Congenital underdevelopment of the thymus. Thymus hypoplasia in children symptoms and treatment

From atrophic (involutive) changes in the thymus, one should distinguish congenital malformations of its development, manifested either by its complete absence - aplasia, agenesis, or underdevelopment with a violation of the formation of lymphocytes in it - hypoplasia, alymphoplasia.

Congenital absence of the thymus may be the only malformation or be combined with other malformations, in particular with congenital absence of the parathyroid glands, which is described in the Anglo-American literature under the name of the Digeorge syndrome (Dodson et al., 1969; Kirkpatrick, Digeorgie, 1969; Lobdell , 1969). Although cases of detection of the complete absence of the thymus gland in children who died in early infancy have been known for a long time (Bischoff, 1842; Friedleben, 1858), until recently the death of such children was not associated with the absence of the thymus gland in them.

With hypoplasia, the thymus gland lags behind in its development from the very beginning and at the birth of a child it turns out to be small, often not exceeding 1-2 g in weight. Microscopically, its lobules also turn out to be reduced in size, and due to the almost complete absence of lymphocytes, their division into the cortical and medulla layers are not observed. Usually there are no Hassall's little bodies in them.

Changes characterizing hypoplasia of the thymus gland have been studied only recently in connection with the description of Glanzmann and Riniker in 1950 of a peculiar disease of early childhood infancy called by them essential lymphocytophthisis. Due to the fact that this disease often has a family character, it was later also described under the names of family (family) lymphopenia (Tobbler, Cottier, 1958) or hereditary lymphoplasmacytic dysgenesis (Hitzig, Willi, 1961).

The disease is manifested by persistent, untreated diarrhea, leading children to exhaustion and death. In the blood, there is a sharp lymphopenia and hypogammaglobulinemia, and an autopsy of the dead reveals a sharp decrease in the size of the spleen and lymph nodes with an almost complete absence of lymphocytes in them. Initially, due attention was not paid to the state of the thymus, although already at the first description of the disease, Glanzmann and Riniker (1950) mention that in one of the two children examined by them, the thymus was small and edematous. However, later changes in the thymus in this disease were studied in more detail (Cottier, 1958; Blackburn, Gordon, 1967; Thompson, 1967; Berry, 1968; Berry, Thompson, 1968), which gave reason to consider the entire disease as a manifestation of primary immunological deficiency. due to hypoplasia or aplasia of the thymus (Good, Martinez, Gabrielsen, 1964; Sell, 1968).

With aplasia or hypoplasia of the thymus, the normal development of the entire lymphoid tissue is disrupted, and therefore the body remains incapable of immunological reactions. As a result, the normal flora of the intestine begins to have a pathogenic effect, causing damage to it and thereby diarrhea, leading to: exhaustion. Often, a secondary infection in the form of candidiasis joins (Glanzmann, Riniker, 1950; Thompson, 1967), pneumocystis pneumonia (Becroft, Douglas, 1968; Berg, Johansson, 1967), etc.

P. With homotransplantation of the skin and other tissues in such patients, there is no rejection reaction (Rosen, Gitlin, Janeway, 1962; Dooren, Bekkum, Cleton, 1968). Thus, the whole picture of the disease is fully consistent with the so-called wasting syndrome that develops in animals after the removal of their thymus gland, produced immediately after birth (Miller, 1961; Good et al., 1962; Metcalf, 1966; Hess, 1968). In some cases, in children with hypoplasia of the thymus, shortly before death, the phenomena of aplastic anemia were also noted (Glanzmann, Riniker, 1950; Thompson, 1967; Dooren et al., 1968) or granulo- and thrombocytopenia (Lamvik, Moe, 1969).

Most children with aplasia or hypoplasia of the thymus die within the first 6 months of life. However, in some cases, a longer course of the disease is also observed - up to 1 year 7 months (Hitzig, Biro et al., 1958) and more. A more detailed immunological examination of such patients made it possible to detect in some of them the preservation of the ability to some extent to some immunological (allergic) reactions (Hitzig, Biro et al., 1958), as well as the preservation of certain fractions of immunoglobulins (Becroft, Douglas, 1968; Berg and Johansson, 1967), which makes it possible to single out the series clinical varieties this disease (Sell, 1968). Obviously, this depends on the degree of hypoplasia (alimphoplasia) of the thymus gland, which can be expressed differently. With a relatively small degree of hypoplasia due to the partial preservation of the body's ability to immune reactions, the disease can take lingering course. An example of this, apparently, is the observation of Grote and Fischer-Wasels (1929) of "total alymphocytosis" in a 39-year-old man who died of exhaustion. At autopsy, atrophy of the spleen (18.0) and other lymphoid organs was found in him. The small intestine had dark pigmented scars, and The lymph nodes the mesentery contained foci of “cheesy necrosis”. The thymus gland, unfortunately, was not examined. In the same respect, one of our observations, which is given below, is of undoubted interest.

Male E., 55 years old. A carpenter. Married, had no children. FROM early childhood he often had diarrhea, in connection with which he strictly observed a diet throughout his life. Smoked a little. He rarely drank alcohol. Within 3 recent years was comprehensively examined in many hospitals in Leningrad, but the diagnosis remained unclear. In connection with the growing exhaustion and suspicion of a tumor in abdominal cavity On 17/V, 1968, he was admitted to the Clinic of Faculty Surgery of the Military Medical Academy, where on 31/V he underwent a diagnostic laparotomy, during which no tumor was found. After the operation, the patient's condition began to deteriorate rapidly. Blood test 17/VI 1968: Er. 3700000, Hb 13.2 g%", bloom, show 1.0, l. 13500, of which s. 45%, p. 37%, s. 7%, lymph. 11%. ROE 10 mm / h. In previous blood tests, the number of lymphocytes fluctuated between 7-14%.At repeated bacteriological studies of feces, pathogenic flora was not detected.The patient died on June 17, 1968 with symptoms of increasing exhaustion and pneumonia. with extreme malnutrition and severe beriberi, condition after diagnostic laparotomy, ascites, pressure ulcers of the sacrum, bilateral pneumonia and pulmonary edema.

At autopsy (prosector T, V. Polozova) there was a sharp exhaustion. Body weight 40 kg with a height of 166 cm. Fresh in the midline of the abdomen postoperative scar. In the area of ​​the sacrum there is a bedsore with a dark gray bottom 5x4 cm. The left pleural cavity is free. The right lung in the upper sections is fused with the parietal pleura. In the region of its apex there are several dense scars and a small encapsulated calcified focus. In the lower part of the left lung, there are multiple gray-red airless foci of compaction measuring 1-1.5 cm in diameter. Inferior branch of the right pulmonary artery thrombosed. In the lower lobe of the right lung under the pleura, there is a black-red airless focus of irregular wedge-shaped shape measuring 5X5X4 cm. The bronchopulmonary lymph nodes are not enlarged, black-gray, with small gray scars. There is a small amount of clear yellowish fluid in the abdominal cavity. On the mucous membrane of the small intestine, transverse superficial ulcers up to 4X2 cm in size with a dark gray pigmented bottom are visible. Two of the same type of ulcer are present in the mucous membrane of the caecum. Peyer's patches and lymphatic follicles are not defined. Lymph nodes of the mesentery up to 1 cm in diameter, in many of them yellowish-gray areas are visible on the cut. The spleen weighs 30.0 with a thickened capsule, dark red in section. Tonsils are small. Inguinal and axillary lymph nodes up to 1 cm in size, gray in section. The heart weighs 250.0, its muscle is brown-red. Liver weighing 1500.0, brown-brown in section. There were multiple small hemorrhages under the pleura of the left lung and in the folds of the gastric mucosa. Other organs and tissues were somewhat reduced in size, otherwise unchanged. Thymus gland in fiber anterior mediastinum not found.

results histological examination.

Small intestine: superficial ulcers with necrotic bottom containing gram-negative rods; in the submucosal and muscular layers - infiltrates of histiocytes and a few lymphocytes. Mesenteric lymph nodes: foci of necrosis are visible among the lymphoid tissue, without cellular reaction around; tubercle bacilli and other microbes are not found in them; an axillary lymph node with sclerosis in the center and a small amount of lymphoid tissue along the periphery (Fig. 10, a). Spleen: lymphatic follicles are very weak, found in small numbers; the pulp is sharply plethoric. Fiber of the anterior mediastinum: among the fatty tissue, there are a few small lobules of the thymus gland, which do not have a division into cortical and medulla layers and do not contain Hassall's bodies; lymphocytes in the lobules are almost completely absent (Fig. 10, b, a), the lobules consist of reticular and epithelial cells, forming in some places separate glandular cells. Liver: fatty degeneration and brown atrophy. Myocardium: brown atrophy. Kidney: hydropic dystrophy. Lung: foci of pneumonia containing gram-positive cocci.

Based on the results of the autopsy and histological examination, a diagnosis of chronic nonspecific ulcerative enterocolitis was made, which led to exhaustion and was complicated by pneumonia. The development of the disease in this case can be associated with the inferior development of the thymus gland and the entire lymphatic apparatus as a whole.

Rice. 10. Alymphoplasia of the thymus.

a - axillary lymph node with sclerosis of the central part and preservation of lymphoid tissue in the form of a narrow layer along the periphery (magnification 60X) "” b-one of the lobules of the extralobular gland with an almost complete absence of lymphocytes (magnification 120X); .400X)..

Recently, transplantation of the thymus from human fetuses has been used with some success for the treatment of such patients (August et al., 1968; Clevelend et al., 1968; Dooren et al., 1968; Good et al., 1969; Koning and others, 1969). At the same time, after transplantation, there is a rapid increase in the number of lymphocytes in the blood, the appearance of immunoglobulins in it. Children acquire the ability to cellular and humoral immune responses, including the rejection of tissue homotransplants (August et al., 1968; Koning" et al., 1969). When examining a biopsied lymph node in one of these patients after transplantation of the thymus gland, the presence of well-defined lymphatic follicles with reproduction centers was found in it (Clevelend, Fogel, Brown, Kay, 1968).

