The ICD systems took more than a hundred years ago at the conference in Paris with the possibility of its revision every 10 years. During the existence, the system was revised ten times.

Since 1993, the Ten code has begun to operate, as part of the disease thyroid glandsuch as chronic autimmune thyroiditis. The main purpose of the application of the ICD was the definition of pathologies, analyzing them and comparing the data obtained in different countries World. Also, this classification allows you to select the most effective treatment for pathologies that are part of the code.

All pathology data is formed in such a way as to create a maximum useful database of diseases, useful for epidemiology, practical medicine.

The following groups of pathologies are included in the ICB-10 code:

• diseases weighing epidemic character;
• common diseases;
• diseases grouped by anatomical localizations;
• development pathology;
• different types of herbs.

This code contains more than 20 groups, among them a group IV, which includes diseases. endocrine system and metabolism.

An autoimmune thyroiditis code on the ICD 10 enters a group of thyroid disease. To write pathologies, codes from E00 to E07 are used. The E06 code reflects the pathology of thyroiditis.

This includes the following subsections:

1. Code E06-0. This code indicates the acute course of thyroiditis.
2. E06-1. This includes a subacute thyroidity of the ICD 10.
3. E06-2. Chronic form thyroiditis.
4. An autoimmune thyroiditis ICBCL Classifies as E06-3.
5. E06-4. Thyroiditis caused by medicines.
6. E06-5. Other types of thyroiditis.

Aukimmune thyroiditis is a dangerous genetic disease that is manifested by a decrease in thyroid hormones. There are two types of pathology denoted by one code.

This is chronic autoimmune thyroiditis Hasimoto and Ridel disease. In the last version of the disease, the parenchyma of the thyroid panels is replaced by a connecting cloth.

International code allows you to determine not only the disease, but also to learn about clinical manifestations of pathologies, as well as determine the methods of diagnosis and treatment.

When identifying symptoms of hypothyroidism, Hasimoto's disease should be assumed. To clarify the diagnosis, the blood test is carried out on TSH and T4. If the laboratory diagnosis shows the presence of antibodies to thyroglobulin, it will talk about the autoimmune nature of the disease.

Ultrasound will help clarify the diagnosis. During this survey, the doctor can see hyperheogenic layers, connecting tissue, clusters of lymphoid follicle. For a more accurate diagnosis, a cytological examination should be conducted, since the E06-3 pathology is similar to malignant education.

The treatment of E06-3 assumes a lifelong reception of hormones. In rare cases, operational intervention is shown.

code on the ICD 10 is the name of the disease in the world classification of disease. The ICD is a huge system that is designed to study the disease in detail and track the trend of the incidence of the population. This classification was accepted more than a century ago in Paris, however, it is changed and complemented every 10 years.

The code under the cipher ten appeared in 1993 and described the disease of the thyroid, namely chronic autoimmune thyroiditis. The meaning of the ICD was determined complex pathologies And the diagnosis, which was subsequently compared in many countries of the world. Thanks to this classification, the optimal treatment system for all pathologies was developed. Each is assigned its code on the ICD 10 system.

All information about diseases is chosen in such a way that it can be the most useful database from it. The ICC 10 code contains such pathologies:

• epidemic diseases;
• common diseases;
• diseases associated with anatomical localization;
• development pathology;
• various types of injuries.

The code contains more than twenty groups. An autoimmune thyroiditis is contained in the group of disorders of the thyroid gland and includes such disease ciphers:

• the sharp, which is indicated by the E06.0 code - it is characterized by an abscess of thyroid and shares on purulent and pyrogen. Sometimes other codes are used to it, namely B95, B96, B97;
• the subacute has encryption E06.1 and is divided into thyroidita de cervane, a giant (cellular), granulated and without pus;
• chronic often moves to thyrotoxicosis and is indicated as E06.2;
• an autoimmune, which is divided by 4 subspecies: Hasimoto Hasitoxicosis (also referred to), lymphocyadomatous goiter, lymphocytic thyroiditis, lymphocytic stream;
• medicinal, encrypted as E06.4, but if necessary, other encodings are used;
• ordinary, which includes chronic, ridiculous, fibroids, threatening Ridel and BDU. Code E06.5;
• unclean, under the sector E06.9.

Hasimoto's disease is a pathology that appears in the event of a rapid drop in the level of hormones, which arises due to the reduction of the volume of tissue producing hormones.

Ridel disease, or as it is also called fibroids, is chronic. Its feature is the replacement of parenchyma by another type of fabric (connective).

And if the subspecies of Hasimoto occurs very often, then the subspecies of the ridel, on the contrary, is very rare.

In the first disease, the disease amazes mostly women whose age has passed over the mark of thirty-five. It appears like this: normal tissues of the thyroid gland disintegrate, and in their place there are new ones.

In other words, due to autoimmune aggression, diffuse infiltration of the thyroid gland with lymphocytes with the formation of lymphoid follicles (lymphocytic thyroiditis), destruction of thyarocytes and proliferation of fibrous tissue are destruction.

The transition phase of hyperthyroidism is closely interconnected with not the functionality of healthy cells of the epithelium of the follicle and the person in the blood of the person has long been synthesized hormones. In the future, this leads to the emergence of hypothyroidism.

