Subacute thyroiditis ICD code 10. Autoimmune thyroiditis (E06.3)

Chronic autoimmune thyroiditis- thyroiditis, usually manifested by goiter and symptoms of hypothyroidism. The risk of malignancy of the thyroid gland is slightly increased, but it is impossible to speak of a significant increase. The predominant age is 40-50 years. Women are observed 8-10 times more often.

Code according to the international classification of diseases ICD-10:

The reasons

Etiology and pathogenesis. An inherited defect in the function of T-suppressors (140300, association with the DR5, DR3, B8, Â loci) leads to stimulation by T-helpers of the production of cytostimulating or cytotoxic antibodies to thyroglobulin, the colloidal component and the microsomal fraction with the development of primary hypothyroidism, an increase in TSH production, and ultimately as a result - goiter. Depending on the predominance of the cytostimulating or cytotoxic action of antibodies, hypertrophic, atrophic and focal forms of chronic autoimmune thyroiditis are distinguished. Hypertrophic. Association with HLA - B8 and - DR5, predominant production of cytostimulating antibodies. Atrophic. Association with HLA - DR3, predominant production of cytotoxic antibodies, TSH receptor resistance. Focal. Damage to one lobe of the thyroid gland. The ratio of AT may be different.

pathological anatomy. Abundant infiltration of the stroma of the gland with lymphoid elements, incl. plasma cells.

Symptoms (signs)

Clinical picture determined by the ratio of cytostimulating or cytotoxic antibodies. Thyroid enlargement is the most common clinical manifestation. Hypothyroidism is found in 20% of patients by the time of diagnosis, but in some it develops later. During the first months of the disease, hyperthyroidism can be observed.

Diagnostics

Diagnostics. Ultrasound - characteristic signs of AIT (heterogeneity of the structure of the thyroid gland, decreased echogenicity, thickening of the capsule, sometimes calcifications in the gland tissue). High titers of antithyroglobulin or antimicrosomal antibodies. The results of thyroid function tests can vary.

Diagnostic tactics. The diagnosis of AIT is made only in the presence of three signs: . hypothyroidism. characteristic changes on ultrasound. high titer of antibodies to thyroid antigen (thyroglobulin and thyroid peroxidase).

Treatment

TREATMENT

Drug therapy

According to current recommendations, thyroxine treatment is indicated only in the presence of hypothyroidism, confirmed clinically and laboratory. Levothyroxine sodium at an initial dose of 25 or 50 mcg / day with further correction until the serum TSH content decreases to the lower limit of normal.

Thiamazole, propranolol - with clinical manifestations of hyperthyroidism.

Concomitant pathology. Other autoimmune diseases (for example, B 12 - deficiency anemia or rheumatoid arthritis).

Synonyms. Hashimoto's disease. Goiter Hashimoto. Hashimoto's thyroiditis. The goiter is lymphomatous. Lymphadenoid goiter. Thyroid blastoma lymphadenoid. Goiter lymphocytic.

ICD-10 . E06.3 Autoimmune thyroiditis

The International Statistical Classification of Diseases and Related Health Problems is a document developed under the leadership of WHO to provide a unified approach to the methods and principles of treating diseases.

Once every 10 years, it is reviewed, changes and amendments are made. To date, there is ICD-10 - a classifier that makes it possible to determine the international protocol for the treatment of a particular disease.

Class IV. E00 - E90. Diseases of the endocrine system, eating disorders and metabolic disorders, also includes diseases and pathological conditions of the thyroid gland. Nosology of the code according to ICD-10 - from E00 to E07.9.

Congenital iodine deficiency syndrome (E00 - E00.9)
Diseases of the thyroid gland associated with iodine deficiency and similar conditions (E01 - E01.8).
Subclinical hypothyroidism due to iodine deficiency (E02).
Other forms of hypothyroidism (E03 - E03.9).
Other forms of non-toxic goiter (E04 - E04.9).
Thyrotoxicosis (hyperthyroidism) (E05 - E05.9).
Thyroiditis (E06 - E06.9).
Other diseases of the thyroid gland (E07 - E07.9).