The child, being in the womb, is completely protected from any adverse environmental factors.

The thymus gland in newborns becomes the first cascade of immune defense. Which protects the child from numerous pathogenic microorganisms. The thymus in children begins to work immediately after birth, when an unfamiliar microorganism enters with the first breath of air.

The thymus gland in children under one year old manages to collect information on almost all pathogenic organisms that we encounter throughout life.

Embryology (development of the thymus in the prenatal period)

The thymus in the fetus is laid already at the seventh - eighth week of development. Even during pregnancy, the thymus gland begins to produce immune cells, by the twelfth week, the precursors of future lymphocytes, thymocytes, are already found in it. By the time of birth, the thymus in newborns is fully formed and functionally active.

Anatomy

To understand, you should attach three fingers to the top of the handle of the sternum (the area between the collarbones). This will be the projection of the thymus gland.

At birth, her weight is 15-45 grams. The size of the thymus in children is normally 4-5 centimeters in length, 3-4 centimeters in width. An intact gland in a healthy child is not palpable.

Age features

The thymus plays a key role in the development of immunity and continues to grow until puberty. At this point, the mass reaches 40 grams. The field of puberty begins reverse development (involution). By old age, the thymus gland is completely replaced by adipose tissue, its mass decreases to 6 grams. In every period of life.

The role of the thymus

The thymus produces hormones necessary for the normal development of the immune system. Thanks to them, the cells of the immune system learn to recognize harmful microorganisms and trigger mechanisms to eliminate them.

Thymus disorders

According to the degree of activity, hypofunction and hyperfunction of the thymus gland are distinguished. According to the morphological structure: (absence), (underdevelopment) and (increase in size).

Congenital pathology of the development of the thymus gland

With anomalies in the genetic code, the laying of the thymus can be disturbed even in the early embryonic period. Such a pathology is always combined with a violation of the development of other organs. There are several genetic abnormalities that cause changes in which the changes are fatal to the immune system. The body loses the ability to fight infection and is not viable.

With genetic defects in development, the whole the immune system. Even with the preservation of partial activity, thymus hypoplasia in newborns leads to a persistent deficiency in the content immune cells in the blood and persistent infections, against which there is a general developmental delay.

Also, genetic malformations include congenital cysts, thymic hyperplasia and thymomas (benign or malignant tumors thymus).

Hypofunction and hyperfunction of the thymus

Functional activity does not always depend on the size of the gland itself. With a thymoma or a cyst, the thymus gland is enlarged, and its activity may be normal or reduced.

Thymus hypoplasia

In the absence of a developmental anomaly, thymus hypoplasia in newborns is extremely rare. This is not an independent disease, but a consequence of a severe infection or prolonged starvation. After the cause is eliminated, its dimensions are quickly restored.

Thymus hyperplasia

There are endogenous hyperplasia, when an increase in the thymus is associated with the performance of its functions ( primary) and exogenous, then the growth is caused by pathological processes in other organs and tissues.

Why does the thymus gland increase in a baby?

Causes of primary (endogenous) thymomegaly:

Causes of exogenous thymomegaly:

• Generalized disorders of the immune system(, autoimmune diseases).
• Violations of the regulatory systems in the brain(hypothalamic syndrome).

Symptoms of hyperplasia

During an external examination, an enlarged thymus gland in an infant is visible when crying, when increased intrathoracic pressure pushes the thymus above the sternum handle.

Enlargement of the thymus gland in children affects appearance child - enlarged facial features, pale skin. There is a delay in general development. Enlargement of the thymus gland in a 2-year-old child, detected during examination, especially with an asthenic physique, should not cause concern. The thymus is a fairly large organ for such a baby and may simply not fit in the space allotted to it.

Enlargement of the thymus gland in infants with transient jaundice of newborns is also not a pathology.

Of clinical importance is the simultaneous detection of several signs characteristic of diseases of the thymus:

• syndrome of compression of nearby organs;
• immunodeficiency syndrome;
• lymphoproliferative syndrome;
• disruption of work endocrine system.

Syndrome of compression of nearby organs

Enlargement of the thymus gland in children causes symptoms of compression of nearby organs. With pressure on the trachea, shortness of breath, breathing noises, dry cough appear. By squeezing the lumen of the vessels, the thymus disrupts the inflow and outflow of blood, pallor of the skin and swelling of the jugular veins are noted.

If an enlarged thymus in a child causes compression vagus nerve, which innervates the heart and digestive tract, there is a persistent slowing of the heartbeat, swallowing disorders, belching, and vomiting. It is possible to change the tone of the voice.

Immunodeficiency Syndrome

When the thymus gland is enlarged in a child against the background of its dysfunction, even the usual diseases proceed differently. Any colds can begin without an increase in temperature, with a sharp jump on the third or fourth day. Such children get sick longer than their peers, and the severity of the disease is higher. Often, the infection passes into the lower parts of the respiratory system with the development of bronchitis and tracheitis.

Lymphoproliferative syndrome

An increase in the production of hormones in the gland causes hyperstimulation of the entire immune system. Lymph nodes are enlarged, the ratio of immune cells with a predominance of lymphocytes is disturbed in the general blood test. Any external stimulus causes an excessive defensive reaction in the form of allergic reactions. A severe reaction to vaccination may occur.

Disruption of the endocrine system

An increase in the thymus in children can lead to malfunctions in the endocrine system, with the development diabetes and disruption thyroid gland.

What is dangerous enlargement of the thymus gland in a child

An increase in the thymus gland in infants, with compression of the trigeminal, disrupts the peristalsis of the esophagus and intestines. The child may have difficulty getting food and spitting air after feeding. When the trachea is compressed, more force is required to inhale, and high blood pressure causes rupture of the alveoli in the lungs with the development of atelectasis.

Diagnostics

With symptoms of an enlarged thymus gland in a child, consultation of several specialists is necessary - an immunologist, an endocrinologist and a pediatrician. It often turns out that an increase in the thymus gland in an infant is not associated with pathology, but is due to individual anatomical features. Often parents panic that the thymus gland is enlarged in a newborn, because when crying, it often protrudes above the handle of the sternum. It is also not worth fearing inflammation of the thymus gland in infants; a huge number of immune cells in it leaves no chance for the development of infection.

To confirm the diagnosis, it is necessary to undergo a thorough examination, including:

• General and detailed blood test.
• Chest x-ray.
• Ultrasound diagnostics.

A blood test can detect a decrease in the level of T-lymphocytes, an imbalance between immunoglobulins.

X-ray of the thymus to the child will allow to exclude anomalies in the structure and location of the thymus gland.

Ultrasound allows you to accurately determine the degree of thymus hyperplasia in newborns. Examination of the adrenal glands, abdominal organs will exclude concomitant pathology.

You may need additional tests for hormone levels.

At dysfunction of T-lymphocytes infectious and other diseases are, as a rule, more severe than with insufficient antibodies. Patients in such cases usually die in the thoracic or early childhood. Damaged gene products have been identified only for some primary disorders of T-lymphocyte function. Thymus transplantation is currently the treatment of choice for these patients. bone marrow from HLA compatible siblings or haploidentical (semi-compatible) parents.

Hypoplasia or aplasia of the thymus(due to violation of its bookmark on early stages embryogenesis) is often accompanied by dysmorphia of the parathyroid glands and other structures that are formed at the same time. Patients have atresia of the esophagus, splitting of the palatine uvula, congenital malformations of the heart and large vessels (defects of the interatrial and interventricular septum, right-sided aortic arch, etc.).

Typical facial features of patients with hypoplasia: shortening of the philtrum, hypertelorism, antimongoloid incision of the eyes, micrognathia, low ears. Often, the first indication of this syndrome is hypocalcemic convulsions in newborns. Similar facial features and anomalies of large vessels extending from the heart are observed in fetal alcohol syndrome.

Genetics and pathogenesis of thymus hypoplasia

DiGeorge Syndrome occurs in both boys and girls. Family cases are rare, and therefore it is not classified as a hereditary disease. However, microdeletions of regions of the qll.2 segment of chromosome 22 (a segment of DNA specific to DiGeorge syndrome) were found in more than 95% of patients. These divisions seem to be more often passed down through the maternal line.

They can be quickly identified by genotyping using PCR microsatellite DNA markers located in the corresponding area. Anomalies of large vessels and division of sections of the long arm of chromosome 22 combine DiGeorge syndrome with velocardiofacial and conotruncal facial syndrome. Therefore, currently they talk about the CATCH22 syndrome (Cardiac, Abnormal facies, Thymic hypoplasia, Cleft palate, Hypocalcemia - heart defects, facial anomalies, thymus hypoplasia, cleft palate, hypocalcemia), including a wide range of conditions associated with 22q deletions. In DiGeorge syndrome and velocardiofacial syndrome, deletions of regions of the p13 segment of chromosome 10 were also found.

Concentration immunoglobulins in serum with thymus hypoplasia is usually normal, but the level of IgA is reduced, and IgE is elevated. The absolute number of lymphocytes is only slightly below the age norm. The number of CD T-lymphocytes is reduced in accordance with the degree of thymic hypoplasia, and therefore the proportion of B-lymphocytes is increased. The response of lymphocytes to mitogens depends on the degree of thymus deficiency.

In the thymus, if present, bodies are found Hassala, normal density of thymocytes and a clear boundary between the cortex and medulla. Lymphoid follicles are usually preserved, but para-aortic lymph nodes and the thymus-dependent region of the spleen are usually depleted.

Clinical manifestations of thymus hypoplasia

More often there is not complete aplasia, but only parathyroid glands, called incomplete DiGeorge syndrome. Such children grow normally and do not suffer too much from infectious diseases. In complete DiGeorge syndrome, as in patients with severe combined immunodeficiency, susceptibility to opportunistic and opportunistic flora, including fungi, viruses, and P. carinii, is increased, and graft-versus-host disease often develops during transfusion of unirradiated blood.

Treatment of thymus hypoplasia - DiGeorge's syndrome

Immunodeficiency with Complete DiGeorge Syndrome corrected by transplantation of thymus tissue culture (not necessarily from relatives) or unfractionated bone marrow from HLA-identical sibs.

