Congenital hypothyroidism consequences. Symptoms and treatment of congenital and acquired hypothyroidism in newborns and children over one year of age. Treatment of congenital hypothyroidism

Congenital hypothyroidism is a group of diseases of various etiologies, manifested by congenital insufficiency of the production of thyroid hormones by the thyroid gland. The disease occurs with a frequency of 1 case per 5,000 newborns, in boys - 2.5-3 times less often than in girls.

A lack of thyroid hormones has a negative impact on the development of the central nervous system. If congenital hypothyroidism is not detected in a timely manner and its treatment is not started, the child develops mental deficiency of varying degrees of severity. Therefore, many countries conduct newborn screening for hypothyroidism. In Russia, since 1997, screening has been carried out in all maternity hospitals.

Long-lasting physiological jaundice is one of the signs of congenital hypothyroidism

Causes and risk factors

In 80-90% of cases, congenital hypothyroidism is caused by malformations of the thyroid gland: for example, hypoplasia, dystopia (displacement) in the sublingual or retrosternal space.

The main risk factors for the formation of congenital hypothyroidism:

• lack of iodine in the body of a pregnant woman;
• exposure to ionizing radiation;
• toxic effects on the developing fetus of chemicals, including some medications;
• infectious and autoimmune diseases of pregnant women.

In approximately 2% of cases, abnormalities in the development of the thyroid gland are caused by mutations in the PAX8, FOXE1, TITF2, TITF1 genes. With congenital hypothyroidism caused by genetic factors, the child often exhibits other developmental anomalies:

• cleft palate (cleft palate);
• cleft lip (cleft lip);
• congenital heart defects.

In 5% of cases, the cause of congenital hypothyroidism is hereditary diseases that lead to disruption of the secretion of thyroid hormones or disrupt their interaction with each other. Such diseases include Pendred syndrome, defects in thyroid hormones and iodine organification. Their inheritance is carried out according to the autosomal recessive type (both parents must be carriers of defective genes).

In other cases, congenital hypothyroidism develops as a result of lesions of the hypothalamic-pituitary system caused by:

• pituitary aplasia;
• asphyxia of the newborn;
• birth trauma;
• tumor processes;
• abnormalities of brain development.

The clinical picture of congenital hypothyroidism may be caused by a resistance syndrome: in some hereditary diseases, the thyroid gland secretes a sufficient amount of thyroid hormones, but the target organs lose sensitivity to them.

Forms of the disease

Depending on the reasons underlying the development of the disease, the following forms of congenital hypothyroidism are distinguished:

• thyroidogenic, or primary – occurs as a result of pathological changes in the thyroid gland;
• secondary - its development is based on a deficiency of TSH (thyroid-stimulating hormone), associated with dysfunction of the adenohypophysis;
• tertiary – the cause is a deficiency of thyrotropin-releasing hormone (a hypothalamic hormone);
• peripheral. The mechanism of its development is associated with the absence or defect of thyroid hormone receptors in tropic tissues. Also, the cause of this form of congenital hypothyroidism can be a violation of the process of converting T4 (thyroxine) into T3 (triiodothyronine).

The most dangerous complication of hypothyroidism is myxedema (hypothyroid) coma. It can be triggered by hypothermia, injuries, and infectious diseases.

Depending on the effectiveness of the treatment, congenital hypothyroidism is divided into:

• for compensated – there are no clinical symptoms of the disease, the concentration in the blood plasma of T4, T3, TSH corresponds to normal values;
• for decompensated – laboratory and clinical manifestations of hypothyroidism persist despite the therapy.

Based on the duration of the flow, two forms are distinguished:

1. Transitional. Insufficiency of thyroid function in a child develops under the influence of maternal antibodies to TSH circulating in his blood. This form of the disease lasts from 7 to 30 days.
2. Permanent. Hormone replacement therapy should be carried out for life.

• latent (subclinical);
• manifest;
• complicated.

Clinical manifestations of latent hypothyroidism are usually absent or nonspecific. Blood tests reveal elevated TSH levels with normal T4 levels.

Complicated hypothyroidism is accompanied by the addition of other diseases (cretinism, polyserositis, heart failure). This form occurs with a sharp deficiency of thyroxine with a very high level of thyroid-stimulating hormone.

Symptoms

Congenital hypothyroidism manifests itself at different ages, depending on the severity of the disease and its form. Thus, with aplasia of the thyroid gland or pronounced hypoplasia, the symptoms of hypothyroidism become clearly visible already in the first week of a child’s life. Slight hypoplasia and dystopia appear clinically after reaching one year of age.

Congenital hypothyroidism occurs with a frequency of 1 case per 5,000 newborns, in boys - 2.5-3 times less often than in girls.

The main signs of congenital hypothyroidism:

• immaturity of a newborn born after the 38th week of gestation;
• delayed passage of meconium;
• large fetus (birth weight exceeds 4 kg);
• long-lasting physiological jaundice;
• muscle atony;
• episodes of apnea (stopping breathing) during feeding;
• hyporeflexia;
• flatulence;
• frequent regurgitation;
• tendency to constipation;
• increase in the size of the tongue (macroglossia);
• apathy;
• slow weight gain;
• swelling of the genitals and limbs;
• coldness of the skin to the touch;
• hip dysplasia;
• increased size of fontanelles.

In the primary form of congenital hypothyroidism and lack of treatment, the severity of the symptoms of the disease increases. The skin becomes dry and compacted, acquiring a yellowish-gray color. Myxedema (swelling of the subcutaneous tissue and skin) develops. Sweat production is reduced. Hair and nail plates atrophy. The voice changes (becomes rough, hoarse and low). There are signs of delayed psychomotor development. If treatment is not started, mental deficiency (oligophrenia) will subsequently develop.

The clinical picture of the central forms (secondary, tertiary) of congenital hypothyroidism is usually unclear. The disease is often combined with a deficiency of other hormones (follicle-stimulating, luteinizing, somatotropic), and abnormalities in the structure of the facial skull.

In 80-90% of cases, congenital hypothyroidism is caused by malformations of the thyroid gland: for example, hypoplasia, dystopia (displacement) in the sublingual or retrosternal space.

Diagnostics

Currently, the diagnosis of congenital hypothyroidism is based primarily on the results of neonatal screening. On the 4-5th day of life, a few drops of blood are taken from the child and applied to filter paper, which is sent to the laboratory to determine the TSH concentration. The diagnosis of congenital hypothyroidism is considered confirmed when the TSH concentration in the test sample exceeds 100 mU/L.

If the TSH content in a dried blood spot is higher than 20 mU/l, then the result is regarded as doubtful and the analysis is repeated. If a similar result is repeated, determination of free T4 and TSH in the blood serum is indicated.

Treatment

Treatment of congenital hypothyroidism should begin immediately after diagnosis. Hormone replacement therapy is carried out for life with synthetic analogues of thyroid hormones. The dosage is selected individually in each specific case. If necessary, the doctor may additionally prescribe symptomatic medications and multivitamins to the sick child. To assess the effectiveness of the treatment, serum concentrations of T4 and TSH are determined.

If therapy is started in the first months of life, then the child’s psychophysical development and intelligence do not suffer.

Possible complications and consequences

If left untreated, congenital hypothyroidism is complicated by damage to the central nervous system with the formation of oligophrenia.