With the second subspecies, healthy parenchyma changes to the fibrium fabric, which causes compression syndrome. This species is very often interrelated with different species Fibridge, namely, with mediastinal and retroperitonal, which makes it possible to explore it within the framework of the Ormond systematic fibrosis syndrome. There is an opinion that Tareloit Ridel - the outcome of thyroidita Hasimoto.

Hasimoto's disease is divided into two forms of development of pathology - hypertrophic and atrophic. The first form is clear, and the second is hidden.

First of all, you need to examine the hassimoto thyroidite when a woman appears at the age of 35-40 years of symptoms:

• began to fall out hair;
• break nails;
• appear face downhow;
• dry skin.

To do this, you must pass the blood for the analysis T and TSH. And the doctor to the touch determines whether the shares of the thyroid gland are increased and they are asymmetrical or not. When carrying out an ultrasound study, the overall picture of the disease is very similar to DTZ - the fabric has many mess and pseudo-nodes.

If the diagnosis is diagnosed with readel, the thyroid will be very dense and involve neighboring organs into the disease. This disease is difficult to distinguish from thyroid cancer.

With autoimmune, lifelong hormone therapy is assigned thyroid code on the ICD 10. The operation is appointed in some cases (large goiter, malignant tumor).

ICB-10 / E90 Class IV Disease of the Endocrine System, Nutrition Disorders and Missing Disrupts / E00-E07 Thyroid Disease / E06 Thyroiditis

Thareloit Hashimoto.

In 2-4% of patients there is a thyrotoxic form of chronic lymphocytic thyroiditis (hashitoxicosis, Khashimoto).

In some of these patients, an unusually dense goiter and high titers of anti-raciferous autoantibodites are found at the primary examination. For such patients, light or moderate thyrotoxicosis caused by thyroidity autoantiboses is characteristic. It is assumed that the thyrotoxic form of the disease is a combination of chronic lymphocytic thyroiditis and diffuse toxic goiter. In other patients, this group thyrotoxicosis develops against the background of the preceding hypothyroidism. Probably, in such cases, thyrotoxicosis is caused by newly emerging B-lymphocyte clones secreting thyroidity by autoantibodies.

Autoimmune thyroiditis: diagnosis

Laboratory and instrumental research

Approximately 80% of patients with chronic lymphocytic thyroiditis at the time of the diagnosis of the levels of the total T4, the total T3 and TG in serum in serum, but the secretory function of the thyroid gland is reduced. This indicates the strengthening of TSH secretion in a sample with Tyrolyberin (to establish a diagnosis of chronic lymphocytic thyroiditis, this test is optional). More than 85% of patients with chronic lymphocytic thyroiditis are detected by autoantilers to thyreoglobulin, to microsomal antigens and yodidperoxidase. These autoantibodies are found in other diseases of the thyroid gland (for example, in 80% of patients with diffuse toxic goiter), but with chronic lymphocytic thyroidity, their titer is usually higher. A significant increase in the titer of autoantibodies is often found in patients with primary lemphoma of the thyroid gland. It is assumed that the mechanisms of autoimmune reactions in chronic lymphocytic thyroid and in the lymphoma are similar. The growing dense goiter in an elderly patient can be a sign of lymphoma and serves as the basis for the biopsy of the thyroid gland if anti-raciferous autoantibodes were detected.

With thyroid scintigraphy, it is usually detected by its symmetric increase with an uneven distribution of isotope. Sometimes a single cold knot is visualized. Absorption radioactive iodine The thyroid gland can be normal, reduced or elevated. It should be noted that the thyroid scintigraphy and the test with the absorption of radioactive iodine in suspected chronic lymphocytic thyroiditis have a slight diagnostic value. However, the value of the results of these samples increases, if a single node is found in the thyroid gland, or if the increase in the thyroid gland continues, despite treatment with thyroid hormones. In these cases, they conduct a thin game biopsy of the node or an increasing site to eliminate the neoplasm.

Autoimmune thyroiditis: treatment

Prevention

Other

Chronic lymphocytic thyroiditis

Etiology and pathogenesis

Chronic lymphocytic thyroiditis is a human-specific autoimmune disease. It is believed that the cd8-lymphocyte defect (T-suppressors) is believed to be the main cause, as a result of which CD4 lymphocytes (T-helpers) are able to interact with thyroid cell antigens. In patients with chronic lymphocytic thyroiditis, HLA-DR5 is often found, which indicates a genetic predisposition to this disease. Chronic lymphocytic thyroiditis can be combined with other autoimmune diseases (see Table 28.5).

Clinical manifestations

The disease most often detected in middle-aged women with asymptomatic goiter. Women make up about 95% of patients. Clinical manifestations are diverse: from a small goiter without symptoms of hypothyroidism to myxedema. The earliest I. characteristic sign Diseases - an increase in the thyroid gland. Ordinary complaints: sensation of pressure, tension or pain on the front surface of the neck. Sometimes there are lightweight dysphagia or voice hoarseness. The unpleasant sensations on the front surface of the neck can be caused by a rapid increase in the thyroid gland, but more often it increases gradually and asymptomatic. The clinical picture at the time of the inspection is determined by the functional state of the thyroid gland (the presence of hypothyroidism, eutiperosis or thyrotoxicosis). Symptoms of hypothyroidism are manifested only with a significant decrease in the levels of T4 and T3.