The child, being in the womb, is completely protected from any adverse environmental factors.

The thymus gland in newborns becomes the first cascade of immune defense. Which protects the child from numerous pathogenic microorganisms. The thymus in children begins to work immediately after birth, when an unfamiliar microorganism enters with the first breath of air.

The thymus gland in children under one year old manages to collect information on almost all pathogenic organisms that we encounter throughout life.

Embryology (development of the thymus in the prenatal period)

The thymus in the fetus is laid already at the seventh - eighth week of development. Even during pregnancy, the thymus gland begins to produce immune cells, by the twelfth week, the precursors of future lymphocytes, thymocytes, are already found in it. By the time of birth, the thymus in newborns is fully formed and functionally active.

Anatomy

To understand, you should attach three fingers to the top of the handle of the sternum (the area between the collarbones). This will be the projection of the thymus gland.

At birth, her weight is 15-45 grams. The size of the thymus in children is normally 4-5 centimeters in length, 3-4 centimeters in width. An intact gland in a healthy child is not palpable.

Age features

The thymus plays a key role in the development of immunity and continues to grow until puberty. At this point, the mass reaches 40 grams. The field of puberty begins reverse development (involution). By old age, the thymus gland is completely replaced by adipose tissue, its mass decreases to 6 grams. In every period of life.

The role of the thymus

The thymus produces hormones necessary for the normal development of the immune system. Thanks to them, the cells of the immune system learn to recognize harmful microorganisms and trigger mechanisms to eliminate them.

Thymus disorders

According to the degree of activity, hypofunction and hyperfunction of the thymus gland are distinguished. According to the morphological structure: (absence), (underdevelopment) and (increase in size).

Congenital pathology of the development of the thymus gland

With anomalies in the genetic code, the laying of the thymus can be disturbed even in the early embryonic period. Such a pathology is always combined with a violation of the development of other organs. There are several genetic abnormalities that cause changes that are fatal to the immune system. The body loses the ability to fight infection and is not viable.

With genetic developmental defects, the entire immune system suffers. Even with the preservation of partial activity, thymic hypoplasia in newborns leads to a persistent deficiency in the content of immune cells in the blood and persistent infections, against which there is a general developmental delay.

Also, genetic malformations include congenital cysts, thymus hyperplasia and thymomas (benign or malignant tumors of the thymus).

Hypofunction and hyperfunction of the thymus

Functional activity does not always depend on the size of the gland itself. With a thymoma or a cyst, the thymus gland is enlarged, and its activity may be normal or reduced.

Thymus hypoplasia

In the absence of a developmental anomaly, thymus hypoplasia in newborns is extremely rare. This is not an independent disease, but a consequence of a severe infection or prolonged starvation. After the cause is eliminated, its dimensions are quickly restored.

Thymus hyperplasia

There are endogenous hyperplasia, when an increase in the thymus is associated with the performance of its functions (primary) and exogenous, then the growth is caused by pathological processes in other organs and tissues.

Why does the thymus gland increase in a baby?

Causes of primary (endogenous) thymomegaly:

Causes of exogenous thymomegaly:

• Generalized disorders of the immune system(, autoimmune diseases).
• Violations of the regulatory systems in the brain(hypothalamic syndrome).

Symptoms of hyperplasia

During an external examination, an enlarged thymus gland in an infant is visible when crying, when increased intrathoracic pressure pushes the thymus above the sternum handle.

Enlargement of the thymus gland in children affects the appearance of the child - enlarged facial features, pale skin. There is a delay in general development. Enlargement of the thymus gland in a 2-year-old child, detected during examination, especially with an asthenic physique, should not cause concern. The thymus is a fairly large organ for such a baby and may simply not fit in the space allotted to it.

Enlargement of the thymus gland in infants with transient jaundice of newborns is also not a pathology.

Of clinical importance is the simultaneous detection of several signs characteristic of diseases of the thymus:

• syndrome of compression of nearby organs;
• immunodeficiency syndrome;
• lymphoproliferative syndrome;
• disruption of the endocrine system.

Syndrome of compression of nearby organs

Enlargement of the thymus gland in children causes symptoms of compression of nearby organs. With pressure on the trachea, shortness of breath, breathing noises, dry cough appear. By squeezing the lumen of the vessels, the thymus disrupts the inflow and outflow of blood, pallor of the skin and swelling of the jugular veins are noted.

If an enlarged thymus in a child causes compression of the vagus nerve, which innervates the heart and digestive tract, a persistent slowing of the heartbeat, swallowing disorders, belching, and vomiting are noted. It is possible to change the tone of the voice.

Immunodeficiency Syndrome

When the thymus gland is enlarged in a child against the background of its dysfunction, even the usual diseases proceed differently. Any catarrhal disease can begin without an increase in temperature, with a sharp jump on the third or fourth day. Such children get sick longer than their peers, and the severity of the disease is higher. Often, the infection passes into the lower parts of the respiratory system with the development of bronchitis and tracheitis.

Lymphoproliferative syndrome

An increase in the production of hormones in the gland causes hyperstimulation of the entire immune system. Lymph nodes are enlarged, the ratio of immune cells with a predominance of lymphocytes is disturbed in the general blood test. Any external irritant causes an excessive protective reaction in the form of allergic reactions. A severe reaction to vaccination may occur.

Disruption of the endocrine system

An increase in the thymus in children can lead to malfunctions of the endocrine system, with the development of diabetes mellitus and disruption of the thyroid gland.

What is dangerous enlargement of the thymus gland in a child

An increase in the thymus gland in infants, with compression of the trigeminal, disrupts the peristalsis of the esophagus and intestines. The child may have difficulty getting food and spitting air after feeding. When the trachea is compressed, more effort is required to inhale, and the increased pressure causes the alveoli in the lungs to rupture with the development of atelectasis.

Diagnostics

With symptoms of an enlarged thymus gland in a child, consultation of several specialists is necessary - an immunologist, an endocrinologist and a pediatrician. It often turns out that an increase in the thymus gland in an infant is not associated with pathology, but is due to individual anatomical features. Often parents panic that the thymus gland is enlarged in a newborn, because when crying, it often protrudes above the handle of the sternum. It is also not worth fearing inflammation of the thymus gland in infants; a huge number of immune cells in it leaves no chance for the development of infection.

To confirm the diagnosis, it is necessary to undergo a thorough examination, including:

• General and detailed blood test.
• Chest x-ray.
• Ultrasound diagnostics.

A blood test can detect a decrease in the level of T-lymphocytes, an imbalance between immunoglobulins.

X-ray of the thymus to the child will allow to exclude anomalies in the structure and location of the thymus gland.

Ultrasound allows you to accurately determine the degree of thymus hyperplasia in newborns. Examination of the adrenal glands, abdominal organs will exclude concomitant pathology.

You may need additional tests for hormone levels.

CONGENITAL (PRIMARY) IMMUNODEFICIENCY Morphological manifestations of primary insufficiency of the immune response are associated, as a rule, with congenital anomalies of the thymus, or a combination of these anomalies with underdevelopment of the spleen and lymph nodes. Aplasia, hypoplasia of the thymus are accompanied by a deficiency of the cellular link of immunity or a combined immune deficiency. With aplasia (agenesis), the thymus is completely absent, with hypoplasia, its size is reduced, the division into the cortex and medulla is disturbed, and the number of lymphocytes is sharply reduced. In the spleen, the size of the follicles is significantly reduced, light centers and plasma cells are absent. In the lymph nodes, there are no follicles and cortical layer (B-dependent zones), only the pericortical layer (T-dependent zone) is preserved. Morphological changes in the spleen and lymph nodes are characteristic of hereditary immunodeficiency syndromes associated with a defect in both humoral and cellular immunity. All types of congenital immunodeficiency are rare. Currently the most studied are:

severe combined immunodeficiency (TCI);

hypoplasia of the thymus (Dai Jodge syndrome);

Nezelof syndrome;

congenital agammaglobulinemia (Bruton's disease);

common variable (variable) immunodeficiency;

isolated IgA deficiency;

immunodeficiencies associated with hereditary diseases (Wiskott-Aldrich syndrome, ataxia-telangiectasia syndrome, Bloom syndrome)

