Iodine deficiency states in children: clinical guidelines. Iodine deficiency diseases in children and adolescents. Iodine preparations for iodine deficiency diseases

Worldwide. Russia belongs to the countries with mild iodine deficiency. The most difficult situation is observed in the countries of Africa and Central Asia.

Iodine deficiency in water, soil and food often leads to the development of iodine deficiency conditions, of which the most common is endemic goiter. Its prevalence among the population fluctuates around 15-40%. The article will tell all the information about iodine deficiency states - description, symptoms, treatment of diseases, their prevention.

Why do you need iodine

Iodine is an essential trace element required by the human body for adequate functioning and vital activity. It is the only one that is part of the thyroid hormones and is directly involved in their synthesis.

The thyroid gland plays a special regulatory role in the human body. Its hormones contribute to the normal growth and development of a person, the proper differentiation of tissues, regulate various chemical reactions of the body, the exchange of energy, vitamins, fats, and proteins. And iodine is involved in all these processes.

Unfortunately, our country belongs to the regions with iodine deficiency. Since Russia has a large territory, the regions also have varying degrees of iodine deficiency. The mountainous regions - the North Caucasus, the Far East, Altai, the Siberian plateau - suffer the most. The regions with a mild degree of deficiency include Moscow and the Moscow Region.

In connection with the urgency of the problem, it is very important to know the causes and signs of iodine deficiency diseases. The main etiological factor in the development of this group of pathologies is considered to be its low concentration in local water bodies, soil and, as a result, insufficient consumption of the trace element with food.

A bit of history

For the first time, our country, still in the form of the young Soviet Union, joined the program for monitoring iodine deficiency conditions at the beginning of the 20th century. In 1927, the first studies in the regions began, according to the results of which the regions with the highest deficit began to receive. Quite quickly, the situation was corrected. In addition, methods of insufficiency have been developed, including in children.

It looks like the problem has been resolved. However, the world began to consider iodine deficiency from a different angle - the amount of the trace element was assessed not in soil or water, as before, but in human urine.

Since then, scientists have discovered that there is also a mild deficiency that can lead to a decrease in mental (cognitive) abilities, as well as various forms of behavioral disorders in old age. Gradually, our country somewhat lagged behind Europe in the prevention of diseases associated with iodine deficiency.

Types of iodine deficiency states

First of all, iodine deficiency is classified according to the degree of its deficiency in the body. This indicator is determined by the amount of trace element in the patient's urine. Separate degrees:

• Light - the amount of iodine in the urine - from 50 to 99 mcg / l.
• Average - from 20 to 49.
• Severe - less than 20.

In iodine deficiency states, an enlargement of the thyroid gland often occurs. To determine its degree, the gland is palpated along the anterior surface of the neck. Allocate:

• zero degree - not enlarged and not palpable;
• 1st degree - palpated and increased to 2 cm;
• 2nd degree - an enlarged thyroid gland is visible when the head is tilted back, the isthmus and its lobes are palpated;
• 3rd degree - goiter.

The spectrum of iodine deficiency states is quite large and is not limited to thyroid diseases. Different age groups have different manifestations of iodine deficiency. In the prenatal period, conditions that can be associated with iodine deficiency include abortion, stillbirth, congenital anomalies, neurological and mexedematous cretinism, and psychomotor disorders.

In newborns, this is neonatal hypothyroidism. In children and adolescents - backwardness in mental and physical development. In adults - goiter with its complications and iodine-induced thyrotoxicosis.

After a full examination and examination, it is important to make the correct diagnosis. In medicine, the entire nomenclature for diseases is presented in the international classification of diseases - ICD-10. Iodine deficiency states are described under the code E00-E02. These include:

• diffuse, nodular endemic goiter;
• subclinical hypothyroidism due to iodine deficiency;
• syndrome of congenital iodine deficiency (neurological, mexedematous and mixed form).

Pregnancy

Pregnant women constitute a special group of health monitoring. Their condition and health is closely monitored throughout the entire 9 months. Gynecologists try to minimize the risks of developing congenital anomalies in a child.

Outside of pregnancy, for normal life, a woman needs from 100 to 150 micrograms of iodine per day, and when carrying a baby, the need for this trace element increases to 250 micrograms. In such an important period of life, the expectant mother takes care of not only herself. Her thyroid gland increases by 16%, but this is not due to increased production of hormones, but to increased blood supply to the organ. A woman is very susceptible to the occurrence of iodine deficiency during pregnancy.