Diagnostics

In physical examination, a symmetric, very dense, movable goiter, often uneven or noded consistency is usually detected. Sometimes a single node is palpped in the thyroid gland.

In the elderly patients (the middle age is 60 years old) sometimes the atrophic form of the disease is encountered - primary idiopathic hypothyroidism. In such cases, the goiter is usually absent, and the deficit of thyroid hormones is manifested by lethargy, drowsiness, voice hoarseness, the edema of the face, bradycardia. It is believed that the primary idiopathic hypothyroidism is caused by the thyroid-blocking autoantoants or the destruction of thyrocytes with cytotoxic anti-rapid autoantaites.

1. Nikolai TF, et al. Postpartum Lymphocytic Thyroiditis: Prevalence, Clinical Course, and Long-Term Follow-Up. Arch Intern MED 147: 221, 1987.

2. Nyulassy S, et al. Subacute (DE QUERVAIN) Thyroiditis: Association with HLA-B35 Antigen and Abnormalities of the Compleden System Immunoglobulins and Other Serum Proteins. J Clin Endocrinol Metab 45: 270, 1977.

3. Vargas MT, et al. Antithyroid Microsomal Autoantibodies and HLA-DR5 Are Associated with Postpartum Thyroid Dysfunction: Evidence Supporting An Autoimmune Pathogenesis. J Clin Endocrinol Metab 67: 327, 1988.

4. VOLPE R. IS SILENT THYROIDITIS AN AUTOIMMUNE DISEASE? Arch Intern MED 148: 1907, 1988.

Pathogenesis of autoimmune thyroiditis

The causes of the organospecific autoimmune process under this pathology are to perceive the immune system of the body of the thyroid cell cells as foreign antigens and the production of antibodies against them. Antibodies begin to "work", and T-lymphocytes (which should recognize and destroy alien cells) rushing in the gland tissue, the launching inflammation is thyroiditis. At the same time, the effector T-lymphocytes penetrate into the parenchyma of the thyroid gland and accumulate there, forming lymphocytic (lymphoplasemic) infiltrates. Against this background, the gland fabrics are destructive changes: the integrity of the membranes of follicles and the walls of thyrocytes (follicular cells producing hormones) are disturbed, part of the iron tissue can be replaced by fibrous. Follicular cells, naturally, are destroyed, their number is reduced, and ultimately there is a violation of the functions of the thyroid gland. This leads to hypothyroidism - reduced level thyroid hormones.

But this does not occur immediately, the pathogenesis of autoimmune thyroiditis is distinguished by a long asymptomatic period (eutheroid phase), when the content of thyroid hormones in the blood is within the normal range. Next, the disease begins to progress, causing a shortage of hormones. This responds to the controlling the work of the thyroid gland the pituitary gland and, increasing the synthesis thyreotropic hormone (TG), some time stimulates thyroxine production. Therefore, months and even years can pass, while the pathology will not be explicitly.

The predisposition to autoimmune diseases is determined by the inherited dominant genetic sign. Studies have shown that half of the nearest relatives of patients having autoimmune thyroiditis, antibodies on the tissue of the thyroid gland are also present in serum. To date, scientists bind the development of autoimmune thyroiditis with mutations in two genes - 8Q23-Q24 on chromosome 8 and 2q33 on chromosome 2.

According to endocrinologists, there are immune diseases that cause autoimmune thyroiditis, more precisely, combined with it: type I diabetes, gluten enteropathy (celiac disease), pernicious anemia, rheumatoid arthritis, system red lupus, Addison disease, Vergood disease, bilyary cirrhosis of the liver (primary) , as well as Down syndromes, Sherchezhevsky-Turner and Klinfelter.

In women, autoimmune thyroiditis arises 10 times more often than in men, and usually manifests itself after 40 years (according to The European Society of Endocrinology, the typical age of the disease manifestation is 35-55 years old). Despite the hereditary nature of the disease, the autoimmune thyroiditis is almost never diagnosed in children under 5 years, but already in adolescents is up to 40% of all thyroid pathologies.

08.12.2017

Manifestation of autoimmune thyroiditis

Autoimmune thyroiditis (AIT) is included in the registry international Classification Diseases (ICD 10) as an endocrine pathology of the thyroid gland and has code E06.3. Thareloit Hashimoto, as it is often called this lymphocytic autoimmune disease, refers to chronic pathology inflammatory genes. Often, autoimmune inflammation of the thyroid gland moves into hypothyroidism - a state of particular danger to children.

For the first time, the disease described the Japanese surgeon with the surname of Hashimoto in the early 20th century, and Zob Hashimoto from now on began to have an identical name. What does autoimmune mean? Translated from Latin "Auuto" means "himself." An autoimmune response of the body is due to the aggression of immune cells to its own, in this case, the thymocytes - thyroid cells. The main difference between autoimmune thyroiditis is that inflammatory process It can be launched both in an enlarged and even unchanged gland tissue.