When the thyroid gland is insufficient, the immune system suffers, so children with congenital hypothyroidism are susceptible to colds and other infectious diseases, which often take on a protracted, chronic nature.

The most dangerous complication of hypothyroidism is myxedema (hypothyroid) coma. It can be triggered by hypothermia, injuries, and infectious diseases.

Forecast

In congenital hypothyroidism, the prognosis largely depends on the time of initiation of hormone replacement therapy. If it starts in the first months of life, then the child’s psychophysical development and intelligence do not suffer. When starting therapy over 3-6 months of age, it is possible to stop further lag in psychomotor development. However, existing intellectual impairments will remain for life.

Prevention

Prevention of congenital hypothyroidism includes:

• prevention of iodine deficiency in a pregnant woman;
• medical and genetic counseling for couples at the stage of pregnancy planning, especially if one of the parents or one of the close relatives suffers from thyroid pathology;
• antenatal protection of the fetus.

Video from YouTube on the topic of the article:

Hormonal diseases of the mother are transmitted to the child. Of course, no one has canceled the influence of unfavorable factors, but it has a lower percentage when diagnosing hypothyroidism in childhood.

More than 85% of newborns have a congenital pathology if their mothers were treated for thyroid diseases during pregnancy. Why hypothyroidism is dangerous, its signs and types, methods of treatment and prevention will be discussed below.

Definition and causes of hypothyroidism in children

A disease in which the thyroid gland is underactive and does not produce enough hormones to keep the body healthy is called hypothyroidism. It affects children of all ages, starting from the period of intrauterine development. Medical statistics state that among newborn babies, one in 5,000 children has congenital hypothyroidism. At the same time, girls are 2 times more likely to suffer from pathology.

Congenital form

Depending on the type of disease, the causes of its occurrence vary. Prerequisites for congenital hypothyroidism (CH):

• genetics, heredity;
• mutations of the thyroid gland - underdevelopment, unnatural location, complete absence of the organ;
• malfunction of the thyroid gland, its resistance to iodine absorption;
• mother living in an environmentally unfavorable region with a high level of radiation pollution;
• overdose and abuse of medications by a pregnant woman if she has thyroid disease;
• serious disorders in the hypothalamic-pituitary system;
• infectious diseases of the mother or fetus.

In general, the causes of CH are thyroid abnormalities and disturbances in the synthesis of hormones, their metabolism, or damage to tissue receptors responsible for sensitivity to the action of hormones. The most severe degree of congenital pathology is cretinism, dementia.

Acquired form

Causes of the acquired form of the disease, the risk of which exists for a child at any age:

• neck injuries;
• absence or deficiency in the diet of foods containing iodine;
• consequences of surgical operations on the thyroid gland;
• tumors, inflammatory processes or injuries in any part of the hypothalamic-pituitary-thyroid triangle;
• autoimmune diseases that lead to malfunctions of the body.

Classification of pathology in children

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The causes of hypothyroidism entail differences in the form, specificity and clinical manifestations of the disease. In addition to disorders of the thyroid gland, hypothyroidism develops with pathologies or diseases of the hypothalamus and pituitary gland, tissue susceptibility to the effects of hormones.

In medical practice, the following classification of pathology is accepted (see table of classification of hypothyroidism in children):

Origin/Character	Kinds	Characteristic
Congenital	Primary (thyroidogenic)	Expressed in a lack of produced hormones thyroxine (T4) and triiodothyronine (T3).
	Secondary (pituitary)	Insufficiency of thyroid-stimulating hormone synthesis. Dysfunction of the pituitary gland provokes disruption of the thyroid gland, a slowdown in metabolic processes in the child’s body, and inhibition of his neurophysical development. Rarely seen.
	Tertiary (hypothalamic)	Disturbances in the activity of the hypothalamus (the controlling structure of the brain) lead to abnormalities in the functioning of the thyroid gland. There is a deficiency of the hormone thyrotropin-releasing hormone.
	Tissue (peripheral)	Change or absence of receptors for the perception of gland hormones.
Acquired		It has a cumulative development due to the influence of negative factors that provoke malfunctions of the thyroid gland, pituitary gland and hypothalamus.
Subclinical (hidden)		It is discovered accidentally during a blood test for TSH, T3 and T4. The internal organs are already suffering from hypothyroidism.
Transitional (transient)		Temporary dysfunction of the thyroid gland. May be congenital or acquired. It goes away quickly on its own or can be treated with short-term treatment. It is characterized by an increased level of thyroid-stimulating hormone against the background of a low concentration of thyroid hormones. Occurs after surgery on the thyroid gland, taking medications that inhibit its function, medications with lithium, potassium perchlorate.
manifest		Deficiency of thyroxine against the background of increased levels of thyroid-stimulating hormone. The disease is accompanied by classic symptoms of hypothyroidism.

Symptoms of hypothyroidism

The pathology clinic is bright. Disturbances in the functioning of the hormonal structure irreversibly lead to changes in both the appearance of the child, his behavior and activity, and in the coherence of the work of internal organs and systems.

The symptoms of hypothyroidism change as the baby gets older, but the general problem with hormonal regulation remains. Therefore, it is important to promptly notice the prerequisites for pathology.

In newborn babies

From the moment a child is born, it is not always possible to suspect hypothyroidism. The most striking manifestations that give rise to an urgent blood test of a newborn will be:

• weight exceeding 4 kg;
• postmaturity of the baby, its appearance after 42 weeks;
• cyanosis of the nose and lips;
• roughness of voice;
• absence of the first cry;
• mouth openness;
• severe swelling of the face;
• compactions in the form of tubercles in the supraclavicular notches;
• lack of ability to maintain a stable body temperature in comfortable conditions;
• persistence of yellowness of the skin for more than a month after birth.

With congenital hypothyroidism, the thyroid gland cannot perform its functions fully

If such signs do not appear in the baby, then after 1 month of life they have the following picture:

• problem with body thermoregulation;
• peeling of the skin and brittle hair;
• teeth erupt later than healthy peers (we recommend reading:);
• loss of appetite, including complete refusal of food and water due to loss or increase in body weight;
• the sucking reflex is weakly expressed;
• tongue size is too large due to swelling;
• swelling of the eyelids;
• weak dynamics of weight gain and growth;
• digestive problems – bloating, constipation;
• malfunctions of the nervous system - whims, lack of reflexes due to age, lethargy, fatigue;
• pathologies in the functioning of the cardiovascular system - weak pulse, low blood pressure;
• poorly and long-healing umbilical wound;
• late closure of the fontanelle;
• voice timbre is rough;
• weakness of muscle tissue - late development of the ability to hold the head, roll over, sit;
• genitals are poorly developed.

If an infant has a disease, it is extremely important to continue breastfeeding, which will have a positive effect on the dynamics of recovery

Breastfeeding provides the baby with less severe symptoms. This is explained by the supply of some hormones with breast milk.

In children from 1 year to 3 years

At the age of one to three years, subclinical hypothyroidism is most often diagnosed in children, when there is no obvious clinical picture. The results of a blood test will show the normal level of the T4 hormone and an increased concentration of TSH. Take your baby to the doctor if you notice most of the following:

• constant apathy, drowsiness, laziness, lethargy, lack of interest in the outside world;
• when in contact with children and adults, the child remains indifferent, silent, and does not talk;
• muscle weakness;
• severe delays in teething, weight gain, height, and skills due to age;
• swelling of the facial muscles, excessively large tongue;
• dry skin, brittle hair;
• violation of body proportions, when the body is long and the limbs are small;
• problems with appetite and digestive system functioning.