complement deficiency

Severe Combined Immunodeficiency (SCI) is one of the most severe forms of congenital immunodeficiency. It is characterized by a defect in lymphoid stem cells (1 in Fig. 5), which leads to impaired production of both T- and B-lymphocytes. The process of lowering the thymus from the neck into the mediastinum is disrupted. It has a sharply reduced number of lymphocytes. They are also few in the lymph nodes (Fig. 6B), spleen, intestinal lymphoid tissue, and peripheral blood. There are no immunoglobulins in the serum (Table 7). Insufficiency of both cellular and humoral immunity is the cause of a variety of severe infectious (viral, fungal, bacterial) diseases (Table 8) that occur immediately after birth, which leads to early death (usually in the first year of life). Severe combined immunodeficiency is a number of different congenital diseases. All of them are characterized by impaired differentiation of stem cells. Most patients have an autosomal recessive form (Swiss type); some have a recessive form associated with the X chromosome. More than half of patients with the autosomal recessive form lack the enzyme adenosine deaminase (ADA) in their cells. In this case, adenosine is not converted to inosine, which is accompanied by the accumulation of adenosine and its lymphotoxic metabolites. Some patients with severe combined immunodeficiency have a deficiency of nucleotide phospholipase and inosine phospholipase, which also leads to the accumulation of lymphotoxic metabolites. The absence of ADA in amniotic cells allows diagnosis in the prenatal period. Bone marrow transplantation is used to treat these patients. Thymus hypoplasia(Dye Jodge's syndrome) is characterized by a lack of T-lymphocytes (2 in Fig. 5) in the blood, in the thymus-dependent zones of the lymph nodes and spleen (Fig. 6B). The total number of lymphocytes in the peripheral blood is reduced. Patients show signs of insufficiency of cellular immunity, which manifest themselves in the form of severe viral and fungal infectious diseases in childhood (Table 8). The development of B-lymphocytes is usually not disturbed. The activity of T-helpers is practically absent, however, the concentration of immunoglobulins in serum is usually normal (Table 7). In thymus hypoplasia, no genetic defects have been identified. This condition is also characterized by the absence of the parathyroid glands, abnormal development of the aortic arch and facial skull. In the absence of parathyroid glands, severe hypocalcemia is observed, leading to death at an early age. T-lymphopenia with Nezelof syndrome associated with dysfunction. It is hypothesized that this occurs as a result of impaired maturation of T cells in the thymus. Nezelof's syndrome differs from Dai Joja's syndrome in the characteristic association of damage to other structures that develop from the third and fourth pharyngeal pouches. Parathyroid glands, with this syndrome are not damaged. Thymic hypoplasia is successfully treated by human embryonic thymus transplantation, which restores T-cell immunity. Congenital agammaglobulinemia(Bruton's disease) is a genetically determined recessive, X-linked disease that occurs mainly in boys and is characterized by a violation of the formation of B-lymphocytes (3 in Fig. 5). Pre-B cells (CD10 positive) are found, but mature B-lymphocytes are absent in the peripheral blood and in the B-zones of the lymph nodes, tonsils, and spleen. There are no reactive follicles and plasma cells in the lymph nodes (Fig. 6D). Insufficiency of humoral immunity is manifested in a marked decrease or absence of immunoglobulins in serum. Thymus and T-lymphocytes develop normally and cellular immunity is not disturbed (Table 7). The total number of lymphocytes in the peripheral blood is within the normal range because the number of T cells, which usually make up 80-90% of blood lymphocytes, is within the normal range. Infectious diseases in a child usually develop in the second half of the first year of life after the level of passively transferred maternal antibodies falls (Table 8). Treatment of such patients is carried out by the introduction of immunoglobulins. common variable immunodeficiency includes several different diseases characterized by a decrease in the level of some or all classes of immunoglobulins. The number of lymphocytes in the peripheral blood, including the number of B cells, is usually normal. The number of plasma cells is usually reduced, possibly as a result of a defect in B-lymphocyte transformation (4 in Fig. 5). In some cases, there is an excessive increase in T-suppressors (5 in Fig. 5), especially in the acquired form of the disease that develops in adults. In some cases, hereditary transmission of the disease with different types of inheritance has been described. Lack of humoral immune response leads to recurrent bacterial infections and giardiasis (Table 8). Prophylactic administration of gammaglobulins is less effective than in Bruton's agammaglobulinemia. Isolated IgA deficiency- the most common immunodeficiency, occurring in one in 1000 people. It results from a defect in terminal differentiation of IgA-secreting plasma cells (4 in Fig. 5). In some patients, this defect is associated with abnormal T-suppressor function (5 in Fig. 5). Most patients with IgA deficiency are asymptomatic. Only a small number of patients have a predisposition to the occurrence of pulmonary and intestinal infections, since they have a lack of secretory IgA in the mucous membranes. In patients with severe IgA deficiency, anti-IgA antibodies are determined in the blood. These antibodies can react with IgA that are present in the transfused blood, leading to the development of type I hypersensitivity.

Immunodeficiencies associated with hereditary diseases Wiskott-Aldrich Syndrome- a hereditary recessive disease associated with the X chromosome, which is characterized by eczema, thrombocytopenia and immunodeficiency. T-lymphocyte deficiency may develop during the course of the disease, with reduced serum IgM levels. Patients develop recurrent viral, fungal, and bacterial infections, often with lymphomas. Ataxia-telangiectasia is a hereditary disease transmitted in an autosomal recessive manner, characterized by cerebellar ataxia, skin telangiectasia, and deficiencies of T-lymphocytes, IgA and IgE. It is possible that this pathology is associated with the presence of a defect in the mechanisms of DNA repair, which leads to the appearance of multiple DNA strand breaks, especially in chromosomes 7 and 11 (T-cell receptor genes). Sometimes these patients develop lymphomas. Bloom syndrome transmitted in an autosomal recessive manner, manifested as other defects in DNA repair. In the clinic, there is a deficiency of immunoglobulin and often lymphomas occur.

Complement deficiency Deficiency of various complement factors is rare. The most common deficiency is factor C2. Manifestations of factor C3 deficiency are clinically similar to those of congenital agammaglobulinemia and are characterized by recurrent bacterial infections in childhood. Deficiency of early complement factors (C1, C4, and C2) is associated with the occurrence of autoimmune diseases, especially systemic lupus erythematosus. Deficiency of complement end factors (C6, C7 and C8) predisposes to recurrent infectious diseases caused by Neisseria.

SECONDARY (ACQUIRED) IMMUNODEFICIENCY Immunodeficiency of varying degrees is quite common. It occurs as a secondary phenomenon in various diseases, or as a result of drug therapy (Table 9) and is very rarely a primary disease.

The morphology of the acquired immunodeficiency syndrome (AIDS) does not have a specific picture and differs at different stages of its development. Changes are observed both in the central and peripheral organs of immunogenesis (the most pronounced changes in the lymph nodes). In the thymus, accidental involution, atrophy can be detected. Accidental involution of the thymus is a rapid decrease in its mass and volume, which is accompanied by a decrease in the number of T-lymphocytes and a decrease in the production of thymic hormones. The most common causes of accidental involution are viral infections, intoxications, and stress. When the cause is eliminated, this process is reversible. With an unfavorable outcome, thymus atrophy occurs. Thymus atrophy is accompanied by a collapse of the network of epithelial cells, a decrease in parenchyma lobules in volume, petrification of thymic bodies, and proliferation of fibrous connective and adipose tissue. The number of T-lymphocytes is sharply reduced. Lymph nodes in the initial period are enlarged in volume, and then undergo atrophy and sclerosis. There are three morphological stages of changes in secondary immunodeficiency:

follicular hyperplasia;

pseudoangioimmunoblastic hyperplasia;

depletion of lymphoid tissue.

Follicular hyperplasia is characterized by a systemic increase in lymph nodes up to 2-3 cm. Many sharply enlarged follicles fill almost the entire tissue of the lymph node. The follicles are very voluminous, with large germinal centers. They contain immunoblasts. Mitoses are numerous. Morphometrically, it is possible to state a violation of the ratio of T-cell subpopulations, but they are variable and have no diagnostic value. Pseudoangioimmunoblastic hyperplasia is characterized by severe hyperplasia of venules (postcapillaries), the structure of follicles is fragmented or not defined. The lymph node is diffusely infiltrated with plasmocytes, lymphocytes, immunoblasts, histiocytes. There is a significant decrease to 30% of T-lymphocytes. There is a disproportionate violation of the ratio of subpopulations of lymphocytes, which depends to some extent on the cause that caused the immunodeficiency. So, for example, in HIV-infected persons, not only a decrease in T-helpers is characteristic, but also a decrease in the CD4 / CD8 ratio (helper-suppressor ratio), which is always less than 1.0. This sign is the main feature of the immunological defect in AIDS, trained HIV infection. This stage of immunodeficiency is characterized by the development of opportunistic infections. Depletion of lymphoid tissue replaces lymphoid hyperplasia at the final stage of immunodeficiency. Lymph nodes at this stage are small. The structure of the lymph node throughout is not determined, only the capsule and its shape are preserved. Sclerosis and hyalinosis of bundles of collagen fibers are pronounced. The population of T-lymphocytes is practically not detected, single immunoblasts, plasmablasts and macrophages are preserved. This stage of immunodeficiency is characterized by the development of malignant tumors. The value of secondary (acquired) immunodeficiency. Immunodeficiency is always accompanied by the development of opportunistic infections and, at the final stage, by the development of malignant tumors, most often Kaposi's sarcoma and malignant B-cell lymphomas. The occurrence of infectious diseases depends on the type of immunodeficiency:

T-cell deficiency predisposes to infectious diseases caused by viruses, mycobacteria, fungi and other intracellular microorganisms, such as Pneumocystis carinii and Toxoplasma gondii.

B-cell deficiency predisposes to purulent bacterial infections.

These infectious diseases reflect the relative importance of cellular and humoral responses in defense against various microbial agents. Kaposi's sarcoma and malignant B-cell lymphomas are the most common malignancies that develop in immunocompromised patients. They can occur in patients with HIV infection, Wiskott-Aldrich syndrome and ataxia-telangiectasia, as well as in patients receiving long-term immunosuppressive therapy after organ transplantation (most often kidney transplantation). The occurrence of malignant neoplasms may be due either to a violation of the immune response aimed at removing developing malignant cells that arise in the body (failure of immune surveillance) or due to immune stimulation of a damaged immune system in which the normal mechanism for controlling cell proliferation is disrupted (this leads to the emergence of B -cell lymphomas). In some cases, especially in ataxia-telangiectasia, immune deficiency is associated with chromosome fragility, which is believed to predispose to the development of neoplasms. Note that epithelioid thymoma, a primary thymic epithelial cell tumor, results in secondary immunodeficiency.

Thymus hypoplasia is a congenital underdevelopment of the organ. Due to the reduced number of T-lymphocytes and thymus hormones, children may die in the first days of life or before 2 years of age. About what thymus hypoplasia is, the role of the organ in the lives of children, the diagnosis of abnormalities, as well as treatment, read further in our article.

Read in this article

The role of the thymus in children

In the thymus, maturation of T-lymphocytes occurs, which are responsible for cellular immunity. Since for the formation of protective proteins (immunoglobulins) by B-lymphocytes, a signal from a T-cell is needed, these reactions (humoral immunity) also suffer when the thymus function is disturbed. Therefore, the gland is considered the main organ that protects the child from the penetration of a foreign antigen protein.

Hormones are also formed in the thymus - thymopoietin, thymulin, thymosin, about 20 biologically active compounds. With their participation, children experience:

• body growth;
• puberty;
• metabolism;
• muscle contractions;
• formation of blood cells in the bone marrow;
• regulation of the pituitary gland, thyroid gland;
• maintaining normal levels of sugar, calcium and phosphorus in the blood and tissues;
• body's immune response.