Causes of autoimmune thyroiditis

It has been established that in the development of the disease plays an important role of heredity. But so that the disease manifested itself to fully, should be accompanied by adverse predisposing factors:

• frequent viral diseases: colds, influenza;
• chronic foci of infection in almonds, carious teeth, nasal sinuses;
• stresses.

How autoimmune thyroiditis develops

How manifolds hashimoto

Ait - the disease is slowly progressive and mostly occurring in people a weak half of humanity. His prevalence in children is equal to a little more than 1% per capita. The fact is that on early stages The clinical picture of the disease may not be exercised in any way, but the symptoms are completely absent. Sometimes there are pain when tamping the thyroid gland. Some patients noted the appearance of articular pains, weakness. Often the first sign of the thyroiditis of autoimmune nature is imperceptible to the external increase in the tissue of the thyroid gland.

Depending on the changes occurring in the organs, the thyroiditis may be euthyroid, hyperthyroid or hypothyroid is the most cunning form of the disease. Each state is characterized by appropriate features. In young people with a healthy strong organism and strong immunity, eutheosis can be diagnosed for a long time - the state when the necessary hormones in the blood is necessary and the optimal amount.

The subclinical picture of the AIT can report changes in the function of the gland not only symptoms, but also laboratory results. There is an increase in the level of thyroxine, and the figures of the thyrotropic hormone are reduced. The hormone-dependent form of Aita - pronounced hypothyroidism and this is the worst, since long-term consequences are possible. Why? The fact is that the hypothyroidism at Aite is the inevitable outcome of the disease in most cases. And many patients are afraid of lifelong reception of hormones, as it is single way out The treatment of AIT with hypothyroidism.

An autoimmune thyroiditis in adults may be the beginning of the eye pathology. Almost all patients appear problems with eyes, the so-called endocrine ophthalmopathy, which can be expressed in bright symptoms:

• suffering eye muscles;
• there is redness in the eyes;
• sand feeling;
• two;
• tear;
• fast fatigue eyeballs.

Diagnosis and treatment of Aita

The diagnosis is established in the presence of an elected history and all necessary research activities:

• general inspection and palpation of gland fabrics by a specialist;
• blood test from veins to the level of hormones TSH and T3, T4;
• detection of antibodies to thyroglobulin and at-TPO.

When Aite is important to protect the body from outbreaks of inflammatory reactions and sluggish chronic processes. If the function of the gland is increased, then soothing drugs are shown, reduced stress levels. In most persons suffering from this pathology, the products of thyroid hormones decrease, therefore, with a tendency to hypothyroidism, replacement hormone therapy and drug reception of L-Troyroxine in doses recommended by the doctor are prescribed as the main treatment.

It is resorted to a surgical method with a fairly extensive growing of gland fabric and in cases where it can put pressure on the respiratory center. Reception of iodine-containing products for the prevention and treatment of hypothyroid form Aita is quite acquitted. The disease occurs with an increase in the function of the thyroid gland requires the exclusion of products rich in iodine, since they will contribute to an even greater increase in the number of thyroid hormones.

When maligning (reincarnation of gland fabric), surgical intervention is prescribed. A favorable effect of both the organism in general and the inflamed thyroid houses are grass, the reception of some vitamins and bodies.

Selenium as an important trace element is needed hardware for its proper functioning. The component can reduce autoimmune attacks on this delicate and susceptible organ. With a lack of selenium in the body, thyroid hormones are not able to fully work, although their development continues. However, the reception of selenium is better to combine with iodine preparations in the absence of disorders of the thyroid function.

Based on use useful products. Leading power principles are based on the restriction of products and dishes that provoke or enhance autoimmune reactions. Aite diet is not a significant factor in curing the ailment, but with the corresponding coordinated diet, it may remove the development of hypothyroidism and improve general state. First of all, it is necessary to achieve the harmonization of the hormonal background.

Each form of AIT requires an individual diet for a patient built, taking into account the recommendations of the nutritionist. The state of the eutheroid does not require any dietary instructions, as they are not justified. So, due to the fact that the main metabolic metabolism in hyperthyroidism is increased, high-calorie food is recommended, providing greater energy consumption. The menu should present a sufficient amount of proteins, fats and vitamins. For patients with elevated gland function, dishes and products that are exciting affecting cardiovascular and nervous Systems. This is coffee, energy, strong tea.

For persons with hypothyroidism, on the contrary, it is important to increase the metabolic level. Fat and carbohydrates are limited, and the amount of protein increases slightly. You need to use easily friendly and useful food.

Among the diseases of the endocrine system, chronic inflammation of the thyroid gland - autoimmune thyroiditis - occupies a special place, since it is a consequence of the body's immune reactions against own cells and fabrics. In the IV class of diseases, this pathology (other names - autoimmune chronic thyroiditis, illness or thyroidita hashimoto, lymphocytic or lymphomatous thyroiditis) has a code on the ICD 10 - E06.3.