In children over 3 years old

After three years of age, hypothyroidism in children takes the form of an acquired form, but it can also be subclinical. It manifests itself as violations:

• weight – obesity (more details in the article:);
• height – dwarfism, disproportion of the body;
• nervous development - outbursts of excitement, mood swings, drowsiness, lethargy;
• facial expressions – they are absent due to swelling of the face;
• attention and thinking are slowed down;
• heart rate – weakness, low frequency;
• skin water balance – dry, flaky;
• hair structures become thinner and break;
• vocal cords – hoarseness and roughness of voice;
• reproductive system – late maturation;
• the size of internal organs is increased.

Diagnosis of hypothyroidism

On days 3-5 after birth in a full-term baby and on days 10-14 in a premature baby, blood is taken for hormone analysis on special filter paper.

Neonatal screening of a newborn (more details in the article:)

The importance of the method is due to the high rate of progression of the disease in the baby, especially in the subclinical form, and the launch of irreversible processes in his body in the absence of a selected treatment regimen. If the result of the blood test is questionable, the child receives an order to visit an endocrinologist.

If there is a clinical diagnosis and suspicion of subclinical or other type of hypothyroidism, the following types of examination are carried out:

• biochemical and clinical blood test;
• blood test for the concentration of T3 and T4, antithyroid antibodies, hormone binding index;
• tests with thyrotropin-releasing hormone;
• scintigraphy and ultrasound of the thyroid gland;
• ECG to identify the dynamics of bradycardia development;
• MRI (CT) of the pituitary gland;
• X-ray examination of the wrist and knee joints for the presence of ossifications, determining the age of the child’s bones.

Treatment methods

The earlier hypothyroidism was identified, the greater the effect of its comprehensive treatment. Children with congenital hypothyroidism show positive results in the growth and development of all organs and systems after therapy. The optimal time to start it is 7-14 days after birth.

Endocrinologists use a number of treatment methods:

• medicinal - with the use of Sodium Levothyroxine drugs, which are indicated for use for life;
• diet and diet adjustments;
• vitamin and mineral complexes;
• surgical intervention in the presence of tumors in the thyroid gland area;
• herbal therapy - decoctions of chamomile, string, sage, St. John's wort.

After a neurologist is involved in the treatment of the disease, massages, exercise therapy, and nootropic drugs appear on the list of mandatory procedures. The criteria for the effectiveness of a combination of methods are the disappearance of all symptoms of hypothyroidism, the normal level of TSH in the blood, and the physical and mental development of children corresponding to their age.

Predictions and prevention

Children whose congenital form of hypothyroidism is diagnosed in the first month of life have a positive prognosis for treatment. If this happened at 3 months or later, then there is a high probability of deviations in further development. A longer delay in diagnosis and treatment is fraught with obvious pathologies of skeletal growth and neuropsychic development. The introduction of hormonal drugs will not improve the child’s condition.

The best prevention is a conscious approach by parents to pregnancy planning. The expectant mother should check her thyroid gland, the level of hormones in her blood, enrich her diet with iodine-containing foods, and perhaps even change her region of residence to a more favorable one. Consult an endocrinologist if you have a family history of thyroid disease or suffer from goiter.

The endocrine system plays an important role in the process of adaptation of a newborn to the conditions of postnatal life.

The birth of a child is accompanied by a transition to pulmonary breathing, activation of mechanisms that provide protection from hypothermia, hypoglycemia, hypocalcemia. The adrenal glands perform an adaptive function from the first minutes of a child’s life. Somewhat later, to maintain energy balance and ionic equilibrium, it is necessary to switch on the mechanisms provided by the endocrine apparatus of the pancreas and the parathyroid glands.

Hypothyroidism is a clinical syndrome caused by a decrease or complete loss of thyroid function, characterized by a decrease in the production of thyroid hormones.

The thyroid gland produces three types of hormones: triiodothyronine, thyroxine and thyrocalcitonin. The first two hormones (triiodothyronine and thyroxine) contain iodine. In the human body, their role changes simultaneously with age: during the period of intrauterine development and early childhood, these hormones promote the development of bones (osteogenesis) and nervous tissue (especially the brain). In an adult, due to the completion of the development of the nervous system and skeleton, the main role of thyroid hormones is to regulate the energy processes of our body. Under the influence of these hormones, our body's cells produce heat when we are cold and also generate energy for other activities. In addition to triiodothyronine and thyroxine, the thyroid gland produces thyrocalcitonin, a hormone that promotes the accumulation of calcium, which is especially important during the growth of the skeleton and teeth.

Thus, the thyroid gland performs the following important functions:

Controls basic metabolism and body temperature.

Regulates the metabolism of proteins, fats and carbohydrates.

Regulates calcium metabolism.

Participates in the formation of human intelligence.

In childhood, the thyroid gland contributes to the growth and harmonious development of the child’s body as a whole. The thyroid gland plays a particularly important role in the development of the nervous system and skeleton.

According to modern concepts, the basis of the action of thyroid hormones on body tissue is the stimulation of oxidative processes in the cell, and above all the absorption of oxygen and the release of carbon dioxide. Such well-known factors as slower growth and differentiation of cartilage tissue, mental retardation, delayed sexual development and others in hypothyroidism are based on the same processes - a decrease in the level of general metabolism. Apparently, thyroid hormones do not specifically regulate the growth and differentiation of the body, but are a factor whose presence is mandatory for these processes, i.e. limiting them. Indeed, with hyperthyroidism, as a rule, gigantism is not observed, there are no cases of accelerated puberty, or accelerated mental development. In a word, an increase in thyroid function, as a rule, does not have a positive physiological effect on the development of the body, but most often leads to pathology. At the same time, ideas about the age-related patterns of functioning of the pituitary-thyroid system in healthy children are undoubtedly of great practical importance, since they make it possible to identify the optimal corridor for the level of hormone secretion, which creates favorable conditions for the growth and development of the entire organism. Etiology and pathogenesis.

Pathogenetically, hypothyroidism syndrome is heterogeneous. Depending on the level of disturbance in the biosynthesis of thyroid hormones, there are:

 Primary (thyroidogenic) hypothyroidism caused by primary pathology of the thyroid gland:

a) as a result of a decrease in the amount of functionally active tissue;

b) as a result of various defects in the biosynthesis of thyroid hormones.

 Secondary (pituitary) hypothyroidism - as a result of a decrease or loss of thyroid-stimulating hormone (TSH) production. Impaired TSH production in adults occurs mainly as a result of a destructive process in the pituitary gland. It may be caused by the results of therapeutic interventions (proton therapy, radiotherapy, hypophysectomy), traumatic damage to the sella turcica, as well as various pituitary tumors (chromophobe adenoma, craniopharyngeoma, cyst, hemachromatosis, tuberculosis, histiocytosis) and metastases of malignant tumors. One of the causes of secondary hypothyroidism in women is postpartum ischemic necrosis of the anterior pituitary gland (Schien's syndrome), when the production of not only TSH, but also gonadotropic hormones, ACTH and growth hormone falls out). Secondary hypothyroidism is rarely isolated; as a rule, hypothyroidism is combined with secondary hypogonadism and secondary hypocortisolism.