All these nosological units are not one disease, but a number of pathological conditions that have their own characteristics - both in the causes of occurrence and in diagnostic methods. Therefore, the treatment protocol is determined by the totality of all factors and taking into account the severity of the condition.

The disease, its causes and classic symptoms

First, remember that the thyroid gland has a special structure. It consists of follicular cells, which are microscopic balls filled with a specific fluid - keloid. Due to pathological processes, these balls begin to grow in size. It is on what nature this growth is, whether it has an effect on the production of hormones by the gland, and the developing disease will depend.

Despite the fact that thyroid diseases are diverse, often the causes of their occurrence are similar. And in some cases, it is not possible to establish it exactly, since the mechanism of action of this gland is still not fully understood.

Heredity is called a fundamental factor in the development of pathologies of the endocrine glands.
Environmental impact - unfavorable environmental conditions, radiological background, iodine deficiency in water and food, the use of food chemicals, additives and GMOs.
Diseases of the immune system, metabolic disorders.
Stress, psycho-emotional instability, chronic fatigue syndrome.
Age-related changes associated with hormonal changes in the body.

Often, the symptoms of thyroid diseases also have a general trend:

discomfort in the neck, tightness, difficulty swallowing;
weight loss without changing the diet;
violation of the sweat glands - excessive sweating or dryness of the skin can be observed;
sudden mood swings, susceptibility to depression or excessive nervousness;
decrease in the sharpness of thinking, memory impairment;
complaints about the work of the digestive tract (constipation, diarrhea);
malfunctions of the cardiovascular system - tachycardia, arrhythmia.

All these symptoms should suggest that you need to see a doctor - at least a local therapist. And he, after conducting primary research, if necessary, will refer to an endocrinologist.

Some thyroid diseases are less common than others due to various objective and subjective reasons. Consider those that are statistically the most common.

Types of thyroid pathologies

Thyroid cyst

A small, benign tumor. It is generally accepted that a cyst can be called a formation that exceeds 15 mm. in diameter. Anything below this limit is an expansion of the follicle.

It is a mature, benign tumor that many endocrinologists classify as a cyst. But the difference is that the cavity of the cystic formation is filled with keloid, and the adenoma is the epithelial cells of the thyroid gland.

Autoimmune thyroiditis (AIT)

A disease of the thyroid gland characterized by inflammation of its tissue caused by a malfunction of the immune system. As a result of such a failure, the body produces antibodies that begin to "attack" their own thyroid cells, saturate them with leukocytes, which causes inflammation. Over time, your own cells are destroyed, stop producing the right amount of hormones and a pathological condition called hypothyroidism occurs.

eutheria

This is an almost normal state of the thyroid gland, in which the function of producing hormones (TSH, T3 and T4) is not impaired, but there are already changes in the morphological state of the organ. Very often, such a condition can be asymptomatic and last a lifetime, and the person will not even be aware of the presence of the disease. This pathology does not require specific treatment and is often detected by accident.

nodular goiter

Nodular goiter code according to ICD 10 - E04.1 (with a single node) - a neoplasm in the thickness of the thyroid gland, which can be either abdominal or epithelial. A single node is rarely formed and indicates the beginning of the process of neoplasms in the form of multiple nodes.

Goiter multinodular

ICD 10 - E04.2 - this is an uneven increase in the thyroid gland with the formation of several nodes, which can be both cystic and epithelial. As a rule, this type of goiter is characterized by increased activity of the endocrine organ.

diffuse goiter

It is characterized by a uniform growth of the thyroid gland, which affects the decrease in the secretory function of the organ.

Diffuse toxic goiter is an autoimmune disease characterized by diffuse enlargement of the thyroid gland and persistent pathological production of excessive amounts of thyroid hormones (thyrotoxicosis).

This is an increase in the size of the thyroid gland, which does not affect the production of normal amounts of thyroid hormones and is not a consequence of inflammation or neoplastic formations.

Thyroid disease caused by iodine deficiency in the body. There are euthyroid (an increase in the size of an organ without affecting hormonal function), hypothyroid (a decrease in hormone production), hyperthyroid (an increase in hormone production) endemic goiter.