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Code of the ICD-10

E06.3 autoimmune thyroiditis

Pathogenesis of autoimmune thyroiditis

The causes of the organospecific autoimmune process under this pathology are to perceive the immune system of the body of the thyroid cell cells as foreign antigens and the production of antibodies against them. Antibodies begin to "work", and T-lymphocytes (which should recognize and destroy alien cells) rushing in the gland tissue, the launching inflammation is thyroiditis. At the same time, the effector T-lymphocytes penetrate into the parenchyma of the thyroid gland and accumulate there, forming lymphocytic (lymphoplasemic) infiltrates. Against this background, the gland fabrics are destructive changes: the integrity of the membranes of follicles and the walls of thyrocytes (follicular cells producing hormones) are disturbed, part of the iron tissue can be replaced by fibrous. Follicular cells, naturally, are destroyed, their number is reduced, and ultimately there is a violation of the functions of the thyroid gland. This leads to hypothyroidism - a reduced level of thyroid hormones.

But this does not occur immediately, the pathogenesis of autoimmune thyroiditis is distinguished by a long asymptomatic period (eutheroid phase), when the content of thyroid hormones in the blood is within the normal range. Next, the disease begins to progress, causing a shortage of hormones. This reacts to the supervision of the thyroid gland the pituitary gland and, increasing the synthesis of thyrotropic hormone (TG), stimulates a thyroxine production for a while. Therefore, months and even years can pass, while the pathology will not be explicitly.

The predisposition to autoimmune diseases is determined by the inherited dominant genetic sign. Studies have shown that half of the nearest relatives of patients having autoimmune thyroiditis, antibodies on the tissue of the thyroid gland are also present in serum. To date, scientists bind the development of autoimmune thyroiditis with mutations in two genes - 8Q23-Q24 on chromosome 8 and 2q33 on chromosome 2.

According to endocrinologists, there are immune diseases that cause autoimmune thyroiditis, more precisely, combined with it: type I diabetes, gluten enteropathy (celiac disease), pernicious anemia, rheumatoid arthritis, system red lupus, Addison disease, Vergood disease, bilyary cirrhosis of the liver (primary) , as well as Down syndromes, Sherchezhevsky-Turner and Klinfelter.

In women, autoimmune thyroiditis arises 10 times more often than in men, and usually manifests itself after 40 years (according to The European Society of Endocrinology, the typical age of the disease manifestation is 35-55 years old). Despite the hereditary nature of the disease, the autoimmune thyroiditis is almost never diagnosed in children under 5 years, but already in adolescents is up to 40% of all thyroid pathologies.

Symptoms of autoimmune thyroiditis

Depending on the level of thyroid hormone deficit, which regulate in the body protein, lipid and carbohydrate exchange, work cardiovascular system, gastrointestinal tract and CNS, symptoms of autoimmune thyroiditis can vary.

At the same time, some people do not feel any signs of the disease, while others have different combinations of symptoms.

For hypothyroidism, in autoimmune, tireoids are characterized by such signs as: fatigue, lethargy and drowsiness; difficulty breathing; hypersensitivity to cold; Pale dry skin; thinning and loss of hair; Nail fragility; Face-faced; hoarseness; constipation; Dustless weight gain; pain in the muscles and stiffness of the joints; Menorragia (in women), depressive state. The goiter can also be formed - swelling in the field of thyroid gland on the front of the neck.

In case of Hashimoto disease, there may be complications: a big goiter makes it difficult to swallowing or breathing; In the blood, the level of low density cholesterol (LDL) increases; There is a long depression, cognitive abilities and libido are reduced. The most serious consequences of autoimmune thyroiditis caused by the critical lack of thyroid hormones - Myxedema, that is, Mudzine swelling, and its result in the form of a hypothyroid coma.

Diagnosis of autoimmune thyroiditis

Endocrinologist specialists are diagnosed with autoimmune thyroiditis (Hashimoto disease), based on patient complaints, symptoms and blood test results.

First of all, blood tests are needed - on the level of thyroid hormones: triiodothyronine (T3) and thyroxine (T4), as well as a pituitary thyrotropic hormone (TSH).

Also, antibodies are defined at autoimmune thyroid:

• antibodies to thyroglobulin (TGAB) - AT-TG,
• antibodies for thyroid peroxidase (TPOAB) - at-TPO,
• antibodies to the thyrotropic hormone receptors (TRAB) - AT-RTTH.

To visualize pathological changes in the structure of the thyroid gland and its tissues, instrumental diagnosis is carried out under the influence of antibodies - ultrasound or computer. Ultrasound allows you to detect and evaluate the level of these changes: damaged tissues in lymphocytic infiltration will give the so-called diffuse hypo echogenicity.

Aspiration puncture biopsy of the thyroid gland and cytological research Bioptata is carried out in the presence of nodes in the gland - to determine oncological pathologies. In addition, the cytogram of autoimmune thyroiditis helps determine the composition of the cells of the gland and reveal the lymphoid elements in its tissues.

Since in most cases of thyroid pathologies, differential diagnosis is required to distinguish autoimmune thyroidity from a follicular or diffuse endemic goiter, toxic adenoma and several tens of other thyroid pathologies. In addition, hypothyroidism can be a symptom of other diseases, in particular, associated with a violation of the functions of the pituitary gland.