 Tertiary (hypothalamic) – as a result of a decrease or loss of thyroid hormone production. The cause of tertiary hypothyroidism may be a decrease or cessation of secretion of the hypothalamic hormone thyrotropin-releasing hormone, which is involved in the regulation of TSH production. The cause of tertiary hypothyroidism can be traumatic brain injury, metastases of malignant tumors from other organs, and neuroinfections.

 Peripheral (tissue) resistance to the action of thyroid hormones.

Each of the listed pathogenetic forms of hypothyroidism has its own spectrum of etiological factors. In addition, hypothyroidism is distinguished with the presence or absence of goiter.

Etiological factors of primary hypothyroidism

Decrease in the amount of functionally active thyroid tissue:

– hypothyroidism caused by subacute thyroiditis (either transient or as a result of a previous illness);

– postoperative hypothyroidism;

– congenital hypothyroidism;

– hypothyroidism due to thyroid tumors;

– hypothyroidism due to impaired biosynthesis of thyroid hormones;

– against the background of iodine deficiency in the environment;

– drug-induced hypothyroidism;

– goiter and hypothyroidism as a result of consumption of food containing goitrogenic factors.

Congenital hypothyroidism This is a chronic disease characterized by disruption of the thyroid gland in newborns and a decrease in the concentration of thyroid hormones in the blood. According to statistics, congenital hypothyroidism occurs with a frequency of 1-2 cases per 5000 newborns, in Europe And North America up to 1 in 6,000–7,000 births. In 90% of cases, the development of congenital hypothyroidism is sporadic, and in 10% it is secondary, associated with congenital disorders of synthesis, secretion and utilization thyroid hormones.

As a rule, girls are more often susceptible to congenital hypothyroidism (2 times more often than boys). The term “congenital hypothyroidism” describes a condition in which a malfunction of the thyroid gland is observed already at the birth of a child, that is, the child is born with a pathology, and does not acquire it during independent life outside the womb. The development of congenital hypothyroidism can be due to various reasons. Main reasons the occurrence of congenital hypothyroidism are:

Hereditary factor. In most cases, the development of congenital hypothyroidism is caused by a violation of the formation of the thyroid gland even before the birth of the child (in the prenatal period) due to certain genetic mutations.

Impaired formation of thyroid hormones (reduced sensitivity of thyroid cells to iodine, impaired iodine metabolism, impaired

reduction in the transport of substances necessary for the synthesis of hormones).

Damage to the hypothalamus (secondary hypothyroidism). The hypothalamus is the center of the nervous system, regulating the functioning of the thyroid gland and other endocrine glands of our body. Lesions of the hypothalamus are usually accompanied by severe endocrine disorders.

Resistance (decreased sensitivity) to thyroid hormones. Most often, a decrease in the sensitivity of cells to thyroid hormones occurs as a result of the mother's use of antithyroid drugs during pregnancy (for example, if a pregnant woman has a goiter).

Main signs and symptoms of congenital hypothyroidism in children Most often, congenital hypothyroidism does not manifest itself in any way in the first weeks of a newborn child’s life, but begins to manifest itself only a few months later, when doctors and parents note a delay in the child’s development. Only a small proportion of children with congenital hypothyroidism experience symptoms of this disease in the first weeks of life.

The most typical signs of congenital hypothyroidism in the first days of life include:

Delay childbirth more than 40 weeks;

Large birth weight (more than 3500g);

The birth of a child with signs of immaturity, despite postmaturity pregnancy; Edema “pads” on the back of the feet and hands, swelling of the face; Swelling in the form of dense “pads” in the supraclavicular fossa;

Poor healing of the umbilical wound, prolonged course of postpartum jaundice; Rough low voice when a newborn cries, apathy, weak breastfeeding; Half-open mouth.

Prolonged course of jaundice.

Cyanosis (blueness) of the nasolabial triangle.

Cold hands and feet, dry skin, brittle and dry hair; Characteristic symptoms of congenital hypothyroidism at 3–4 months of a child’s life are: decreased appetite; chronic constipation in a child; peeling of the child's skin; decrease in the child’s body temperature; brittle hair in a child.

Child 1.5 months (6 weeks) - clinic of congenital hypothyroidism: yellowness of the skin, umbilical hernia, increased in size language.

Methods for diagnosing congenital hypothyroidism in children To diagnose CH in newborns, the Apgar scale is used:

Table 1

Congenital hypothyroidism should be suspected if the total score is more than 5.

At a later date, characteristic signs of congenital hypothyroidism are:

Late teething in a child and closure of fontanelles

Delayed physical development of the child

Delayed mental development of a child

It should be noted that it is very rarely possible to identify congenital hypothyroidism in the first days of a child’s life, only on the basis of the presence of symptoms of this disease. This task is much more successfully accomplished by early screening for congenital hypothyroidism, which is carried out in all newborns.

A timely diagnosis of congenital hypothyroidism can be made during early examination (screening) of newborns. Screening for hypothyroidism in newborns was first performed in Canada in 1971. It is known that hypothyroidism is characterized by a low level of thyroid hormones in the blood simultaneously with an increase in the level of thyroid-stimulating hormone (TSH, a hormone of the hypothalamus that stimulates the thyroid gland). The purpose of screening is to identify newborns with elevated TSH levels. As a rule, to diagnose congenital hypothyroidism in children, blood is taken from the heel 3–4 days after birth. The content of the hormone (TSH) is determined in a blood sample. A TSH concentration above 50 mU/L suggests hypothyroidism. A level of 20-50 nmol/l - the result is considered doubtful, and the study must be repeated. Testing for hypothyroidism takes several weeks. The results of the analysis are reported only to those parents whose children may have hypothyroidism.

It is very difficult to diagnose hypothyroidism before birth - amniocentesis (puncture and collection of amniotic fluid using a long needle) is necessary to study thyroid hormones.

During pregnancy, thyroid-stimulating hormones TSH and T4 should be examined at 8–12 weeks, when the effect of hormonal abnormalities on the fetus is especially unfavorable.

An ultrasound scan of the thyroid gland, as well as determination of the level of other thyroid hormones, can confirm or refute the diagnosis. A more detailed examination is carried out for children only after 3 years of age (at this time a short-term interruption of treatment is relatively safe).

Early detection of congenital hypothyroidism and initiation of treatment (in the first 3–4 weeks) is of great importance to ensure normal growth and development of the child. A lack of thyroid hormones during the first weeks of a child’s life can lead to irreversible damage to the development of the nervous system, so treatment for children with congenital hypothyroidism should begin no later than a month after birth.

Treatment of congenital hypothyroidism in children.

If proper treatment for congenital hypothyroidism is started on time, the physical and mental development of the child occurs normally. Treatment should be started immediately after the diagnosis of congenital hypothyroidism is made. The main method of treating congenital hypothyroidism in children is replacement therapy with sodium levothyroxine (Eutyrox, L-thyroxine, thyro-4, L-thyroxine-Acri, L-thyroxine-Farmak). In small doses, levothyroxine has an anabolic effect (promotes the formation of substances and the growth of the body). In medium doses, levothyroxine promotes the growth and development of the body, increases the need for oxygen in tissues, and affects the metabolism of proteins, fats and carbohydrates. A positive effect is observed already 7–12 days after the start of treatment with levothyroxine. As a rule, in developed countries, treatment begins no later than the first month of a child’s life (in Germany, in children with congenital hypothyroidism, treatment begins on the 7–8th day of life, in England on the 10–15th day).