Manifestations of underdevelopment of the thymus gland

The complete absence of the thymus (aplasia) can cause the death of a child in the first days of life or stillbirth. Surviving infants have severe, persistent diarrhea that is difficult to treat. They lead to progressive exhaustion. Especially dangerous is the addition of any, even the most insignificant infection.

When the thymus is reduced in size, the development of the entire lymphatic system. The body cannot cope not only with external pathogens, but also its own intestinal microflora can cause inflammatory process. Against the background of low immunity, fungi multiply rapidly, causing candidiasis (thrush), pneumocysts that affect the lungs.

Most children with greatly reduced thymus do not survive beyond 2 years of age without treatment due to severe infections.

With a slight decrease in the size of the organ, manifestations of immune deficiency can occur in adulthood. Signs of disorders of the thymus are:

• frequent viral and bacterial infections;
• tendency to recurrent fungal infections of the skin, mucous membranes of the mouth and genitals, lungs, intestines;
• periodically aggravated herpes;
• severe course of "children's" diseases (measles, rubella, mumps);
• a pronounced reaction to vaccinations (temperature, convulsive syndrome);
• the presence of tumor processes.

The condition of patients is aggravated by the presence of changes in the liver, spleen and bone marrow, which occur due to insufficient function of the thymus.

Diagnosis of the disease

Suspicion of hypoplasia of the thymus appears with a combination of:

• frequent viral diseases;
• persistent thrush;
• diarrhea that is difficult to treat;
• pustular skin lesions;
• severe course of infectious diseases with drug resistance.

To examine the thymus in children, ultrasound is used, and in adults, computed, magnetic resonance imaging is more informative.

What to do if the thymus gland is reduced

In children, the most radical treatment is a thymus transplant. Parts of the thymus or a whole organ from stillborn fetuses with a normal structure of the organ are sutured into the region of the rectus abdominis muscles, thighs.

With a successful and timely operation, the content of lymphocytes and immunoglobulins in the blood increases, and the ability to immune reactions appears. Bone marrow transplantation, the introduction of drugs that stimulate the development of T-lymphocytes outside the thymus - Neupogen, Leukomax - can also be successful.

In less complex cases, symptomatic therapy of infections with antibiotics, antiviral and antifungal agents. To correct the insufficient function of the thymus, T-activin, Timalin, Timogen, immunoglobulin are administered intravenously.

Thymus hypoplasia is a dangerous pathology in children. With a slight decrease in size, there is a tendency to frequent infections, their severe course, resistance to antibacterial and antifungal agents.

With a significant or complete absence of the gland, children can die before 2 years of age. The disease can be suspected by the persistent course of thrush and diarrhea. To detect hypoplasia of the gland, ultrasound, tomography, and immunological blood tests are performed. In severe cases, only an organ transplant can help, less complex variants of the disease require symptomatic treatment, the introduction of thymus extracts.

Useful video

Watch the video about the syndrome of Di George, Di George, Di Georgie, parathyroid gland aplasia, dysembryogenesis syndrome 3-4 gill arch:

Similar articles

Mostly ultrasound of the thymus is performed in children, especially infants. In adults, CT is more informative, since age-related changes organs can distort the picture or completely hide the organ.

Content

People don't know everything about their body. Where the heart, stomach, brain and liver are located is known to many, and the location of the pituitary gland, hypothalamus or thymus is not known to many. However, the thymus or thymus gland is a central organ and is located in the very center of the sternum.

Thymus gland - what is it

Iron got its name due to the shape resembling a two-pronged fork. However, a healthy thymus looks like this, and a sick one takes on the appearance of a sail or a butterfly. For its proximity to the thyroid gland, doctors used to call it the thymus gland. What is thymus? This is the main organ of vertebrate immunity, in which the production, development and training of T-cells of the immune system takes place. The gland begins to grow in a newborn baby before the age of 10, and after the 18th birthday it gradually decreases. The thymus is one of the main organs for the formation and activity of the immune system.

Where is the thymus located

The thymus can be identified by placing two folded fingers on the top of the sternum below the clavicular notch. The location of the thymus is the same in children and adults, but the anatomy of the organ has age-related features. At the time of birth, the mass of the thymus organ of the immune system is 12 grams, and by puberty it reaches 35-40 g. Atrophy begins at about 15-16 years. By the age of 25, the thymus weighs about 25 grams, and by 60 it weighs less than 15 grams.

By the age of 80, the weight of the thymus gland is only 6 grams. The thymus by this time becomes elongated, the lower and lateral parts of the organ atrophy, which are replaced by adipose tissue. This phenomenon is not explained by official science. Today it is the biggest mystery of biology. It is believed that opening this veil will allow people to challenge the aging process.

The structure of the thymus

We have already found out where the thymus is located. The structure of the thymus gland will be considered separately. This small-sized organ has a pinkish-gray color, soft texture, and a lobed structure. The two lobes of the thymus are completely fused or closely adjacent to each other. The upper part of the body is wide, and the lower one is narrower. The entire thymus gland is covered with a capsule of connective tissue, under which there are dividing T-lymphoblasts. The jumpers that depart from it divide the thymus into lobules.

The blood supply to the lobular surface of the gland comes from the internal mammary artery, thymic branches of the aorta, branches of the thyroid arteries and the brachiocephalic trunk. Venous outflow of blood is carried out through the internal thoracic arteries and branches of the brachiocephalic veins. In the tissues of the thymus, the growth of various blood cells occurs. The lobular structure of the organ contains cortex and medulla. The first looks like a dark substance and is located on the periphery. Also, the cortical substance of the thymus gland contains:

• hematopoietic cells of the lymphoid series, where T-lymphocytes mature;
• hematopoietic macrophage series, which contain dendritic cells, interdigitating cells, typical macrophages;
• epithelial cells;
• supporting cells that form the hemato-thymic barrier, which form the tissue framework;
• stellate cells - secreting hormones that regulate the development of T-cells;
• baby-sitter cells in which lymphocytes develop.

In addition, the thymus secretes the following substances into the bloodstream:

• thymic humoral factor;
• insulin-like growth factor-1 (IGF-1);
• thymopoietin;
• thymosin;
• thymalin.

What is responsible for

Thymus in a child forms all the systems of the body, and in an adult it maintains good immunity. What is the thymus responsible for in the human body? The thymus gland performs three important functions: lymphopoietic, endocrine, immunoregulatory. It produces T-lymphocytes, which are the main regulators of the immune system, that is, the thymus kills aggressive cells. In addition to this function, it filters the blood, monitors the outflow of lymph. If any malfunction occurs in the work of the organ, then this leads to the formation of oncological and autoimmune pathologies.

In children

In a child, the formation of the thymus begins at the sixth week of pregnancy. The thymus gland in children under one year old is responsible for the production of T-lymphocytes by the bone marrow, which protect the child's body from bacteria, infections, and viruses. An enlarged goiter (hyperfunction) in a child does not affect health in the best way, as it leads to a decrease in immunity. Children with this diagnosis are susceptible to various allergic manifestations, viral and infectious diseases.

In adults

The thymus gland begins to involute with age, so it is important to maintain its functions in a timely manner. Thymus rejuvenation is possible with low calorie diet, taking Ghrelin and using other methods. The thymus gland in adults is involved in modeling two types of immunity: a cell-type response and a humoral response. The first forms the rejection of foreign elements, and the second manifests itself in the production of antibodies.

Hormones and functions

The main polypeptides produced by the thymus gland are thymalin, thymopoietin, thymosin. By their nature, they are proteins. When lymphoid tissue develops, lymphocytes get the opportunity to take part in immunological processes. Thymus hormones and their functions have a regulatory effect on all physiological processes in the human body:

• reduce cardiac output and heart rate;
• slow down the work of the central nervous system;
• replenish energy reserves;
• accelerate the breakdown of glucose;
• increase the growth of cells and skeletal tissue due to increased protein synthesis;
• improve the work of the pituitary gland, thyroid gland;
• produce the exchange of vitamins, fats, carbohydrates, proteins, minerals.

Hormones

Under the influence of thymosin, lymphocytes are formed in the thymus, then with the help of the influence of thymopoietin blood cells partially change the structure to ensure maximum protection of the body. Timulin activates T-helpers and T-killers, increases the intensity of phagocytosis, accelerates regeneration processes. Thymus hormones are involved in the work of the adrenal glands and genital organs. Estrogens activate the production of polypeptides, while progesterone and androgens inhibit the process. A glucocorticoid, which is produced by the adrenal cortex, has a similar effect.

Functions

Proliferation of blood cells occurs in the tissues of the goiter gland, which enhances immune reactions organism. The resulting T-lymphocytes enter the lymph, then colonize in the spleen and lymph nodes. Under stressful influences (hypothermia, starvation, severe trauma, and others), the functions of the thymus gland weaken due to the massive death of T-lymphocytes. After that, they undergo positive selection, then negative selection of lymphocytes, then regenerate. The functions of the thymus begin to fade by the age of 18, and fade almost completely by the age of 30.

Thymus gland diseases

As practice shows, diseases of the thymus are rare, but always accompanied by characteristic symptoms. The main manifestations include severe weakness, an increase in lymph nodes, a decrease in the protective functions of the body. Under the influence of developing diseases of the thymus, lymphoid tissue grows, tumors are formed that cause swelling of the limbs, compression of the trachea, borderline sympathetic trunk or vagus nerve. Malfunctions in the work of the body are manifested with a decrease in function (hypofunction) or with an increase in the work of the thymus (hyperfunction).

magnification

If the ultrasound photo showed that the central organ of lymphopoiesis is enlarged, then the patient has thymus hyperfunction. Pathology leads to the formation of autoimmune diseases (lupus erythematosus, rheumatoid arthritis, scleroderma, myasthenia). Hyperplasia of the thymus in infants is manifested in the following symptoms:

• decrease in muscle tone;
• frequent regurgitation;
• weight problems;
• heart rhythm failures;
• pale skin;
• profuse sweating;
• enlarged adenoids, lymph nodes, tonsils.

hypoplasia

The central organ of human lymphopoiesis may have congenital or primary aplasia (hypofunction), which is characterized by the absence or weak development of the thymic parenchyma. Combined immunological deficiency is diagnosed as congenital disease Di George, in which children have heart defects, convulsions, anomalies of the facial skeleton. Hypofunction or hypoplasia of the thymus may develop against the background of diabetes mellitus, viral diseases or alcohol consumption by a woman during pregnancy.