An increase in the size of the organ, which can be observed both in a sick person and in a healthy one. The neoplasm is benign and is not considered a tumor. It does not require specific treatment until changes in the organ or an increase in the size of the formation begin.

Separately, it is necessary to mention such a rare disease as thyroid hypoplasia. This is a congenital disease that is characterized by underdevelopment of the organ. If this disease occurs during life, then it is called thyroid atrophy.

thyroid cancer

One of the rare pathologies that is detected only by specific diagnostic methods, since the symptoms are similar to all other thyroid diseases.

Diagnostic methods

Almost all pathological neoplasms rarely develop into a malignant form (thyroid cancer), only with very large sizes and untimely treatment.

For diagnostics, the following methods are used:

medical examination, palpation;
if necessary, fine-needle biopsy.

In some cases, treatment may not be required at all if the size of the neoplasms is very small. The specialist simply observes the condition of the patient. Sometimes neoplasms spontaneously resolve, and sometimes they rapidly begin to increase in size.

The most effective treatments

Treatment can be conservative, that is, medication. Drugs are prescribed in strict accordance with laboratory tests. Self-treatment is unacceptable, since the pathological process requires the control and correction of a specialist.

If there are clear indications, surgical measures are taken when the part of the organ that is subject to the pathological process is removed, or the entire organ.

Treatment of autoimmune diseases of the thyroid gland has several differences:

medication - aimed at destroying excess hormones;
radioactive iodine treatment or surgery - leads to the destruction of the gland, which entails hypothyroidism;
computer reflexology is designed to restore the functioning of the gland.

Thyroid disease, especially in the modern world, is a fairly common phenomenon. If you turn to a specialist in time and carry out all the necessary therapeutic measures, you can significantly improve the quality of life, and in some cases completely get rid of the disease.

Deals with issues of prevention, diagnosis and treatment of diseases of the endocrine system: thyroid gland, pancreas, adrenal glands, pituitary gland, sex glands, parathyroid glands, thymus gland, etc.

Autoimmune thyroiditis, ICD code 10 - the name of the disease according to the International Classification of Diseases or ICD. The ICD is a whole system designed specifically to study diseases and track the stage of their development in the world's population.

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

Since 1993, code ten has come into effect, which includes thyroid diseases, such as chronic autoimmune thyroiditis. The main purpose of using the ICD was to identify pathologies, analyze them and compare the data obtained in different countries of the world. Also, this classification allows you to select the most effective treatment regimens for pathologies that are part of the code.

All data on pathologies are formed in such a way as to create the most useful database of diseases, useful for epidemiology and practical medicine.

The ICD-10 code includes the following groups of pathologies:

diseases of an epidemic nature;
general diseases;
diseases grouped by anatomical localization;
pathology of development;
different types of herbs.

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

Autoimmune thyroiditis, ICD code 10, is included in the group of thyroid diseases. To record pathologies, codes from E00 to E07 are used. Code E06 reflects the pathology of thyroiditis.

This includes the following subsections:

Code E06-0. This code indicates the acute course of thyroiditis.
E06-1. This includes subacute thyroiditis mkb 10.
E06-2. Chronic form of thyroiditis.
Autoimmune thyroiditis is classified as E06-3.
E06-4. Drug-induced thyroiditis.
E06-5. Other types of thyroiditis.

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

These are Hashimoto's chronic autoimmune thyroiditis and Riedel's disease. In the latter variant of the disease, the thyroid parenchyma is replaced by connective tissue.

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

If symptoms of hypothyroidism are identified, Hashimoto's disease should be suspected. To clarify the diagnosis, a blood test for TSH and T4 is performed. If laboratory diagnostics show the presence of antibodies to thyroglobulin, then this will indicate the autoimmune nature of the disease.

Ultrasound will help clarify the diagnosis. During this examination, the doctor can see hyperechoic layers, connective tissue, accumulations of lymphoid follicles. For a more accurate diagnosis, a cytological examination should be performed, since on ultrasound the pathology of E06-3 is similar to a malignant tumor.