The chemical structure of levothyroxine is similar to the thyroid hormone (thyroxine), which is its main advantage over other drugs. After taking levothyroxine, a certain concentration of the drug is created in the child’s body, which is consumed as needed. Accordingly, it is possible to avoid high levels of the hormone in the blood.

The daily dose of levothyroxine for congenital hypothyroidism should be given to the child in the morning an hour before breakfast, with a small amount of liquid. Children in the first weeks of life should be given levothyroxine during the morning feeding.

Criteria adequate treatment with levothyroxine for congenital hypothyroidism in children are:

Normal serum TSH level

In children of the first year of life - thyroxine level. Control determinations of thyroxine level concentrations should be carried out in the first year of life every 2–3 months of life, after 1 year – every 3–4 months.

Data on the dynamics of physical development at different periods of a child’s life.

Data on the dynamics of a child’s mental development

Skeletal growth indicators.

As a rule, the level of thyroxine in the blood of a child with congenital hypothyroidism normalizes 10–14 days after the start of treatment. The child’s TSH level returns to normal 2–3 weeks after the start of treatment. The dosage of levothyroxine sodium is selected individually for each child, taking into account clinical and laboratory data. Levothyroxine is available in various dosages - 25, 50 and 100 mcg per tablet. Parents need to know the prescribed dose of levothyroxine in mcg, not just tablet parts.

Basic principles of levothyroxine dosing.

With congenital hypothyroidism in the first weeks of life (per 1 sq.m. of body surface):

initial dose – 12.5–50 mcg/day;

maintenance – 100–150 mcg.

For congenital hypothyroidism in children under 6 months of age: 8–10 mcg/kg/day.

For congenital hypothyroidism in children aged 6–12 months: 6–8 mcg/kg/day.

For congenital hypothyroidism in children under 5 years of age: 5–6 mcg/kg/day.

For congenital hypothyroidism in children aged 6–12 years: 4–5 mcg/kg/day.

Treatment of children with congenital hypothyroidism is carried out exclusively

endocrinologist. Monitoring of children with congenital hypothyroidism

carried out by an endocrinologist, pediatrician, neurologist.

With proper and timely treatment, children with congenital hypothyroidism develop well.

Severe forms of untreated hypothyroidism in children are cretinism.

Fortunately, in our time, most children with congenital hypothyroidism receive the necessary treatment that compensates for the lack of thyroid hormones. In the absence of treatment, a child with congenital hypothyroidism develops a pronounced lag in intellectual and physical development - cretinism. Signs of cretinism are short stature, twisted limbs, deformed face, low level of intelligence, and a tendency to chronic diseases.

For differential diagnosis it is necessary to note signs of thyroid dysfunction and clinical features

manifestations in various forms of deviations of hormonal homeostasis.

Children have more older manifestations of hypothyroidism often occur as a clinical syndrome caused by a decrease or complete loss of thyroid function, characterized by a decrease in the production of thyroid hormones.

The most common cause of primary hypothyroidism in older children is autoimmune thyroiditis (AIT). This number includes patients with both the presence of goiter and its absence. The largest number of patients with hypothyroidism, reaching 90-100%, is detected in the atrophic form of autoimmune thyroiditis.

The pathogenesis of hypothyroidism is caused by an autoimmune process in the thyroid gland, leading to degeneration of follicular cells and a decrease in functionally active gland tissue, which is replaced by fibrous tissue. In the atrophic form of autoimmune thyroiditis, follicular tissue is practically absent.

The presence of goiter in AIT is caused by fibrous changes in the thyroid tissue, as well as inclusions of plasma cells, leukocytes, macrophages, and the remaining follicular tissue does not have sufficient hormonal activity.

In 10% of those who have had subacute thyroiditis, persistent hypothyroidism develops. Thyroidectomy in 100% of cases leads to the development of persistent hypothyroidism. Post-radiation hypothyroidism (after treatment with DTZU 131) is observed in 20–30% of patients.

The clinical manifestations of various forms of hypothyroidism can be almost the same, however, with primary hypothyroidism, the most pronounced and typical symptoms are observed.

With the aim of differential diagnosis it is necessary to conduct a syndromic analysis of changes in organs and systems.

The initial manifestations of hypothyroidism are characterized by scanty symptoms and nonspecific disorders (weakness, fatigue, pain in the heart, dizziness, etc.), and patients can be unsuccessfully observed for a long time by various specialists for “cerebral sclerosis,” “pyelonephritis,” “anemia”, “angina pectoris”, “depression”, “osteochondrosis”, etc.

1. Hypoenergetic syndrome.

Weakness, low body temperature, chilliness, cold parts of the body, loss of appetite, weight gain. This symptomatology occurs with a decrease in basal metabolism, incl. lipid metabolism. In contrast to patients with atherosclerosis, the level of high-density lipids in hypothyroidism is normal, which may explain the relative rarity of myocardial infarction. Weight gain should be differentiated from other types of obesity (nutritional-constitutional, hypothalamic-pituitary, etc.).

With the types of obesity mentioned above, there will be no known symptoms of hypothyroidism.

2. Edema-dystrophic syndrome.

With severe hypothyroidism, the appearance of patients with a pale, puffy face is very typical.

Skin that is cold to the touch is dry and flaky. Particularly characteristic are areas of increased dryness and keratinization of the skin on the feet, the front surface of the lower leg, knees, elbows, and hands.

The swelling of the skin is dense and does not leave marks when pressed.

The edematous component should be differentiated from kidney pathology and symptoms of heart failure.

Kidney pathology is characterized by hypothyroid habitus: pale, puffy face, swelling of the eyelids, “congestive” limbs. But with pyelo- and glomerulonephritis there will be no pronounced degenerative changes (brittle nails, hyperkeratosis, dry and brittle hair, thinning hair on the head, in the armpits, on the pubis and hair loss in the outer third of the eyebrows.

With hypothyroidism, there is swelling of the vocal cords and tongue, which leads to slow, unclear speech, and the voice becomes low and rough. This type of disorder often leads patients to a phoniatrist. The phoniatrist should be focused on the clinic of hypothyroidism. A diagnosis of vocal cord paresis is often made.

People who have dentures often believe that the denture is not suitable and are treated by dentists to no avail, whereas this is a hypothyroid enlargement of the swollen tongue.

There may be hearing loss due to swelling in the middle ear. This phenomenon is often considered as hearing loss and the patient is seen by an audiologist.

Yellowness of the skin is often observed, which occurs due to a violation of the transition of B-carotene to vitamin A and hypercarotenemia. It is in this regard that chronic hepatitis is mistakenly diagnosed.

4. Cardiovascular syndrome.

In the vast majority of patients, symptoms of damage to the cardiovascular system appear in the early stages of the disease and largely determine its severity. A number of metabolic changes caused by a deficiency of thyroid hormones, namely dysproteinemia, fatty tissue infiltration and specific mucoid edema, hypoxia. Increased vascular permeability and electrolyte imbalance lead to morphological and functional changes in the myocardium and pericardium and the clinical symptom complex of the hypothyroid heart.

