The eyes are called the mirror of the soul, and the physical state of the human body is often reflected in the eyes. For example, if the yolks of the eyes have changed color and acquired a yellowish tint, then a serious pathology may be occurring. Diseases that are accompanied by such characteristic feature, can even be fatal. If you do not start treating the patient in a timely manner, the course of the disease can be unpredictable.

Quite often, people whose whites of their eyes have turned yellow do not bother to find the cause of such a pathological change. This indifference is due to the fact that this symptom does not bring pain and is not perceived by the patient as an alarming symptom. However, this approach is incorrect and dangerous. It is imperative to establish the reason for the change in shell color, even if only some areas have acquired a yellow tint. Such transformations can occur against the background of:

• Various types of infections;
• Viral hepatitis;
• Pathological changes in liver tissue;
• Diseases of the biliary tract;
• The appearance of neoplasms of benign and malignant nature.

Only a doctor's opinion

In order to determine whether the change in color of the whites of the eyes is pathological, you need to consult a doctor and conduct a full examination. After this, we can already talk about whether it is worth panicking or whether there is no danger in the yellowing of the sclera. Interestingly, in some cases this color change is a consequence of congenital characteristics.

Below are the main reasons why yellow membranes of the eye may form.

Option #1. The problem is related to internal pathology body

Typically, yellow whites of the eyes tell the patient that some pathological changes are occurring in his body. More often than others, liver diseases are diagnosed. Due to the fact that the cells of this organ bear a colossal load, the liver is very important for the normal functioning of the entire body. Therefore, at the slightest suspicion of its damage, you should visit a doctor.

For hepatitis of any type characteristic symptom is jaundice. This condition is also accompanied not only by a change in the color of the skin, but also the mucous membrane of the eye. Most often, jaundice appears with hepatitis type A, but can accompany the acute stage of hepatitis C or B.

Option number 2: changes in the color of the sclera in a newborn

In newborn babies, yellowing of the whites of the eyes is very common. This is due to the fact that after birth the child’s intrauterine hemoglobin, which has a slightly different structure, begins to decompose. As a result, a large amount of bilirubin is released into the baby's blood. It is this pigment that gives the yellow tint to the skin and eyes. After a couple of weeks everything returns to normal and the signs physiological jaundice in newborns they disappear without a trace. The sclera of the eyes becomes white again.

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“Jaundice,” that is, the appearance of a yellow color on the skin or mucous membranes, is not an independent disease. This is a symptom, that is, the result of an emerging pathology. Yellowing of the white of the eye itself is often not painful. In this case, it is often ignored. The patient does not consider it necessary to seek advice about the causes of his condition, since the change in color is not perceived as a dangerous problem. But sometimes yellowing of the eyes is combined with quite unpleasant symptoms: skin itching, bitter taste in the mouth, headache, nausea, weakness, insomnia.

However, even in the absence of painful manifestations, such a condition should in no case be neglected. Sometimes a yellowish tint to the white of the eye can be explained natural causes. But in such cases, the shade remains permanently, throughout life. And, most definitely, we are talking about a light shade, and not definitely yellow. In cases where the whites of the eyes have recently turned yellow, it is important to pay close attention to this change. “Jaundice” is a signal indicating the emergence of a serious problem or illness.

Causes

If we talk about the symptom of yellowing eyes, then this condition may look different: the color varies from yellowish to bright yellow. Sometimes not the entire white part of the eye turns yellow. The patient notices the appearance or even “growths” of the corresponding color. Due to the fact that yellowing of the eyes may indicate the most various diseases, the reasons for the color change are also different. The most common cause of jaundice is high level bilirubin(from Latin bilis - bile and ruber - red) - one of the main components of bile.

Bilirubin is a pigment and is yellow in color. He formed by the breakdown of proteins, for example, hemoglobin, released during the breakdown of red blood cells. During normal functioning of the body, the end products of hemoglobin breakdown (including bilirubin) must enter the bile and be excreted naturally. If the process of removing bilirubin is disrupted or its amount is excessively increased, this leads to the coloring of the eyes in the color of this pigment: the proteins acquire a yellow tint. In this case, not only the whites of the eyes can turn yellow, but also other tissue structures of the body.

Read also about yellow eye color.

A change in eye color may indicate either a pathology leading to excessive destruction of red blood cells, or problems in neutralizing and removing bilirubin from the body. Thus, the most common cause of “jaundice” is the following processes:

• Increased destruction of red blood cells(for example, in case of poisoning or blood diseases);
• Liver diseases leading to the inability to neutralize bilirubin;
• Gallbladder diseases, that is, insufficient or impossible excretion of bilirubin.

Another reason for the yellow color appearing on proteins may be a change in lipid metabolism in the body. This leads to the formation of yellowish wen in the eye area. An extremely dangerous pathology that cause yellowness of the whites of the eyes are of various types malignant neoplasms conjunctiva.

The causes of “jaundice” are sometimes infections, manifestations of subconjunctival hemorrhages, and even bad habits.

Possible diseases

Yellowing of the eyes is a symptom, not a disease itself. There are a huge number of ailments that cause such discoloration. They can be divided into separate groups:

• Liver diseases;
• Blood diseases;
• Problems arising in the biliary tract;
• Metabolic disorders in the body;
• Diseases of the pancreas;
• Diseases of the organs of vision.

Read also about why the white of the eye is yellow.

Pathological problems in the liver that lead to “jaundice” include the following diseases: hepatitis, cirrhosis and liver cancer, Ziewe syndrome, echinococcosis, amebiasis and sarcoidosis of the liver. When problems arise in the functioning of the liver, the binding of indirect bilirubin from the blood is disrupted due to damage to liver cells. Upon reaching high concentration of bilirubin, it penetrates the sclera of the eyes and is deposited in them.

Blood diseases, leading to the development of “jaundice”: malaria, erythrocyte membranopathies, enzymopathies, hemoglobinopathies, autoimmune hemolytic anemia, babesiosis, poisoning with hemolytic poisons.

When blood diseases occur, significant destruction of erythrocytes (red blood cells) occurs. This causes an increase in hemoglobin concentration.

Hemoglobin, breaking down, forms a large amount of bilirubin, which the liver is not able to neutralize.

In diseases of the biliary tract, a significant amount of bilirubin accumulates in the blood. This is due to the fact that the flow of bile from the liver to the duodenum is disrupted. Most famous Cause of yellowing of the whites of the eyes in these cases it is cholelithiasis. However, “jaundice” can also be caused by primary sclerosing cholangitis, opisthorchiasis, and cancer. Metabolic disorders that can cause yellowing of proteins can be divided into three types:

• Violation of metal metabolism;
• Bilirubin metabolism disorder;
• Protein metabolism disorder.

Such pathological processes lead to the development a number of diseases, such as amyloidosis, hemochromatosis, Wilson-Konovalov's disease, Gilbert's disease and others, accompanied by yellowing of the eyes.

There are also diseases of the organs of vision, which are accompanied by the appearance of yellow color in the whites of the eyes.

These are melanomas and malignant conjunctivitis. Yellowness in the form of individual spots is caused by such ophthalmic diseases as pterygium and pinguecula.

Pterygium manifests itself as a consequence of conjunctivitis. The pinguecula becomes the result of lipid metabolism and the appearance of yellow wen on the protein.

Read why a newborn has yellow whites of his eyes.

Diagnostic methods

Diagnosis of the causes of yellowness in the whites of the eyes includes a significant number of methods. This is due to the fact that there are many reasons for the manifestation of such a symptom. For establishing accurate diagnosis apply:

• Clinical methods;
• Radiation studies;
• Laboratory research.

The doctor turns to basic diagnostic methods, such as finding out the most complete history of the development of the disease and the patient. Radiation research methods involve the use of computed tomography of internal organs and ultrasound. When determining the cause of “jaundice,” an important method is various types of laboratory tests:

• General blood test;
• Biochemical blood test;
• Toxicological blood test;
• Stool analysis;
• Urinalysis;
• Immunological and genetic tests.

What does a person look like with increased level bilirubin

It is assumed that there is a need to obtain data on the condition of the liver, pancreas and biliary tract.

Should you immediately call an ambulance if the whites of your eyes turn yellow and get ready to treat 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 sign, and not all require hospitalization.

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

There are also absolutely “harmless” reasons for this condition that do not require urgent treatment, but gradually undermine the body from the inside - chronic lack of sleep, constant sitting in front of 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 fever or nausea. It is always necessary to find out why the eyeballs have changed their color. The chance of eliminating ophthalmological diseases at the first sign of a change in the color of the eye whites is almost 100% - if the symptom is neglected, you can lose your vision.

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

Impaired bilirubin production indicates liver pathologies of various types.

Highlight the following types 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.

He is called:

• Viral lesions. Symptoms of the disease with various strains of viruses: chills, headache, fever, febrile state, abdominal pain, nausea, loss of appetite, enlarged liver, change in the color of stool 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 increases, hemoglobin levels decrease, and thrombocytopenia occurs. The liver enlarges from the first days of the disease.
• Toxic hepatitis develops acutely, and symptoms resemble viral hepatitis. The kidneys may be affected at the same time, resulting in renal failure. Liver function is impaired.
• The symptoms of acute alcoholism resemble the development of viral hepatitis.

Additional symptoms are diarrhea, ascites.

