biliary dyskinesia, scars and adhesions in the bile ducts

), inflammatory processes in the biliary tract (

inflammation of the lining of the gallbladder or bile ducts

), diseases of the endocrine system (

diabetes mellitus, hypothyroidism

obesity

Wrong diet (

excessive consumption of fatty foods

pregnancy

Certain medications (

estrogens, clofibrate, etc.

), liver disease (

hepatitis, cirrhosis, liver cancer

), hemolytic anemia (

pathology associated with a decrease in the number of red blood cells due to their destruction

Stones formed during gallstone disease can be located in the so-called blind spots in the biliary system (

for example, in the body or the bottom of the gallbladder

). In such cases, this disease does not manifest itself clinically, since the stones do not clog 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, intrahepatic bile ducts are destroyed inside the liver, and bile enters directly into the bloodstream.

Due to the fact that bile contains a large amount of bilirubin (

), then its concentration in the blood increases. Moreover, such an increase is always proportional to the duration of blockage of the bile ducts by a stone. At a certain concentration in the blood of direct bilirubin, it penetrates the skin and whites of the eyes and stains them yellow.

The organs of the biliopancreatoduodenal zone include the extrahepatic bile ducts, gallbladder, pancreas, and duodenum. These organs are very close to each other in the upper floor of the abdominal cavity. In addition, they are functionally interconnected, so the 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 in their presence there is a mechanical blockage of the extrahepatic bile ducts (

or gallbladder

) and the 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 with stagnation of bile in them are able to break, as a result of which it penetrates into the blood. Bilirubin (

), which is part of its composition, gradually accumulates in the skin and the white of the eyes and stains them yellow.

pancreatic cancer

Which accounts for 50% of all tumors of the biliopancreatoduodenal zone, mechanical obstruction (

blockage

) of the biliary tract occurs outside, that is, a growing tumor of the pancreas from the side of the abdominal cavity compresses the main extrahepatic bile duct. Cancer of the bile ducts of the extrahepatic ducts and the gallbladder accounts for approximately 30% of all cases of tumors of the organs of the biliopancreatoduodenal zone. Cancer of these organs is accompanied by internal blockage of their lumen. With cancer of Vater's nipple (

) and duodenum (

occur in 15% of cases

) blocking the outflow of bile occurs in the area of ​​​​emission into it (

) bile from the main bile duct.

cat fluke

). This infection is transmitted by food, most often through the use of thermally improperly cooked fish of the carp family (

crucian carp, carp, tench, vobla, bream, ide, etc.

they grow connective tissue

), their lumen narrows. All this (

accumulation of worms in the bile intrahepatic tract and deformation of the walls of the bile ducts

) leads to difficulty in the outflow of bile from the liver. Bile stasis provokes rupture of the smallest bile capillaries, as a result of which bile begins to flow into the blood, which leads to the accumulation of bilirubin in it (

) and its partial deposition in the skin and the white of the eyes (

), which is accompanied by their yellowing.

There are certain pathologies

hemochromatosis, Wilson-Konovalov disease, Gilbert's disease, Crigler-Najjar syndrome, Dubin-Johnson syndrome, amyloidosis

), in which there are violations of metabolic processes in the body. Such disorders may be associated with the metabolism of bilirubin, proteins, and certain metals (

iron, copper

Hemochromatosis is a congenital disease in which there is a violation of iron metabolism in the body, and it accumulates in large quantities in various tissues and organs. With this disease, too much iron is absorbed in the intestines from the food that a person normally consumes. After the intestines, this iron is absorbed into the blood and through it is transported to various organs. With hemochromatosis, cirrhosis of the liver quite often develops, since this organ is one of the first where the accumulation of excess amounts of iron entering the body occurs.

The occurrence of cirrhosis of the liver with hemochromatosis is due to the fact that this chemical element, penetrating into the liver, causes free radical oxidation reactions in it, as a result of which the membranes of hepatocytes are damaged (

liver cells

). Damage to the membranes of hepatocytes subsequently leads to their destruction. Liver cells die. Connective tissue appears in their place. Such substitution is a characteristic morphological sign of liver cirrhosis. With the development of cirrhosis, the liver loses the ability to neutralize toxic elements circulating in the blood and, in particular, bilirubin, which, as this pathology develops, accumulates in the blood and then penetrates the skin and sclera of the eyes, turning them yellow.

Wilson-Konovalov disease is a chronic hereditary disease associated with impaired copper metabolism in the body. The reason for its development is a defect in the gene that encodes the synthesis of a transport protein (

), which regulates the binding of copper to ceruloplasmin in the liver (

blood plasma protein

), as well as removing excess copper that enters it from the intestines. Violation of the synthesis of this protein leads to the accumulation of copper in the liver. Since this element is toxic, under conditions of its excess, damage to the liver tissues occurs, as a result of which their inflammation develops, and then their replacement with connective tissue. Therefore, one of the main manifestations of Wilson-Konovalov's disease is cirrhosis of the liver.

With cirrhosis of the liver, a decrease in its detoxification function is observed (

as her cells are destroyed

), therefore, various metabolites accumulate in the blood of such patients (

which the liver must normally detoxify

), including bilirubin (

indirect

). An increase in the concentration of this substance in the blood leads to its deposition in the skin and sclera of the eyes, which is accompanied by their yellowing. It should be noted that in Wilson-Konovalov disease, copper accumulation is observed not only in the liver, but also in other organs, such as the brain, kidneys, and eyes. Deposition of copper in the region of the Descemet's membrane of the eyes, accompanied by the appearance of yellowish-green pigmentation along the periphery of the irises (

on the border between the sclera and cornea of ​​each eye

). This pigmentation is called Kaiser-Fleischer rings.

Gilbert's disease is an inherited disease of the liver in which liver cells (

hepatocytes

) are unable to bind indirect bilirubin circulating in the blood, as well as transport it intracellularly to microsomes (

elements of the endoplasmic reticulum - one of the cell organelles of hepatocytes

), in which it binds to glucuronic acid. As a result of these disorders, the liver loses the ability to neutralize indirect bilirubin, and it gradually accumulates in the blood. If its concentration in the blood plasma reaches high values, then it begins to migrate into the skin and sclera of the eyes, as a result of which they turn yellow.

Jaundice (

i.e. yellowing of the whites of the eyes and skin

) in Gilbert's disease is practically the main and only manifestation. However, this symptom is not permanent. It usually occurs under the influence of certain provoking factors. These include starvation,

Crigler-Najjar syndrome is an inherited liver disease in which there is a defect in the gene encoding the amino acid sequence of the enzyme (

uridine-5-diphosphate glucuronyltransferase

) 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 excretion 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-Najjar 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 glucuronyl transferase

), which binds indirect bilirubin. This type of Crigler-Najjar syndrome usually results in the 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 with the norm, is much lower. In 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-Najjar 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-Najjar syndrome are observed much more often than in patients with Gilbert's disease.

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 detoxified bilirubin (

), 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 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 whites of the eyes, which causes them to turn yellow.

The first signs of Dubin-Johnson syndrome in patients usually appear at a young age (

predominantly in men

). Jaundice is almost always permanent 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

). If the disease goes into remission (

asymptomatic course

), then it can quickly worsen if the patient is exposed to various provoking factors (

heavy physical exertion, stress, alcohol consumption, fasting, injuries, viral or bacterial infections, etc.

Amyloidosis is a systemic disease resulting in various organs (

kidneys, heart, esophagus, liver, intestines, spleen, etc.

) accumulates an abnormal protein - amyloid. The reason for 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 plasma proteins

Amyloid itself is not toxic to the body, but its deposition in organs causes a violation of their structure and function. This happens due to the fact that amyloid is deposited in the tissues, displacing them. As a result, inside the organs, normal functional tissue is gradually replaced by non-functional tissue. This results in multiple organ failure

functional insufficiency of several organs

). If amyloid is deposited in the liver, then its function is also impaired. The more amyloid accumulates in it, the more pronounced

liver failure

With this insufficiency, the liver does not neutralize indirect bilirubin circulating in the blood. This leads to its accumulation in the blood plasma and its deposition in the skin and sclera of the eyes, which causes them to turn yellow.

Pancreatitis is a disease of the pancreas characterized by inflammation of its parenchyma (

). The mechanism of development of this pathology is associated with the activation of enzymes (

chymotrypsin, trypsinogen, proelastase, phospholipase, etc.