Treatment for E06-3 involves lifelong hormone therapy. In rare cases, surgery is indicated.

Among 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 its own cells and tissues. In the IV class of diseases, this pathology (other names are autoimmune chronic thyroiditis, Hashimoto's disease or thyroiditis, lymphocytic or lymphomatous thyroiditis) has the ICD code 10 - E06.3.

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ICD-10 code

E06.3 Autoimmune thyroiditis

The pathogenesis of autoimmune thyroiditis

The causes of the organ-specific autoimmune process in this pathology are the perception by the body's immune system of thyroid cells as foreign antigens and the production of antibodies against them. Antibodies begin to "work", and T-lymphocytes (which must recognize and destroy foreign cells) rush into the tissues of the gland, triggering inflammation - thyroiditis. At the same time, effector T-lymphocytes penetrate into the parenchyma of the thyroid gland and accumulate there, forming lymphocytic (lymphoplasmacytic) infiltrates. Against this background, the tissues of the gland undergo destructive changes: the integrity of the membranes of the follicles and the walls of thyrocytes (follicular cells that produce hormones) are violated, part of the glandular tissue can be replaced by fibrous tissue. Follicular cells are naturally destroyed, their number is reduced, and as a result, there is a violation of the functions of the thyroid gland. This leads to hypothyroidism - low levels of thyroid hormones.

But this does not happen immediately, the pathogenesis of autoimmune thyroiditis is characterized by a long asymptomatic period (euthyroid phase), when the levels of thyroid hormones in the blood are within the normal range. Further, the disease begins to progress, causing a deficiency of hormones. The pituitary gland, which controls the work of the thyroid gland, reacts to this and, by increasing the synthesis of thyroid-stimulating hormone (TSH), stimulates the production of thyroxine for some time. Therefore, it can take months and even years until the pathology becomes apparent.

Predisposition to autoimmune diseases is determined by an inherited dominant genetic trait. Studies have shown that half of the next of kin of patients with autoimmune thyroiditis also have antibodies to thyroid tissue in their blood serum. To date, scientists have associated the development of autoimmune thyroiditis with mutations in two genes - 8q23-q24 on chromosome 8 and 2q33 on chromosome 2.

As endocrinologists note, there are immune diseases that cause autoimmune thyroiditis, more precisely, combined with it: type I diabetes, celiac disease (celiac disease), pernicious anemia, rheumatoid arthritis, systemic lupus erythematosus, Addison's disease, Werlhof's disease, biliary cirrhosis of the liver (primary) , as well as Down syndrome, Shereshevsky-Turner and Klinefelter.

In women, autoimmune thyroiditis occurs 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 disease manifestation is 35-55 years). Despite the hereditary nature of the disease, autoimmune thyroiditis is almost never diagnosed in children under 5 years of age, but in adolescents it accounts for up to 40% of all thyroid pathologies.

Symptoms of autoimmune thyroiditis

Depending on the level of deficiency of thyroid hormones, which regulate protein, lipid and carbohydrate metabolism in the body, the work of the cardiovascular system, gastrointestinal tract and central nervous system, the symptoms of autoimmune thyroiditis may vary.

However, some people do not feel any signs of the disease, while others experience various combinations of symptoms.

Hypothyroidism in autoimmune thyroiditis is characterized by such signs as: fatigue, lethargy and drowsiness; difficulty breathing; hypersensitivity to cold; pale dry skin; thinning and hair loss; fragility of nails; puffiness of the face; hoarseness; constipation; unreasonable weight gain; muscle pain and joint stiffness; menorrhagia (in women), depression. A goiter, a swelling in the area of the thyroid gland on the front of the neck, may also form.

There can be complications with Hashimoto's disease: a large goiter makes swallowing or breathing difficult; the level of low-density cholesterol (LDL) rises in the blood; prolonged depression sets in, cognitive abilities and libido decrease. The most serious consequences of autoimmune thyroiditis, caused by a critical lack of thyroid hormones, are myxedema, that is, mucinous edema, and its result in a hypothyroid coma.