The microelement plays a crucial role in maintaining pregnancy in the early stages. Thanks to him, the ratio of the luteinizing and follicle-stimulating functions of the pituitary gland changes in favor of the first. Thus, the development of the corpus luteum of pregnancy in the ovary is stimulated, which prevents miscarriage.

With iodine deficiency, there is a high probability of not only premature termination of pregnancy, but also stillbirth. There are also frequent cases of the development of various developmental anomalies, such as endemic cretinism (a pronounced form of mental and physical retardation), neonatal goiter and others.

The trace element plays an important role in the development of bone and cartilage tissue, the formation of the lungs and kidneys, the central nervous system, and the development of intelligence. With an insufficient amount of thyroid hormones, the weight of the fetal brain decreases.

The process of formation of red blood cells - erythropoiesis - is also under the control of the thyroid gland. Due to the sufficient presence of iodine in the body, the absorption of iron in the gastrointestinal tract and the synthesis of transferrin, the protein responsible for its transportation to the hematopoietic organs, increase.

In the fetus, the first rudiments of the gland are formed at the 3-4th week. On the 8th it starts to function. From the 12th week, the first hormones are already formed. Since that time, the ratio of maternal and own hormones is 50/50% and practically remains the same until the end.

As you can see, good nutrition and prevention of iodine deficiency diseases of the thyroid gland during pregnancy can significantly reduce the risks of conditions that threaten the life and health of the unborn baby.

In children

In Russia, goiter is already detected in 20-40% of the child population. While in the absence of iodine deficiency, the disease occurs only in 5% of children. With age, the risk of developing diseases caused by iodine deficiency only increases. So in children under 1 year old, the risk is about 2%, in adolescents it rises to 30-50%.

Insufficiency of iodine intake with food contributes to a decrease in neuropsychic, mental development, impaired cognitive functions, puberty, and the development of speech and hearing is reduced. Doctors noted a 2-fold increase in mental retardation in iodine-deficient areas. A 15% decrease in school performance was also found there.

In the course of research, iodine deficiency conditions in children clearly correlate with an increase in the incidence of infectious, cardiovascular diseases, gastrointestinal diseases, and allergic rhinitis. The listed pathologies occur 2 times more often with a lack of this most important trace element. Curvature of the spine is found 4 times more often than in children without goiter.

Children, of course, are extremely susceptible to the development of diseases. Constant growth and development, accelerated metabolism require a huge amount of resources. Including iodine. Diagnosis of iodine deficiency states in children is carried out by the same methods as in adults.

Symptoms

With moderate iodine deficiency, people experience difficulties in solving logical problems, there is a decrease in cognitive functions: memory worsens, working capacity decreases, attention is scattered. Such symptoms of iodine deficiency conditions are especially noticeable in children. In addition, patients often complain of apathy, spleen, constant fatigue, sleep disturbances, a feeling of constant lack of sleep, and headaches.

Since thyroid hormones primarily regulate metabolism, when they are deficient, it slows down, which leads to weight gain, despite the diet. Dry skin, brittle nails and hair are common. It is possible to increase blood pressure, cholesterol levels in the blood. In women, in most cases, menstrual irregularities and infertility are observed.

Due to iodine deficiency, the synthesis of thyroid hormones decreases, the body lacks them for normal functioning. Therefore, to compensate, an increase in the gland occurs - it develops, which contributes to the normalization of the level of thyroid hormones. The only symptoms of this disease may be signs of compression of the organs in the neck, for example, a violation of the act of swallowing, a feeling of a lump in the throat. There is also an increase in the thyroid gland, which can create discomfort due to appearance.

Diagnostics

Any examination consists of successive stages: questioning, examination, palpation, laboratory and instrumental examinations. The survey is conducted to determine the symptoms of iodine deficiency diseases of the thyroid gland. It is the basis of all diagnostics. Knowing the symptoms that torment the patient, the doctor narrows the circle of possible pathology.

The next step is inspection. If you suspect a deficiency of iodine or thyroid hormones, first of all, they examine the neck area for a visible increase in the organ, then look for additional signs: they determine the condition of the hair, nails, skin, and visible mucous membranes. Then proceed to palpation of the thyroid gland. The specialist carefully probes the isthmus, both lobes, evaluates their structure and density. Thus, it is possible to identify small nodules in the thickness of the tissue.

For laboratory diagnosis, an indicator of TSH (thyroid-stimulating hormone) is used. According to the mechanism of negative feedback, it can increase with a reduced content of thyroid hormones or decrease with their increase. If TSH is in normal values, then free T4 and T3 fractions become the main thing in making a diagnosis. Their decrease indicates hypothyroidism. Low levels of TSH are combined with a high level of thyroid hormones in the blood and indicate hyperthyroidism, which is also possible with the formation of goiter.