) within the gland itself, resulting in autolysis (

self-digestion or self-destruction

With pancreatitis, an increase in the pancreas in size is almost always observed, due to its edema (swelling is associated with inflammatory processes occurring inside this organ). An enlarged pancreas often compresses the common bile duct (choledochus), which transports bile from the gallbladder to the duodenum. This is accompanied by difficulty in the outflow of bile from the liver to the intestines and its stagnation in the bile ducts (gall bladder, intrahepatic and extrahepatic bile ducts). Violation of the outflow of bile, in the end, leads to rupture of the bile capillaries (due to high pressure in the bile ducts) and the penetration of bile into the blood.

Since one of the main components of bile is bilirubin (

), 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 in the 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.

To diagnose the causes of yellowness of the eyes, various types of studies can be used (

clinical, radiation, laboratory

). The main clinical diagnostic methods are the collection of anamnesis (

clarification of the entire history of the development of the disease

) in the patient and his examination. Of the radiation methods of research, doctors most often prefer ultrasound and

computed tomography

abdominal organs (

in case of suspicion of any pathology of the liver, pancreas or biliary tract

). In the diagnosis of 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

urine tests

The main symptoms of liver diseases are pain in the right hypochondrium, increased

temperature

Feeling of bitterness in the mouth, loss of appetite, jaundice (

yellowing of the eyes and skin

), headache, general weakness, decreased performance, insomnia, nausea, vomiting, liver enlargement,

flatulence

Also, depending on the disease, these patients may experience additional symptoms. For example, with liver echinococcosis, various allergic reactions on the skin are often observed (

skin rashes, itching, skin redness, etc.

). In liver sarcoidosis, there may be

in the chest, joints, muscles, shortness of breath, cough, hoarseness, an increase in the size of peripheral lymph nodes (

inguinal, occipital, elbow, cervical, axillary, etc.

joint inflammation

), deterioration

visual acuity

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 meet

diarrhea with blood and mucus

False desires, dehydration of the body, hypovitaminosis. Patients with cirrhosis often experience

nosebleeds bleeding gums

Skin itching, palmar erythema (

small red rash on palms

), gynecomastia (

an increase in the size of the mammary glands in men

), spider veins on the skin,

In addition to symptoms in patients with liver disease, it is important to conduct a quality collection of anamnestic data that the doctor receives in the process of questioning the patient. These data will allow the attending physician to suspect a certain pathology of the liver. This is especially true of medicinal, alcoholic, infectious, toxic hepatitis (

inflammation of the liver

), Zieve syndrome, liver amoebiasis, 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 functioning of the liver, the doctor concludes that the possible pathology due to which the patient turned to him is drug-induced hepatitis.

The most common CBC changes in patients with liver disease are anemia (

), leukocytosis (

), increase

ESR (erythrocyte sedimentation rate) thrombocytopenia

), sometimes leukopenia (

) and lymphopenia (

). With echinococcosis and sarcoidosis of the liver, eosinophilia is possible (

). It is worth noting that based on the results of a complete blood count, a definitive diagnosis of any specific liver disease cannot be made.

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 activity

alanine aminotransferase (ALT), aspartate aminotransferase (AST)

Gamma-glutamyl transpeptidase, alkaline phosphatase, decrease in the amount of albumin, prothrombin index. Hypercalcemia can be seen in sarcoidosis (

increase in blood calcium

) and an increase in ACE (

angiotensin converting enzyme

An immunological blood test is most often given to patients with suspected viral hepatitis (

conduct a study on hepatitis markers - HbsAg, anti-Hbs, HBeAg, anti-Hbc IgG, etc.

), liver echinococcosis (

prescribe a test for antibodies to echinococcus

), amoebiasis of the liver (

prescribe a test for anti-amoebic 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 on alpha-fetoprotein - one of the oncomarkers

Infectious mononucleosis

test for antibodies to the Epstein-Barr virus

), cytomegalovirus infection (

test for antibodies to the cytomegalovirus virus

In some cases, patients with infectious liver diseases (

for example, with viral hepatitis, amoebiasis, cytomegalovirus infection, etc.

) appoint

PCR (polymerase chain reaction)

- one of the methods of laboratory diagnostics, which allows to identify DNA particles (

genetic material

) harmful pathogens in the blood. One of the most important methods for diagnosing liver diseases are radiation research methods - ultrasound (

) and computed tomography (

The main pathological changes that detect radiation methods of research in liver diseases

According to certain indications (

for example, enlargement of the liver and spleen of unclear etiology, conflicting laboratory results, etc.

) in patients with liver disease, a percutaneous liver biopsy is performed (

insertion through the skin into the liver of a needle 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, a liver biopsy is performed in order to confirm the presence of a malignant tumor in the liver, liver sarcoidosis, to establish the cause of hepatitis (

or cirrhosis of the liver

), its stage, severity.

In addition to yellowing of the albuginea (

) eyes and skin with blood diseases, there may also be an increase in the liver and spleen, fever,

General weakness, fatigue, shortness of breath, palpitations, dizziness, possible development

thrombosis

Nausea, vomiting, drowsiness, dark urine and stool,

convulsions

In case of poisoning with hemolytic poisons, the clinical picture depends entirely on the type of hemolytic poison, on the route of its entry into the body and concentration. Therefore, it is quite difficult to predict what kind of symptoms a patient will have in such cases.

Important information for the diagnosis of blood diseases is provided by the collection of anamnesis, in which doctors quite often establish their possible causes of 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, constant use of certain medications, etc.

). With hereditary pathologies (

erythrocyte membranopathies, erythrocyte enzymopathies, erythrocyte hemoglobinopathies, congenital autoimmune hemolytic anemias

) yellowness of the sclera of the eyes in patients appears periodically, often from birth and is often associated with various provoking factors (

for example, physical activity, 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 (

). 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 red blood cells.

In a biochemical blood test in patients with blood diseases, an increase in the content of total bilirubin is most often detected (

due to fraction of indirect bilirubin

), free hemoglobin, iron, increased activity of lactate dehydrogenase (

), a decrease in the content of haptoglobin. 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 erythrocytes. In case of poisoning with hemolytic poisons, a toxicological study of blood is carried out to identify toxins in its plasma that can damage red blood cells.

Immunological examination of blood in blood diseases is also no less important. It helps to detect antibodies against pathogens of malaria and babesiosis, to detect autoantibodies to erythrocytes in autoimmune hemolytic anemia (

AIHA with thermal 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

), which cause yellowing of the eyes. These methods help to establish the presence of defects in various genes encoding membrane proteins or erythrocyte enzymes. As an additional study for erythrocyte hemoglobinopathies,

electrophoresis

hemoglobin (

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 diseases is confirmed by ultrasound or computed tomography. In some cases, they are prescribed a puncture of the ilium or sternum to take the bone marrow. The formation of all erythrocytes that circulate in the blood takes place 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 erythrocytes.

For diseases of the biliary tract, yellowing of the sclera of the eyes and skin, skin itching, pain in the right hypochondrium are characteristic,

weight loss

Fever, heaviness in the abdomen, flatulence, nausea, vomiting, general malaise, myalgia (

muscle pain

), arthralgia (

joint pain

), hepatomegaly (

liver enlargement

), splenomegaly (

enlargement of the spleen

), headache.

These patients often show anemia on a complete blood count (

decrease in the number of red blood cells and hemoglobin in the blood

), leukocytosis (

an increase in the number of leukocytes in the blood

), an increase in 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 (

), aspartate aminotransferase (

), gamma-glutamyl transpeptidase.

Esophagogastroduodenoscopy (

) allows you to detect a tumor in the duodenum, assess the functional state of the papilla of Vater (

place in the wall of the duodenum where the common bile duct opens into it

). Also, with the help of this study, a biopsy can be performed (

select a piece of pathological tissue for cytological examination

) duodenal tumors. To assess the condition of the bile 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 of diagnosing gallstone disease are cholecystography (

x-ray method of examination of the gallbladder

) and ultrasound. 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, to identify the presence of tumors and foreign bodies in them. Ultrasound is also often prescribed to patients with suspected pancreatic tumor, opisthorchiasis.

Computed tomography and magnetic resonance imaging are commonly used in the diagnosis of tumors of the organs of the biliopancreatoduodenal zone (

extrahepatic bile ducts, gallbladder, pancreas and duodenum

). These methods allow to determine with high accuracy the presence of a tumor, its size, localization, stage of cancer, as well as to identify the presence of various complications.