1. Cholestatic jaundice. The bile ducts become blocked by stones or stagnation of bile, which causes nausea, dizziness, and pain in the right hypochondrium.
2. Enzymopathic jaundice. Due to a hereditary defect in the body's enzyme system, bilirubin synthesis is insufficient.

Jaundice in newborns rarely leads to pathological changes in the liver. It occurs in the first days after birth due to adaptation to the extrauterine period. Before birth, a huge number of red blood cells enter the fetal blood, and the liver cannot cope with the processing of bilirubin, which is released during their breakdown. Jaundice in newborns usually goes away on its own by 10-12 days of life.

Jaundice in newborns is dangerous if the parents' Rh factor is incompatible. In this case, infants require treatment.

Chronic liver diseases may have following symptoms: pain in the right hypochondrium, nausea, enlarged spleen, low-grade fever, varicose veins esophageal veins, ascites, anemia and others.

Treatment of all liver diseases is the prerogative of the doctor. In this case traditional methods may only have additional effects.

Yellowness of the eyeball and iris can be caused by malignant formations of the tissues of the organ of vision - most often the conjunctiva. Yellowness is one of the symptoms of melanoma in the eye area. So don’t delay visiting an ophthalmologist if you have 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.

Whites 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 disorder of lipid metabolism in the body on the eyeball.

Pterygium is a growth of the conjunctiva of the eye (popularly the disease is called “wild meat”). It begins to extend onto the sclera and reduces the field of view.

Treatment of pinguecula and pterygium is surgical. Pterygium can only be eliminated by initial stage. If the conjunctiva grows so large that it closes the pupil, then reverse restoration is impossible.

All eye diseases are a reason to consult an ophthalmologist.

This disease also has a second name – constitutional jaundice. Boys get sick 5 times more often than girls. If we consider only the 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, the frequency of manifestations increases.

Yellowness of the sclera does not always appear, but only when feeding is delayed, due to which hemolysis increases. That is, in the absence of fasting, 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 gentle diet, the use of choleretic drugs and soy emulsion.

Smoking itself does not affect the color of the sclera, but you need to take into account that constantly feeding the body with nicotine increases the load on the liver.

In addition to nicotine, when smoking, other combustion products, tars and toxins enter the body. The liver cleanses the body, and overload negatively affects its function.

This is why long-term smokers have yellowish whites of their 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 regime, 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 , nicotine 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 - if the color of the sclera changes - you need to consult a doctor. This condition 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

liver diseases blood diseases

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

bilirubin

Jaundice is accompanied by more than just yellowing of the eyes. With it, the skin often turns yellow, skin

Fever, pain in the right hypochondrium, sensation

bitterness in the mouth, loss of appetite

Appears

nausea,vomiting,headache

weaknessinsomnia

The liver increases in size and

spleen

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

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

There are three main membranes in the eyeball:

• outer (fibrous) membrane of the eyeball;
• middle (choroid) layer of the eyeball;
• inner (sensitive) lining of the eyeball.

Outer shell of the eyeball The outer shell of the eyeball consists of two important sections, which differ from each other in their anatomical structure and functions. The first section is called the cornea of ​​the eye. The cornea of ​​the eye is located in the front central part of the eyeball. Due to the absence of blood vessels and the homogeneity of its tissue, the cornea is transparent, so the pupil and iris of the eye can be seen through it.

The cornea consists of the following layers:

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

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

The cornea of ​​the eye is the most convex part of the eyeball. Along the periphery, the cornea of ​​the eye smoothly passes into the sclera of the eyeball, which is the second important section of the outer shell of the eye. This section occupies most of the area of ​​the outer shell of the eye. The sclera of the eye is represented by dense fibrous connective tissue, consisting of bundles of collagen fibers with an admixture of elastic fibers and fibroblasts (

connective tissue cells

). The outer surface of the sclera is covered in front by the conjunctiva, and the back by endothelium. Conjunctiva (

conjunctiva

) is a relatively thin membrane that consists of columnar stratified epithelium. This membrane covers the eyelids from the inside (

secular part of the conjunctiva

) and the eyeball outside (

ocular part of the conjunctiva

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

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

Middle layer of the eyeball

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

back, middle and front

). Of all the parts of the middle shell, only the iris can be visually seen (

anterior part of the middle shell of the eyeball

), which is located between the pupil and the sclera of the eyes. It is the iris that gives the eyes specific color. It consists of loose connective tissue, blood vessels, smooth muscles, nerves and pigment cells. Iris of the eye (

unlike the other two parts of the middle shell

) is not adjacent to the outer shell of the eyeball and is separated from the cornea by the anterior chamber of the eye, which contains intraocular fluid. Behind the iris is the posterior chamber of the eye, which separates the lens from each other (

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

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

Rear end The middle layer of the eyeball is called the choroid proper of the eyeball. It is located directly under the white membrane of the eye in the back part. It consists of a large number of vessels, connective tissue fibers, pigment and endothelial cells. The main function of this anatomical structure is to provide nutrients to the retinal cells (

inner lining of the eyeball

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

A little in front of her (

posterior part of the middle shell

), in the form of a ring, the ciliary body (

middle part of the medial 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 included in the ciliary (

ciliary

) the body includes special epithelial cells that produce intraocular fluid that fills the anterior and posterior chambers of the eye.

The inner lining of the eyeball (

or retina

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

) part of the retina. The remaining, posterior, larger part of the retina is called visual. This part of the retina perceives light entering the eyeball. This perception is possible due to the presence of special photoreceptor cells inside the retina. The retina itself consists of ten layers, which differ from each other in different anatomical structures.

In liver cells, indirect bilirubin binds with glucuronic acid (a chemical substance necessary to neutralize bilirubin), and it turns into direct bilirubin (neutralized bilirubin). Next, direct bilirubin is transported by liver cells into bile, through which it is excreted from the body. In some cases, some of it may be absorbed back into the blood. Therefore, two main fractions of bilirubin are always present in the blood - direct bilirubin and indirect bilirubin. These two fractions together make up the total bilirubin in the blood. Indirect bilirubin accounts for about 75% of total bilirubin. The reference (limit) values ​​for the concentration of total bilirubin in the blood 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

). At mild degree the concentration of total bilirubin in the blood reaches 86 µmol/l. At medium degree in the patient’s blood the level of bilirubin is in the range from 87 to 159 µmol/l. With severe severity, its concentration in the blood plasma is above 159 µmol/l.

Causes of yellowing of the sclera of the eyes

Cause	The mechanism of formation of yellowness of the whites of the eyes
Liver diseases	In liver diseases, there is a violation of the binding of indirect (not associated with glucuronic acid) bilirubin from the blood and the release of direct bilirubin from it, due to damage to hepatocytes (liver cells). Slowing the removal of indirect bilirubin from the blood and the entry of direct bilirubin into it (it enters the blood as a result of damage to liver cells) leads to its accumulation in it. When it reaches high concentrations, it leaves the vessels and penetrates the sclera of the eyes, where it is deposited. This deposition is accompanied by a yellow coloration of the white membrane of the eyes.
Blood diseases	In case of blood diseases, pronounced hemolysis (destruction) of erythrocytes (red blood cells) is observed, which leads to an increase in the concentration in the blood of hemoglobin (a protein that transports oxygen), which is contained in large quantities in erythrocytes. Subsequently, this hemoglobin undergoes breakdown and indirect bilirubin is formed from it. Since in blood diseases much more indirect bilirubin is formed (due to breakdown in the blood large quantity hemoglobin), which the liver is able to neutralize, it gradually accumulates in the blood, and then penetrates into the sclera of the eyes, turning them yellow.
Biliary tract diseases	Yellowing of the whites of the eyes in diseases of the biliary tract is associated with the accumulation of a significant amount of direct bilirubin in the blood. With these pathologies, the outflow of bile from the liver into the duodenum is disrupted. As a result, the intrahepatic bile ducts, through which bile is removed from the liver, rupture. Because of this, bile components penetrate into the blood. Since one of its main components is direct bilirubin, its concentration in the blood plasma increases significantly. This bilirubin then penetrates the sclera of the eyes and turns them yellow.
Disturbance of metabolic processes in the body	There are at least three types of metabolic disorders that lead to yellowing of the whites of the eyes (metabolism disorders of metals, bilirubin and proteins). When the metabolism of iron (hemochromatosis) or copper (Wilson-Konovalov disease) is impaired, they accumulate in the liver, which leads to damage to its tissues (since in high concentrations these metals are toxic to body tissues) and the development of liver cirrhosis. With cirrhosis, the detoxification function of the liver is impaired, as a result of which it does not remove indirect bilirubin from the blood. As the disease progresses, it accumulates in the skin and sclera of the eyes and turns them yellow. For some hereditary diseases liver (Gilbert's disease, Crigler-Najjar syndrome, Dabin-Johnson syndrome) there is a violation of bilirubin metabolism, and it accumulates in the blood and peripheral tissues (skin and sclera of the eyes). With amyloidosis (a pathology associated with impaired protein metabolism), amyloid (abnormal protein) is deposited in the liver, which causes a disruption of its structure and function, as a result of which it gradually loses the ability to remove indirect bilirubin from the blood, as a result of which it accumulates in the skin and tunica albuginea eyes, giving them a yellow tint.
Acute or chronic pancreatitis	In acute or chronic pancreatitis (inflammation of the pancreas), an increase in the size of the pancreas is often observed, due to its inflammatory edema. Since the common bile duct (common bile duct) is located near the pancreas, in such cases, mechanical compression from the side often occurs. abdominal cavity enlarged pancreas. Mechanical blockage of the common bile duct is accompanied by stagnation of bile in the biliary tract and rupture of intrahepatic bile capillaries, as a result of which the components (including direct bilirubin) of bile enter the blood. Therefore, in acute or chronic pancreatitis, patients have increased levels of direct bilirubin in the blood and have jaundice (yellowing of the skin and sclera of the eyes).