Diagnosis of autoimmune thyroiditis

Autoimmune thyroiditis (Hashimoto's disease) is diagnosed by endocrinologists based on the patient's complaints, symptoms, and blood test results.

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

Antibodies are also necessarily determined in autoimmune thyroiditis:

antibodies to thyroglobulin (TGAb) - AT-TG,
antibodies to thyroid peroxidase (TPOAb) - AT-TPO,
antibodies to thyroid-stimulating hormone receptors (TRAb) - AT-rTTG.

To visualize pathological changes in the structure of the thyroid gland and its tissues under the influence of antibodies, instrumental diagnostics are performed - ultrasound or computer. Ultrasound allows you to detect and assess the level of these changes: damaged tissues with lymphocytic infiltration will give the so-called diffuse hypoechogenicity.

An aspiration puncture biopsy of the thyroid gland and a cytological examination of the biopsy are performed if there are nodes in the gland - to determine oncological pathologies. In addition, a cytogram of autoimmune thyroiditis helps to determine the composition of gland cells and identify lymphoid elements in its tissues.

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

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They cannot cure autoimmune thyroiditis, but by increasing the level of thyroxine, they alleviate the symptoms caused by its deficiency.

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

There were no cases of spontaneous regression of autoimmune thyroiditis, although the size of the goiter may decrease significantly over time. Removal of the thyroid gland is performed only in case of its hyperplasia, which prevents normal breathing, compression of the larynx, and also when malignant neoplasms are detected.

Lymphocytic thyroiditis is an autoimmune condition and cannot be prevented, therefore, the prevention of this pathology is impossible.

The prognosis for those who treat their health correctly, is registered with an experienced endocrinologist and follows his recommendations, is positive. Both the disease itself and the methods of its treatment still raise many questions, and even a doctor of the highest qualification will not be able to answer the question of how long people live with autoimmune thyroiditis.

RCHD (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical Protocols of the Ministry of Health of the Republic of Kazakhstan - 2017

Autoimmune thyroiditis (E06.3)

Endocrinology

general information

Short description

Approved
Joint Commission on the quality of medical services
Ministry of Health of the Republic of Kazakhstan
dated August 18, 2017
Protocol No. 26

Autoimmune thyroiditis- organ-specific autoimmune disease, which is the main cause of primary hypothyroidism. It has no independent clinical significance in the absence of thyroid dysfunction.

INTRODUCTION

ICD-10 code(s):

ICD-10
The code	Name
E 06.3	Autoimmune thyroiditis

Date of development/revision of the protocol: 2017

Abbreviations used in the protocol:

AIT	-	autoimmune thyroiditis
St. T4	-	free thyroxine
svt3	-	free triiodothyronine
TSH	-	thyroid-stimulating hormone
TG	-	thyroglobulin
TPO	-	thyroperoxidase
thyroid	-	thyroid
AT to TG	-	antibodies to thyroglobulin
AT to TPO	-	antibodies to thyroperoxidase

Protocol Users: therapists, general practitioners, endocrinologists.

Evidence level scale:

BUT	High-quality meta-analysis, systematic review of RCTs, or large RCTs with a very low probability (++) of bias whose results can be generalized to an appropriate population.
AT	High-quality (++) systematic review of cohort or case-control studies or High-quality (++) cohort or case-control studies with very low risk of bias or RCTs with low (+) risk of bias, the results of which can be generalized to the appropriate population .
FROM	Cohort or case-control or controlled trial without randomization with low risk of bias (+). The results of which can be generalized to the relevant population or RCTs with a very low or low risk of bias (++ or +), the results of which cannot be directly generalized to the appropriate population.
D	Description of a case series or uncontrolled study or expert opinion.
GPP	Best Clinical Practice.

Classification

Classification:

atrophic form;
hypertrophic form.

Clinical variants are juvenile thyroiditis and focal (minimal) thyroiditis.

Histologically, lymphoid and plasmacytic infiltration of the thyroid tissue, oncocytic transformation of thyrocytes (Gürthle cells), destruction of follicles, a decrease in colloid reserves and fibrosis are determined. Juvenile thyroiditis is manifested by moderate lymphoid infiltration and fibrosis. In focal thyroiditis, parenchymal destruction and lymphoid infiltration are minimal, and Hürthle cells are absent.