Tumor

Thymomas (tumors of the thymus) occur at any age, but more often such pathologies affect people from 40 to 60 years old. The causes of the disease have not been established, but it is believed that a malignant tumor of the thymus arises from epithelial cells. It has been noticed that such a phenomenon occurs if a person has suffered chronic inflammation or viral infections or exposed to ionizing radiation. Depending on which cells are involved in the pathological process, the following types of tumors of the goiter gland are distinguished:

• spindle cell;
• granulomatous;
• epidermoid;
• lymphoepithelial.

Symptoms of thymus disease

When the work of the thymus changes, an adult feels a violation of breathing, heaviness in the eyelids, muscle fatigue. The first signs of thymus disease are a long recovery after the simplest infectious diseases. When cellular immunity is impaired, symptoms of a developing disease begin to appear, for example, multiple sclerosis, Basedow's disease. With any decrease in immunity and the corresponding signs, you should immediately contact the doctor.

Thymus gland - how to check

If a child has frequent colds that turn into severe pathologies, there is a greater predisposition to allergic processes, or lymph nodes are enlarged, then a diagnosis of the thymus gland is needed. For this purpose, a sensitive, high-resolution ultrasound machine is needed, since the thymus is located near the pulmonary trunk and atrium, and is closed by the sternum.

In case of suspicion of hyperplasia or aplasia after a histological examination, the doctor may refer to computed tomography and examination by an endocrinologist. The tomograph will help to establish the following pathologies of the thymus gland:

• MEDAC syndrome;
• DiGeorge syndrome;
• myasthenia gravis;
• thymoma;
• T-cell lymphoma;
• pre-T-lymphoblastic tumor;
• neuroendocrine tumor.

Norms

In a newborn baby, the size of the thymus gland is on average 3 cm wide, 4 cm long and 2 cm thick. The average size of the thymus is normally presented in the table:

Pathology of the thymus

In violation of immunogenesis, changes in the gland are observed, which are represented by such diseases as dysplasia, aplasia, accidental involution, atrophy, hyperplasia with lymphoid follicles, thymomegaly. Often, thymus pathology is associated either with an endocrine disorder, or with the presence of an autoimmune or oncological disease. most common cause the decline in cellular immunity is an age-related involution, in which there is a deficiency of melatonin in the pineal gland.

How to treat the thymus

As a rule, thymus pathologies are observed up to 6 years. Then they disappear or turn into more serious diseases. If the child has an enlarged goiter gland, then a phthisiatrician, immunologist, pediatrician, endocrinologist and otolaryngologist should be observed. Parents should take precautions respiratory diseases. If symptoms such as bradycardia, weakness and/or apathy are present, urgent medical attention is required. Treatment of the thymus gland in children and adults is carried out with medication or surgical method.

Medical treatment

When the immune system is weakened, to maintain the body, it requires the introduction of biologically active substances. These are the so-called immunomodulators that thymus therapy offers. Treatment of the goiter gland in most cases is carried out on an outpatient basis and consists of 15-20 injections that are injected into the gluteal muscle. The treatment regimen for thymus pathologies may vary, depending on the clinical picture. In the presence of chronic diseases therapy can be carried out for 2-3 months, 2 injections per week.

Intramuscularly or subcutaneously, 5 ml of thymus extract isolated from the peptides of the goiter gland of animals is injected. It is a natural biological raw material without preservatives and additives. Noticeable improvement in 2 weeks general condition patient, because during the treatment, protective blood cells are activated. Thymus therapy has a long-term effect on the body after the therapy. A second course can be carried out after 4-6 months.

Operation

Thymectomy or removal of the thymus is indicated if the gland has a tumor (thymoma). The operation is performed under general anesthesia, which keeps the patient asleep during the entire operation. There are three types of thymectomy:

1. Transsternal. An incision is made in the skin, after which the sternum is separated. The thymus is separated from the tissues and removed. The incision is closed with staples or sutures.
2. Transcervical. An incision is made along the lower part of the neck, after which the gland is removed.
3. Video assisted surgery. Several small incisions are made superior mediastinum. A camera is inserted through one of them, displaying the image on the monitor in the operating room. During the operation, robotic arms are used, which are inserted into the incisions.

diet therapy

Diet therapy plays an important role in the treatment of thymus pathologies. Foods rich in vitamin D should be introduced into the diet: egg yolk, brewer's yeast, dairy products, fish fat. The use of walnut, beef, liver is recommended. When developing a diet, doctors advise including in the diet:

• parsley;
• broccoli, cauliflower;
• oranges, lemons;
• sea ​​buckthorn;
• syrup or decoction of wild rose.

Alternative treatment

Children's doctor Komarovsky advises to warm up the thymus with a special massage to increase immunity. If an adult has an unreduced gland, then he should maintain immunity for prevention by taking herbal preparations with rose hips, black currants, raspberries, and lingonberries. Thymus treatment folk remedies it is not recommended to carry out, since the pathology requires strict medical supervision.

Video

Attention! The information presented in the article is for informational purposes only. The materials of the article do not call for self-treatment. Only a qualified doctor can make a diagnosis and give recommendations for treatment based on the individual characteristics of a particular patient.

Medical and social expertise and disability in thymus hypoplasia

THYM GLAND APLASIA (hypoplasia) (Dee George's syndrome) - congenital underdevelopment of the thymus gland as a result of a violation of the normal embryogenesis of the thymus, accompanied by a violation of the formation of neighboring organs - the parathyroid glands, aorta and other developmental anomalies, which is clinically manifested by primary immunodeficiency and hypoparathyroidism.

Epidemiology: frequency in children has not been established, but the frequency of all defects T cell immunity is 5-10% in the structure of primary immunodeficiencies, and the total frequency of primary forms of immunodeficiencies is 2:1000.

Etiology and pathogenesis. The disease is associated with impaired intrauterine development of the fetus for a period of about 8 weeks; under the influence of a teratogenic factor, the laying of organs developing during this period from the 3rd-4th pharyngeal fissures is disrupted: the thymus, parathyroid glands, aorta, as well as the facial skull, the central nervous system. In 80-90% of children with this syndrome, a deletion of the 22nd chromosome is detected (partial monosomy on the 22nd chromosome - a deficiency of genetic material), combined with a symptom complex: congenital heart defects, "cleft palate" and other defects of the facial skeleton, thymus hypoplasia and hypocalcemia due to hypolalasia of the parathyroid glands.

clinical picture.
From birth, the child has hypocalcemia syndrome (typical hypocalcemic convulsions), recurrent oral candidiasis with transformation into chronic candidiasis of the skin and mucous membranes, anomaly of the aorta (its arch is turned to the right), sepsis. There may be a congenital heart disease with a corresponding clinical picture, anomaly of the facial skull; in the future - a decrease in mental abilities, delayed sexual development.

Complications: HF, impaired mental development of varying severity, defeat internal organs Candida fungi (candidiasis bronchitis, esophagitis with subsequent development of esophageal stricture).

Laboratory and instrumental methods confirming the diagnosis:
1) study of the content of parathyroid hormone in the blood;
2) biochemical blood test (decreased calcium content in the blood);
3) ECG, echocardiography;
4) consultation of a psychologist, neurologist, psychiatrist;
5) mycological examination;
6) immunogram (decrease in the number and function of T-lymphocytes).

Treatment: compensation of insufficiency of the thyroid glands with vitamin D preparations, transplantation of the fetal thymus gland, the use of thymus hormones for replacement purposes, bone marrow transplantation, correction of congenital heart disease, the use of antimycotic agents for the treatment of candidiasis.

The prognosis is relatively favorable - children are viable, do not suffer from viral and bacterial infections, but have chronic candidiasis of the skin and mucous membranes with damage to internal organs, and need constant treatment with antimycotic drugs; hypoparathyroidism also requires constant replacement therapy vitamin D preparations; in addition, children lag behind in mental development.

Disability criteria: mental retardation, requiring the child to study in a special school, NC from 1-2st. and higher with congenital heart disease, recurrent candidiasis of the bronchi, esophagus and other internal organs with a violation of their functions.

Rehabilitation: medical rehabilitation during periods of exacerbations; social, psychological, pedagogical and professional habilitation during the remission of the disease.

Description:

Thymus aplasia is a group of diseases caused by genetic defects in the immune system.

Symptoms:

1. Di-George syndrome. Along with aplasia of the gland, aplasia of the parathyroid glands with manifestations is possible. In pathogenesis, there is a deficiency of circulating T-lymphocytes, a sharp inhibition of the reaction of cellular immunity, a relative increase in the number of B-lymphocytes and the preservation of the response of humoral immunity ( normal level immunoglobulins in the blood).
Characteristic signs of the disease are, starting from the neonatal period, recurrent infections of the respiratory and digestive systems. Usually associated with malformations of the aortic arch, mandible, earlobes, with hypoplasia of the lymph nodes and underdevelopment of thymus-dependent zones.

2. Nezelof's syndrome - autosomal recessive aplasia of the thymus with lymphopenia, without aplasia of the parathyroid glands, but with underdevelopment of thymus-dependent zones in the lymph nodes and spleen.
A sharp decrease in the reactivity of T-lymphocytes (deficiency of the cellular immune system) is also revealed.
Since the neonatal period, recurrent bronchitis, enterocolitis of viral or fungal etiology, herpetic rashes, have been noted. Deficiency of T-lymphocytes and inhibition of the reaction of cellular immunity are more pronounced than in DiGeorge's syndrome. Patients die at an early age.