The size of the heart in most patients is increased due to the accumulation of mucopolysaccharides, fluid retention and disturbances in electrolyte metabolism. The reason for the “increase” in the size of the heart is often the accumulation of mucinous fluid in the pericardium, which can reach significant sizes. A direct relationship between the presence of hydropericardium and the severity of hypothyroidism has not been established. In elderly patients, in addition to hydropericardium, pleurohydropericardium or ascites, it is often regarded as a manifestation of heart failure.

If these changes are present, the remaining symptom complexes of hypothyroidism should be taken into account.

Dystrophic processes, accumulation of fluid and mucoid substance in the myocardium and pericardium lead to an enlargement of the right parts of the heart and expansion of its boundaries. The heartbeat is almost undetectable. Muffled tones are heard. A set of characteristic ECG changes is determined. Changes in the terminal part of the ventricular complex, i.e. reduction or inversion of the T wave and depression of the ST interval are equally characteristic of coronary atherosclerosis and hypothyroidism.

It is these ECG changes, combined with pain and sometimes with arterial hypertension, that provide grounds for overdiagnosis of coronary heart disease.

The best evidence of the metabolic, rather than atherosclerotic, coronarogenic nature of cardiac symptoms is the disappearance of pain and positive ECG dynamics during effective treatment with thyroid hormones.

Bradycardia is observed in 30–50% of patients with hypothyroidism, and the pulse may be small and soft. The vast majority of patients have a pulse in

within normal limits.

10% of patients have tachycardia without other signs of cardiovascular

insufficiency. Blood pressure can be low, normal, and in 20% of patients it can be elevated, which is something that therapists should especially pay attention to.

A feature of hypertension in the majority of patients with hypothyroidism under the age of 50 years is its reversible nature, i.e. decrease or normalization due to thyroid replacement therapy. In people over 50 years of age, one should pay attention to the clinical syndromes of diabetes in the stream of hypertensive patients.

5. Gastrointestinal syndrome.

Characteristic of gastrointestinal disorders. Patients complain of decreased appetite, nausea, flatulence, and constipation. A decrease in the tone of the muscles of the intestines and biliary tract leads to stagnation of bile in the bladder and contributes to the formation of stones, the development of megacolon and sometimes intestinal obstruction with a picture of an “acute abdomen”. In addition, patients with hypothyroidism often develop atrophic anacid gastritis (most often of an autoimmune nature), which in turn aggravates the anemia characteristic of hypothyroidism. Sometimes it is with anacid gastritis that the path to the diagnosis of hypothyroidism begins.

6. Psychoneurological syndrome.

One degree or another of mental disorders is observed in all patients, and sometimes they dominate clinical symptoms. Characterized by lethargy, apathy, memory impairment, indifference to the environment; The ability to concentrate, the acuity of perception and reaction decreases. Often such patients are admitted to psychiatric hospitals with a diagnosis of endogenous depression. The ongoing psychotropic antidepressant and neuroleptic therapy aggravates the course of the emotional sphere in hypothyroidism. With undiagnosed hypothyroidism, sleep is further distorted: drowsiness during the day and insomnia at night. With a long-term untreated disease, hypothyroid psychosis develops, its structure approaching endogenous ones (schizophrenia, manic-depressive psychosis, involutional psychosis, etc.).

Changes in the bioelectrical activity of the brain (slowdown of the main -rhythm of the EEG) and the nature of its recovery during the diagnostic process, as well as the effectiveness of therapy, occur when the dose of thyroid drugs is adequate. Mental disorders of adults with hypothyroidism are completely or almost completely corrected by successful replacement therapy.

Children who did not receive thyroid therapy in the first years of life and illness may experience irreversible lag in mental functions up to severe dementia.

Disorders of the peripheral nervous system are manifested by parasthesias, neuralgia, and slowed tendon reflexes, which must be taken into account by neurologists focused on the polymorphic picture of hypothyroidism.

7. Changes in other organs and systems.

In patients with hypothyroidism, antibodies to the parietal cells of the stomach are detected, which reduces the absorption of vitamin B12, a decrease in its content in the blood and the development of pernicious anemia. Anemia can be hypochromic, normochromic and even hyperchromic. Anemia of autoimmune origin accompanies severe autoimmune forms of hypothyroidism. And again, doctors often go from anemia and hypothyroidism syndrome to the correct diagnosis of thyroid disease. Patients are prone to hypercoagulation, as plasma tolerance to heparin is increased and the amount of free fibrinogen increases. Hypercholesterolemia is very characteristic (sometimes reaching 15–17 mmol/l).

Neurologists should pay attention to signs of polyneuropathy, characterized by sensory disturbances in the form of parasthesias, decreased vibration and tactile sensitivity.

The numbness of the hands and parasthesia that patients present with are caused by compression of the nerve trunks in the osteoligamentous canals (mucinous edema) - tunnel syndrome.

Muscle changes in hypothyroid myopathy are characterized by their enlargement and thickening. A significant increase in skeletal muscles in women gives the impression of masculinization in the absence of hypertrichosis and virilization of the clitoris. Patients often complain of muscle soreness upon palpation and movement.

Hypothyroid myopathy often has to be differentiated from dermatomyositis, tetany and myopathy of unknown origin. With hypothyroidism, in addition to muscle changes, the main syndromes of hypothyroidism will be evident.

To summarize the differential diagnosis of hypothyroidism, it should be noted the difference between primary and secondary hypothyroidism. Hypothyroidism in Sheehan's syndrome is combined with hypogonadism and hypokarticism. Thyroid insufficiency in various hypothalamic-pituitary diseases (pituitary dwarfism, acromegaly, adiposogenital dystrophy, etc.) is combined with impaired growth, sexual development, pathology of fat metabolism, and diabetes insipidus. Currently, there are a number of optimal studies that help register the pathology of the thyroid gland - T 3, T 4, TSH, ultrasound, computed tomography of the pituitary gland.

The diagnosis of “congenital hypothyroidism” is not a death sentence. Modern treatment completely restores the required amount of hormones. If therapy is started in a timely manner, children are no different from their peers in mental and physical development. The criterion for correct treatment is a normal TSH level for age.

Insufficient formation of the hormones thyroxine (T4) and triiodothyronine (T3) in the thyroid gland (hypothyroidism) in children has several clinical forms depending on the level of damage and the course of the disease: congenital, primary, central (pituitary or secondary), peripheral, transient, subclinical, manifest.

In most newborns(up to 90% of all cases of disease) the primary form occurs. Causes in children under one year of age: defects in organ development, infections, autoimmune lesions, use of medications by a pregnant woman, exposure to chemicals, radiation exposure, iodine deficiency in the diet, thyroiditis, endemic goiter, gene mutations, disruption of hormone formation due to a defect in the absorption of iodine by the thyroid gland, hereditary developmental anomaly - Pendred's syndrome (deafness and enlarged thyroid gland).

Central forms of hypothyroidism (secondary and tertiary) appear due to brain pathology - cysts, developmental defects, benign or malignant neoplasms, trauma during childbirth, suffocation due to entanglement of the umbilical cord. Cause of peripheral form is a genetic defect that is inherited. Acquired occurs due to a brain tumor, skull injury, surgery, lack of iodine in food and water.

All symptoms of thyroid deficiency can be divided into initial (nonspecific) and consequences in the form of delayed psychomotor development, which become noticeable over time.

Acquired forms of the disease, especially after 2 years of age, are less dangerous. Mental development does not suffer with them. Possible obesity, stunted growth, delayed puberty, slow thinking, and poor performance at school.

