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 one cannot speak of a significant increase. The predominant age is 40-50 years. In women it is observed 8-10 times more often.

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

Causes

Etiology and pathogenesis. An inherited defect in the function of T - suppressors (140300, association with loci DR5, DR3, B8, Â) leads to stimulation by T - helpers of the production of cytostimulating or cytotoxic antibodies to thyroglobulin, the colloid 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 effect of AT, hypertrophic, atrophic and focal forms of chronic autoimmune thyroiditis are distinguished. Hypertrophic. Association with HLA - B8 and - DR5, preferential production of cytostimulating antibodies. Atrophic. Association with HLA - DR3, preferential production of cytotoxic antibodies, TSH receptor resistance.. Focal. Damage to one lobe of the thyroid gland. The AT ratio may be different.

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

Symptoms (signs)

Clinical picture determined by the ratio of cytostimulating or cytotoxic antibodies. Enlarged thyroid gland is the most common clinical manifestation. Hypothyroidism is found in 20% of patients at 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. Thyroid function test results may vary.

Diagnostic tactics. The diagnosis of AIT is made only if three signs are present: . hypothyroidism. characteristic changes on ultrasound. high titer of antibodies to thyroid antigens (thyroglobulin and thyroid peroxidase).

Treatment

TREATMENT

Drug therapy

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

Thiamazole, propranolol - for clinical manifestations of hyperthyroidism.

Concomitant pathology. Other autoimmune diseases (eg B 12 deficiency anemia or rheumatoid arthritis).

Synonyms. Hashimoto's disease. Hashimoto's goiter. Hashimoto's thyroiditis. Lymphomatous goiter. Lymphadenoid goiter. Lymphadenoid blastoma of the thyroid gland. Lymphocytic goiter.

ICD-10 . E06.3 Autoimmune thyroiditis

The International Statistical Classification of Diseases and Related Health Problems is a document developed under the guidance of WHO to provide a uniform approach to the methods and principles of disease treatment.

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

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

Congenital iodine deficiency syndrome (E00 – E00.9)
Thyroid diseases 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 whole series of pathological conditions that have their own characteristics - both in the causes of occurrence and in diagnostic methods. Consequently, the treatment protocol is determined based on the totality of all factors and taking into account the severity of the condition.

The disease, its causes and classic symptoms

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

Despite the fact that thyroid diseases are varied, their causes are often similar. And in some cases it is not possible to establish it precisely, 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, 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 tendency:

feeling of discomfort in the neck, tightness, difficulty swallowing;
losing weight without changing your diet;
disruption of the sweat glands - excessive sweating or dry skin may occur;
sudden mood swings, susceptibility to depression or excessive nervousness;
decreased thinking acuity, memory impairment;
complaints about the gastrointestinal tract (constipation, diarrhea);
disruptions in the functioning of the cardiovascular system - tachycardia, arrhythmia.

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

Some thyroid diseases are less common than others due to various objective and subjective reasons. Let's look at 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. Everything below this border is an expansion of the follicle.

This is a mature benign tumor, which 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 made up of 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 this failure, the body produces antibodies that begin to “attack” its own thyroid cells, saturate them with leukocytes, which causes inflammatory processes. Over time, your own cells are destroyed, they stop producing the required amount of hormones, and a pathological condition called hypothyroidism occurs.

Eutheriosis

This is an almost normal condition 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, this condition can be asymptomatic and last a lifetime, and the person will not even suspect the presence of the disease. This pathology does not require specific treatment and is often detected by chance.

Nodular goiter

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

Multinodular goiter

ICD 10 - E04.2 is an uneven enlargement of the thyroid gland with the formation of several nodes, which can be either cystic or epithelial. As a rule, this type of goiter is characterized by increased activity of the internal secretion organ.

Diffuse goiter

It is characterized by 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 (increase in organ size without affecting hormonal function), hypothyroid (decreased hormone production), hyperthyroid (increased 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, mention should be made of such a rare disease as thyroid hypoplasia. This is a congenital disease, which is characterized by underdevelopment of the organ. If this disease occurs during life, it is called atrophy of the thyroid gland.

Thyroid cancer

One of the less common pathologies, which is detected only through 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 if they are very large in size and untimely treatment.

The following methods are used for diagnosis:

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

In some cases, treatment may not be required at all if the tumors are very small. The specialist simply monitors the patient's condition. Sometimes the 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-medication is unacceptable, since the pathological process requires monitoring and correction by a specialist.

If there are clear indications, surgical measures are carried out when a part of an organ that is susceptible to a pathological process, or the entire organ, is removed.