The main symptoms of pathologies associated with impaired metabolic processes in the body are jaundice (

yellowing of the 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, tremor of the extremities , peripheral edema, mental retardation, psychosis. It is important to note that in most of these pathologies (

amyloidosis, Wilson-Konovalov disease, hemochromatosis, Crigler-Najjar syndrome, Dubin-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 be significantly expanded (

depending on the number of affected organs and the severity of their damage

Since almost all pathologies associated with impaired metabolic processes in the body are hereditary (

with the exception of 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-Najjar syndrome, Dubin-Johnson syndrome, or Gilbert's disease than amyloidosis, hemochromatosis, and Wilson-Konovalov disease. Jaundice in these last three pathologies appears later. In 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, heavy physical exertion, drinking excess alcohol, mechanical injuries, taking medications (

antibiotics, glucocorticoids, cytostatics, hormones, anticonvulsants, etc.

), smoking. With hemochromatosis, Wilson-Konovalov's disease and amyloidosis, yellowness of the sclera of the eyes is most often constant. Transmission of all hereditary diseases (

Crigler-Najjar syndrome, Dubin-Johnson syndrome, Gilbert's disease, amyloidosis, hemochromatosis, Wilson-Konovalov's 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 taking an anamnesis (

questioning the patient

In the general blood test 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 (

decrease in the number of red blood cells and hemoglobin in the blood

), an 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

). In a biochemical blood test in such patients, 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 (

), alanine aminotransferase (

), alkaline phosphatase, gamma-glutamyl transpeptidase, decrease in the amount of albumin, prothrombin index.

Based on the results of ultrasound or computed tomography, one can only suspect liver damage in a patient. Therefore, in order 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 the histological examination, a genetic examination is carried out, which is mainly used in the diagnosis of Crigler-Najjar syndrome, Dubin-Johnson syndrome, Gilbert's disease and hemochromatosis. This study identifies mutations characteristic of these pathologies (

) in the genes.

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 girdle character, nausea, vomiting, loss of appetite,

belchingheartburn

Diarrhea with steatorrhea

feces fetid, mushy, sticky, with a greasy sheen

), 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 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 detect 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

), which cause jaundice in these patients.

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, 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 access to these highly specialized doctors, then you can simply go to see 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 for different groups of pathologies (

diseases of the liver, diseases of the biliary tract, blood diseases, pancreatitis, metabolic disorders

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

Ziwe syndrome The main treatment for Ziwe syndrome is complete abstinence from alcohol. 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 has arisen on 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 agents. With autoimmune cirrhosis, immunosuppressants are prescribed, that is, agents that reduce the activity of immune reactions in the body. If cirrhosis appeared against the background of Wilson-Konovalov's 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 excrete 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 drugs, stop treatment with these drugs. In Budd-Chiari disease (

pathology in which blockage of the hepatic veins occurs

) patients are prescribed anticoagulants and thrombolytic agents. These drugs speed up the absorption

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 very early stages. In the later stages, this pathology is practically incurable. A variety of methods are used to treat liver cancer, 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.).

Sarcoidosis of the liver Sarcoidosis of the liver is treated with immunosuppressants and cytostatics. These drugs suppress immune responses in the body, reduce the formation of inflammatory granulomatous infiltrates, inhibit the reproduction of immunocytes (cells of the immune system) 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.

Amoebiasis of the liver With amoebiasis of the liver, amebocides are prescribed (drugs that destroy harmful amoebae). 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).

Blood diseases 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, erythrocyte hemoglobinopathies, autoimmune hemolytic anemias

) cannot be completely cured, therefore, symptomatic treatment is prescribed for such patients.

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, infusions of erythrocyte mass (drugs containing donor erythrocytes) or whole blood, hemodialysis, oxygen therapy are prescribed.

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

Erythrocyte enzymopathies Currently, there is no treatment method that would allow the patient to get rid of any kind of erythrocyte enzymopathy, so these pathologies are treated only symptomatically. They are usually given transfusions of red blood cells (a preparation containing donor red blood cells) or whole blood 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.

Erythrocyte hemoglobinopathies Treatment of erythrocyte hemoglobinopathies should be aimed at correcting the deficiency of hemoglobin, erythrocytes in the blood, iron deficiency in the body, the treatment of oxygen deficiency and the avoidance of provoking hemolytic crises (periods of breakdown of erythrocytes in the blood) factors (smoking, alcohol consumption, certain drugs, ionizing radiation, severe exercise, 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 (a drug containing donor red blood cells), 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 erythrocyte hemoglobinopathies may undergo surgical bone marrow transplantation or removal of the spleen.

Autoimmune hemolytic anemias 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 make up for the deficiency of destroyed red blood cells, patients are infused with red blood cells (a preparation containing donor red blood cells) or whole blood. To neutralize harmful products released from hemolyzed erythrocytes, detoxification therapy is carried out (gemodez, albumin, rheopolyglucin, plasmapheresis are prescribed). To prevent thrombosis, which often occurs in such patients, anticoagulants (anticoagulants) are prescribed.

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 detoxifying substances and hemodialysis (blood purification using a special device), which are designed to remove both the poisons themselves and the decay products of their own red blood cells from the blood. Washing the gastrointestinal tract is carried out only if the poisoning happened after eating the poison.

The main objective of the treatment of 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, cholelithiasis. With these pathologies, etiotropic treatment is often prescribed together with symptomatic treatment, which improves the outflow of bile through the biliary tract, but does not neutralize the very cause of bile stasis. Symptomatic treatment is 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. Etiotropic treatment against 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 stagnation of bile inside the liver. For this purpose, anticholestatics are used (cholestyramine, ursodeoxycholic acid, bilignin, etc.). These same drugs have a hepatoprotective property, that is, they protect liver cells from damage.

Cholelithiasis Gallstone disease is treated with various methods. First of all, such patients are prescribed a diet with the exception 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, these drugs are usually not prescribed for all patients. Drug therapy is 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 clog the bile ducts). According to the same indications, lithotripsy is performed - the destruction of stones under the action of specially created shock waves. With blockage of bile duct stones, the presence of jaundice and cholecystitis (inflammation of the mucous membrane of the gallbladder), surgery is often performed to remove the gallbladder.

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

The main direction of treatment of such pathologies is the appointment of all patients with detoxifying agents capable of removing various metabolites (

metabolic products

) from body tissues. Detoxifying therapy is performed in patients with hemochromatosis, Wilson-Konovalov's disease, Gilbert's disease, Crigler-Najjar syndrome, Dubin-Johnson. With amyloidosis, such treatment is not performed, since amyloid deposits are firmly deposited in the liver tissues and cannot be removed from the body by detoxifying methods.

Hemochromatosis In the presence of hemochromatosis, the patient is prescribed detoxifying drugs (deferoxamine), which are able to bind iron well in the blood and excrete it through the kidneys. In addition to drugs, such patients are often prescribed a diet that excludes the intake of foods containing large amounts 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 bloodletting 500 ml of blood, about 250 mg of iron is instantly removed from the human body.

Wilson-Konovalov disease In 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), which 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 responses in the body), choleretic drugs (improve the excretion of bile from the liver) .

Gilbert's disease 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), vitamins of group B. 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 increase the level of indirect bilirubin in the blood.

Crigler-Najjar Syndrome With Crigler-Najjar syndrome, various methods of detoxifying the body are used (prescription of barbiturates, heavy drinking, 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, and liver transplantation.

Dubin-Johnson Syndrome Patients with Dubin-Johnson syndrome are prescribed B vitamins and choleretic agents (they help to remove bile from the liver). They are contraindicated 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, starvation, trauma, viral or bacterial infections, etc.).

Amyloidosis 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). In some forms of amyloidosis, a liver transplant is performed.

If acute pancreatitis occurs or recurs (

re-exacerbation

) of chronic pancreatitis in the first few days, fasting is prescribed, that is, at this time the patient should not eat. He is switched to parenteral nutrition (

that is, he is injected with 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 stimulant for the production of gastric juice in the stomach and pancreatic juice in the pancreas.

Painkillers are usually prescribed for all pancreatitis (

analgin, drotaverine, baralgin, morphine, etc.

) means and inhibitors of proteolysis (

gordox, aprotinin, contrical, etc.