The course of the disease is long, in the phase of euthyroidism asymptomatic. AIT, as a rule, is diagnosed at the stage of primary hypothyroidism and less often (in 10% of cases) debuts with transient (no more than 6 months) thyrotoxicosis.
Manifest hypothyroidism that developed in the outcome of AIT indicates persistent and irreversible destruction of the thyroid parenchyma and requires lifelong replacement therapy.

Diagnostics

METHODS, APPROACHES AND DIAGNOSIS PROCEDURES

Diagnostic criteria

Complaints and anamnesis:
During the first years, complaints and symptoms are usually absent. Over time, there may be complaints of swelling of the face, limbs, drowsiness, depression, weakness, fatigue, in women - menstrual irregularities. It should be borne in mind that not all patients develop hypothyroidism, approximately 30% may only have antibodies to the thyroid gland.

Physical examination: in the hypertrophic form of AIT, the thyroid gland is enlarged, of a dense consistency, its surface is "uneven"; in atrophic form of AIT, the thyroid gland is not enlarged.

Laboratory research:
Hormonal profile: study of TSH, fT3, fT4, antibodies to thyroperoxidase, antibodies to thyroglobulin

Instrumental studies:
Ultrasound of the thyroid gland - a cardinal ultrasound sign - a diffuse decrease in tissue echogenicity;
· Fine-needle puncture biopsy - according to indications.

Indications for consultation of specialists: no.

Diagnostic algorithm

The "major" diagnostic signs, the combination of which makes it possible to establish AIT, are primary hypothyroidism (manifest or subclinical), the presence of antibodies to thyroid tissue, as well as ultrasound signs of autoimmune pathology.

Differential Diagnosis

Differential Diagnosisand rationale for additional research

Treatment abroad

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Treatment

Treatment (ambulatory)

TACTICS OF TREATMENT AT OUTPATIENT LEVEL:
Currently, there are no methods of influencing the actual autoimmune process in the thyroid gland. Drug therapy (levothyroxine preparations) is prescribed only when hypothyroidism is detected.

Non-drug treatment
Mode: IV
Table: diet number 15

Medical treatment: the only drug is levothyroxine sodium tablets.
Starting daily dose for overt hypothyroidism:
In patients under 60 years of age - 1.6-1.8 mcg / kg;
In patients with concomitant diseases of the cardiovascular system and older than 60 years - 12.5-25 mcg, followed by an increase of 12.5-25 mcg every 6-8 weeks.
Take in the morning on an empty stomach no later than 30 minutes before a meal. After taking thyroid hormones, avoid taking antacids, iron and calcium preparations within 4 hours.

The selection of the maintenance dose is carried out under the control of the general condition, pulse rate, dynamic determination of the level of TSH in the blood. The first determination is made no earlier than 6 weeks from the start of therapy, then until the effect is achieved - 1 time in 3 months.

In subclinical hypothyroidism (increased TSH levels in combination with a normal T4 level in the blood and the absence of a hypothyroidism clinic), it is recommended:
· repeated hormonal study after 3 - 6 months to confirm the persistent nature of the dysfunction of the thyroid gland; if subclinical hypothyroidism is detected during pregnancy, levothyroxine therapy at a full replacement dose is prescribed immediately;

List of Essential Medicines(having a 100% cast chance):

List of additional medicines: no.

Surgical intervention: no.

Further management:
· After reaching the clinical and laboratory effect to determine the adequacy of the dose of levothyroxine 1 every 6 months, a TSH study is performed. The criterion for the adequacy of replacement therapy for subclinical hypothyroidism is the stable maintenance of a normal level of TSH in the blood (0.5-2.5 mIU / l).

Patients with concomitant diseases of the cardiovascular system and over 60 years of age should be treated with doses of levothyroxine that maintain the state of subclinical hypothyroidism.

NB! The study of the dynamics of the level of antibodies to the thyroid gland in order to assess the progression of AIT has no diagnostic and prognostic value.