In addition to laboratory tests, the doctor without fail prescribes an ultrasound of the thyroid gland. This examination method allows you to assess the structure of tissue, nodes, their size, the presence of increased blood flow in the organ. But unfortunately, ultrasound is not able to determine the possible malignancy of formations.

For this, a fine-needle aspiration puncture biopsy is used. This is a piercing with a needle of the thyroid gland, followed by taking a tissue sample. The procedure is carried out under the control of ultrasound, because it is very important to get into the focus of the altered tissue. Then the biopsy is examined under a microscope and a conclusion is issued about the malignancy or benign formation.

Another research method is scintigraphy. It shows the intensity of hormone formation in the thyroid gland and has clear indications:

• node of average size in hyperthyroidism;
• a large nodule the size of half a lobe or more (blood tests in this case do not matter);
• incorrect location of the thyroid gland or its tissue.

The procedure involves the introduction of radioisotope iodine, which accumulates in the thyroid gland. During certain periods of time, images of the organ are taken, which are then studied. The doctor makes a conclusion about the presence of so-called hot nodes that accumulate the isotope, and cold nodes - without it.

Treatment

With endemic goiter of the 1st degree, only iodine preparations are prescribed. At the 2nd degree, there are 3 treatment regimens. The doctor can prescribe only iodine preparations. If they do not help, then L-thyroxine is prescribed instead of the previous medication or together with it as replacement therapy. The described schemes should reduce the size of the thyroid gland. In this case, the patient continues to take only iodine preparations.

Conservative or drug therapy is effective only in the case of a diffuse or mixed form of the disease. Therapy or L-thyroxine, as a rule, does not give an effect.

There is also a surgical method of treatment that can be used in case of failure of drug therapy. It is also chosen for suspected malignant degeneration of the goiter, in the presence of symptoms of compression of neighboring organs, with the rapid growth of the goiter. After the operation, the person is put on lifelong hormone replacement therapy.

It should be noted that the treatment of iodine deficiency conditions in children obtained in the prenatal period is not carried out. Such consequences of iodine deficiency are irreversible.

Condition Prevention

Conditions caused by a lack of iodine intake in the human body are the second most common among endocrine diseases after diabetes mellitus. However, unlike it, a micronutrient deficiency is much easier to prevent.

Prevention of iodine deficiency states can be mass, group or individual. Mass is carried out by adding iodine to various foods: bread, eggs, salt. Some countries even add the trace element to farm animal feed.

The population most vulnerable to such conditions are pregnant and lactating women, children and adolescents. It is in relation to them that measures are primarily aimed at preventing diseases caused by a lack of the most important microelement. This is group prevention.

Individual conducts for himself each person independently. If he understands the importance of iodine, knows what its deficiency leads to, and takes care of his health, then he makes the right decision to introduce the necessary foods into his diet.

It is possible to fill the deficiency not only with the help of products with the artificial introduction of iodine into their composition, but also by eating food that is initially rich in it. This is primarily marine products: shrimp, crabs, squid, fish, sea kale.

It is easy to trace a small pattern. In countries where the food culture is centered around seafood, such as Greece, Italy, Japan, there are very few iodine deficiency conditions among the population. And in most of the territory of our country, due to the lack of full access to the above provisions, almost everywhere there are increased rates of iodine deficiency. Therefore, in Russia, iodine deficiency diseases are the second most common among endocrine pathologies.

But the easiest way to prevent is to replace regular table salt with iodized salt. This method is considered the cheapest and most affordable for our country.

MINISTRY OF HEALTH OF THE REPUBLIC OF BELARUS

BELARUSIAN STATE MEDICAL UNIVERSITY

1st DEPARTMENT OF CHILDREN'S DISEASES

A. V. Solntseva, N. I. Yakimovich

IODINE DEFICIENCY IN CHILDREN

Teaching aid

Minsk BSMU 2008

UDC 616.441–002–053.2 (075.8) LBC 57.33 i 73

Approved by the Scientific and Methodological Council of the University as a teaching aid on June 25, 2008, Protocol No. 10

Reviewers: Ph.D. honey. Sciences, Assoc. 1st department internal diseases of the Belarusian State Medical University ZV Zabarovskaya; cand. honey. Sciences, Assoc. 1st department internal diseases of the Belarusian State Medical University A. P. Shepelkevich

Solntseva, A. V.