). The latter block the work of activated pancreatic enzymes that cause autolysis (

self-digestion

) of pancreatic tissue and, thereby, reduce the intensity of inflammatory processes in it. Also, with pancreatitis, substitution therapy is prescribed, which includes drugs (

festal, pancreatin, mezim, creon, panzinorm, cholenzim, etc.

antiemetics

metoclopramide, domperidone, etc.

). These drugs have not only antiemetic properties, but also improve motility in the gastrointestinal system.

There are the following main causes of the appearance of yellow sclera of the eyes in newborns:

• Crigler-Najjar syndrome. Crigler-Najjar 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.
• Dubin-Johnson Syndrome. Dubin-Johnson syndrome is a congenital disease in which the excretion of direct bilirubin from liver cells is impaired, due to which there is a violation of the removal of bilirubin from the liver and the whole organism.
• Physiological jaundice of newborns. During intrauterine development, the fetus has a large amount of fetal hemoglobin in erythrocytes. When a child is born, this type of hemoglobin is replaced with ordinary hemoglobin (HbA-hemoglobin), which is the dominant (predominant) form in all children and adults. Such a change is accompanied by yellowing of the skin and sclera of the eyes in a newborn and lasts the first 7-8 days of his life.
• Nuclear jaundice. Nuclear jaundice 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 incompatibility of the mother and fetus by blood groups, hereditary erythrocyte membranopathies, Hirschsprung's disease, congenital pyloric stenosis (obstruction of the pylorus), etc.
• infectious hepatitis. Infectious hepatitis in newborns is most common in cases where their mothers during pregnancy are not observed by doctors and do not undergo various laboratory tests for infections (toxoplasmosis, herpes, cytomegalovirus, hepatitis B, etc.).

How to clean the whites of the eyes from yellowness? It is possible to clean the whites of the eyes from yellowness forever only by curing those pathologies (diseases of the liver, biliary tract, blood, etc.) that cause it. There is no other way of such purification, since yellowness is usually caused by the deposition of bilirubin in the white of the eyes, where it is brought from the blood.

Alcoholic drinks contain ethyl alcohol, which is toxic to liver cells. When it is consumed excessively, liver cells are damaged, and toxic hepatitis occurs (

inflammation of the liver tissue

). With it, part of the liver cells die, as a result of which the liver loses the ability to neutralize all the indirect bilirubin that circulates in the blood, as a result of which it accumulates in it. Also, when liver cells are damaged, direct bilirubin is released into the blood, which these cells have already managed to create from indirect bilirubin. Therefore, when taking alcohol in the blood of a person, the level of direct and indirect bilirubin rises, which leads to their penetration into the sclera of the eyes, due to which the latter turn yellow.

There are no such drops. There is simply no point in developing these drops, since they will act for a very short time, because with pathologies that cause yellowing of the whites of the eyes, bilirubin, which is in the blood in high concentrations, will constantly penetrate into the white of the eyes and stain it yellow. Therefore, in order to get rid of the yellowness of the whites of the eyes, it is necessary to eliminate the main cause of the increase in bilirubin in the blood.

NOTE!

learn more If a person has yellow whites of the eyes, the reasons may lie in the appearance of various serious ailments, for example, diseases of the internal organs are possible. It is recommended to immediately seek help from doctors, since it is desirable to detect pathology at the initial stage of its development.

Yellowing of the whites of the eyes can mean the occurrence of diseases such as viral hepatitis, conjunctivitis, or even a cancerous tumor. A person alone will not be able to establish the exact cause, so it is better to immediately consult a doctor, conduct an examination, and begin treatment.

If the whites of the eyes turn yellow in a patient, then the following reasons for this phenomenon are possible:

1. Most often, a change in the color of proteins in front of a person's eyes occurs with liver damage.
2. Newborn babies may have yellow eyeballs for 3 to 5 days after birth. This phenomenon is called "jaundice in infants".
3. If the patient has yellow eyes, the cause may lie in the development of a malignant tumor on the conjunctiva.
4. Another option for why the whites of the eyes turn yellow is that the patient has an ailment that affects the eyes themselves. Most often, these are specific diseases that develop on the visual organs.
5. Yellowness in the eyes may develop from fatigue after intense intellectual work. Most often, this phenomenon is observed in people who sit in front of a computer monitor for days.

   The yellowness of proteins is striking

   The yellowness of the whites of the eyes can also appear under the influence of other factors.

   In any case, the clarification of the cause and treatment of the above pathologies should occur under the supervision of a physician.

   Self-diagnosis and taking medications is unacceptable, as it can provoke serious complications.

   If the white of the eye is yellow in a person who has applied to the clinic, this may mean hepatitis or other damage to the structures of the liver.

   The body has a special enzyme that is found in red blood cells.

   It is called bilirubin and is produced by the liver. When, under the influence of microorganisms that have entered the liver structures, this substance breaks down, the whites of the eyes turn yellow. In this case, yellowness due to processes in the liver extends to the entire human body.

   Newborn jaundice passes under UV irradiation

   Symptoms of such a lesion:

   1. The whites of the eyes are yellow.
   2. The liver is enlarged.
   3. Temperature rise is possible.
   4. The whole body of the patient is covered with yellow spots or completely painted in this color.
   5. Loss of appetite, general weakness.

   If the patient has these symptoms, you should immediately call a doctor or take the person to the hospital. As a rule, hepatitis is detected, most often type A. This is a group of serious diseases. Most common in children (jaundice). Its development at the initial stage can be detected precisely with the help of yellowed eye proteins (some types of this disease do not cause complete yellowing of the patient's body).

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   This symptom is clearly manifested in such ailments as echinococcosis or opisthorchiasis. Diseases are caused by various types of worms that settle in the liver and lay eggs there. Their larvae feed in this organ, and then, having matured, move to other parts of the human body.

   Many new mothers wonder why the whites of their newly born baby are yellow. This phenomenon - jaundice - is typical for babies. It develops due to the saturation of the baby's blood with a large number of red blood cells during development in the womb. After birth, he does not need such a volume of red blood cells, so they begin to decay. Because of this, the baby's eyes and body skin turn yellow.

   Moms rush to the doctors asking what to do. There is no need to worry, usually this phenomenon disappears by itself within 7-12 days. If this does not happen, then perhaps the child has another disease that caused similar symptoms. Then you need to seek help from a doctor.

   The white of the eye may turn slightly yellowish (slightly at the edges) or completely change color due to the development of various tumor neoplasms on the conjunctiva. Most often this occurs when melanoma occurs. This disease is quite difficult to diagnose. This type of cancer can lead to serious consequences, so you need to be treated for the disease in specialized clinics. For more information about the treatment of melanoma, see this video:

   In other diseases of the eye, its protein turns slightly yellow or can completely turn into various shades of this color. Usually such signs are inherent in diseases such as pterygium or pinguecula.

   The second disease develops due to a violation of lipid metabolism, which leads to the appearance of yellow wen in the eyes.

   A pterygium is an overgrowth of the conjunctiva. If this phenomenon spreads to the pupil, the patient may lose sight in one or both eyes. Therefore, if there are problems with the eyes, you should immediately contact the specialists.

   Doctors have determined that sometimes a patient develops a yellow tint on the proteins of the visual organs due to malnutrition. In order for everything to return to normal, doctors recommend a special diet to such a patient.

   It provides for the following measures:

   1. A person should completely refrain from drinking alcohol.
   2. The patient is forbidden to eat salty or spicy food.
   3. Fried foods and various flour products should be excluded from the diet.
   4. The daily menu should include a large number of fruits and foods that are rich in ascorbic acid.

   Sometimes men or women who have yellowness on the whites of their eyes due to fatigue come to the doctor for an appointment. This usually happens if a person does not get enough sleep or sits at a computer for a long time. The problem can be provoked by the solution of some complex intellectual problem, the presence of dry air in the room. The eyes are inflamed. These people need a little rest. You can apply sedative lotions. It is recommended to walk more in the fresh air. Usually, after 2-3 days of such a rest, the eyes return to normal, and the whites of the eyes acquire a natural color. For more information about dealing with the problem, see this video:

   If none of the above reasons is suitable to explain the change in the color of the proteins, then you should urgently consult a doctor, as this may be a warning of serious systemic disorders in the body that need to be treated.