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In principle, this problem of all autoimmune human diseases. And drugs for immune correction, taking into account the genetic nature of the disease, are also powerless.

Cases of spontaneous regression of autoimmune thyroiditis were not fixed, although the size of the goiter over time can significantly decrease. The removal of the thyroid gland is performed only with its hyperplasia that impedes normal breathing, grinding compression, as well as when detecting malignant neoplasms.

The lymphocytic thyroiditis is an autoimmune state and cannot be prevented, therefore, the prevention of this pathology is impossible.

The forecast for those who are correct to their health is on a dispensary accounting with an experienced endocrinologist and fulfills its recommendations positive. And the disease itself, and methods of his treatment still cause many questions, and even the doctor of the highest qualification will not be able to answer the question of how many live with autoimmune thyroiditis.

It's important to know!

Chronic nonspecific thyroidites include autoimmune and fibrous. Fibrous thyroiditis almost does not occur in childhood. Autoimmune thyroiditis - most frequent disease thyroid gland in children and adolescents. The disease is determined by an autoimmune mechanism, but the main immunological defect is unknown.

Chronic autoimmune thyroiditis, autoimmune lymphocytic thyroiditis, thyroiditelite Hashimoto, lymphoacedomatous goiter, lymphomatousine.

Version: MedElement disease reference

Aukimmune thyroiditis (E06.3)

Endocrinology

general information

Short description

Autimmune thyroiditis- chronic inflammatory disease of the thyroid gland (thirting) autoimmune genesis, in which, as a result of chronically progressive lymphoid infiltration, there is a gradual destruction of the tissue of the pin, most often leading to the development of primary hypothyroidism Hypothyroidism - thyroid deficiency syndrome characterized by neuropsychiatric disorders, edema of face, limbs and torso, bradycardia
.

The disease was first described in 1912 by the Japanese surgeon, it develops more often in women after 40 years. There is no doubt the genetic conditionality of the disease, implemented when exposed to environmental factors (long-term reception of an excessive amount of iodine, ionizing radiation, the influence of nicotine, interferon). The hereditary genesis of the disease is confirmed by the fact of its association with certain antigens of the HLA system, more often than with HLA DR 3 and DR 5.

Classification

Aukimmune thyroiditis (AIT) is divided into:

1. Hypertrophic AIT(Khashimoto, the classic option) is characterized by an increase in the volume of the thyroid gland, massive lymphoid infiltration with the formation of lymphoid follicles, oxyphyl transformation of thyrocytes, is characterized by the thyroid tissue.

2. Atrophic AIT- It is characterized by a decrease in the volume of the threshold, in the histological picture signs of fibrosis prevail.

Etiology and pathogenesis

An autoimmune thyroiditis (AIT) is developing against the background of a genetically deterministic defect of an immune response, leading to T-lymphocytic aggression against its own tyrocytes, ending with their destruction. The genetic conditionality of development is confirmed by the AIT association with certain antigens of the HLA system, more often than with HLA DR 3 and DR 5.
In 50% of cases, the relatives of patients with Ait detected circulating antibodies to the thyroid gland. In addition, there is a combination of AIT in the same patient or within one family with other autoimmune diseases - type 1 type, vitiligo Vitiligo - idiopathic skin dyschromy, characterized by the appearance of depigmented spots of various sizes and outlines of milk-white color with the surrounding zone of moderate hyperpigmentation
, pernicious anemia, chronic autoimmune hepatitis, rheumatoid arthritis and etc.
The histological picture is characterized by lymphocytic and plasmocyte infiltration, oncocyte transformation of thyrocytes (the formation of Gürtle-Ashkenazi cells), follicle destruction and proliferation Proliferation - an increase in the number of cells of any tissue due to their reproduction
Fibrous (connective) fabric, which replaces the normal imaging structure.

Epidemiology

Women meets 4-6 times more often than men. The ratio of persons aged 40-60 years suffering from autoimmune thyroiditis, between men and women is 10-15: 1.
Among the population of various countries, AIT is found in 0.1-1.2% of cases (in children), children for 3 sick girls account for one boy. Ait is rarely found in children under 4 years of age, the maximum of morbidity falls on the middle of the publity period. 10-25% of practically healthy people with eutheyosis Eutheosis - normal functioning of the thyroid gland, no symptoms of hypo- and hyperthyroidism
Antiteroid antibodies can be detected. The incidence is higher in individuals with HLA DR 3 and DR 5.

Risk factors and groups

At-risk groups:
1. Women over 40 years old, with the hereditary predisposition to the diseases of the thyroid gland or if there are those of the next relatives.
2. Persons with HLA DR 3 and DR 5. Atrophic version of autoimmune thyroiditis is associated with haplotype Haplotype - a set of alleles on the locus of one chromosome ( various forms same gene located in the same sections) commonly inherited together
HLA DR 3, and hypertrophic version with DR 5 HLA systems.

Risk factor:long-term reception of large doses of iodine with sporadic goiter.

Clinical picture

Cymptoms, flow

The disease is developing gradually - for several weeks, months, sometimes years.
The clinical picture depends on the stage of the autoimmune process, the degree of damage to the thyroid gland.