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

hepatitis

inflammation of the liver tissue

amebiazechinococcosis

liver. Non-communicable diseases liver may have toxic hepatitis, cirrhosis,

liver cancer sarcoidosis

liver, Zieve syndrome.

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

). 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.

amebiasis, echinococcosis, ascariasis, schistosomiasis, etc.

toxins

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

). Therefore, depending on the etiology (

reasons of origin

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

or medicinal

All of these factors (

viruses, bacteria, etc.

) cause damage to liver cells, resulting in their gradual destruction, which is accompanied by the appearance of inflammation in the liver. This is accompanied by a violation of its full function and loss of the ability to neutralize indirect bilirubin coming from the blood to the liver for processing. In addition, with hepatitis, direct bilirubin also accumulates in the blood (

since the liver cells are destroyed, and it is released from them into the surrounding space

). The accumulation of direct and indirect bilirubin in the blood contributes to their deposition in various tissues and, in particular, in

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

Ziewe syndrome is a rare syndrome (

totality pathological signs

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

yellowing of the sclera and skin

), enlarged liver, hemolytic anemia (

), hyperbilirubinemia (

increase in bilirubin levels in the blood

) and hyperlipidemia (

increased blood fat levels

). This syndrome is observed in people who abuse alcohol. The yellowing of the white of the eyes in Zieve syndrome is caused by an increase in bilirubin levels (

mainly due to indirect

) in the blood, due to the destruction of red blood cells and liver dysfunction. In most cases, such patients develop fatty liver disease (

dystrophy

) liver, that is, pathological deposition inside the parenchyma (

) liver fat.

Liver cirrhosis is a pathology in which the liver is damaged and its normal tissue is replaced by pathological connective tissue. With this disease, connective tissue begins to grow in the liver, which gradually replaces the normal liver tissue, as a result of which the liver begins to function poorly. It loses its ability to neutralize various compounds harmful to the body (

ammonia, bilirubin, acetone, phenol, etc.

). Violation of the detoxifying ability of the liver leads to the fact that these toxic metabolic products begin to accumulate in the blood and have an adverse effect on the organs and tissues of the body. Bilirubin (

indirect

), circulating in large quantities in the bloodstream, is gradually deposited in the skin, white membrane of the eyes, brain and other organs. The deposition of bilirubin in the tissues gives them a yellow color, therefore, with cirrhosis of the liver, icterus is noted (

yellowing

) sclera and skin.

Liver cirrhosis is usually the most adverse complication various hepatitis (

liver inflammation

). The most common reasons which lead to the development of liver cirrhosis 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 mucous membrane of the bile ducts

), drug-induced hepatitis (

in the background long-term use 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

for example, 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. As the tumor increases in size, it displaces normal liver tissue, which is why the liver quickly 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 bilirubin levels in the blood

). When the level of bilirubin in the blood is high, it begins to be deposited in the skin and white of the eyes, causing the patient to develop jaundice (

yellowing of the skin and sclera

Echinococcus granulosus

), which is a type of tapeworm (

). Human infection with echinococcosis occurs through consumption of food or water contaminated with the eggs of these worms or through contact with infected animals (

dogs, horses, pigs, cows, etc.

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

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 shaped like a bubble filled with liquid with numerous echinococcal embryos.

If the disease is not treated for a long time, the hydatid cyst begins to gradually increase in size and put pressure on the surrounding liver tissue, causing them to die (

atrophy of the liver parenchyma

). As a result, mechanical replacement of normal liver tissue occurs, in place of which a cyst appears. In some certain moment, when the cyst reaches a large size, the liver loses the ability to bind and neutralize indirect bilirubin in the blood, as a result of which it accumulates first in it, and then in the skin and in the white of the eyes, giving them a characteristic yellow color.

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

lungs, liver, kidneys, intestines, etc.

) granulomas appear. Granuloma is a focus of accumulation

lymphocytes

Macrophages and epithelioid cells. Granulomas in sarcoidosis appear as a result of an inadequate immune response of the body to certain antigens (

foreign particles

). This is facilitated by various infectious diseases (

viruses, bacteria

) and non-infectious factors (

genetic predisposition, human contact with toxic substances etc.

As a result of the impact of such factors on human tissue, the work of immune system. If it detects some antigens in the tissues, then hyperimmune (

excessive immune

) response and in the places where such antigens are localized, cells of the immune system begin to accumulate, resulting in small foci of inflammation. These lesions visually look like nodules (

or granulomas

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

especially if the disease is not treated

The constant growth of existing granulomas and the emergence of new pathological foci in various organs disrupts their normal architecture (

structure

) and work. Organs gradually lose their functions due to the fact that granulomatous infiltrates replace their normal parenchyma (

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

and they are most often damaged by this disease

), then the patient experiences

cough, shortness of breath, pain in chest

Excessive fatigue due to lack of air. If the liver is damaged, then, first of all, its detoxifying and protein-synthetic functions are disrupted (

the synthesis of blood proteins is disrupted in the liver

) functions.

When the detoxifying function of the liver is impaired, various metabolites accumulate in the blood, which the liver must absorb and neutralize. This explains the fact that with liver sarcoidosis, patients have high levels of bilirubin in their 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 yellowing of the eyes.

Entamoeba histolytica

inflammation of the colon mucosa

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

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

), when amoebas 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 tissue damage there. Hepatitis occurs first

inflammation of the liver tissue

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

and inflammation

) can form inside the liver

abscesses

cavities filled with pus

). There can be a large number of such abscesses. In the absence of treatment, liver amebiasis disrupts its various functions, including the neutralization of bilirubin in the blood (

indirect bilirubin

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

direct bilirubin

) back into the blood. Therefore, with liver amebiasis in a patient’s 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.

Red blood cells (

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 life span (

about 125 days

). When this period comes to an end, red blood cells are destroyed. The hemoglobin contained in them is released into the surrounding space and then breaks down into protein and heme parts. Heme is further converted into indirect bilirubin, which must be neutralized in the liver.

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

Plasmodium vivax, Plasmodium ovale, Plasmodium falciparum, Plasmodium malariae

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

malaria mosquitoes

), which are unique carriers and distributors of this infectious disease. Getting into the human blood when

tissue schizogony

), after which merozoites are formed (

mononuclear Plasmodium individuals

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

erythrocyte schizogony

). At the end of erythrocyte schizogony, the infected erythrocytes are completely destroyed and release large numbers of multiplied merozoites, which re-enter new erythrocytes to reproduce. Thus, this process occurs cyclically. Each new destruction of erythrocytes is accompanied by the release into the blood of not only new populations of malarial merozoites, but also the rest of the erythrocyte contents and, in particular, the protein - hemoglobin. The breakdown of this protein produces bilirubin (

indirect

), which must be neutralized in the liver.

The problem is that with malaria, a very significant number of red blood cells are destroyed and a huge amount of indirect bilirubin is formed in the blood, which the liver does not have time to process. Therefore, with malaria, patients develop hyperbilirubinemia (

increase in blood bilirubin levels

) and jaundice (

yellowing of the skin and sclera of the eyes

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

Erythrocyte membranopathies are a set of hereditary pathologies based on congenital defects of genes encoding proteins (

glycophorin C, alpha spectrin, etc.

), which are part of the membranes of erythrocytes. Such defects lead to disruption of the production of membrane proteins during the formation of red blood cells in the bone marrow, causing the membranes of older red blood cells circulating in the blood to change their shape. In addition, with these pathologies, their membranes become defective, they have improper permeability to various substances and low resistance to damaging factors, and therefore such red blood cells are quickly destroyed and do not live long.

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

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, frequent destruction of defective red blood cells occurs in the blood, which is accompanied by the release of large amounts of hemoglobin, which is then converted into indirect bilirubin. The liver cannot immediately process large amounts of indirect bilirubin and remove it from the blood. Therefore, this metabolite (

product of exchange

) accumulates in the blood and subsequently settles in the tissues, causing yellowing of the white membrane of the eyes and skin.

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

proteins that accelerate biochemical reactions

), controlling the course of metabolic reactions (

exchange reactions

). This leads to inferior energy metabolism, accumulation of intermediate reaction products and energy deficiency in the red blood cells themselves. Under conditions of energy deficiency in red blood cells, the transport of various substances through their membrane slows down, which contributes to their wrinkling and destruction. There are also certain erythrocyte membranopathies in which there may be a deficiency of red blood cell antioxidant enzymes (

for example, pentose phosphate cycle, glutathione system

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

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

a pathology in which there is a deficiency of red blood cells and hemoglobin in the blood resulting from the destruction of red blood cells

) and jaundice. The appearance of the latter is due to the fact that the liver does not have time to quickly process and remove indirect bilirubin from the blood, which is formed in huge quantities during the breakdown of hemoglobin. Therefore, indirect bilirubin is deposited in the skin and white of the eyes and causes them to turn yellow.