Treatment effectiveness indicators: complete elimination of clinical and laboratory signs of hypothyroidism in young people, a decrease in its severity in the elderly.

Hospitalization

Indications for planned hospitalization: no.
Indications for emergency hospitalization: no.

Information

Sources and literature

Minutes of the meetings of the Joint Commission on the quality of medical services of the Ministry of Health of the Republic of Kazakhstan, 2017
1. 1) Fadeev V.V., Melnichenko G.A. Hypothyroidism. Guide for doctors. - M., 2002. - 218 p. 2) Bravermann L.I. Diseases of the thyroid gland. - M.: Medicine. 2000. - 417 p. 3) Kotova G.A. Diseases of the endocrine system. Under the editorship of Dedov I.I. - M.: Medicine. - 2002. - 277 p. 4) Lavin N. Endocrinology. – M.: Practice. - 1999. - 1127 p. 5) Balabolkin M.I., Klebanov E.M., Kreminskaya V.M. Differential diagnosis and treatment of endocrine diseases. - M.: Medicine, 2002. - 751 p. 6) Melnichenko G.A., Fadeev V.V. Diagnosis and treatment of hypothyroidism  Physician. - 2004. - No. 3. - S. 26-28. 7) Fadeev V.V. Iodine deficiency and autoimmune diseases in the region of mild iodine deficiency: Abstract of the thesis. … doc. honey. Sciences. - Moscow. - 2004. - 26 p. 8) M.A. Paltsev, O.V. Zairatyants, P.S. Vetshev. et al. Autoimmune thyroiditis: pathogenesis, morphogenesis and classification // Archives of Pathology. - 1993. - No. 6 - S. 7-13. 9) Khmelnitsky O.K., Eliseeva N.A. Thyroiditis of Hashimoto and De Quervain // Archives of Pathology. – M.: Medicine. - 2003. - No. 6. - S. 44-49. 10) Kalinin A.P., Kiseleva T.P. Autoimmune thyroiditis. Guidelines. - Moscow. -1999. - 19 p. 11) Petunina N.A. Clinic, diagnosis and treatment of autoimmune thyroiditis // Problems of endocrinol. - 2002. -T48, No. 6. - S. 16-21. 12) Kaminsky A.V. Chronic autoimmune thyroiditis (etiology, pathogenesis, radiation aspects) // Med. hour-painting Ukraine. -1999. - No. 1(9). - P.16-22. 13) Kandror V.I., Kryukova I.V., Krainova S.I. Antithyroid antibodies and autoimmune diseases of the thyroid gland // Problems of Endocrinology. - 1997. - V.43, No. 3. - S. 25-30. 14) American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for the Diagnosis and Management of Thyroid Nodules // AACE/AME Task Force on Thyroid Nodules. - Endocr. Pract. - 2006. - Vol. 12. - P. 63-102.

Information

ORGANIZATIONAL ASPECTS OF THE PROTOCOL

List of protocol developers with qualification data:
1) Taubaldieva Zhannat Satybaevna - Candidate of Medical Sciences, Head of the Department of Endocrinology, National Scientific Medical Center JSC;
2) Madiyarova Meruert Shaizindinovna - Candidate of Medical Sciences, Head of the Department of Endocrinology, CF "UMC" Republican Diagnostic Center;
3) Smagulova Gaziza Azhmagievna - Candidate of Medical Sciences, Associate Professor, Head of the Department of Propaedeutics of Internal Diseases and Clinical Pharmacology of the Republican State Enterprise on the REM “West Kazakhstan State Medical University named after M.O. Ospanov".

Indication of no conflict of interest: No.

Reviewers:
1) Bazarova Anna Vikentievna - Candidate of Medical Sciences, Associate Professor of the Department of Endocrinology of JSC "Astana Medical University";
2) Temirgaliyeva Gulnar Shakhmievna - Candidate of Medical Sciences, endocrinologist of Meyirim Multidisciplinary Medical Center LLP.

Indication of the conditions for revising the protocol: revision of the protocol 5 years after its publication and from the date of its entry into force or in the presence of new methods with a level of evidence.

Attached files

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