   DO YOU STILL THINK IT IS DIFFICULT TO CORRECT YOUR VISION? Judging by the fact that you are now reading these lines, victory in the fight against deteriorating vision is not yet on your side ... And have you already thought about surgical intervention? It is understandable, because the eyes are a very important organ, and their proper functioning is the key to a full, healthy and happy life. Loss of vision, redness and sharp pain in the eyes, constant wearing of lenses ... All this is familiar to you firsthand. But perhaps it is more correct to treat not the consequence, but the cause? We recommend reading the story of the host of the program "Live Healthy" - Elena Malysheva, how she restored her vision ... Read the article >>

   The white of the human eye is not absolutely white, as it is imagined by designers who process pictures of models in a photo editor for gloss. A healthy protein color is slightly yellowish, but uniform, without streaks, spots, darkening. If the proteins turn yellow or become stained, this means that a person has problems with the state of internal organs, eye diseases, or he leads an unhealthy lifestyle. Most often, this is almost certainly a signal of a disease, so you should immediately consult a doctor and diagnose the disease.

   The whites of the eyes are yellow: causes and how to treat

   Why does the sclera turn yellow

   The white membrane, which is called the sclera, turns yellow most often imperceptibly to the person himself. This process does not cause pain or discomfort, and it may take some time before a person notices yellowing when looking at himself in a mirror, or someone tells him about it. Yellowing - sclera icterus - means the presence of pathology.

   Icteric sclera

   By the way. There are people who have a yellow tunic from birth. This is due to genetics, and does not mean disease. But if the color has changed, that is, the proteins have turned yellow, or blotches, fragments, darkening have appeared on them, it is urgent to go to the doctor.

   Metabolism of bilirubin

   There are several shades of yellow in which protein can be painted - from light to ocher or almost orange. It depends on the disease itself and on what stage the disease is in, that is, how badly the body has suffered from it. Diseases and other reasons due to which the color of the albuginea changes can be divided into three groups.

   Table. Causes of yellowing of the sclera in groups.

   Gilbert's syndrome

   Internal illnesses

   As a rule, yellowness in the eyes is observed due to an excess in the blood of a substance called bilirubin. It is a multiple compound that is yellow-brown in color and is an integral part of the bile that is produced in the body.

   Important! Bilirubin is formed after the destruction of the protein structure. Hemoglobin, cytochrome, myoglobin break down, and free bilirubin remains. This is a toxin that must be neutralized. This function is performed by the liver, which contains an acid that neutralizes the toxicity of bilirubin. The direct compound, which is no longer dangerous, is then sent to the bile ducts to exit the body.

   Yellow whites of the eyes

   Hepatic pathologies

   If the liver experiences overload, there is a malfunction in its work of any nature, bilirubin rises in the blood, since the unhealthy organ cannot cope with its task. Decay occurs, but the removal of the toxin is not carried out, accumulating in the body. Because of this, all the integuments of the body turn yellow, and since yellowing occurs first on the sclera, and such a phenomenon as yellow squirrels is observed.

   Hepatitis symptoms

   Echinococcosis

   A disease resulting from penetration into the body and effects on the liver of echinococci. This is one of the modifications of helminthic infestations that can be found in worm-infected food, drink, or pass from animals.

   Echinococcus

   cirrhosis

   This pathology entails multiple lesions of the liver tissue, replacing healthy tissue with a pathologically altered one. In damaged tissue, the ability to neutralize the toxicity of bilirubin decreases and is completely canceled. It accumulates in the tissues, leaving the outer integument and mucous membranes. Cirrhosis can occur:

   • due to alcoholism;
   • as a post-hepatitis complication;
   • due to venous insufficiency;
   • a consequence of prolonged use of antibiotics;
   • due to diseases in which a suspension of heavy metals accumulates in the tissues.

   Cirrhosis of the liver

   Crayfish

   The disease is marked by the appearance and progressive growth of tissue inflammation, which develops into a tumor that destroys healthy liver cells. Because of this, the body loses the ability to function and, in particular, neutralize bilirubin.

   Cholangiocarcinoma of the liver

   Microorganisms

   These infections include:

   • worms are flat;
   • epistorchiasis;
   • opisthorchiasis;
   • echinococcosis.

   Worms in the liver

   By the way. Opisthorchiasis, characterized by cloudy yellow proteins, causes a type of worm that can appear in the body after eating insufficiently cooked fish. They, multiplying, block the walls of the liver ducts, disrupting the excretion of bile. After that, the substance enters the blood, and the appearance of yellowness on the sclera.

   Opisthorchiasis

   Blood diseases

   The internal ailments that cause the yellowness of the peripupillary zone include diseases of the circulatory apparatus. They always cause erythrocyte annihilation, which immediately increases the amount of bilirubin. The body begins not to cope with its excretion, even with a healthy liver, so the toxin is deposited and gives the tissues a characteristic yellowness.

   1. Malaria.
   2. Congenital pathologies.
   3. Babesiosis.
   4. Sickle cell poisons that affect the body.

   Symptoms of malaria

   Malaria

   Gained immense popularity, but spread only in those parts of the world where malarial mosquitoes live. It is their bite that charges the blood with malarial bacteria. The infected organism transports it directly to the liver, where they multiply intensively. Having increased the population to a critical one, they again penetrate into the blood, destroying the structural bodies and causing the breakdown of erythrocytes, stimulating the hyperformation of bilirubin.

   Babesiosis in humans

   By the way. With stable and high immunity, the susceptibility to this disease in humans is very low, almost zero. But if immunity is reduced, a tick bite will certainly cause jaundice of the sclera.

   There is a whole group of hereditary diseases that pass as genetic traits and cause yellowness of the albuginea. These include the following:

   • erythrocyte membraneopathy;
   • hemoglobinopathy;
   • enzymopathy and others.

   Hereditary enzymopathies are diseases caused by hereditary disorders of biosynthesis

   All of them are characterized by an effect on blood cells, leading to their disintegration. During the process, there is an excess of bilirubin in the blood. The liver ceases to cope with it, and its cells capture the entire body, including the eye sclera.

   We are talking about letting into the blood of hemolytic poisons, called sickle-shaped. It provokes hemolysis of blood, causing a shortage of red blood cells. As a result, there is a state of anemia, and yellowness of the eyes. Poisons of this class include:

   • arsenic;
   • copper connections;
   • benzene;
   • chloroform;
   • nitrate compounds;
   • mercury and others.

   By the way. The class of these toxins also includes the venom of bees and snakes, poisonous spiders and other insects, and substances contained in poisonous mushrooms, berries and other plants.

   Since unnecessary and dangerous substances leave the body through the exit routes of bile, problems in the routes cause transportation problems. To get into the intestines, bile goes a long way, during which, in the presence of failures and narrowing of the ducts, an accumulation of a substance is formed at one point. This causes a rupture at this point, after which bile enters the bloodstream. Further, everything, as with other internal diseases - hyperbilirubin is reflected in the color of the sclera. Pathologies that trigger these processes include the following.

   1. Cholelithiasis.
   2. Cholangitis.
   3. Jaundice.
   4. Cancers of the pancreas.

   Primary sclerosing cholangitis

   Sclerosing cholangitis

   The origin of the disease is not clear. In the course of the disease, irritation of the bile ducts occurs, inflammation occurs, transformation of the walls of the passage, and blockages. It is difficult for bile to enter the intestines, instead it is absorbed by the blood. Since bile contains conjugated bilirubin, external tissues stain.

   Gallstone disease occurs due to the formation of stones, which are soldered particles of cholesterol and other solid substances and sediments. When formed, they clog the bile ducts and provoke the release of bile into the blood.

   Cholelithiasis

   Crayfish

   Not only a tumor in the liver, but also its formation in the bile duct demonstrates the yellowness of the protein. As the tumor grows, bile with bilirubin stagnates. It goes out into the break and becomes an integral part of the blood flow.

   About this disease, which has the medical name hepatitis A, it is necessary to talk in detail. Jaundice is very dangerous for humans. And yellowness of the eyes is the first in a series of signs of this disease.

   Hepatitis A

   Depending on how slowly or quickly bilirubin breaks down and is excreted (since different processes affect the output in different ways), the disease is divided into three types.

   1. Hemolytic.
   2. cholestatic.
   3. Hepatic.

   Table. Types of hepatitis A.