Erythrocyte hemoglobinopathies are a group of congenital diseases, the origin of which is based on genetically mediated defects in the formation of hemoglobin in erythrocytes. Some of the most common hemoglobinopathies are sickle cell anemia, alpha thalassemia and beta thalassemia. With these pathologies, red blood cells contain abnormal hemoglobin, which does not perform its function well (

oxygen transfer

), and the red blood cells themselves lose strength and shape, as a result of which they quickly undergo lysis (

destruction

) and have a short lifespan in the blood.

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

decrease in the level of red blood cells in the blood due to their destruction

), jaundice and oxygen deficiency (

due to disruption of oxygen transport by hemoglobin

). The occurrence of jaundice can be explained by the fact that with erythrocyte hemoglobinopathies there is a significant release of pathological hemoglobin into the blood from decaying red blood cells. This hemoglobin subsequently undergoes breakdown and turns into indirect bilirubin. Since in these pathologies a large number of red blood cells are destroyed, then, accordingly, there will be a lot of indirect bilirubin in the blood, which the liver is not able to quickly neutralize. This leads to its accumulation in the blood and other tissues and organs. If this bilirubin penetrates the skin and white of the eyes, they turn yellow. Yellowing of the whites of the eyes and skin is called jaundice.

Autoimmune hemolytic anemia is a group of pathologies in which red blood cells are damaged due to their binding to autoimmune (

pathological

) antibodies (

protective protein molecules that circulate in the blood and are directed against the body's own cells

). These antibodies begin to be synthesized by cells of the immune system when its proper functioning is disrupted, which can be caused by genetic defects in immunocytes (

cells of the immune system

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

for example, viruses, bacteria, toxins, ionizing radiation etc.

When normal red blood cells bind to autoimmune ones (

pathological

) antibodies destroy them (

). The destruction of a large number of red blood cells leads to hemolytic anemia (

that is, a decrease in red blood cells due to their sudden intravascular destruction

). This anemia is completely called autoimmune hemolytic anemia (

). Depending on the type of autoimmune antibodies that cause destruction of red blood cells in the blood, all autoimmune hemolytic anemias are divided into types (

for example, AIHA with warm hemolysins, AIHA with incomplete cold agglutinins, Fisher-Evans syndrome, etc.

). All autoimmune hemolytic anemias are accompanied by an increase in the concentration of indirect bilirubin in the blood (

due to increased release of hemoglobin from damaged red blood cells

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

Babesiosis is an infectious disease that occurs as a result of human infection with protozoa of the genus Babesia (

). Transmission mechanism

infections

transmissible, that is, a person acquires this disease from tick bites (

genera Dermacentor, Hyalomma, Rhipicephalus

). The disease mainly affects people who are constantly in contact with pets and have a fairly pronounced immunodeficiency (

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

). A man 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 blood, which breaks down and turns into bilirubin (

indirect

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

Hemolytic poisons are a group of chemical compounds that, when entering the human body, cause severe 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 sclera of the eyes

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

Most hemolytic poisons are represented by artificially synthesized chemicals (

benzene, phenol, aniline, nitrites, chloroform, trinitrotoluene, phenylhydrazine, sulfapyridine, hydroquinone, potassium bromate, arsenic, lead, copper, etc.

), which are used in various industries (

chemical, medical, fuel, etc.

). Therefore, most of the poisoning with hemolytic poisons occurs among workers of industrial enterprises who are constantly in contact with these toxic substances.

Under the influence of hemolytic poisons, the membranes of red blood cells are deformed, as a result of which they are destroyed. There are also some hemolytic poisons that block the course of enzymatic processes inside red blood cells, which is why their energy metabolism or their antioxidant capacity is disrupted (

resistance to oxygen free radicals

), as a result of which they are destroyed. Certain chemicals can change the structure of red blood cell membranes in such a way that it becomes unrecognizable and foreign to cells of the immune system. This is how acquired autoimmune hemolytic anemias arise. With them, the immune system destroys the patient’s own red blood cells, so their number in the blood decreases significantly.

Thus, in case of poisoning with hemolytic poisons due to various mechanisms massive destruction of red blood cells occurs inside the vessels. This is accompanied by the release of a large amount of hemoglobin into the blood, which is subsequently converted into bilirubin (

indirect

). High concentrations of this bilirubin in the blood lead to its deposition in the skin and sclera of the eyes, which is accompanied by yellowing of the eyes.

Bile is biological fluid yellow-brown in color, which is produced in the liver and secreted into the duodenum. Bile plays an important role in digestive processes, occurring in the intestines. Also, along with bile, various harmful substances unnecessary for the body (

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

). Before reaching the intestines, bile passes through the biliary tract (

intrahepatic and extrahepatic

). With diseases of these pathways, it becomes difficult to transport bile to the duodenum due to their partial or complete blockage. This is accompanied by an increase in pressure in the bile ducts located above the blockage. In those places where the wall of these ducts is thinnest, it ruptures, and part of the bile enters the blood. Therefore, for diseases of the biliary tract (

primary sclerosing cholangitis, cholelithiasis, tumors of the organs of the biliopancreatoduodenal zone, opisthorchiasis

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

Primary sclerosing cholangitis is a disease of unknown origin 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, become rough and deformed. As the disease progresses, the lumen of the affected biliary tract is completely obliterated (

closes

). Such pathways become completely non-functional; bile does not move through them from the liver to the duodenum. The more such ducts are affected, the more difficult it is for bile to be transported to the intestines. If a large number of bile ducts are damaged inside the liver, bile stagnation occurs (

cholestasis

), which is accompanied by its partial penetration into the blood. Since bile contains direct bilirubin, it gradually accumulates in the skin and sclera of the eyes, causing them to turn yellow.

Gallstone disease is a pathology in which stones appear in the gallbladder or bile ducts. The reason for its occurrence is a violation of the ratio of substances (

cholesterol, bilirubin, bile acids

) in bile. In such cases, some substances (

for example cholesterol

) becomes larger than all the others. The bile becomes oversaturated with them, and they precipitate. The sediment particles gradually stick together and overlap each other, resulting in the formation of stones.

The development of this disease can be facilitated by stagnation of bile (

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

), inflammatory processes in the biliary tract (

inflammation of the mucous membrane of the gallbladder or bile ducts

), diseases of the endocrine system (

diabetes mellitus, hypothyroidism

obesity

Poor nutrition (

excessive consumption of fatty foods

pregnancy

Certain medications (

estrogens, clofibrate, etc.

), liver diseases (

hepatitis, liver cirrhosis, liver cancer

), hemolytic anemia (

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

Stones formed during cholelithiasis may be located in the so-called blind spots in the biliary system (

for example, in the body or bottom of the gallbladder

). In such cases, this disease does not manifest itself clinically, since the stones do not block the bile ducts, and the outflow of bile through the biliary system is preserved. If these stones suddenly fall from the gallbladder into the bile ducts, then the movement of bile through them slows down sharply. Bile accumulates in large volumes in parts of the biliary system located above the obstruction. This leads to increased pressure in the bile ducts. Under such conditions, the intrahepatic bile ducts inside the liver are destroyed, and bile goes directly into the blood.

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

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

The organs of the biliopancreatoduodenal zone include the extrahepatic bile ducts, gallbladder, pancreas and duodenum. These organs are located very close to each other in the upper floor of the abdominal cavity. In addition, they are functionally interconnected, so tumors of all these organs have similar symptoms. With tumors of the organs of the biliopancreatoduodenal zone, yellowing of the skin and sclera of the eyes is very often observed. This is explained by the fact that if they are present, there is a mechanical blockage of the extrahepatic bile ducts (

or gallbladder

) and bile entering them (

into the ducts

) from the liver stagnates. Such stagnation is observed not only in the extrahepatic ducts, but also in the intrahepatic ducts, which are very thin and fragile. Intrahepatic ducts, when bile stagnates in them, can rupture, as a result of which it penetrates into the blood. Bilirubin (

), which is part of it, gradually accumulates in the skin and white of the eyes and colors them yellow.

pancreatic cancer

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

blockage

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

) and duodenum (

occur in 15% of cases

) blocking the outflow of bile occurs in the area where it is released (

) bile from the main bile duct.

cat fluke

). This infection is transmitted through food, most often through the consumption of thermally incorrectly prepared fish of the carp family (

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

connective tissue grows in them

), their lumen narrows. All this (

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

) leads to difficulty in the outflow of bile from the liver. Stagnation of bile 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 white membrane of the eyes (

), which is accompanied by their yellowing.

There are certain pathologies (

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

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

iron, copper

Hemochromatosis is a congenital disease in which iron metabolism in the body is disrupted, 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 would normally consume. After the intestines, this iron is absorbed into the blood and through it transported to various organs. With hemochromatosis, cirrhosis of the liver quite often develops, since this organ is one of the first where excess amounts of iron entering the body accumulate.

The occurrence of liver cirrhosis 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 hepatocyte membranes subsequently leads to their destruction. Liver cells die. In their place connective tissue appears. This replacement is a characteristic morphological sign of liver cirrhosis. With the development of cirrhosis, the liver loses its 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 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, in conditions of its excess, damage to the liver tissue 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 disease is liver cirrhosis.