Diagnosis of the condition: screening (selection test) for hypothyroidism is performed. It provides taking blood for TSH. For full-term babies, the optimal time is the 5th day after birth, and for premature babies - the second week of life. The upper limit for the indicator is 20 μ/U per ml. If this value is exceeded, .

If it is below 120 nmol/l, then a diagnosis of congenital hypothyroidism is made and replacement therapy is prescribed. To clarify, additional methods of examining the child are prescribed.

To avoid severe mental retardation, treatment of congenital hypothyroidism should begin no later than 10 days after birth. If it develops, then drug therapy does not completely restore brain function, but only slows down the progression of developmental abnormalities.

Most children with congenital and acquired forms of the disease are prescribed levothyroxine (Euthyrox, L-thyroxine) for lifelong use. Start with a minimum dosage - 8 mcg per 1 kg of weight per day. If correction of the disease is insufficient, the doctor can increase it to 10-15 mcg/kg. If the pulse increases, sweating, or diarrhea, reduce the dose.

Read more in our article about hypothyroidism in children, its consequences and treatment.

Read in this article

Classification

Insufficient formation of the hormones thyroxine (T4) and (T3) has several clinical forms. They are distinguished depending on the level of damage and the course of the disease.

Congenital

The diagnosis of congenital hypothyroidism is made if thyroid insufficiency is detected in a newborn immediately after birth. It occurs in fetal development and can be primary, central (secondary, tertiary) and peripheral according to the level of cell damage. Symptoms of the disease can be transient, permanent, and the course of hypothyroidism can be subclinical or manifest, complicated.

Primary

This hypothyroidism is called true or thyrogenic. This means that low levels of thyroid hormones T4 and T3 are associated with pathology of the thyroid gland itself.

Central

The work of secretory cells that produce thyroxine and triiodothyronine is regulated by the pituitary gland using the thyroid-stimulating hormone - TSH. With its insufficient synthesis, the production of T3 and T4 decreases. This type of disease is called pituitary or secondary. Above the pituitary gland in the hormonal “hierarchy” is located. With the help of thyrotropin-releasing hormone, it accelerates the formation of TSH. Hypothalamic failure is called tertiary.

Peripheral

If the hormonal activity of the thyroid gland, pituitary gland and hypothalamus is normal, but tissue receptors lose sensitivity to hormones or their number is much lower than normal, then such hypothyroidism is called peripheral. This also includes a violation of the conversion of thyroxine to triiodothyronine.

Transitory

Caused by the mother's antibodies, which were formed to the thyroid-stimulating hormone of the child's pituitary gland. Its duration is usually 1-3 weeks. The second development option is transition to a permanent form. In this case, periods of improvement alternate with an increase in symptoms, which requires lifelong use of hormones in tablets.

Subclinical

Develops with elevated TSH and normal thyroxine formation. Not accompanied by clinical manifestations or few of them. Such latent (hidden) hypothyroidism usually has nonspecific symptoms.

manifest

A pronounced lack of hormones. Thyroid-stimulating hormone is higher than normal, and the thyroid gland produces little thyroxine. Causes a complete, detailed picture of hypothyroidism, and with a severe T 4 deficiency – complications. These may include circulatory failure, mental retardation,.

Causes of hypothyroidism before one year of age

In most newborns (up to 90% of all cases of disease) the primary form occurs. It can be called:

• defects in organ development - displacement behind the sternum, under the tongue, insufficient formation (hypoplasia), less often, complete absence of the thyroid gland;
• infections acquired in utero;
• autoimmune lesions;
• the use of medications by a pregnant woman that impair development (cytostatics, lithium salts, bromine, tranquilizers);
• exposure to chemicals;
• radioactive exposure;
• iodine deficiency in the mother's diet, endemic goiter;
• gene mutations (usually combined with heart defects and skeletal structure);
• disruption of hormone formation due to a defect in the absorption of iodine by the thyroid gland;
• hereditary developmental anomaly - Pendred syndrome (deafness and enlargement of the thyroid gland).

Central forms of hypothyroidism (secondary and tertiary) appear with brain pathology - cysts, developmental defects, benign or malignant neoplasms, trauma during childbirth, suffocation due to entanglement of the umbilical cord.

The peripheral form occurs when the formation of receptor proteins that are located on cell membranes and connect to thyroid hormones is disrupted. The reason for this is a genetic defect that is inherited, and the consequence is the formation of resistance to hormones (resistance syndrome). In this case, the hormonal levels in the blood are normal or even slightly elevated, but the cells do not respond to T3 and T4.

The causes of acquired hypothyroidism in children can be:

• brain tumors;
• skull injuries, surgeries;
• lack of iodine in food and water (endemic iodine deficiency).

Symptoms of hypothyroidism

All manifestations of thyroid deficiency can be divided into initial (nonspecific) and consequences in the form of delayed psychomotor development, which become noticeable over time.

First signs in children

Recognizing hypothyroidism in a newborn baby can be quite difficult. Primary signs are not specific and are found in pathologies of internal organs and other developmental anomalies. Indirect symptoms may include:

• post-term pregnancy (40-42 weeks);
• large fruit (from 3.5 kg);
• enlarged tongue;
• swelling on the face, especially in the eyelid area;
• swelling of the fingers and toes;
• labored breathing;
• low timbre of crying (rough voice);
• umbilical hernia, slow healing of the umbilical wound;
• prolonged jaundice of newborns;
• rapid fatigue when feeding;
• the appearance of cyanosis and breathing problems when sucking.

If the child is breastfed, clinical symptoms may subside. But such children often lag behind the age norm in weight gain and have problems digesting food - bloating, constipation, poor appetite. They have an enlarged fontanel, insufficient fusion of the skull bones, and impaired formation of the hip joints.

Psychomotor development of children

The most severe consequences of hypothyroidism affect the nervous system. From the neonatal period, signs of lag in psychomotor development appear:

• general weakness, lethargy;
• indifference to the environment - the child does not try to make sounds, walk, does not respond to speech addressed to him;
• when hungry or wet diapers, remains motionless for hours;
• movements are poor, lethargy and muscle weakness are noted;
• starts to hold his head up late, rolls over in bed, and does not sit up.

Children with hypothyroidism are prone to frequent colds, their skin is dry, pale and cold, their hair grows poorly, and teeth erupt late. The face is swollen, puffy, the eyes are widely spaced, the bridge of the nose is widened and flattened, and the lips are thickened.

If congenital hypothyroidism progresses, then dementia (cretinism) develops, the psyche, hearing and speech are impaired. Such symptoms can be visible already from the second half of the year with a sharp deficiency of hormones. Less severe cases are hidden and are discovered only by the age of 5-6 years or even during puberty.

Acquired forms of the disease, especially after 2 years of age, are less dangerous. Mental development does not suffer with them. Possible obesity, stunted growth, delayed puberty, slow thinking, and poor performance at school.

Diagnosis of the condition

Since it is impossible to suspect hypothyroidism based on symptoms, and its consequences are irreversible if detected late, screening (selection test) for hypothyroidism has been carried out since 1995. It involves taking blood for TSH.