From 60 Iodine deficiency states in children: textbook.-method. allowance / A. V. Solntseva, N. I. Yakimovich. - Minsk: BSMU, 2008. - 28 p.

ISBN 978-985-462-872-1.

Modern aspects of etiopathogenesis, classification, clinical manifestations, diagnosis, prevention and treatment of iodine deficiency diseases in children of different ages are summarized.

It is intended for students of pediatric and medical faculties, trainee doctors.

List of abbreviations

WHO - World Health Organization IDD - iodine deficiency IDD - iodine deficiency diseases

FAB - fine needle aspiration biopsy TRH - thyrotropin-releasing hormone TSH - thyroxin-binding globulin TSH - thyroid stimulating hormone T3 - triiodothyronine T4 - thyroxine

st3 - free triiodothyronine st4 - free thyroxine Ultrasound - ultrasound examination of the thyroid gland - thyroid gland

Introduction

Chronic iodine deficiency and related diseases determine a wide range of medical and social problems due to their high prevalence and serious clinical complications. According to the World Health Organization, more than a third of the inhabitants of the Earth are deficient in iodine, 740 million people have an enlarged thyroid gland (endemic goiter), 43 million suffer from mental retardation, which has developed as a result of a lack of this trace element.

In the practice of a pediatrician, the main problem of ID is not the obvious manifestation of the latter (an increase in the size / volume of the thyroid gland), but the negative impact of iodine deficiency on the developing brain of the fetus and newborn and the subsequent intellectual development of the child.

Against the background of chronic iodine deficiency, endemic goiter and neonatal hypothyroidism, the maturation and differentiation of the child's brain are disrupted with the manifestation of various pathological conditions: from a mild decrease in intelligence to severe forms of myxedematous and neurological cretinism. Studies have shown that in children born under conditions of ID, the IQ is 10–15 points lower than that of their peers from iodine-provided areas.

ID also causes disruption of puberty and reproductive function, the formation of congenital developmental anomalies, and an increase in perinatal and infant mortality.

For Belarus, the problem of iodine deficiency is extremely relevant. According to the results of a large-scale study (A. N. Arinchin et al., 2000), conducted jointly with WHO and the International Council for the Control of Iodine Deficiency Diseases, Belarus is classified as a country with mild and moderate natural iodine deficiency (median iodine 12,000 examined children in the country was 44.5 mcg; the constant consumption of iodized salt ranged from 35.4 to 48.1%). The results obtained formed the basis for the development of a state strategy for the elimination of ID in our country, which is currently ongoing.

The physiological role of iodine in the child's body

Iodine is one of the vital trace elements. Being a structural component of thyroid hormones, it is involved in almost all metabolic processes of the human body. This trace element is part of many natural organic compounds or is present in inorganic salts in the form of iodide anion.

Iodine enters the body in inorganic and organic forms (Fig. 1). It is completely absorbed in the small intestine (100% bioavailability). In the gastrointestinal tract, the organic "carrier" of the trace element is hydrolyzed, and iodide enters the bloodstream. Iodine circulates in the blood as iodide or in a protein-bound state. The concentration of the trace element in the blood plasma with adequate intake is 10–15 µg/L. From the blood, it easily penetrates into various tissues and organs. A significant part of the absorbed iodine (up to 17% of the administered amount) is selectively absorbed by the thyroid gland. Partially, iodine accumulates in the organs that excrete it from the body: in the kidneys, salivary and mammary glands, and the gastric mucosa.

Rice. one . The exchange of iodine in a healthy person when receiving 150 mcg per day

Two-thirds of the incoming trace element is excreted in the urine (up to 70% of the administered amount), feces, saliva, and sweat.

Iodine, which enters the body through the gastrointestinal tract, makes up a large part of the extracellular pool. An additional pool of inorganic extracellular iodine is formed as a result of deiodination of thyroid hormones in tissues and the thyroid gland and during the release of iodine by thyrocytes. The total extracellular pool of iodine is about 250 mcg.

The main depot of the trace element is the thyroid gland. After entering the blood, inorganic iodine is actively absorbed by the thyroid against a concentration gradient under the action of iodide/sodium symporter and ATP. The transport of iodine in iron is regulated by the body's need for this trace element.