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

as her cells are destroyed

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

which the liver should 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 yellowing of the eyes. It should be noted that in Wilson-Konovalov disease, copper accumulation is observed not only in the liver, but also in other organs, for example, the brain, kidneys, and eyes. Copper deposition in the Descemet's membrane area of ​​the eyes is accompanied by the appearance of yellowish-green pigmentation along the periphery of the irises (

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

). This pigmentation is called Kayser-Fleischer rings.

Gilbert's disease is a hereditary liver disease in which its 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 cellular organelles of hepatocytes

), in which it binds to glucuronic acid. As a result of these disorders, the liver loses its 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 (

that is, yellowing of the white membrane of the eyes and skin

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

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

uridine 5-diphosphate 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 removal of indirect bilirubin from the blood is impaired. It accumulates in the blood, and then in the skin and sclera of the eyes, causing them to turn yellow.

There are two types of Crigler-Najjar syndrome. The first type is characterized by severe clinical symptoms and severe jaundice. With it, the liver cells completely lack the enzyme (

uridine 5-diphosphate glucuronyltransferase

), binding indirect bilirubin. This type of Crigler-Najjar syndrome usually causes death in patients at a very early age.

In the second type, which is also called Arias syndrome, this enzyme is present in hepatocytes, but its amount, compared to the norm, is significantly lower. With this type, 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-Nayjar syndrome a little later (

during the first years of life

). Clinical course this type is chronic, with periods of exacerbations and remissions (

asymptomatic

). Exacerbations in patients with Crigler-Najjar syndrome are observed much more often than in patients with Gilbert's disease.

Dubin-Johnson syndrome is also an inherited liver disease. With this pathology, the release process is disrupted (

into the bile ducts

) from liver cells of neutralized bilirubin (

), as a result of which it first accumulates in them (

in liver cells

), and then gets into the blood. The cause of this disorder is a hereditary defect in the gene, which is responsible for the synthesis of direct bilirubin transport proteins localized on the hepatocyte membrane (

liver cells

). The accumulation of direct bilirubin in the blood gradually leads to its retention in the skin and white of the eyes, which is why they turn yellow.

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

predominantly in men

). Jaundice is almost always constant and is often associated with various dyspeptic diseases (

nausea, vomiting, abdominal pain, poor appetite, diarrhea, etc.

) and asthenovegetative (

headache, dizziness, weakness, depression, etc.

) symptoms. This syndrome does not affect life expectancy, but in such patients its quality is significantly reduced (

due to the persistence of symptoms of the disease

). If the disease goes into remission (

asymptomatic

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

heavy physical activity, stress, alcohol consumption, fasting, injury, viral or bacterial infections, etc.

Amyloidosis – systemic disease, as a result of which in various organs (

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

) an abnormal protein – amyloid – accumulates. The cause of amyloid is a disorder of protein metabolism in the body. There are acquired (

for example, ASC1 amyloidosis, AA amyloidosis, AH amyloidosis, etc.

) and hereditary (

AL amyloidosis

) forms of this pathology. The chemical structure of amyloid and its origin depend on the form of amyloidosis. For example, in AL amyloidosis, the amyloid consists of accumulations of light chains (

fragments

) immunoglobulins (

protective molecules that circulate in the blood

). In AH amyloidosis, amyloid deposits are composed of beta-2 microglobulin (

one of the blood plasma proteins

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

functional failure of several organs

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

liver failure

With this deficiency, 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.

) inside the gland itself, resulting in autolysis (

self-digestion or self-destruction

With pancreatitis, an increase in the size of the pancreas is almost always observed, due to its swelling (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 biliary tract (gallbladder, intrahepatic and extrahepatic biliary tract). Impaired bile outflow ultimately leads to rupture of bile capillaries (due to high pressure in the biliary tract) 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 promotes its penetration and retention in peripheral tissues (

especially in the skin and sclera of the eyes

), which leads to their yellowing. Jaundice (

yellowing of the skin and whites of the eyes

) can be observed in both acute and chronic pancreatitis.

To diagnose the causes of yellow eyes, various types of tests can be used (

clinical, radiation, laboratory

). The main clinical diagnostic methods are taking anamnesis (

clarification of the entire history of the development of the disease

) in the patient and his examination. Of the radiation research methods, doctors most often give preference to ultrasound and

computed tomography

abdominal organs (

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

). In diagnosing yellow 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 disease are pain in the right hypochondrium, increased

temperature

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

yellowing of the sclera of the eyes and skin

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

flatulence

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

skin rashes, itching, redness of the skin, etc.

). In liver sarcoidosis, there may be

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

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

joint inflammation

), deterioration

visual acuity

In patients with liver amebiasis, pain 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 liver cirrhosis often experience

nosebleeds bleeding gums

Skin itching, palmar erythema (

small red rash on the palms of the hands

), gynecomastia (

increase in the size of the mammary glands in men

), spider veins on the skin,

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

liver inflammation

), Zieve syndrome, liver amoebiasis, liver echinococcosis. So, for example, if a patient, in a conversation with a doctor, mentions that before the symptoms of the disease appeared, he had been using certain types of drugs for a long time (

paracetamol, tetracycline, aminazine, methotrexate, diclofenac, ibuprofen, nimesulide, etc.

), which may adversely affect liver function, the doctor concludes that possible pathology The reason the patient came to him was drug-induced hepatitis.

The most common changes in the general blood test 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 general blood test, 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, and an increase in the activity of

alanine aminotransferase (ALT), aspartate aminotransferase (AST)

Gamma-glutamyl transpeptidase, alkaline phosphatase, decrease in the amount of albumin, prothrombin index. Hypercalcemia may occur in sarcoidosis (

increase in blood calcium levels

) and increase in ACE (

angiotensin converting enzyme

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

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

), liver echinococcosis (

a test for antibodies to echinococcus is prescribed

), liver amoebiasis (

a test for anti-amebic antibodies is prescribed

), autoimmune hepatitis (

study for the presence of circulating immune complexes, antinuclear, antimitochondrial autoantibodies, antibodies to smooth muscles, to deoxyribonucleoprotein, etc.

), liver cancer (

test for alpha-fetoprotein - one of the tumor markers

infectious mononucleosis

test for antibodies to Epstein-Barr virus

), cytomegalovirus infection (

test for antibodies to cytomegalovirus virus

In some cases, patients with infectious diseases liver (

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

) appoint

PCR (polymerase chain reaction)

- one of the methods laboratory diagnostics, allowing detection of 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 are detected by radiation research methods in liver diseases

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

For certain indications (

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

) patients with liver disease undergo percutaneous liver biopsy (

insertion of a needle through the skin into the liver under local anesthesia

), which allows you to take a piece of liver tissue from them for histological examination (

examining tissue under a microscope in the laboratory

). Most often, a liver biopsy is performed to confirm that a patient has malignant tumor in the liver, liver sarcoidosis, establish the cause of hepatitis (

or cirrhosis of the liver

), its stage, severity.

In addition to yellowing of the tunica albuginea (

) eyes and skin with blood diseases, an enlargement of the liver and spleen, an increase in temperature,

General weakness, increased fatigue, shortness of breath, rapid heartbeat, 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, the route of its entry into the body and its concentration. Therefore, it is quite difficult to predict exactly what symptoms the patient will have in such cases.

Important information for diagnosing blood diseases is provided by taking an anamnesis, in which doctors quite often establish them possible reasons development. Anamnestic data are especially important when diagnosing malaria or babesiosis (

for example, the patient’s stay in endemic areas of these infections

), poisoning with hemolytic poisons (

working with toxic substances, constant use of certain medications, etc.

). For hereditary pathologies (

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

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

for example, physical activity, taking medications, stress, drinking alcohol, hypothermia, etc.

In a general blood test for blood diseases that cause yellowing of the eyes, a decrease in the number of red blood cells and hemoglobin, an increase in ESR (

erythrocyte sedimentation rate

), reticulocytosis (

an increase in the content of reticulocytes in the blood - young red blood cells

), thrombocytopenia (

). Microscopy of blood products can reveal poikilocytosis (

change in the shape of red blood cells

) and anisocytosis (

change in red blood cell size

). To diagnose malaria and babesiosis, the thick drop and thin smear method is used to identify the causative agents of these diseases inside red blood cells.

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

due to the fraction of indirect bilirubin

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

), decrease in haptoglobin content. With erythrocyte enzymopathies, a decrease in the concentration or complete absence of some enzymes can be detected (

for example, glucose-6-phosphate dehydrogenase, pyruvate kinase, etc.

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

Immunological blood testing for blood diseases is also equally important. It helps to detect antibodies against pathogens of malaria and babesiosis, to identify autoantibodies to red blood cells in autoimmune hemolytic anemia (

AIHA with warm hemolysins, AIHA with incomplete cold agglutinins, Fisher-Evans syndrome, etc.

). Genetic research methods are mainly used in diagnostics congenital pathologies blood (

erythrocyte membranopathies, erythrocyte enzymopathies, erythrocyte hemoglobinopathies

), which cause yellowing of the eyes. These methods help determine the presence of defects in various genes encoding membrane proteins or red blood cell enzymes. As additional research for erythrocyte hemoglobinopathies

electrophoresis

hemoglobin (

protein that carries oxygen in red blood cells

). This study reveals the presence pathological forms hemoglobin.

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

Diseases of the biliary tract are characterized by yellowing of the sclera of the eyes and skin, itching, pain in the right hypochondrium,

weight loss

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

muscle pain

), arthralgia (

joint pain

), hepatomegaly (

liver enlargement

), splenomegaly (

enlarged spleen

), headache.