Eutheroid phase Many years or decades may continue, or even throughout life.
Further, as the process is progressing, namely, gradual lymphocytic infiltration of the pin and destruction of its follicular epithelium, the number of cells producing thyroid hormones decreases. Under these conditions, in order to provide the body with a sufficient amount of thyroid hormones, the production of TSH (thyrotropic hormone) is enhanced, which hypersulates the pin. Due to this hyperstimulation for an indefinite time (sometimes tens of years), it is possible to maintain the products of T 4 at a normal level. it Phase of subclinical hypothyroidismwhere there are no obvious clinical manifestations, but the level of TSH is increased with normal values T 4.
With further damage to the pin, the number of functioning thyroidocytes falls below critical level, Concentration T 4 in the blood decreases and manifests hypothyroidism, manifested phase of obvious hypothyroidism.
Quite rare ait can manifest transient thyrotoxic phase (hashi-toxicosis). The cause of hashi-toxicosis can be both the destruction of the threshold and its stimulation due to the transient generation of stimulating antibodies to the TTG receptor. In contrast to thyrotoxicosis during graves (diffuse toxic goiter), Hashi-toxicosis in most cases does not have a pronounced clinical picture of thyrotoxicosis and proceeds as subclinical (reduced TSH at normal values \u200b\u200bof T 3 and T 4).

The main objective feature of the disease is goiter(increase in the thyroid gland). Thus, the main complaints of patients are associated with an increase in the volume of the brief:
- feeling difficulty in swallowing;
- difficulty breathing;
- Often small soreness in the area of \u200b\u200bthe pin.

For hypertophroic formThe brush is visually enlarged, when palpation has a dense, inhomogeneous ("uneven") structure, not fasting with surrounding tissues, painless. Sometimes it may be regarded as a nodal goiter or an eye cancer. The tension and small soreness of the pin may be occurring during a rapid increase in its size.
For atrophic formthe volume of the brush is reduced, during palpation is also determined by heterogeneity, moderate density, with the surrounding tissues of the pin is not fast.

Diagnostics

The diagnostic criteria for autoimmune thyroiditis include:

1. Increasing the level of circulating antibodies to the thyroid gland (antibody to thyroperoxidase (more informative) and antibodies to thyroglobulin).

2. Detection of typical ultrasonic data AIT (diffuse decrease in the echogenicity of the tissue of the pin and an increase in its volume in hypertrophic form, during atrophic form - a decrease in the volume of the thumbnail, usually less than 3 ml, with hypo echogenicity).

3. Primary hypothyroidism (manifest or subclinical).

In the absence of at least one of the listed criteria, the diagnosis of AIT is probabilistic.

The punkey biopsy of the pin to confirm the diagnosis of the AIT is not shown. It is carried out for differential diagnosis with nodal goiter.
After establishing a diagnosis, a further study of the dynamics of the level of circulating antibodies to the chart to assess the development and progression of AIT, has no diagnostic and prognostic value.
In women planning a pregnancy, when the antibodies are detected to the tissue of the pin and / or with ultrasonic signs of AIT, it is necessary to investigate the imaging function (determining the level of TSH and T4 in blood serum) before the conception of conception, as well as in each trimester of pregnancy.

Laboratory diagnostics

1. General analysis Blood: normal or hypochromic anemia.

2. Biochemical analysis Blood: Changes are characteristic of hypothyroidism (increasing the level of total cholesterol, triglycerides, a moderate increase in creatinine, aspartate transaminase).

3. Hormonal research: various options for violation of the chart function are possible:
- increase in TSH level, content T 4 within the norm (subclinical hypothyroidism);
- raising the level of TSH, reduction T 4 (manifestic hypothyroidism);
- Reducing the level of TSH, concentration T 4 within the norm (subclinical thyrotoxicosis).
Without hormonal changes, the imaging function is not permanified.

4. Detection of antibodies to the tissue of the pin: as a rule, an increase in the level of antibodies to thyroperoxidase (TPO) or thyreoglobulin (TG) is noted. The simultaneous rise of the titer of antibodies to TPO and TG indicates the presence or a high risk of autoimmune pathology.

Differential diagnosis

Differential-diagnostic search for autoimmune thyroid should be carried out depending on the functional state of the pin and the characteristics of the goiter.

Hyperthyroid phase (hashi-toxicosis) should be differentiated with diffuse toxic goiter.
In favor of autoimmune thyroiditis, testify:
- the presence of an autoimmune disease (in particular AIT) in close relatives;
- subclinical hyperthyroidism;
- Moderate severity clinical symptoms;
- short period of thyrotoxicosis (less than six months);
- lack of increasing the titer of antibodies to the TSG receptor;
- Characteristic ultrasound painting;
- the rapid achievement of eutheroid when appointing minor doses of thyreostatics.

The euticoid phase should be differentiated with diffuse non-toxic (endemic) goiter (especially in areas with iodine deficiency insufficiency).