Secretion and metabolism of thyroid hormones

The thyroid gland secretes 90–110 μg T4 and 5–10 μg T3 per day. The following phases of thyroid hormone biosynthesis are distinguished:

– the first is the retention of iodides in the basement membrane of thyrocytes through active transport with the participation of iodide / sodium symporter

and ATP (iodine mechanism);

– the second is the oxidation of iodide to molecular iodine under the action of the enzyme peroxidase and hydrogen peroxide;

– the third is the organization of iodine (iodination of tyrosine residues in thyroglobulin). Iodine in molecular form is highly active and quickly binds to the tyrosine amino acid molecule embedded in thyroglobulin. Depending on the quantitative ratio between iodine

and Free tyrosyl radicals bind one or two iodine atoms to one tyrosine molecule. Monoiodotyrosine or diiodotyrosine is formed;

– the fourth is condensation. At the stage of oxidative condensation, the main product T4 is formed from two diiodotyrosine molecules, and T3 is formed from monoiodotyrosine and diiodotyrosine. In the blood and various body fluids, under the action of deiodinase enzymes, T4 is converted to more active T3. Approximately 80% of the total amount of T3 is formed as a result of T4 deiodination in peripheral tissues (mainly in the liver and kidneys), 20% is secreted by the thyroid gland. The hormonal activity of T3 is 3 times higher than that of T4. Deiodination of T4 at position 5" - increases biological efficiency, deiodination at position 3" - cancels biological activity. Biologically active are only L-isomers of thyroid hormones.

An alternative pathway of T4 metabolism is the formation of a positional T3 isomer - reverse T3. The latter does not have hormonal activity and does not inhibit the secretion of TSH. The total daily production of reverse T3 is 30 mcg. With all violations of the formation of T3 from T4, the content of reverse T3 in serum increases.

Free and bound thyroid hormones. Thyroid mountains

Monas are present in the blood serum in free and bound forms. Only free T3 and T4 have hormonal activity. The content of free fractions is respectively 0.03 and 0.3% of their total serum concentration.

The predominant amount of T3 and T4 is associated with transport proteins, primarily with thyroxin-binding globulin (75% of bound T4 and more than 80% of bound T3). Other proteins - transthyretin (thyroxine-binding prealbumin) and albumin bind approximately 15 and 10% of T4, respectively.

Changes in the concentrations of binding proteins affect the levels of thyroid hormones. With an increase in TSH values, serum indicators of the general forms of T4 and T3 increase, and with its deficiency, they decrease.

There is a dynamic balance between the content of total and free fractions of thyroid hormones. Increasing the concentration of TSH initially leads to a short-term decrease in fT4 and fT3. The secretion of T3 and T4 is increased compensatory. The total content of thyroid hormones in serum rises until normal levels of fT4 and fT3 are restored. In this way, serum free T3 and T4 levels do not change, therefore, the intensity of the processes regulated by them in target tissues is also preserved. Factors affecting the concentration of TSH are given in table. one.

Table 1

Factors affecting the content of thyroxine-binding globulin

Fluctuations in the concentrations of transthyretin or albumin change the levels of thyroid hormones less due to a lower affinity for these proteins than for TSH.

Hypothalamic-pituitary-thyroid system. The main stimulus

The source of T4 and T3 production is TSH. In turn, TSH secretion is controlled by the mechanisms shown in Fig. 2.

The peptide hormone thyroliberin (TRH) is produced in the nuclei of the hypothalamus and enters the portal system of the pituitary gland. TRH and TSH secretion is regulated by a negative feedback mechanism and is closely related to T3 and T4 levels. Thyroid hormones directly inhibit TSH production in a negative feedback manner by acting on the thyroid-stimulating cells of the adenohypophysis. In addition to TRH and thyroid hormones, other factors (estrogens, glucocorticoids, growth hormone, somatostatin) directly or indirectly affect TSH secretion, but their role is not so significant.

- thyroid pathology, which develops as a result of a lack of iodine in the body. Signs of iodine deficiency can be an increase in the size of the thyroid gland, dysphagia, memory impairment, weakness, chronic fatigue, dry skin, brittle nails, weight gain. Iodine deficiency diseases of the thyroid gland are diagnosed by an endocrinologist based on laboratory data (TSH levels and thyroid hormones), ultrasound of the thyroid gland, fine needle biopsy. Therapy for iodine deficiency diseases may include potassium iodide monotherapy, the appointment of L-thyroxine, or combined treatment (L-thyroxine + iodine preparations).

General information

Iodine deficiency diseases of the thyroid gland include a number of pathological conditions caused by a lack of iodine in the body, the occurrence and development of which can be prevented by sufficient consumption of this trace element. Iodine deficiency diseases include not only the pathology of the thyroid gland, but also conditions caused by a deficiency of thyroid hormones.