   Hemolytic Cholestatic Hepatic Facts about viral hepatitis A By the way. There is also jaundice diagnosed in newborns. It is not a disease or pathology. The phenomenon is explained by the fact that in the process of intrauterine formation, the embryo receives an excess amount of red blood cells from the mother. Then, in order to rid the body of it, nature arranges for the breakdown of blood cells, replacing them with bilirubin cells. One to two weeks after birth, the color indicators of the skin and sclera of the baby acquire a normal color. If this does not happen, a consultation with a pediatrician is necessary. Of the ophthalmic pathologies that cause yellowing of the albuginea, not so many diseases can be listed as internal ones. However, some eye problems lead to this phenomenon - icterus of the sclera. Pingueculitis. Gilbert's syndrome. Melanoma. Malignant conjunctivitis. Pterygium. Yellow whites of the eyes - causes Pinguecula formation In a simple way, this is a wen, which is formed on the conjunctiva, mainly due to disorders of fat metabolism. It can be large and colored in a shade of yellow. It appears for several reasons: aging; eye irritation from smoke or wind; prolonged exposure to the sun. Pinguecula (fat on the eye) This formation does not affect vision in any way, but when it is detected, it is worthwhile to see an ophthalmologist in order to exclude yellowing of the sclera for another reason. Also, if the tissue around the wen becomes inflamed and begins to cause discomfort, an operation to remove it may be indicated. Wen is a benign formation, unlike melanoma, which is malignant. With it, the white membranes also turn yellow. And it can have various modifications. Flat spot. Convex or bumpy spot. Color yellow to brown. Colorless. Blue-eyed people are at higher risk for melanoma Pathology is formed in the inner corner of the eye, it is considered a rare disease that is difficult to diagnose. With this pathology, the conjunctiva grows. Soon it forms a rim, advancing on the albuginea. In this case, the color of the latter changes, becoming cloudy yellow. There is discomfort in the eye. Education is treated surgically, and the effectiveness of treatment depends on timely detection. The course of pterygium Important! If the growth of the conjunctiva is not stopped, it will close the entire pupil completely, and the person will stop seeing. This disease can be attributed to genetic. The syndrome is not even considered a pathology, rather, a physiological feature, but it can also cause yellow eyes. With this feature in the blood of a person, the concentration of bilirubin is constantly increased, as a result, his eyes are constantly yellow. What does Gilbert's syndrome mean and how is it treated? Having a syndrome, the patient must avoid situations of release of bilirubin in even greater quantities due to stress, overload or viral diseases. This is a serious cause of yellowing of the eyes, especially if a person has it wrong. Bad habits and addictions, abuse and processing, an insufficient amount of useful substances entering the body - all this can be the reason for the acquisition of an unhealthy yellow tint by the protein coat. What do you want in this case? Take steps to improve your lifestyle. Change the diet by removing flour, salty, spicy, fried. Exclude alcohol. Vitaminize food. Relax, sleep, walk. Refusal of alcohol As you can see, there are many causes of yellow whites of the eyes, and the main ones are serious illnesses. How to treat them? Depending on which group the disease belongs to, the manifestation of which was yellowing of the eyes, the treatment is prescribed either by an ophthalmologist, or a therapist, or a doctor of another narrow specification. In any case, it is necessary, having discovered the yellowness of the protein, which suddenly appeared, or the intensification of the hue from the nature of the yellowish color, immediately undergo a consultation. The first doctor is an ophthalmologist who will refer the patient to other specialists for tests and ultrasound. Examination by an ophthalmologist To prevent diseases that cause yellowing of the sclera, first of all, it is necessary to increase the level of general health and avoid infection with viral infections. The liver must be protected and supplied with all the necessary elements for uninterrupted operation, which is achieved by a balanced diet. Best Foods for Liver Health You should engage in physical activity or at least take walks. It is helpful to take a multivitamin from time to time. Make sure that there is rest in work, sleep remains healthy and in sufficient quantity.

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

There are three main membranes in the eyeball:

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

Outer shell of the eyeball

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 the endothelium.

The cornea 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 section of the outer shell of the eye. This department occupies most of the area of ​​the 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 anteriorly by the conjunctiva, and the posterior by the endothelium. conjunctiva ( conjunctiva) is a relatively thin shell, which consists of a cylindrical stratified epithelium. This sheath covers the inside of the eyelids ( secular part of the conjunctiva) and the eyeball outside ( ocular part of the conjunctiva). Moreover, this structure does not cover the cornea.

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

Middle shell of the eyeball

The back part of the middle shell of the eyeball is called the own choroid of the eyeball. It is located directly under the white of the eye in the back of it. 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 cells of the retina ( inner lining of the eyeball) eyes. The posterior part of the middle shell lines almost two-thirds of the entire area of ​​the sclera, and therefore is the largest of all three parts of the middle shell.

A little ahead of her back of 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) of the body includes special epithelial cells that are engaged in the production of intraocular fluid that fills the anterior and posterior chambers of the eye.

The inner lining of the eyeball

Causes of yellow eyes

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). With a mild degree, the concentration in the blood of total bilirubin reaches 86 µmol / l. With an average degree in the blood of a patient, the level of bilirubin 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 of these listed 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 a 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 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 liver damage, yellowing of the skin and albuginea occurs ( sclera) eye.

Ziwe syndrome

Cirrhosis of the liver

If the disease is not treated for a long time, then the echinococcal cyst begins to gradually increase in size and compress the surrounding liver tissues, causing them to die ( atrophy of the liver parenchyma). As a result of this, there is a mechanical replacement of normal hepatic tissue, in place of which a cyst appears. At a certain moment, 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 of the eyes, giving them a characteristic yellow color.

Sarcoidosis of the liver

As a result of the impact of such factors on human tissues, the functioning of the immune system is disrupted. If it detects some antigens in 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 foci visually look like nodules ( or granulomas), different from normal tissues. Granulomas may vary in size and location. Inside such foci, the cells of the immune system, as a rule, act inefficiently, so these granulomas persist for a long time, and in some cases they can increase in size. In addition, new granulomas constantly appear in sarcoidosis ( especially if left untreated).

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 function as granulomatous infiltrates replace their normal parenchyma ( the cloth). If, for example, sarcoidosis affects the lungs ( and they are most often damaged in 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 ( in the liver, the synthesis of blood proteins is disrupted) functions.

The main manifestation of extraintestinal amebiasis is liver damage. When pathogenic amoebas enter the liver, they cause damage to its tissues there. Hepatitis occurs first inflammation of the liver tissue). Some time later, 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 may be a large number of such abscesses. In the absence of treatment for liver amoebiasis, its various functions are violated, 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 the erythrocyte schizogony, the infected erythrocytes are completely destroyed and release a large number of proliferating merozoites, which again enter new erythrocytes for reproduction. Thus, this process proceeds 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 contents of erythrocytes and, in particular, the protein - hemoglobin. When this protein breaks down, bilirubin is formed ( indirect), which must be detoxified 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, patients with malaria develop hyperbilirubinemia ( an increase in the level of bilirubin in the blood) and jaundice ( yellowing of the skin and eyes), which occurs due to the partial deposition of bilirubin in the tissues.

Erythrocyte membranopathies

The best-known erythrocyte membranopathies are Minkowski-Chauffard disease, hereditary elliptocytosis, hereditary stomatocytosis, hereditary acanthocytosis, and hereditary pyropoykylocytosis. All these pathologies are characterized by a triad of clinical signs - jaundice, hemolytic anemia ( a 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 there is a frequent destruction of defective erythrocytes in the blood, which is accompanied by the release of a large amount of hemoglobin, which then turns into indirect bilirubin. The liver cannot immediately process huge 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 whites of the eyes and skin.

Erythrocyte enzymopathies

In any case, enzyme deficiency 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 ( a 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 indirect bilirubin from the blood, which was formed in large quantities during the breakdown of hemoglobin. Therefore, indirect bilirubin is deposited in the skin and whites of the eyes and causes them to turn yellow.

Erythrocyte hemoglobinopathies

Therefore, patients suffering from one of these diseases often have hemolytic anemia ( 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 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 collapsing erythrocytes. This hemoglobin is subsequently broken down and converted into indirect bilirubin. Since with these pathologies there is a destruction of a large number of red blood cells, 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 in other tissues and organs. If this bilirubin penetrates the skin and whites of the eyes, they turn yellow. Yellowing of the whites of the eyes and skin is called jaundice.