3. Louis-Bar syndrome - immunological deficiency with -telangiectasia, characterized by autosomal recessive inheritance of aplasia of the gland, occurs with a decrease in lymphocytes in the thymus-dependent zones of the lymph nodes and the spleen, demyelination in the cerebellum.
Multisystem Complex Disorders:
1) neurological (ataxia, impaired coordination, etc.);
2) vascular (telaniectasia of the skin and conjunctiva);
3) mental (mental retardation);
4) endocrine (impaired functions of the adrenal glands, gonads). Recurrent sino-pulmonary infections appear from early childhood.
Violation of cellular immunity is accompanied by damage to the T- and B-systems of immunity, deficiency of IgA. In the blood serum, emorional fir-trees (α- and β-fetoproteins) are found. In such patients, malignant neoplasms (more often, lymphogranulomatosis) develop more often.

4. "Swiss syndrome" - autosomal recessive severe combined immunological deficiency. Lymphopenic agammaglobulinemia, aplasia or hypoplasia of the thymus are combined with hypoplasia of the entire lymphoid tissue. Sharp hypoplasia of the thymus gland, hypoplasia of the lymph nodes and lymphoid formations of the spleen, intestines.
Since the neonatal period, recurrent fungal, viral and bacterial lesions of the skin and mucous membranes of the nasopharynx, respiratory tract, intestines. In these children, the thymus gland is difficult to identify.
Along with a sharp inhibition of reactions of cellular immunity, a deficiency of humoral immunity (deficiency of T- and B-lymphocytes) is revealed. Children usually die in the first six months of life.

Causes of occurrence:

This group of diseases is caused by genetic defects in the immune system.
Congenital, or primary, aplasia (or hypoplasia) of the thymus gland is characterized by the complete absence of the thymic parenchyma or its extremely weak development, which determines the presence of severe combined immunological deficiency due to a sharp decrease in the content of T- and B-lymphocytes and the absence of thymus bodies.
All these diseases are accompanied by recurrent inflammatory diseases, more often pulmonary or intestinal localization, which are often the direct cause of death of patients. Therefore, children, especially young children, suffering from recurrent inflammatory diseases, should be carefully examined for the functional state of the thymus.
Similar changes are found in children with a number of diseases united in the immunodeficiency group. The most pronounced defects in the development of the thymus were found in the following syndromes.

Treatment:

– genetic disease, belonging to the group of primary immunodeficiencies and, along with weakened immunity, characterized by numerous malformations. Symptoms of this condition are frequent bacterial infections with a tendency to severe course, congenital heart defects, facial abnormalities and other disorders. Diagnosis of DiGeorge syndrome is based on the study of the heart, thyroid and parathyroid glands, the study of the immunological status and the data of molecular genetic analyzes. Treatment is only symptomatic, including surgical correction of heart defects and facial anomalies, immunological replacement therapy, and the fight against bacterial and fungal infections.

General information

DiGeorge syndrome (hypoplasia of the thymus and parathyroid glands, velocardiofacial syndrome) is a genetic disease caused by a violation of the embryonic development of the third and fourth pharyngeal sacs. This condition was first described in 1965 by the American pediatrician Angelo Di Giorgi, who classified it as congenital aplasia of the thymus and parathyroid glands. Further research in the field of genetics helped to determine that the disorders in this disease go far beyond the primary immunodeficiency. This gave rise to another name for the DiGeorge syndrome. Given the most commonly affected organs (palate, heart, face), some experts call this pathology velocardiofacial syndrome. A number of modern researchers distinguish between these two conditions and believe that the "true" velocardiofacial syndrome is not accompanied by severe immunological disorders. The incidence of DiGeorge syndrome is 1:3,000-20,000 - such a significant discrepancy in the data is due to the fact that a reliable and clear boundary between this disease and velocardiofacial syndrome has not yet been established. Therefore, the same patient, according to different experts, may have either a primary immunodeficiency, accompanied by concomitant disorders, or more numerous malformations against the background of a decrease in immunity.

Causes of DiGeorge Syndrome

The genetic nature of DiGeorge syndrome is damage to the central part of the long arm of chromosome 22, where genes encoding a number of important transcription factors are presumably located. One of these genes, TBX1, was identified; its expression product is a protein called T-box. It belongs to a family of proteins that control the processes of embryogenesis. Evidence of the relationship between DiGeorge syndrome and TBX1 is the fact that a small percentage of patients do not have pronounced damage to the 22nd chromosome, only mutations in this gene are present. There are also suggestions about the role of deletions of other chromosomes in the development this disease. So, manifestations similar to the DiGeorge syndrome were detected in the presence of damage to the 10th, 17th and 18th chromosomes.

In most cases of DiGeorge syndrome, the deletion of the 22nd chromosome captures about 2-3 million base pairs. Most often, this genetic defect occurs spontaneously during the formation of male or female germ cells - that is, it is germinal in nature. Only a tenth of all cases of the disease is a familial form with an autosomal dominant pattern of inheritance. The pathogenesis of the DiGeorge syndrome is reduced to a violation of the formation of special embryonic formations - the pharyngeal sacs (mainly the 3rd and 4th), which are the precursors of a number of tissues and organs. They are mainly responsible for the formation of the palate, parathyroid glands, thymus, mediastinal vessels and the heart, therefore, with DiGeorge's syndrome, malformations of these organs occur.

Symptoms of DiGeorge Syndrome

Many manifestations of the DiGeorge syndrome are determined immediately after the birth of a child, individual malformations (for example, of the heart) can be detected even earlier - on preventive ultrasound examinations. Most often, anomalies in the development of the face are the first to be detected - a splitting of the palate, sometimes in combination with a “cleft lip”, prognathism of the lower jaw. Babies with DiGeorge Syndrome often have a small mouth, a small nose with an enlarged bridge of the nose, and deformed or underdeveloped cartilage. auricles. With a relatively mild course of the disease, all of the above symptoms can be expressed rather weakly, even splitting of the hard palate can occur only in its back part and be detected only with a thorough examination by an otolaryngologist.

In the first months of life of a patient with DiGeorge syndrome, manifestations of congenital heart defects come to the fore - it can be both Fallot's tetrad and individual disorders: ventricular septal defect, cleft ductus arteriosus and a number of others. They are accompanied by cyanosis, cardiovascular insufficiency and, in the absence of qualified medical care(including surgical) can lead to early death of patients. Seizures and tetany due to parathyroid hypoplasia and subsequent hypocalcemia are considered to be another common disorder in children with DiGeorge syndrome.

The next most important manifestation of DiGeorge syndrome, which distinguishes it from other varieties of velocardiofacial syndrome, is a pronounced primary immunodeficiency. It develops due to aplasia or underdevelopment of the thymus and therefore affects cellular immunity to a greater extent. However, due to the close relationship between the humoral and cellular sections of the immune system, this leads to a general weakening of the body's defenses. Patients with DiGeorge syndrome are extremely sensitive to viral, fungal and bacterial infections, which often take a protracted and severe course. Some researchers note the presence mental retardation varying degrees, sometimes there may be seizures of neurological origin.

Diagnosis of DiGeorge Syndrome

To determine the DiGeorge syndrome, the method of a physical general examination, cardiological studies (EchoCG, electrocardiogram), ultrasound of the thyroid gland and thymus, and immunological tests are used. A supporting role is played by the general and biochemical analyzes blood, the study of the patient's history, genetic studies. When examining patients with DiGeorge syndrome, disorders characteristic of the disease can be determined - splitting of the hard palate, anomalies in the structure of the face, pathology of the ENT organs. In the anamnesis, as a rule, frequent episodes of viral and fungal infections that take a severe course are detected, convulsions caused by hypocalcemia, and extensive carious lesions of the teeth are often detected.

Ultrasound examinations of the thymus show a significant decrease in mass or even complete absence organ (agenesis). Echocardiography and other cardiac diagnostic methods reveal numerous heart defects (for example, ventricular septal defect) and mediastinal vessels. Immunological studies confirm a significant drop in the level of T-lymphocytes. The same phenomenon is observed in peripheral blood and is often combined with a decrease in the concentration of immunoglobulin proteins. Biochemical study of blood indicates a decrease in the level of calcium and parathyroid hormones. A geneticist can search for deletions on chromosome 22 using fluorescent DNA hybridization or multiplex polymerase chain reaction.

Treatment of DiGeorge Syndrome

There is currently no specific treatment for DiGeorge syndrome, only palliative and symptomatic techniques are used. It is very important to identify congenital heart defects as early as possible and, if necessary, to perform their surgical correction, since it is cardiovascular disorders that are the most common cause of neonatal death in this disease. A significant danger is convulsive seizures caused by hypocalcemia, which requires timely correction of the electrolyte balance of blood plasma. The help of surgeons with DiGeorge syndrome may also be required to eliminate malformations of the face and palate.

Due to severe immunodeficiency, any signs of a bacterial, viral or fungal infection are a reason for the urgent use of appropriate drugs (antibiotics, antiviral and fungicidal agents). To improve the immune status of a patient with DiGeorge syndrome, a replacement infusion of immunoglobulins obtained from donor plasma can be performed. In some cases, a thymus transplant was performed, which stimulated the formation own T-lymphocytes This contributed to the improvement of the quality of life of patients.

Forecast and prevention of DiGeorge's syndrome

The prognosis of DiGeorge syndrome is assessed by most researchers as uncertain, since this disease is characterized by a significant variability in symptoms. In severe cases, there is a high risk of early neonatal death due to a combination of cardiovascular and immunological disorders. More benign forms of DiGeorge syndrome require fairly intensive palliative care, it is especially important to pay attention to the treatment and prevention of viral and fungal infections. The intellectual development of patients is somewhat slowed down, however, with the correct pedagogical and psychological correction, the manifestations of developmental delay can be leveled. Due to the frequent spontaneous nature of mutations, the prevention of DiGeorge syndrome has not been developed.

The child, being in the womb, is completely protected from any adverse environmental factors.

The thymus gland in newborns becomes the first cascade of immune defense. Which protects the child from numerous pathogenic microorganisms. The thymus in children begins to work immediately after birth, when an unfamiliar microorganism enters with the first breath of air.