Iodine is an essential trace element for the functioning of the body. The body of a healthy person contains 15-20 mg of iodine, 70-80% of which accumulates in the thyroid gland and serves as a necessary component for the synthesis of thyroid hormones, consisting of 2/3 of iodine: triiodothyronine (T3) and thyroxine (T4). The need for a daily norm of iodine is from 100 to 200 micrograms, and a person consumes 1 teaspoon of iodine (3-5 g) in his life. Periods of increased need for iodine for the body are puberty, pregnancy and breastfeeding.

Iodine deficiency in the environment (in soil, water, food) and, consequently, insufficient natural intake of it into the body causes a complex chain of compensatory processes designed to support the normal synthesis and secretion of thyroid hormones. Persistent and prolonged lack of iodine is manifested by the occurrence of a number of iodine deficiency diseases of the thyroid gland (diffuse and nodular goiter, hypothyroidism), miscarriage, perinatal mortality, physical and mental retardation of children, and endemic cretinism.

Types of iodine deficiency

Most often, iodine deficiency in the body is manifested by the development of diffuse euthyroid goiter - a uniform increase (hyperplasia) of the thyroid gland. Diffuse goiter occurs as a compensatory mechanism that ensures sufficient synthesis of thyroid hormones in conditions of iodine deficiency.

Diffuse goiter that develops in people living in an area with iodine deficiency is called endemic, and in an area with sufficient iodine content - sporadic. According to WHO criteria, if more than 10% of the region's population suffers from diffuse thyroid hyperplasia, then this region is recognized as endemic for goiter. Much less often, the development of endemic goiter is associated not with iodine deficiency, but with the action of chemical compounds: thiocyanates, flavonoids, etc. To date, endocrinology does not have accurate data on the mechanism of occurrence of sporadic goiter. This question is understudied. It is believed that in most cases sporadic goiter is associated with congenital disorders of the enzymatic systems that synthesize thyroid hormones.

The second most common iodine deficiency disease of the thyroid gland among the adult population is nodular goiter - uneven, nodular hyperplasia of the thyroid gland. In the early stages, nodular goiter does not lead to dysfunction of the thyroid gland, however, when taking iodine preparations, it can cause the development of thyrotoxicosis. The extreme degree of iodine deficiency manifests itself in the form of hypothyroidism, due to a sharp decrease in the level of thyroid hormones in the body.

The most vulnerable category of the population with iodine deficiency are pregnant women and children. Iodine deficiency experienced during pregnancy is especially dangerous, because in this condition, the thyroid glands of the mother and fetus are affected. With iodine deficiency diseases of the thyroid gland in pregnant women, the risk of spontaneous miscarriages, congenital malformations of the fetus increases, and in newborn children - the development of hypothyroidism and mental disability.

In the fetus, the production of its own hormone T4 by the thyroid gland begins at 16-18 weeks. prenatal development, while before this period the development of all systems is carried out through the use of maternal thyroid hormones. Therefore, already in the first trimester, the secretion of T4 in a pregnant woman increases by almost 40%.

With severe iodine deficiency and a decrease in the level of T4 in a woman already at the time of pregnancy, the deficiency of thyroid-stimulating hormones during fetal development is so pronounced that it leads to severe consequences for the child and the occurrence of neurological cretinism - an extreme degree of mental and physical retardation associated with intrauterine iodine deficiency and lack of thyroid hormones.

Mild iodine deficiency, easily compensated in the absence of pregnancy and not leading to a decrease in the level of thyroid hormones, but manifested by a decrease in T4 production during pregnancy, is regarded as a syndrome of relative gestational hypothyroxinemia. Hypothyroxinemia that develops during pregnancy can lead to intellectual disabilities that do not reach a severe degree of oligophrenia.

Classification of iodine deficiency

According to the classification of ICCIDD (International Council on Iodine Deficiency) and WHO, the degree of enlargement of the thyroid gland caused by iodine deficiency is determined by the following dimensions:

• Grade 0 - the thyroid gland is not enlarged and is not normally palpable;
• Grade 1 - the thyroid gland is palpable the size of the first phalanx of the thumb;
• Grade 2 - the thyroid gland is determined by eye when the head is thrown back, the isthmus and lateral lobes of the gland are palpated;
• Grade 3 - euthyroid goiter.

Iodine deficiency experienced by the body is determined by the amount of iodine in the urine and can be:

• light - when the content of iodine in the urine is from 50 to 99 mcg / l;
• moderate - with iodine content in urine from 20-49 mcg / l;
• severe - with the content of iodine in the urine< 20 мкг/л.