The pseudo-node form of autoimmune thyroiditis is differentiated with nodal goiter, thyroid cancer. Penal biopsy in this case is informative. A typical morphological feature for AIT is the local or widespread infiltration lymphocyte lymphocytes (foci of lesion consist of lymphocytes, plasma cells and macrophages, there is a penetration of lymphocytes to the cytoplasm of acinar cells, which is not typical for the normal impact structure), as well as the presence of large Gürtle- oxifices Ashkenazi.

Complications

The only clinically significant problem to which the ait can lead is hypothyroidism.

Treatment abroad

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Treatment

Treats of treatment:
1. Compensation of the function of the thyroid gland (maintaining the concentration of TSH in the range of 0.5 - 1.5 MME / L).
2. Correction of disorders associated with an increase in the volume of the thyroid gland (if available).

Currently, it is recognized in an ineffective and inappropriate use of levothyroxine sodium in the absence of violations of the functional state of the threshold, as well as glucocorticoids, immunosuppressants, plasmafezes / hemosorption, laser therapy in order to correct anti-immediate antibodies.

The dose of Levothyroxine sodium, requiring substitution therapy in hypothyroidism on the background of the AIT, is an average of 1.6 μg / kg body weight per day or 100-150 μg / day. Traditionally, during the selection of individual therapy, L-thyroxine is prescribed, starting with relatively small doses (12.5-25 μg / day), gradually increasing them until the eutheroid state is reached.
Levothyroxin sodium inside in the morning on an empty stomach, for 30 minutes. Before breakfast, 12.5-50 μg / day., with a subsequent increase in the dose of 25-50 μg / day. up to 100-150 μg / day. - life (under the control of the level of TSH).
A year later, an attempt is made to cancel the drug to eliminate the transient nature of violations of the imaging function.
The effectiveness of therapy is evaluated by the level of TSH: when appropriate, the total substitution dosage is in 2-3 months, then 1 time in 6 months, in the future - 1 time per year.

According to the clinical recommendations of the Russian Association of Endocrinologists, the physiological doses of iodine (about 200 μg / day) do not provide negative influence On the imaging function with already existing hypothyroidism caused by AIT. When appointing drugs containing iodine, one should remember possible increase Needs in thyroid hormones.

In the hyperthyroid phase, the AIT should not be prescribed by thyaretics, it is better to do symptomatic therapy (ß-adrenoblays): propronolol inside 20-40 mg 3-4 times a day, until the clinical symptoms are eliminated.

Operational treatment is shown at a significant increase in pin with signs of compression of the surrounding organs and tissues, as well as fast Growth The sizes of the bridge against the background of a long-term moderate increase in the brief.

Forecast

The natural flow of autoimmune thyroid is the development of persistent hypothyroidism, with the appointment of lifelong substitution hormone therapy with Levothyroxin sodium.

The probability of the development of hypothyroidism in a woman with an elevated level of at-TPO and a normal level of TSH is about 2% per year, the likelihood of explicit hypothyroidism in a woman with subclinical hypothyroidism (TTG is raised, t 4 in normal) and increased level AT-TPO is 4.5% per year.

Women carrier at-TPOs without violating the function of the threshold, when pregnancy, the risk of the development of hypothyroidism and the so-called gestational hypothiocynemia increases. In this regard, such women require control of the chart of the pin in the early periods of pregnancy, and if necessary, at later deadlines.

Hospitalization

The term of stationary treatment and surveys about hypothyroidism - 21 days.

Prevention

Prevention is absent.

Information

Sources and literature

1. Braverman L. Diseases of the Thyroid. - Humana Press, 2003
2. Balabolkin M.I., Klebanova E.M., Kreminskaya V.M. Differential diagnosis and the treatment of endocrine diseases. Guide, M., 2002
   1. p. 258-270
3. Grandfall I.I, Melnichenko G.A. Endocrinology. National leadership, 2012.
   1. p. 515-519
4. Dedov I.I., Melnichenko G.A., Gerasimov G.A. and etc. Clinical recommendations The Russian Association of Endocrinologists in the diagnosis and treatment of autoimmune thyroiditis in adults. Clinical thyroid, 2003
   1. T.1, p. 24-25
5. Dedov I.I., Melnichenko G.A., Andreeva V.N. Rational pharmacotherapy of diseases of the endocrine system and metabolic disorders. Guide for practicing doctors, M., 2006
   1. p. 358-363.
6. Dedov I.I., Melnichenko G.A., Pronin V.S. Clinic and diagnostics of endocrine disorders. Educational and methodical manual, M., 2005
7. Dedov I.I., Melnichenko G.A., Fadeev V.V. Endocrinology. Textbook for universities, M., 2007
   1. p. 128-133
8. Efimov A.S., Bodnar P.N., Zelinsky B.A. Endocrinology, K, 1983
   1. p. 140-143.
9. Starkova N.T. Guide on Clinical Endocrinology, St. Petersburg, 1996
   1. p. 164-169.
10. Fadeev V.V., Melnichenko G.A. Hypothyroidism: Guide for Doctors, M.: RCCs perfect, 2002
11. Fadeev V.V., Melnichenko G.A., Gerasimov G.A. Aukoimmune thyroiditis. The first step towards consensus. Endocrinology problems, 2001
    1. T.47, №4, p. 7-13

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