A general blood test often reveals anemia in such patients (

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

), leukocytosis (

increase in the number of leukocytes in the blood

), increase in ESR (

erythrocyte sedimentation rate

), eosinophilia (

increase in the number of eosinophils in the blood

). The most common pathological changes in biochemical blood tests in patients with biliary tract diseases are an increase in total bilirubin (

mainly due to direct bilirubin

), bile acids, cholesterol, triglycerides, increased activity of alkaline phosphatase, alanine aminotransferase (

), aspartate aminotransferase (

), gamma-glutamyl transpeptidase.

Esophagogastroduodenoscopy (

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

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

). Also using this study a biopsy can be performed (

select a piece of pathological tissue for cytological examination

) tumors of the duodenum. To assess the condition of the bile ducts and pancreas, endoscopic retrograde cholangiopancreatography is performed. In opisthorchiasis, primary sclerosing cholangitis, and tumors of the organs of the biliopancreatoduodenal zone, these ducts are often damaged.

The main methods for diagnosing cholelithiasis are cholecystography (

X-ray method for examining the gallbladder

) and ultrasound examination. These methods most accurately detect the presence of stones in the gallbladder and blockage of the bile ducts. In addition, these two methods allow you to evaluate the correct functioning of the gallbladder and biliary tract, their shape, structure, size, and identify the presence of a tumor in them, foreign bodies. Ultrasound examination is also often prescribed to patients with suspected pancreatic tumors or opisthorchiasis.

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

extrahepatic bile ducts, gallbladder, pancreas and duodenum

). These methods make it possible to accurately determine the presence of a tumor, its size, location, stage of cancer, and also identify the presence of various complications.

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

yellowing of eyes and skin

), pain in the right hypochondrium, in the joints, weakness, lethargy, decreased ability to work, enlarged liver and spleen, nausea, vomiting, poor appetite, diarrhea, headache, dizziness, bleeding gums, nosebleeds, skin sensitivity disorders, convulsions, tremors of the limbs , peripheral edema, slowing mental development, psychoses. It is important to note the fact that in most of these pathologies (

amyloidosis, Wilson-Konovalov disease, hemochromatosis, Crigler-Nayjar syndrome, Dabin-Johnson syndrome

) affects not only the liver, but also other organs (

brain, heart, kidneys, eyes, intestines, etc.

). Therefore, the list of the above symptoms can expand significantly (

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

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

except for some forms of amyloidosis

), then 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. For pathologies associated with impaired bilirubin metabolism (

Crigler-Najjar syndrome, Dubin-Johnson syndrome, Gilbert's disease

), the eyes usually begin to turn yellow due to various provoking factors - fasting, stress, heavy physical exertion, drinking excessive amounts of alcohol, mechanical injuries, taking medications (

antibiotics, glucocorticoids, cytostatics, hormones, anticonvulsants etc.

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

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

) comes from parents, so the presence of any genetic disease in one of them can serve as an important diagnostic sign. The doctor takes these features into account when collecting anamnesis (

questioning the patient

In a general blood test in patients with pathologies associated with metabolic disorders in the body, leukocytosis is the most common (

increase in the number of leukocytes in the blood

), anemia (

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

), increase in ESR (

erythrocyte sedimentation rate

), lymphopenia (

decrease in the number of lymphocytes in the blood

), thrombocytopenia (

decrease in the number of platelets in the blood

), sometimes leukopenia (

decrease in the number of leukocytes in the blood

). A biochemical blood test in such patients can reveal a decrease in the amount of ceruloplasmin, cholesterol, an increase in the amount of copper, total bilirubin, globulins, glucose, and an increase in the activity of aspartate aminotransferase (

), alanine aminotransferase (

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

Based on the results of an ultrasound or computed tomography, one can only suspect liver damage in a patient. Therefore, to more accurately confirm the presence of pathologies associated with metabolic disorders, patients usually undergo a biopsy (

taking a piece of tissue for histological examination

). In parallel with histological examination carry out genetic testing, which is mainly used in the diagnosis of Crigler-Najjar syndrome, Dabin-Johnson syndrome, Gilbert's disease and hemochromatosis. This study identifies mutations characteristic of these pathologies (

) in 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 girdling nature, nausea, vomiting, loss of appetite,

burpingheartburn

Diarrhea with steatorrhea (

feces are foul-smelling, mushy, sticky, with a greasy sheen

), weight loss. A general blood test can reveal leukocytosis (

increase in the number of leukocytes in the blood

) and increase in ESR (

erythrocyte sedimentation rate

), in severe clinical cases anemia is possible (

decrease in the number of red blood cells and hemoglobin

In a biochemical blood test in such patients, an increase in the activity of certain enzymes can be detected (

alpha-amylase, lipase, elastase, trypsin

), an increase in the concentration of total bilirubin, alkaline phosphatase, gamma-glutamyl transpeptidase, glucose, a decrease in albumin, calcium and an increase in the concentration of acute phase proteins (

C-reactive protein, orosomucoid, etc.

). Instrumental research methods (

ultrasound, computed tomography

) make it possible to identify certain pathological changes in the pancreas (

proliferation of connective tissue, presence of cysts, increase in size, etc.

), their localization and various complications (

including compression of the extrahepatic bile ducts

), which causes jaundice in these patients.

In the vast majority of cases, yellowness in the eyes occurs as a result of one or another pathology of the digestive system (

liver, pancreas, biliary tract

). Therefore, if this symptom appears, it is better to seek help from a gastroenterologist. In some cases, yellowing of the eyes can be caused by blood diseases, which are treated and diagnosed by a hematologist. If the patient does not have the opportunity to contact these highly specialized doctors, then you can simply go to see family doctor or a 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 (

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

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

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

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

For primary sclerosing cholangitis, bile acid sequestrants are prescribed - drugs that bind bile acids. In case of liver cirrhosis caused by taking medications, stop treatment with these drugs. For Budd-Chiari disease (

pathology in which blockage of the hepatic veins occurs

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

in liver tissues and improve venous outflow from the liver.

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

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

Amebiasis of the liver For liver amebiasis, amoebicides (medicines that destroy harmful amoebas) are prescribed. Most often they are metronidazole, emetine, tinidazole, ornidazole, etofamide, chloroquine. These drugs also have anti-inflammatory and antibacterial effect. When abscesses form inside the liver, it is also sometimes carried out surgical treatment, 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, poisoning with hemolytic poisons

) can be cured by prescribing etiotropic drugs to the patient that can eliminate the cause of the disease. Other pathologies (

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

) cannot be completely cured, so such patients are prescribed symptomatic treatment.

Malaria Malaria is treated with antimalarial drugs (chloroquine, quinine, artemether, halofantrine, mefloquine, fansidar, etc.). These drugs are prescribed according to special therapeutic treatment regimens, which are selected depending on the type of malaria, its severity and the presence of complications. In severe cases, in the presence of complications, detoxifying, rehydrating (normalize the total volume of fluid in the body), antibacterial, anticonvulsant, anti-inflammatory drugs, infusions of red blood cells (preparations containing donor red blood cells) 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), infusions of red blood cells (a drug containing donor red blood cells), and administration of vitamins B12 and B9. In some cases, they are transfused whole blood, and also prescribe steroidal anti-inflammatory drugs and cholekinetics (drugs that accelerate the excretion of bile from the liver).

Erythrocyte enzymopathies Currently, there is no treatment method that would allow the patient to get rid of any type of erythrocyte enzymopathy, therefore these pathologies are treated only symptomatically. They usually prescribe transfusions of red blood cells (a drug containing donor red blood cells) or whole blood during 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 hemoglobin deficiency, red blood cells in the blood, iron deficiency in the body, treating oxygen deficiency and avoiding factors that provoke hemolytic crises (periods of breakdown of red blood cells in the blood) factors (smoking, drinking alcohol, certain medications, ionizing radiation, severe physical activity, drugs, etc.). To compensate for the deficiency of red blood cells and hemoglobin in the blood, all patients are prescribed infusions of whole blood or packed red blood cells (a preparation containing donor red blood cells), as well as vitamins B9 and B12. Iron supplements are prescribed to correct iron deficiency. In some cases, for certain clinical indications, patients with erythrocyte hemoglobinopathies may undergo surgical transplantation bone marrow or remove the spleen.

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

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

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

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

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

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

The main direction of treatment of such pathologies is the appointment of detoxifying agents to all patients that can remove various metabolites (

products of exchange

) from body tissues. Detoxifying therapy is carried out in patients with hemochromatosis, Wilson-Konovalov disease, Gilbert's disease, Crigler-Nayyar syndrome, Dabin-Johnson. For 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 If hemochromatosis is present, the patient is prescribed detoxifying drugs (deferoxamine), which are able to bind iron well in the blood and remove it through the kidneys. Except medicines such patients are often prescribed a diet that excludes the intake of foods containing large quantities of iron, as well as bloodletting, through which it is possible to quickly remove a certain amount of iron from the body. It is believed that when 500 ml of blood is bled, about 250 mg of iron is immediately removed from the human body.

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

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

Crigler-Najjar syndrome For 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, and liver transplantation.