The thymus gland in children under one year old manages to collect information on almost all pathogenic organisms that we encounter throughout life.

Embryology (development of the thymus in the prenatal period)

The thymus in the fetus is laid already at the seventh - eighth week of development. Even during pregnancy, the thymus gland begins to produce immune cells, by the twelfth week, the precursors of future lymphocytes, thymocytes, are already found in it. By the time of birth, the thymus in newborns is fully formed and functionally active.

Anatomy

To understand, you should attach three fingers to the top of the handle of the sternum (the area between the collarbones). This will be the projection of the thymus gland.

At birth, her weight is 15-45 grams. The size of the thymus in children is normally 4-5 centimeters in length, 3-4 centimeters in width. An intact gland in a healthy child is not palpable.

Age features

The thymus plays a key role in the development of immunity and continues to grow until puberty. At this point, the mass reaches 40 grams. The field of puberty begins reverse development (involution). By old age, the thymus gland is completely replaced by adipose tissue, its mass decreases to 6 grams. In every period of life.

The role of the thymus

The thymus produces hormones necessary for the normal development of the immune system. Thanks to them, the cells of the immune system learn to recognize harmful microorganisms and trigger mechanisms to eliminate them.

Thymus disorders

According to the degree of activity, hypofunction and hyperfunction of the thymus gland are distinguished. According to the morphological structure: (absence), (underdevelopment) and (increase in size).

Congenital pathology of the development of the thymus gland

With anomalies in the genetic code, the laying of the thymus can be disturbed even in the early embryonic period. Such a pathology is always combined with a violation of the development of other organs. There are several genetic abnormalities that cause changes that are fatal to the immune system. The body loses the ability to fight infection and is not viable.

With genetic developmental defects, the entire immune system suffers. Even with the preservation of partial activity, thymic hypoplasia in newborns leads to a persistent deficiency in the content of immune cells in the blood and persistent infections, against which there is a general developmental delay.

Also, genetic malformations include congenital cysts, thymus hyperplasia and thymomas (benign or malignant tumors of the thymus).

Hypofunction and hyperfunction of the thymus

Functional activity does not always depend on the size of the gland itself. With a thymoma or a cyst, the thymus gland is enlarged, and its activity may be normal or reduced.

Thymus hypoplasia

In the absence of a developmental anomaly, thymus hypoplasia in newborns is extremely rare. This is not an independent disease, but a consequence of a severe infection or prolonged starvation. After the cause is eliminated, its dimensions are quickly restored.

Thymus hyperplasia

There are endogenous hyperplasia, when an increase in the thymus is associated with the performance of its functions (primary) and exogenous, then the growth is caused by pathological processes in other organs and tissues.

Why does the thymus gland increase in a baby?

Causes of primary (endogenous) thymomegaly:

Causes of exogenous thymomegaly:

• Generalized disorders of the immune system(, autoimmune diseases).
• Violations of the regulatory systems in the brain(hypothalamic syndrome).

Symptoms of hyperplasia

During an external examination, an enlarged thymus gland in an infant is visible when crying, when increased intrathoracic pressure pushes the thymus above the sternum handle.

Enlargement of the thymus gland in children affects the appearance of the child - enlarged facial features, pale skin. There is a delay in general development. Enlargement of the thymus gland in a 2-year-old child, detected during examination, especially with an asthenic physique, should not cause concern. The thymus is a fairly large organ for such a baby and may simply not fit in the space allotted to it.

Enlargement of the thymus gland in infants with transient jaundice of newborns is also not a pathology.

Of clinical importance is the simultaneous detection of several signs characteristic of diseases of the thymus:

• syndrome of compression of nearby organs;
• immunodeficiency syndrome;
• lymphoproliferative syndrome;
• disruption of the endocrine system.

Syndrome of compression of nearby organs

Enlargement of the thymus gland in children causes symptoms of compression of nearby organs. With pressure on the trachea, shortness of breath, breathing noises, dry cough appear. By squeezing the lumen of the vessels, the thymus disrupts the inflow and outflow of blood, pallor of the skin and swelling of the jugular veins are noted.

If an enlarged thymus in a child causes compression of the vagus nerve, which innervates the heart and digestive tract, a persistent slowing of the heartbeat, swallowing disorders, belching, and vomiting are noted. It is possible to change the tone of the voice.

Immunodeficiency Syndrome

When the thymus gland is enlarged in a child against the background of its dysfunction, even the usual diseases proceed differently. Any catarrhal disease can begin without an increase in temperature, with a sharp jump on the third or fourth day. Such children get sick longer than their peers, and the severity of the disease is higher. Often, the infection passes into the lower parts of the respiratory system with the development of bronchitis and tracheitis.

Lymphoproliferative syndrome

An increase in the production of hormones in the gland causes hyperstimulation of the entire immune system. Lymph nodes are enlarged, the ratio of immune cells with a predominance of lymphocytes is disturbed in the general blood test. Any external irritant causes an excessive protective reaction in the form of allergic reactions. A severe reaction to vaccination may occur.

Disruption of the endocrine system

An increase in the thymus in children can lead to malfunctions of the endocrine system, with the development of diabetes mellitus and disruption of the thyroid gland.

What is dangerous enlargement of the thymus gland in a child

An increase in the thymus gland in infants, with compression of the trigeminal, disrupts the peristalsis of the esophagus and intestines. The child may have difficulty getting food and spitting air after feeding. When the trachea is compressed, more effort is required to inhale, and the increased pressure causes the alveoli in the lungs to rupture with the development of atelectasis.

Diagnostics

With symptoms of an enlarged thymus gland in a child, consultation of several specialists is necessary - an immunologist, an endocrinologist and a pediatrician. It often turns out that an increase in the thymus gland in an infant is not associated with pathology, but is due to individual anatomical features. Often parents panic that the thymus gland is enlarged in a newborn, because when crying, it often protrudes above the handle of the sternum. It is also not worth fearing inflammation of the thymus gland in infants; a huge number of immune cells in it leaves no chance for the development of infection.

To confirm the diagnosis, it is necessary to undergo a thorough examination, including:

• General and detailed blood test.
• Chest x-ray.
• Ultrasound diagnostics.

A blood test can detect a decrease in the level of T-lymphocytes, an imbalance between immunoglobulins.

X-ray of the thymus to the child will allow to exclude anomalies in the structure and location of the thymus gland.

Ultrasound allows you to accurately determine the degree of thymus hyperplasia in newborns. Examination of the adrenal glands, abdominal organs will exclude concomitant pathology.

You may need additional tests for hormone levels.

The immune system of a child begins to form long before it is born. At the sixth week of pregnancy, the fetus already has thymus is the central organ of human immunogenesis. Due to the fact that it is shaped like a fork, the thymus is also called thymus. The younger the child and the more often he gets sick, the more actively the thymus works, and, accordingly, the more intensively it grows. The growth of the thymus gland slows down when the child is 12 years old. His immune system by this time is already considered formed. In adults, only a reminder remains of the thymus gland in the form of a small lump of adipose tissue. And by old age, the thymus in a person is almost absorbed.

The thymus gland in children - what is it, what is it responsible for and where is it located

The size of the thymus in children: the norm (photo)

The thymus of a healthy child should be no more than CTTI 0.33(CTTI - cardiothymic thoracic index - this is how the thymus is measured). If this index is higher, fixed thymomegaly ( increase) , which can be of three degrees:

I. CTTI 0.33-0.37;

II. CTTI 0.37-0.42;

III. CTTI more than 0.42.

Among the factors that have a direct impact on the increase in the thymus, one can name the pathology of the development of the fetus during, gene anomalies, late pregnancy, infectious diseases suffered by the expectant mother.

ultrasound

Theoretically, it is possible to determine the size of the thymus using radiography and ultrasound examination of the thymus gland. For diagnosis in children, x-rays are used only as a last resort, due to the risk of exposing the child. Usually, ultrasound is enough to get the desired results.

Immunity and thymus: Komarovsky (video)

Hyperplasia and hypoplasia of the thymus

Among diseases of the thymus gland, in addition to thymomegaly, in children one can also find hyperplasia and hypoplasia of the thymus. Hyperplasia of the thymus- this is the growth of its tissues with the formation of neoplasms. BUT hypoplasia- this is a violation of the function of T-lymphocytes due to congenital pathologies of development. These diseases are recorded much less often than thymomegaly, but they require more serious medical intervention.

Thymomegaly: symptoms to see a doctor

What could be the reason for going to the doctor? What symptoms may indicate an enlarged thymus gland in a child?

1. The baby is rapidly gaining (or losing) weight.
2. After feeding, the baby often spits up.
3. The child begins to cough when he lies down (false croup).
4. Often sick with colds.
5. When a baby cries, its skin turns blue-violet.
6. On the chest - a venous mesh, and skin covered with the so-called marble pattern.
7. With an enlarged thymus, the tonsils, adenoids, or lymph nodes can also increase in size.
8. Often in children, arrhythmia and reduced muscle tone are observed.

Treatment of an enlarged gland

Often, with an increase in the thymus gland, drug treatment not required. The exception is rare complex cases of thymomegaly.

But you should make every effort to. Doctors recommend:

• Taking vitamins and a diet rich in proteins.
• Hardening and sports.
• Compliance with the daily routine.
• Vaccinations for thymomegaly can be done, only you must first give the child antihistamine appointed by the pediatrician.
• Contact with SARS patients should be avoided.
• Avoid eating allergenic food.

And very important point. If your child has an enlarged thymus gland, he should not take acetylsalicylic acid as an antipyretic. Aspirin can speed up the growth of thymus cells.

Forecasts

The thymus gland works and grows intensively in the first years of a child's life. Then she gets relatively little work. Accordingly, the rate of its growth is markedly reduced. Therefore, an enlarged thymus does not require serious treatment, most often, and up to two years it is considered the norm. By the age of 5-6, usually, the thymus stops growing. But this does not mean that she should be left without proper supervision. After all, the formation of immunity of your child and his health in the future depends on it.