Symptoms of thyroid iodine deficiency

Usually diffuse euthyroid goiter develops asymptomatically. Sometimes there are unpleasant sensations in the neck, and with a significant increase in the size of the thyroid gland, symptoms of compression of neighboring structures of the neck are noted: a feeling of "coma in the throat", difficulty swallowing. An increase in the thyroid gland, noticeable to the eye, can create cosmetic inconvenience and become a reason for contacting an endocrinologist.

Neurological cretinism is manifested by severe dementia, speech impairment, strabismus, deafness, gross developmental disorders of the musculoskeletal system, and dysplasia. The growth of patients does not exceed 150 cm, there is a disharmony of physical development: a violation of the proportions of the body, the severity of the deformity of the skull. There are no signs of hypothyroidism. If the patient continues to experience iodine deficiency, then he develops a goiter. The level of thyroid-stimulating hormones during the formation of goiter can remain unchanged (state of euthyroidism) or increased (state of hyperthyroidism), but more often it decreases (state of hypothyroidism).

Even against the background of moderate iodine deficiency, patients experience a decrease in mental abilities by 10-15%: memory worsens (especially visual), auditory perception of information decreases and its processing slows down, absent-mindedness, apathy, weakness, a feeling of chronic lack of sleep, constant headaches. Due to the slowdown in metabolic processes, an increase in body weight occurs, even when dieting. The skin becomes dry, hair and nails become brittle. Arterial hypertension is often observed, an increase in blood cholesterol levels, which increases the risk of developing coronary heart disease and atherosclerosis. The development of biliary dyskinesia and cholelithiasis is characteristic, in women - uterine fibroids, mastopathy, menstrual disorders and infertility.

The consequences of iodine deficiency are due to its severity and the age at which iodine deficiency develops. The most severe consequences are caused by iodine deficiency, which developed in the early stages of the body's formation: from intrauterine to the age of puberty.

Diagnostics

In a patient with iodine deficiency diseases of the thyroid gland, they find out information about the presence of thyroid pathology in close relatives, assess the size of the neck, pay attention to dysphonia (hoarseness), dysphagia (swallowing disorder). When evaluating the patient's complaints, attention is paid to manifestations of hypo- or hyperthyroidism.

During palpation of the thyroid gland, its density, location, and the presence of a nodular formation are taken into account. When a goiter is detected by palpation, an ultrasound of the thyroid gland is performed to determine the degree of hyperplasia. The normal volume of the thyroid gland in men does not exceed 25 ml, and in women 18 ml. According to the indications, a fine-needle biopsy of the thyroid gland is performed.

To assess the functional state of the thyroid gland, the level of TSH is determined. In the presence of diffuse euthyroid goiter, the enlargement of the thyroid gland occurs due to both lobes, and the patient's TSH level is within the normal range. Low levels of TSH (less than 0.5 mU / l) suggest hyperthyroidism and require a study of the blood levels of thyroid hormones (T4 and T3).

Treatment of iodine deficiency diseases of the thyroid gland

Minor hyperplasia of the thyroid gland, found in elderly patients, is not accompanied by functional disorders, usually does not require drug therapy. Active therapy for iodine deficiency diseases of the thyroid gland is indicated for young patients. In an area endemic for iodine deficiency, treatment of a patient begins with the appointment of iodine preparations in doses not exceeding the daily norm, followed by a dynamic assessment of the volume of the thyroid gland. In most cases, within six months, the size of the thyroid gland decreases or returns to normal.

If the desired result is not achieved, treatment is continued with L-thyroxine (levothyroxine), sometimes in combination with potassium iodide. Usually this treatment regimen causes a decrease in the size of the thyroid gland. In the future, monotherapy with potassium iodide preparations continues. Neurological disorders that develop during embryogenesis and lead to neurological cretinism are irreversible and cannot be treated with thyroid hormones.

Forecast and prevention

Acquired iodine deficiency is reversible in most cases. The therapy allows to normalize the volume and function of the thyroid gland. In regions where there is mild iodine deficiency, the development of diffuse euthyroid goiter in patients rarely reaches a significant degree. In a number of patients, nodules may form, leading in the future to functional autonomy of the thyroid gland. Psycho-neurological disorders caused by iodine deficiency are irreversible.

Prevention of iodine deficiency can be carried out by individual, group and mass methods. Individual and group prophylaxis includes the use of potassium iodide preparations in physiological doses, especially during those periods when the need for additional iodine increases (childhood and adolescence, pregnancy, breastfeeding). Mass prevention of iodine deficiency involves the use of iodized table salt.