Dubin-Johnson syndrome Patients with Dubin-Johnson syndrome are prescribed B vitamins and choleretic agents (promote the removal of bile from the liver). Insolation (prolonged exposure to sunlight) is contraindicated for them. Whenever possible, such patients are advised to avoid provoking factors (heavy physical exertion, stress, alcohol consumption, hepatotoxic drugs, fasting, 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 cellular pressure in tissues), hepatoprotectors (protect liver cells from damage). For some forms of amyloidosis, a liver transplant is performed.

If acute pancreatitis occurs or recurs (

re-exacerbation

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

that is, 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 stimulator of production in the stomach. gastric juice and pancreatic juice in the pancreas.

For all pancreatitis, painkillers are usually prescribed (

analgin, drotaverine, baralgin, morphine, etc.

) proteolysis agents and inhibitors (

gordox, aprotinin, contrical, etc.

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

self-digestion

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

Festal, Pancreatin, Mezim, Creon, Panzinorm, Cholenzym, etc.

antiemetics

metoclopramide, domperidone, etc.

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

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

• Crigler-Najjar syndrome. Crigler-Najjar syndrome is a pathology in which the liver cells lack the enzyme (glucuronyl transferase), which converts indirect bilirubin into direct bilirubin, as a result of which the former accumulates in the blood, penetrates the sclera of the eyes and stains them yellow.
• Dubin-Johnson syndrome. Dubin-Johnson syndrome is a congenital disease in which the removal of direct bilirubin from liver cells is impaired, resulting in impaired removal of bilirubin from the liver and the entire body.
• Physiological jaundice of newborns. During intrauterine development, the fetus contains a large amount of fetal hemoglobin in its red blood cells. When a child is born, this type of hemoglobin is replaced with regular hemoglobin (HbA-hemoglobin), which is the dominant (predominant) form in all children and adults. This change is accompanied by yellowing of the skin and sclera of the eyes in a newborn and lasts the first 7–8 days of his life.
• Kernicterus. Kernicterus is a pathological condition in which the level of indirect bilirubin in the blood of newborns sharply increases (more than 300 µmol/l). The reason for this increase may be incompatibility of mother and fetus in blood groups, hereditary erythrocyte membranopathies, Hirschsprung's disease, congenital pyloric stenosis (obstruction of the pylorus), etc.
• Infectious hepatitis. Infectious hepatitis in newborns most often occurs in cases where their mothers are not observed by doctors during pregnancy and do not undergo various laboratory tests for the presence of infections (toxoplasmosis, herpes, cytomegalovirus, hepatitis B, etc.).

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

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

inflammation of the liver tissue

). With it, some of the liver cells die, as a result of which the liver loses the ability to neutralize all 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 drinking alcohol, the level of direct and indirect bilirubin in a person’s blood increases, which leads to their penetration into the sclera of the eyes, which is why 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 in pathologies that cause yellowing of the whites of the eyes, bilirubin, which is in high concentrations in the blood, will constantly penetrate the white membrane of the eyes and color it yellow. Therefore, in order to get rid of the yellowness of the whites of the eyes, it is necessary to eliminate main reason increase in blood bilirubin.

PLEASE NOTE!

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

Yellowing of the whites of the eyes may indicate the occurrence of diseases such as viral hepatitis, conjunctivitis, or even cancer. A person will not be able to determine the exact cause on his own, so it is better to immediately consult a doctor, conduct an examination, and begin treatment.

If the patient’s whites of the eyes turn yellow, 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 due to liver damage.
2. Newly born babies may have yellow eyeballs for 3 to 5 days after birth. This phenomenon is called “jaundice in babies.”
3. If the patient has yellow eyes, the reason may lie in the development of a malignant formation on the conjunctiva.
4. Another option why the whites of the eyes turn yellow is that the patient has an illness that has affected the eyes themselves. Most often these are specific diseases that develop in the visual organs.
5. Yellowness in the eyes can 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 the whites is striking

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

   In any case, determining the cause and treating the above pathologies should occur under the supervision of a doctor.

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

   If a person who comes to the clinic has yellow white eyes, this may mean hepatitis or other damage to liver structures.

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

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

   Jaundice of newborns undergoes UV irradiation

   Symptoms of such a lesion:

   1. The whites of the eyes are yellow.
   2. The liver is enlarged in size.
   3. Possible increase in temperature.
   4. The patient's entire body 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 often found in children (jaundice). Its development at the initial stage can be detected precisely with the help of yellowed eye whites (some types of this disease do not cause complete yellowing of the patient’s body).

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   This symptom clearly manifests itself in diseases such as echinococcosis or opisthorchiasis. Diseases are caused various types 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 young mothers are interested in why their whites are just born child painted yellow. This phenomenon - jaundice - is typical for infants. 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 as much red blood cells, so they begin to disintegrate. Because of this, the baby's eyes and body skin turn yellow.

   Mothers rush to doctors asking what to do. There is no need to worry; usually this phenomenon goes away on its own within 7 to 12 days. If this does not happen, then perhaps the child has another disease that caused similar signs. 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 growths 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 treatment for the disease must be done in specialized clinics. For more information about the treatment of melanoma, watch this video:

   With other eye diseases, the whites of the eye turn slightly yellow or may completely turn into different shades of this color. Typically, such signs are characteristic of diseases such as pterygium or pinguecula.

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

   Pterygium is a growth of the conjunctiva. If this phenomenon spreads to the pupil, the patient may lose vision in one or both eyes. Therefore, if problems with the eyes appear, you should immediately contact a specialist.

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

   It provides for the following measures:

   1. A person should completely stop drinking alcohol.
   2. The patient is prohibited from eating salty or spicy foods.
   3. Should be excluded from the diet fried foods and various flour products.
   4. The daily menu should include a large amount of fruits and foods that are rich in ascorbic acid.

   Sometimes men or women come to the doctor for an appointment with yellow discoloration in the whites of their eyes due to fatigue. This usually happens if a person does not get enough sleep or sits at the computer for a long time. The problem can be triggered by solving some complex intellectual problem or the presence of dry air in the room. The eyes become inflamed. Such people need a little rest. You can use soothing lotions. It is recommended to walk more in the fresh air. Usually, after 2 - 3 days of such rest, the eyes return to normal, and the whites of the eyes acquire a natural color. For more information about combating the problem, watch this video:

   If none of the above reasons are suitable to explain the change in the color of 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 THAT CORRECTING YOUR VISION IS DIFFICULT? Judging by the fact that you are reading these lines now, victory in the fight against deteriorating vision is not yet on your side... And you have already thought about surgical intervention? This 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 would be more correct to treat not the effect, but the cause? We recommend reading the story of the host of the “Live Healthy” program, Elena Malysheva, how she restored her vision... Read the article >>

   Protein human eye is not absolutely white, as it is imagined by designers who process photographs of models in a photo editor for gloss. Healthy color the squirrel is slightly yellowish, but uniform, without streaks, spots, or darkening. If the whites turn yellow or become stained, this means that the person has problems with the condition of internal organs, eye diseases, or leads an unhealthy lifestyle. Most often, this is almost certainly a signal of some 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, called the sclera, most often turns yellow unnoticed by the person himself. This process is not painful or inconvenient, and it may take some time before a person notices the yellowing when looking at themselves in the mirror, or someone tells them about it. Yellowing - icterus of the sclera - means the presence of pathology.

   Icteric sclera

   By the way. There are people who have a yellow tunica from birth. This is genetically determined and does not mean a disease. But if the color has changed, that is, the whites have turned yellow, or inclusions, fragments, or darkening have appeared on them, you need to urgently go to the doctor.

   Metabolism of bilirubin

   There are several shades of yellow that squirrels can turn into - from light to ocher or almost orange. It depends on the disease itself and on what stage the disease is in, that is, how much the body has suffered from it. Diseases and other reasons that cause the color of the tunica albuginea to change can be divided into three groups.

   Table. Causes of yellowing of the sclera by group.

   Gilbert's syndrome

   Internal diseases

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

   Important! Bilirubin is formed after the destruction of the protein structure. Hemoglobin, cytochrome, myoglobin disintegrate, leaving free bilirubin. 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. Then direct connection, which is no longer dangerous, is sent to the biliary tract to exit the body.

   Yellow whites of eyes

   Liver pathologies

   If the liver is overloaded, there is a malfunction of any kind in its work, bilirubin in the blood increases, since the unhealthy organ cannot cope with its task. Disintegration occurs, but the toxin is not removed, accumulating in the body. Because of this, all the integuments of the body turn yellow, and since yellowing occurs on the sclera first, such a phenomenon as yellow whites is observed.

   Symptoms of hepatitis

   Echinococcosis

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

   Echinococcus

   Cirrhosis

   This pathology causes multiple lesions of the liver tissue, replacing healthy tissue with pathologically altered ones. In damaged tissue, the ability to neutralize the toxicity of bilirubin is reduced or completely eliminated. It accumulates in tissues, reaching the outer integument and mucous membranes. Cirrhosis can occur:

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

   Cirrhosis

   Cancer

   The disease is marked by the appearance and progressive growth of tissue inflammation, developing into a tumor that destroys healthy liver cells. Because of this, the organ loses the ability to function and, among other things, neutralize bilirubin.

   Liver cholangiocarcinoma

   Microorganisms

   These infections include:

   • flatworms;
   • epistorchiasis;
   • opisthorchiasis;
   • echinococcosis.

   Worms in the liver

   By the way. Opisthorchiasis, characterized by dull yellow proteins, is caused by a type of worm that may appear in the body after eating insufficient fish heat treatment. As they multiply, they block the walls of the liver ducts, disrupting the excretion of bile. After this, the substance enters the blood and yellowness appears on the sclera.