Autoimmune hemolytic anemias

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). This anemia is fully 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 thermal 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 erythrocytes). Being deposited in the tissues, this chemical metabolite causes them to turn yellow, therefore, with these pathologies, patients often have yellow skin and sclera of the eyes.

babesiosis

Most of the hemolytic poisons are 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 the poisoning with hemolytic poisons occurs in industrial workers who are constantly in contact with these toxic substances.

Under the influence of hemolytic poisons, the membranes of erythrocytes are deformed, as a result of which they are destroyed. There are also some hemolytic poisons that block the flow of enzymatic processes inside red blood cells, due to which they disrupt energy metabolism or their antioxidant capacity ( resistance to oxygen free radicals), causing them to collapse. Certain chemicals are able to 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 anemia occurs. With them, the immune system destroys the patient's own red blood cells, so their number in the blood is significantly reduced.

Thus, in case of poisoning with hemolytic poisons, due to various mechanisms, massive destruction of erythrocytes inside the vessels occurs. 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 their yellowing.

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

Primary sclerosing cholangitis

Cholelithiasis

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

Stones formed during gallstone disease can be located in the so-called blind spots in the biliary system ( for example, in the body or the bottom of the gallbladder). In such cases, this disease does not manifest itself clinically, since the stones do not clog 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, intrahepatic bile ducts are destroyed inside the liver, and bile enters directly into the bloodstream.

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 blockage of the bile ducts by a stone. At a certain concentration in the blood of direct bilirubin, it penetrates the skin and whites of the eyes and stains them yellow.

Tumors of the organs of the biliopancreatoduodenal zone

Crigler-Najjar Syndrome

There are two types of Crigler-Najjar 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 glucuronyl transferase), which binds indirect bilirubin. This type of Crigler-Najjar syndrome usually results in the 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 with the norm, is much lower. In 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-Najjar 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-Najjar syndrome are observed much more often than in patients with Gilbert's disease.

Dubin-Johnson Syndrome

The first signs of Dubin-Johnson syndrome in patients usually appear at a young age ( predominantly in men). Jaundice is almost always permanent 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). If the disease goes into remission ( asymptomatic course), then it can quickly worsen if the patient is exposed to various provoking factors ( heavy physical exertion, stress, alcohol consumption, fasting, injuries, viral or bacterial infections, etc.), which should be avoided if possible.

Amyloidosis

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 in the 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

Diagnosis of liver diseases

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 have diarrhea with blood and mucus, false urges, dehydration of the body, hypovitaminosis. Patients with cirrhosis of the liver often experience epistaxis, bleeding gums, pruritus, palmar erythema ( small red rash on palms), gynecomastia ( an increase in the size 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 conduct a quality collection of anamnestic data that the doctor receives in the process of questioning the patient. These data will allow the attending physician to suspect a certain pathology of the liver. This is especially true of medicinal, alcoholic, infectious, toxic hepatitis ( inflammation of the liver), Zieve syndrome, liver amoebiasis, 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 functioning of the liver, the doctor concludes that the possible pathology due to which the patient turned to him is drug-induced hepatitis.

The most common CBC changes in patients with liver disease are anemia ( ), leukocytosis ( an increase in the number of leukocytes in the blood), an 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 ( an increase in the number of eosinophils in the blood). It is worth noting that based on the results of a complete blood count, a definitive diagnosis of any specific liver disease cannot be made.

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, decreased albumin, prothrombin index. Hypercalcemia can be seen in sarcoidosis ( increase in blood calcium) and an increase in ACE ( angiotensin converting enzyme).

An immunological blood test is most often given to patients with suspected viral hepatitis ( conduct a study on hepatitis markers - HbsAg, anti-Hbs, HBeAg, anti-Hbc IgG, etc.), liver echinococcosis ( prescribe a test for antibodies to echinococcus), amoebiasis of the liver ( prescribe a test for anti-amoebic 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 on alpha-fetoprotein - one of the oncomarkers), Infectious mononucleosis ( test for antibodies to the Epstein-Barr virus), cytomegalovirus infection ( test for antibodies to the cytomegalovirus virus).

In some cases, patients with infectious liver diseases ( for example, with viral hepatitis, amoebiasis, cytomegalovirus infection, etc.) appoint PCR ( polymerase chain reaction) is one of the methods of laboratory diagnostics, which makes it possible to detect DNA particles ( genetic material) harmful pathogens in the blood. One of the most important methods for diagnosing liver diseases are radiation research methods - ultrasound ( ultrasound) and computed tomography ( CT).

The main pathological changes that detect radiation methods of research in liver diseases

Diagnosis of blood diseases

Important information for the diagnosis of blood diseases is provided by the collection of anamnesis, in which doctors quite often establish their possible causes of 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, constant use of certain medications, etc.). With hereditary pathologies ( erythrocyte membranopathies, erythrocyte enzymopathies, erythrocyte hemoglobinopathies, congenital autoimmune hemolytic anemias) yellowness of the sclera of the eyes in patients appears periodically, often from birth and is often associated with various provoking factors ( for example, physical activity, 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 ( decrease in blood platelets). 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 red blood cells.

In a biochemical blood test in patients with blood diseases, an increase in the content of total bilirubin is most often detected ( due to 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 some enzymes can be detected ( for example, glucose-6-phosphate dehydrogenase, pyruvate kinase, etc.) inside erythrocytes. In case of poisoning with hemolytic poisons, a toxicological study of blood is carried out to identify toxins in its plasma that can damage red blood cells.

Immunological examination of blood in blood diseases is also no less important. It helps to detect antibodies against pathogens of malaria and babesiosis, to detect autoantibodies to erythrocytes in autoimmune hemolytic anemia ( AIHA with thermal 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), which cause yellowing of the eyes. These methods help to establish the presence of defects in various genes encoding membrane proteins or erythrocyte enzymes. As an additional study for erythrocyte 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 diseases is confirmed by ultrasound or computed tomography. In some cases, they are prescribed a puncture of the ilium or sternum to take the bone marrow. The formation of all erythrocytes that circulate in the blood takes place 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 erythrocytes.

Diagnosis of diseases of the biliary tract

These patients often show anemia on a complete blood count ( decrease in the number of red blood cells and hemoglobin in the blood), leukocytosis ( ), an increase in 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 papilla of Vater ( place in the wall of the duodenum where the common bile duct opens into it). Also, with the help of this study, a biopsy can be performed ( select a piece of pathological tissue for cytological examination) duodenal tumors. To assess the condition of the bile 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 of diagnosing gallstone disease are cholecystography ( x-ray method of examination of the gallbladder) and ultrasound. 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, to identify the presence of tumors and foreign bodies in them. Ultrasound is also often prescribed to patients with suspected pancreatic tumor, opisthorchiasis.

Computed tomography and magnetic resonance imaging are commonly used in the diagnosis of tumors of the organs of the biliopancreatoduodenal zone ( extrahepatic bile ducts, gallbladder, pancreas and duodenum). These methods allow to determine with high accuracy the presence of a tumor, its size, localization, stage of cancer, as well as to identify the presence of various complications.

Diagnosis of pathologies associated with impaired metabolic processes in the body

Since almost all pathologies associated with impaired metabolic processes in the body are hereditary ( with the exception of 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-Najjar syndrome, Dubin-Johnson syndrome, or Gilbert's disease than amyloidosis, hemochromatosis, and Wilson-Konovalov disease. Jaundice in these last three pathologies appears later. In 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, heavy physical exertion, drinking excess alcohol, mechanical injuries, taking medications ( antibiotics, glucocorticoids, cytostatics, hormones, anticonvulsants, etc.), smoking. With hemochromatosis, Wilson-Konovalov's disease and amyloidosis, yellowness of the sclera of the eyes is most often constant. Transmission of all hereditary diseases ( Crigler-Najjar syndrome, Dubin-Johnson syndrome, Gilbert's disease, amyloidosis, hemochromatosis, Wilson-Konovalov's 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 taking an anamnesis ( questioning the patient).

In the general blood test 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 ( decrease in the number of red blood cells and hemoglobin in the blood), an 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). In a biochemical blood test in such patients, 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, decrease in the amount of albumin, prothrombin index.

Based on the results of ultrasound or computed tomography, one can only suspect liver damage in a patient. Therefore, in order 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 the histological examination, a genetic examination is carried out, which is mainly used in the diagnosis of Crigler-Najjar syndrome, Dubin-Johnson syndrome, Gilbert's disease and hemochromatosis. This study identifies mutations characteristic of these pathologies ( defects) in the genes.