Foods containing high concentrations of iodine are useful: seaweed, sea fish, seafood, fish oil. Before planning and during pregnancy, a woman needs to determine the thyroid status. To ensure the daily physiological need for iodine for children and adults, as well as for risk groups for the development of iodine deficiency diseases, the World Health Organization in 2001 determined the following norms for the use of iodine:

• infants - (0-23 months) - 50 mcg per day;
• young children (2-6 years old) - 90 mcg per day;
• children of primary and secondary school age (6-11 years old) - 120 mcg per day;
• adolescents and adults (12 years and older) - 150 mcg per day;
• pregnant and lactating women - 200 mcg per day.

Pathology name: Iodine deficiency diseases (IDD)

ICD-10 code: E00. Congenital iodine deficiency syndrome (00.0 - neurological form, 00.1. - myxedematous form, 00.2. - mixed form).

E01. Diseases of the thyroid gland (TG) associated with iodine deficiency and similar conditions [E01.0. - diffuse (endemic) goiter associated with iodine deficiency; E01.1. - multinodular (endemic) goiter associated with iodine deficiency] E02. Subclinical hypothyroidism due to iodine deficiency.

Brief epidemiological data
According to the WHO, about 2 billion inhabitants of the Earth live in conditions of iodine deficiency. Inadequate iodine intake threatens the health of more than 100 million Russians, including posing a threat to the normal physical and mental development of 32.8 million children living in the Russian Federation (Dedov I.I., Melnichenko G.A., Troshina E.A. and others, 2004). Diffuse euthyroid goiter is detected on average in 20% of Russians. The frequency of nodular colloid goiter associated with iodine deficiency in women over 30 years old in the Russian Federation reaches 30%.

Classification
The spectrum of iodine deficiency pathology in the population is very wide and includes (WHO, 2001):

In the prenatal period - intrauterine death (abortions), stillbirths, congenital anomalies, increased perinatal and infant mortality, neurological cretinism (mental retardation, deafness, strabismus), myxedematous cretinism (mental retardation, hypothyroidism, dwarfism), psychomotor disorders;
- in newborns - neonatal hypothyroidism;
- in children and adolescents - disorders of mental and physical development;
- in adults - goiter and its complications, iodine-induced thyrotoxicosis;
- at any age - hypothyroidism, impaired cognitive function, increased absorption of radioactive iodine in nuclear disasters [Dedov I.I., Melnichenko G.A., Fadeev V.V., 2000; Gerasimov G.A. et al., 2002; Melnichenko G.A. et al., 2005].

In this section, we will consider the issues of iodine prophylaxis and management of women with diffuse euthyroid and nodular/multinodular colloid goiter during pregnancy. [Melnichenko G.A., Fadeev V.V., Dedov I.I., 2003].

Diagnostics

Treatment

LITERATURE

1. Algorithms for the prevention and treatment of iodine deficiency diseases [Text] / Ed. G.A. Melnichenko. - M.: [b.i.], 2005. - 48 p.
2. Dedov I.I. Endocrinology [Text] / I.I. Dedov, G.A. Melnichenko, V.V. Fadeev. - M.: Medicine, 2000. - 632 p.
3. Iodine deficiency diseases in Russia. A simple solution to a complex problem [Text] / G.A. Gerasimov [i dr.]. - M.: Adamant, 2002. - 168 p.
4. Clinical guidelines of the Russian Association of Endocrinologists (RAE) for the diagnosis and treatment of nodular goiter [Text] / I.I. Dedov [et al.] // Clinical thyroidology. - 2004. - V.2, No. 4. - S. 47-52.
5. Melnichenko, G.A. Thyroid disease during pregnancy. Diagnosis, treatment, prevention [Text]: a guide for doctors / G.A. Melnichenko, V.V. Fadeev, I.I. Dedov. - M.: MedExpertPress, 2003. - 48s.
6. Prevention and treatment of iodine deficiency diseases in high-risk groups [Text] / I.I. Dedov [and others]. - M.: [b.i.], 2004. - 56 p.
7. Modern concepts of clinical endocrinology [Text]. Abstracts of the Fifth Moscow City Congress of Endocrinologists (March 23-24, 2006) / M .: Geos, 2006. - 134 p.
8. American Association of Clinical Endocrinologists and Assocazione Medici Endocrinologi medical guidelines for clinical practice for the diagnosis and management of thyroid nodules. Endocr Pract., 2006 - V. 12, No. 1. - P. 63-102.