   Opisthorchiasis

   Blood diseases

   Internal ailments that cause yellowness of the peripillary zone include diseases of the circulatory system. They always cause red blood cell cancellation, which immediately increases the amount of bilirubin. The body begins to be unable to cope with its elimination, even with a healthy liver, so the toxin is deposited and gives the tissues a characteristic yellow color.

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

   Symptoms of malaria

   Malaria

   It gained enormous popularity, but became widespread only in those parts of the world where malaria mosquitoes live. It is their bite that charges the blood with the malarial bacterium. The infected organism transports it directly to the liver, where they multiply intensively. Having increased the population to a critical level, they re-enter the blood, destroying structural bodies and causing the breakdown of red blood cells, stimulating the hyperproduction of bilirubin.

   Babesiosis in humans

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

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

   • erythrocyte membranopathy;
   • 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 stops coping with it, and its cells take over the entire body, including the eye sclera.

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

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

   By the way. Also included in the class of these toxins are the venom of bees and snakes, poisonous spiders and other insects, and substances contained in poisonous mushrooms, berries and other plants.

   Since unnecessary and hazardous substances,path problems cause transportation problems. To reach the intestines, bile passes long haul, during which, in the presence of failures and narrowing of the ducts, an accumulation of substance is formed at one point. This causes a rupture at this point, after which the bile enters the bloodstream. Then everything is the same as with the others internal diseases– hyperbilirubin is reflected in the color of the sclera. Pathologies that trigger these processes include the following.

   1. Gallstone disease.
   2. Cholangitis.
   3. Jaundice.
   4. Pancreatic cancer.

   Primary sclerosing cholangitis

   Sclerosing cholangitis

   The origin of the disease is not clear. During the course of the disease, irritation of the bile ducts occurs, inflammation occurs, transformation of the walls of the duct, and blockages occur. It is difficult for bile to enter the intestines and is instead absorbed into the blood. Because bile contains conjugated bilirubin, external tissues become stained.

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

   Gallstone disease

   Cancer

   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 comes out into the breakthrough and becomes an integral part of the blood flow.

   About this disease, which has medical name hepatitis A, we need to talk in detail. Jaundice is very dangerous for humans. And yellowness of the eyes is the first sign of this disease.

   Hepatitis A

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

   1. Hemolytic.
   2. Cholestatic.
   3. Hepatic.

   Table. Types of hepatitis A.

   Hemolytic Cholestatic Hepatic Facts about hepatitis A virus By the way. There is also jaundice, diagnosed in newborns. This is not a disease or pathology. The phenomenon is explained by the fact that during 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 and their replacement with bilirubin cells. One to two weeks after birth, the color indicators of the baby’s skin and sclera acquire a normal color. If this does not happen, consultation with a pediatrician is necessary. Of the ophthalmological pathologies that cause yellowing of the tunica albuginea, not as many diseases can be listed as internal ones. However, some eye problems lead to this phenomenon - scleral icterus. Pingueculitis. Gilbert's syndrome. Melanoma. Malignant conjunctivitis. Pterygium. Yellow whites of the eyes - causes Formation of the pinguecula Simply put, it is a wen that forms on the conjunctiva, mainly due to disorders of fat metabolism. It can be large and colored a shade of yellow. Appears for several reasons: aging; eye irritation from smoke or wind; prolonged exposure to the sun. Pinguecula (wen on the eye) This formation does not affect vision in any way, but if it is detected, you should see an ophthalmologist to rule out yellowing of the sclera for another reason. Also, if the tissue near the wen becomes inflamed and begins to cause discomfort, surgery 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 different modifications. Smooth spot. A raised or bumpy spot. Color ranges from yellow to brown. Colorless. People with blue eyes are at greater risk of developing melanoma The pathology forms in the inner corner of the eye and is considered a rare disease that is difficult to diagnose. With this pathology, the conjunctiva grows. Soon it forms a rim advancing on the tunica albuginea. At the same time, the color of the latter changes, becoming dull yellow. There is an unpleasant sensation in the eye. The formation is treated surgically, and the effectiveness of treatment depends on timely detection. Course of pterygium Important! If the growth of the conjunctiva is not stopped, it will completely close the entire pupil, and the person will stop seeing. This disease can be classified as genetic. The syndrome is not even considered a pathology, rather, physiological feature, but can also cause yellow eyes. With this feature, the concentration of bilirubin in a person’s blood is constantly increased, as a result, his eyes are constantly yellow. What does Gilbert's syndrome mean and how is it treated? Having the syndrome, the patient should avoid situations where bilirubin is released 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 the wrong color. Bad habits and addictions, abuse and overwork, insufficient quantity useful substances entering the body - all this can cause the tunica albuginea to acquire an unhealthy yellow tint. What do you want in this case? Take measures to normalize your lifestyle. Change your diet by removing flour, salty, spicy, fried foods. Avoid alcohol. Fortify food. Relax, get enough sleep, go for a walk. Quitting alcohol As you can see, there are many reasons for yellow whites of the eyes, and the main ones are serious illnesses. How to treat them? Depending on which group the disease, the manifestation of which is yellowing of the eyes, belongs to, treatment is prescribed either by an ophthalmologist, or a therapist, or a doctor of another narrow specification. In any case, it is necessary to immediately undergo a consultation upon discovering yellowness of the white that has suddenly appeared, or an increase in the naturally yellowish tint. 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, it is first of all necessary to improve the level of general health and avoid infection viral infections. The liver must be protected and supplied with all the necessary elements for uninterrupted operation, which is achieved by nutritional balance. Best Foods for Liver Health Should be engaged physical activities or at least arrange hiking. Taking a multivitamin from time to time is helpful. Make sure that there is rest during work and that sleep remains healthy and in sufficient quantity.

Yellow whites of the eyes may indicate liver disease, infection, viral hepatitis, malignant neoplasms or conjunctiva. Yellowing of the whites of the eyes can also be caused by problems with the gallbladder and biliary tract.

Yellowing of the whites of the eyes due to liver disease

When the whites of the eyes acquire a yellow tint, it makes sense to be wary. Such changes may indicate liver disease. Since in the human body, namely in red blood cells, there is bilirubin - an enzyme during the breakdown of which, the formation of yellow spots. Bilirubin is produced in the liver, so when the whites of the eyes turn yellow, it is assumed that this organ is affected by the disease.

Yellow whites of the eyes can also signal liver problems such as hepatitis - serious illness, a characteristic feature of which is yellowing of the skin, as well as the whites of the eyes. With jaundice, the tissues of the entire body turn yellow, thanks to the yellow pigment formed during the breakdown of bilirubin. During this process, a substance harmful to the body is released that negatively affects nervous system.

Eye diseases characterized by yellowing of the whites

The whites of the eyes may take on a yellow tint due to the presence of neoplasms of the conjunctiva, such as melanoma. This disease is very serious, difficult to diagnose and difficult to treat. This disease is a type of cancer, and in mandatory Treatment must be carried out by appropriate specialists; independent actions in treatment are not allowed.

The whites of the eyes can take on a yellow tint if the visual organs themselves are diseased. Such ailments include pinguecula (the appearance of a yellow wen) and pterygium (overgrowth of the conjunctiva). These diseases may be associated with disruption of lipid metabolism.

Sometimes the whites of the eyes become yellowish when overworked and tired. Lack of sleep, dry indoor air and prolonged work at the computer can also be the reasons for this phenomenon.

Recommendations in such cases are fresh air and special soothing lotions for the eyes. Such yellowness of the whites of the eyes is easily removable, but in serious cases, with various liver diseases and other pathologies, the yellowing of the whites does not go away until the underlying disease is eliminated.

3967 03/19/2019 5 min.

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

Symptom Definition

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

Causes

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

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

Jaundice (yellowing of the sclera of the eyes and skin of the body) begins when the bilirubin concentration is more than 30-35 µmol/l. This occurs because at such concentrations, bilirubin begins to diffuse (that is, penetrate) into peripheral tissues and stain them. There are three degrees of severity of the disease - mild, moderate and severe. In mild cases, the bilirubin concentration is up to 86 µmol/l, and in severe cases – 159 µmol/l or more.

Possible diseases

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

Liver diseases

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

Blood diseases

In blood diseases, severe hemolysis (or destruction) of red blood cells is observed. As a result, the content of hemoglobin increases, which then breaks down to form indirect bilirubin. The concentration of this element becomes too high and the liver cannot neutralize it.

Biliary tract problems

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

Metabolic disorders

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

• proteins;
• bilirubin;
• metals

If there are problems with the metabolism of copper or iron, these elements begin to accumulate in the liver and damage its tissue, causing cirrhosis. With amyloidosis (a protein metabolism disorder), abnormal amyloid protein begins to deposit in the liver, destroying the structure of the organ. As a result, the liver begins to work incorrectly, ceasing to remove indirect bilirubin.

Pancreatitis (acute and chronic)

For acute or chronic form pancreatitis (pancreatitis - inflammation of the pancreas) swelling and, accordingly, enlargement of the pancreas occurs. It begins to put pressure on the bile duct (choledochus), as a result of which the work of the latter is disrupted. Bile stagnates in the biliary tract, intrahepatic capillaries rupture, and bile components enter the blood.

Jaundice of newborns

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

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