Diagnosis of acute or chronic pancreatitis

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 detect 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), which cause jaundice in these patients.

Treatment of pathologies leading to yellowness of the eyes

Treatment of liver diseases

Ziwe syndrome
The main treatment for Ziwe syndrome is complete abstinence from alcohol. 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 arose on 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 agents. With autoimmune cirrhosis, immunosuppressants are prescribed, that is, agents that reduce the activity of immune reactions in the body. If cirrhosis appeared on 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 excrete 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 drugs, stop treatment with these drugs. In 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 very early stages. In the later stages, this pathology is practically incurable. A variety of techniques are used to treat liver cancer, which may include surgery ( mechanical removal of the tumor, liver transplantation, cryodestruction, etc.), radial ( irradiation of the tumor with ionizing radiation, radioembolization, etc.) and chemical methods ( injection of acetic acid, ethanol into the tumor, etc.).

Sarcoidosis of the liver
Sarcoidosis of the liver is treated with immunosuppressants and cytostatics. These drugs suppress immune reactions in the body, reduce the formation of inflammatory granulomatous infiltrates, inhibit the reproduction of immunocytes ( immune system cells) and 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.

Amoebiasis of the liver
For 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. 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

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 erythrocytes) or whole blood, hemodialysis, oxygen therapy.

Erythrocyte membranopathies
Patients with erythrocyte membranopathies are given symptomatic treatment, which most often consists of splenectomy ( removal of the spleen), infusions of erythrocyte mass ( ), prescribing vitamins B12 and B9. In some cases, whole blood is transfused, and steroidal anti-inflammatory drugs and cholekinetics are also prescribed ( drugs that speed up 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 kind of erythrocyte enzymopathy, so these pathologies are treated only symptomatically. They are usually treated with red blood cell transfusions ( preparation containing donor erythrocytes) or whole blood in 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.

Erythrocyte hemoglobinopathies
Treatment of erythrocyte hemoglobinopathies should be aimed at correcting the deficiency of hemoglobin, erythrocytes in the blood, iron deficiency in the body, treating oxygen deficiency and avoiding provoking hemolytic crises ( periods of breakdown of erythrocytes in the blood) factors ( smoking, drinking alcohol, certain drugs, ionizing radiation, heavy physical exertion, 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 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 erythrocyte hemoglobinopathies may undergo surgical bone marrow transplantation or removal of the spleen.

Autoimmune hemolytic anemias
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, patients are infused with erythrocyte mass ( preparation containing donor erythrocytes) or whole blood. To neutralize harmful products released from hemolyzed erythrocytes, detoxification therapy is carried out ( prescribe gemodez, albumin, reopoliglyukin, plasmapheresis). Anticoagulants are prescribed to prevent thrombosis, which is common in these patients ( 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 detoxifying agents and hemodialysis ( blood purification with a special device), which are designed to remove from the blood both the poisons themselves and the decay products of their own red blood cells. Washing 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
Primary sclerosing cholangitis is a rapidly progressive disease that usually leads to the development of biliary cirrhosis. Etiotropic treatment against 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 stagnation of bile inside the liver. For this purpose, anticholestatic drugs are used ( cholestyramine, ursodeoxycholic acid, bilignin, etc.). These same drugs have a hepatoprotective property, that is, they protect liver cells from damage.

Cholelithiasis
Gallstone disease is treated with various methods. First of all, such patients are prescribed a diet with the exception of very fatty and high-calorie foods. Secondly, they are prescribed drugs ( chenodeoxycholic and ursodeoxycholic acids), which can dissolve stones directly in the gallbladder. However, these drugs are usually not prescribed for all patients. Drug therapy is indicated only in cases where gallbladder function and biliary tract patency are preserved ( that is, stones do not clog the bile ducts). According to the same indications, lithotripsy is performed - the destruction of stones under the action of specially created shock waves. With blockage of bile duct stones, the presence of jaundice and cholecystitis ( inflammation of the mucous membrane of the gallbladder) quite often perform surgery to remove the gallbladder.

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

Hemochromatosis
In the presence of hemochromatosis, the patient is prescribed detoxifying drugs ( deferoxamine), which are able to bind iron well in the blood and excrete it through the kidneys. In addition to drugs, such patients are often prescribed a diet that excludes the intake of foods containing large amounts 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 bloodletting 500 ml of blood, about 250 mg of iron is instantly removed from the human body.

Wilson-Konovalov disease
In 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, 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 intestine), anti-inflammatory agents, 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), vitamins of group B. 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, fasting, heavy physical exertion, drinking alcohol, smoking, etc.), which can increase the level of indirect bilirubin in the blood.

Crigler-Najjar Syndrome
With Crigler-Najjar syndrome, various methods of detoxifying the body are used ( prescription of barbiturates, heavy drinking, plasmapheresis, hemosorption, administration of albumin). 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 cholagogues ( promote the excretion of bile from the liver). They are contraindicated insolation ( prolonged exposure to sunlight). To the extent possible, such patients are advised to avoid precipitating factors ( heavy physical exertion, stress, alcohol consumption, hepatotoxic drugs, fasting, injuries, viral or bacterial infections, etc.).

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

Treatment of acute or chronic pancreatitis

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

Often, people are very carelessly in no hurry to look for the causes of yellowed whites of the eyes, and in vain. Even if such a state does not yet bring tangible discomfort, it is simply necessary to wonder why this happened. After all, the following factors can serve as reasons:

• infectious diseases;
• Viral hepatitis;
• Liver disease;
• gallbladder problems;
• Neoplasms, including malignant ones.

Liver disease

Most often, the yellowness of the whites of the eyes signals a violation in the liver, which, most likely, requires urgent treatment. After all, this organ performs very important functions that ensure the viability of the body.

For example, yellow proteins are a symptom of any type of hepatitis, although group A disease is most likely. In addition to yellowing of the eyes, it has spots on the skin of the same color or a shade of yellowness throughout the skin.

Newborn jaundice

Newborns also have a yellow color of proteins. True, this situation should not cause alarm. The reasons for its occurrence are banal - during the development of the embryo in the womb, a large number of red blood cells enter its bloodstream, which, after the birth of the child, begin to disintegrate, staining the skin, including the eyes, yellow. After ten to fourteen days, after the complete disintegration of the pigment, the color of the eyes becomes normal, as well as the rest of the baby's body.

Malignant conjunctivitis

Yellow colored squirrels may be a symptom or another malignant type. The particular danger of this disease is its relative rarity, which complicates the correct diagnosis and the choice of effective treatment.

Therefore, it is especially important to get to the doctor on time, to identify this type of cancer as early as possible and get rid of it safely.

Other eye diseases

Often, the eyes change shade under the influence of diseases of the organs of vision, for example, such as and.

The cause of the disease in the first case is changes in lipid metabolism, leading to the development of yellow wen.

In the second case, with pterygium, we are talking about increasing and affecting a large area of ​​the eyeball conjunctivitis. In this case, treatment should be started immediately, since due to its spread directly to the pupil, a complete loss of the ability to see is possible.

Bad habits

There are also bad habits, whose manifestations are reflected in the color of the eye proteins.

True, contrary to popular belief, smoking cannot change the shade of the eyes, even though it is incredibly harmful. Unlike an incorrectly composed diet, therefore, having noticed the yellowness of the eyes, be prepared to switch to a strict diet at least for a while:

• Refuse salty;
• Exclude acute;
• Remove fried, flour from the diet;
• Significantly limit alcohol consumption.

It is very important to consume foods rich in vitamin C.

Eye strain

Excessive strain on vision can also be a factor influencing changes in eye color, including:

• Prolonged daily work at the computer;
• Chronic sleep deprivation;
• Reading lying down and in low light, etc.

Therefore, walk outdoors as much as possible. This not only contributes to the rest of the organ of vision, but also serves as an excellent prevention of many diseases.

Try to use medical methods of care, including drops, lotions, etc. But do not neglect your health, and when the first signs of a change in the color of the whites of the eyes appear, be sure to contact a qualified specialist for a thorough examination and examination.

As already mentioned, the cause of the appearance of yellow eyes can be eye pathologies that require the participation of an ophthalmologist in the treatment. In this case, it is important to choose an eye clinic where you will really be helped, and not "swept aside" or will "pull" money without solving the problem. The following is a rating of specialized ophthalmological institutions where you can undergo examination and treatment if you have been diagnosed with yellow whites of the eyes.