For full-term babies, the optimal time is the 5th day after birth, and for premature babies - the second week of life. The upper limit for the indicator is 20 μ/U per ml. If this value is exceeded, thyroxine is determined. If it is below 120 nmol/l, then a diagnosis of congenital hypothyroidism is made and replacement therapy is prescribed. With low TSH and T4, the cause of the disorders is in the brain (pituitary gland or hypothalamus). Ultrasound of the thyroid gland

• administration of radioisotopes with scanning (scintigraphy);
• radiography of skeletal bones (detects a lag in their development from the age norm);
• ECG – low-amplitude waves, bradycardia, wide ventricular complex;
• CT and MRI of the brain in the central form.

Treatment of hypothyroidism

In order to avoid severe mental retardation, treatment of congenital hypothyroidism should be started no later than 10 days after birth. If cretinism develops, then drug therapy does not completely restore brain function, but only slows down the progression of developmental abnormalities.

Most children with congenital and acquired forms of the disease are prescribed levothyroxine (Euthyrox, L-thyroxine) for lifelong use. Start with a minimum dosage - 8 mcg per 1 kg of weight per day. The child requires medical supervision and laboratory diagnostics to correctly select the dose.

If correction of the disease is insufficient, the doctor can increase it to 10-15 mcg/kg. If the pulse increases, sweating, or diarrhea, reduce the dose.

In addition, vitamins, means to improve metabolism in the brain (Nootropil, Encephabol), massage, and physical therapy can be used. In the absence of symptoms and a mild form, observation and the use of potassium iodide for iodine deficiency are indicated.

Watch the video about the treatment of hypothyroidism in children:

Disease prevention

Prevention of congenital hypothyroidism is carried out through group prevention of iodine deficiency in endemic areas (low iodine content in water), as well as identification of individual risk factors when planning pregnancy. The expectant mother is recommended:

• replace table salt with iodized salt (add only to prepared dishes);
• increase the proportion in the diet of foods containing iodine - sea fish, seafood, algae, cod liver, fish oil, seaweed, feijoa, kiwi, apples;
• undergo a blood test for thyroid hormone levels and an examination by an endocrinologist;
• take medications or vitamin complexes with iodine (Vitrum prenatal forte, Multi Tabs intensive, Multimax for pregnant women, Perfectil, Pregnakea) as prescribed by your doctor.

Hypothyroidism in children is most often congenital. It is caused by genetic mutations, iodine deficiency in the mother's diet, infectious and autoimmune processes. At birth, nonspecific manifestations are noted; as they grow older, untreated forms of the disease lead to dementia and deformation of skeletal bones.

To detect hypothyroidism, newborns are screened for thyroid-stimulating hormone. Treatment should be started as early as possible. Children are prescribed lifelong levothyroxine replacement therapy.

Congenital hypothyroidism refers to diseases that have a chronic nature. For those who don’t know, experts associate this type of disease with a dysfunction of the thyroid gland, which affects newborn babies.

Regarding the reasons why this type of disease begins to develop in babies even in the womb, we can say that there are several of them. As a rule, diagnosis of this type of disease is carried out among newborn babies in the maternity hospital around the fourth birthday.

Hypothyroidism in newborns is treated with drugs that replace thyroid hormones. According to medical data, a correct diagnosis and adequate treatment help to avoid irreversible consequences, and the baby develops normally, otherwise everything ends very sadly for both the parents and the child himself.

The frequency of diagnosed cases is approximately two children out of five thousand. It is also interesting that congenital hypothyroidism is most often detected in young women than in boys.

Congenital hypothyroidism in children can occur for many reasons, let’s look at them in more detail:

• Genetic predisposition. Most often, the development of this type of disease is associated with a violation of the correct formation of the gland long before the birth of the child; as a rule, this happens even during the period when the baby is still in the mother’s stomach; various mutations at the gene level may be to blame;
• A disorder that is associated with the normal production of thyroid hormones;
• Damage to the hypothalamus or, as it is also called, secondary hypothyroidism. As a rule, such a lesion is accompanied by various severe disorders in the endocrine system;
• Significant decrease in sensitivity to thyroid hormones. This deviation most often occurs due to the fact that the mother, while still pregnant, used antithyroid drugs. The use of such medications can be prescribed by a doctor and only if the pregnant girl suffers from goiter.

In addition to the above reasons, there are several other factors that can have a negative impact on the unborn baby. First, do not forget about toxic damage. This term refers to the consumption of alcoholic beverages and smoking, which the expectant mother did not give up even during pregnancy. Secondly, radiation also affects the development of the disease.

Well, we should not forget that living in regions where the situation in terms of iodine content in food and water is considered unfavorable, also has a detrimental effect on the health of not only the mother, but also the baby.

Unfortunately, it is almost impossible to avoid the last point, therefore, while carrying a child, the expectant mother should devote as much time as possible to her health and do not forget to visit an endocrinologist.

Main symptoms

Most often, congenital hypothyroidism passes without any visible symptoms and does not manifest itself in any way, especially in the first weeks of the baby’s life. The first signs indicating the development of the disease become noticeable after about a few months, usually at this time both doctors and parents begin to notice that their child is significantly behind in development from his peers. According to statistics, only in a small number of babies the first symptoms become visible in the first weeks of life.

So, typical symptoms of the disease:

• Post-term pregnancy that lasts more than forty weeks;
• At birth, the baby weighs more than 3500 grams;
• Swelling of the face;
• A large tongue causes the baby to constantly have a half-open mouth;
• Rough and hoarse voice when crying;
• Protracted jaundice.

These symptoms indicate congenital hypothyroidism in recently born babies, which is detected almost immediately after birth. It should be noted that the first signs indicating the development of the disease in children in the fourth month of life differ from those found in newborns.

Firstly, such children’s appetite decreases. Secondly, parents notice that their baby suffers from constipation. Thirdly, the child’s skin begins to peel off greatly. Fourthly, body temperature decreases and, as a rule, stops at a level below normal.

And lastly, newly grown hair becomes brittle and thin. Despite all modern technologies, it is quite difficult to detect congenital hypothyroidism in children after a few days of life. Today, almost every child receives exactly the treatment that will help him in his full development, as a result of which he will grow up and enjoy life just like all his peers.

Necessary treatment

As mentioned earlier, if the disease is detected in a timely manner and the correct treatment is prescribed, congenital hypothyroidism can be corrected quite well. Please note that if for any reason the disease is diagnosed later than the first three weeks of life, the child will suffer irreversible brain damage.

At the moment when the child already has visible symptoms indicating illness, it is no longer possible to restore normal brain function, as a result of which the child becomes disabled. But children whose congenital hypothyroidism was detected at an early stage continue to grow and develop as their peers should.

Of course, there can be no talk of any independent treatment; in this case, therapy should be carried out only under the supervision of the attending physician. Only the doctor chooses the dosage necessary for the baby and strictly monitors his condition using a blood test. As a rule, before prescribing any medication to a child, the doctor tells the parents in detail about it, who in the future must strictly adhere to all recommendations received.

There is no need to panic; with the right course of treatment, congenital hypothyroidism will not bother your child in any way, and he will continue to develop as a completely normal and healthy boy or girl. The most important task facing the parents of such a child is to provide him with the most correct treatment, because this is what his further development will depend on.

Now you know the main reasons for the development of this disease. When you are pregnant, try to take extra care of yourself whenever possible. Many expectant mothers are able to avoid most of the reasons why their baby may have health problems after birth. Don’t abuse bad habits; it’s better to spend more time walking in the fresh air and eating right.