Treatment of autoimmune thyroid diseases has several differences:

medicinal – aimed at destroying excess hormones;
treatment with radioactive iodine or surgery leads to destruction of the gland, which leads to hypothyroidism;
Computer reflexology is designed to restore the functioning of the gland.

Thyroid diseases, especially in the modern world, are quite common. If you consult a specialist in time and carry out all the necessary therapeutic measures, you can significantly improve your 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, gonads, parathyroid glands, thymus gland, etc.

Autoimmune thyroiditis ICD code 10 is the name of the disease according to the International Classification of Diseases or ICD. The ICD is an entire system designed specifically for studying diseases and tracking the stage of their development in the world population.

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

Since 1993, code ten began to operate, which includes diseases of the thyroid gland, 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. This classification also allows you to select the most effective treatment regimens for the pathologies included in the code.

All data on pathologies is generated 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 location;
developmental pathologies;
various 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 denotes acute thyroiditis.
E06-1. This includes subacute thyroiditis ICD 10.
E06-2. Chronic form of thyroiditis.
Autoimmune thyroiditis is classified by the microbiome 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 chronic autoimmune Hashimoto's 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 methods of diagnosis and treatment.

If symptoms of hypothyroidism are detected, Hashimoto's disease should be considered. To clarify the diagnosis, a blood test is performed for TSH and T4. If laboratory diagnostics show the presence of antibodies to thyroglobulin, 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, and clusters 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 formation.

Treatment of E06-3 involves lifelong use of hormones. 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 class IV diseases, this pathology (other names are autoimmune chronic thyroiditis, Hashimoto's disease or thyroiditis, lymphocytic or lymphomatous thyroiditis) has an ICD 10 code - E06.3.

, , , , ,

ICD-10 code

E06.3 Autoimmune thyroiditis

Pathogenesis of autoimmune thyroiditis

The reasons for the organ-specific autoimmune process in this pathology are that the body’s immune system perceives thyroid cells as foreign antigens and produces antibodies against them. Antibodies begin to “work”, and T-lymphocytes (which must recognize and destroy foreign cells) rush into the gland tissue, triggering inflammation - thyroiditis. In this case, effector T-lymphocytes penetrate into the parenchyma of the thyroid gland and accumulate there, forming lymphocytic (lymphoplasmacytic) infiltrates. Against this background, the glandular tissues undergo destructive changes: the integrity of the membranes of the follicles and the walls of thyrocytes (follicular cells that produce hormones) is disrupted, and part of the glandular tissue can be replaced by fibrous tissue. Follicular cells are naturally destroyed, their number is reduced, and as a result, thyroid dysfunction occurs. 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 blood levels of thyroid hormones are within normal limits. Then the disease begins to progress, causing hormone deficiency. The pituitary gland, which controls the functioning 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, months and even years may pass until the pathology becomes obvious.

Predisposition to autoimmune diseases is determined by an inherited dominant genetic trait. Studies have shown that half of the immediate relatives of patients with autoimmune thyroiditis also have antibodies to thyroid tissue in their blood serum. Today, scientists associate 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, or more precisely, those combined with it: type I diabetes, gluten enteropathy (celiac disease), pernicious anemia, rheumatoid arthritis, systemic lupus erythematosus, Addison's disease, Werlhoff's disease, biliary cirrhosis of the liver (primary) , as well as Down, Shereshevsky-Turner and Klinefelter syndromes.

In women, autoimmune thyroiditis occurs 10 times more often than in men, and usually appears after 40 years (according to The European Society of Endocrinology, the typical age of manifestation of the disease 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 already 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 functioning of the cardiovascular system, gastrointestinal tract and central nervous system, the symptoms of autoimmune thyroiditis may vary.

However, some people experience no signs of illness, while others experience varying combinations of symptoms.

Hypothyroidism with autoimmune thyroiditis is characterized by such symptoms as: fatigue, lethargy and drowsiness; difficulty breathing; hypersensitivity to cold; pale dry skin; thinning and hair loss; brittle nails; puffiness of the face; hoarseness; constipation; causeless 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.

Hashimoto's disease can have complications: a large goiter makes swallowing or breathing difficult; the level of low-density cholesterol (LDL) increases in the blood; Long-term 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 the form of hypothyroid coma.

Diagnosis of autoimmune thyroiditis

Endocrinologist specialists diagnose autoimmune thyroiditis (Hashimoto's disease) based on patient complaints, existing symptoms and blood test results.

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

Antibodies are also required for autoimmune thyroiditis:

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

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 makes it possible to detect and evaluate 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 sample is carried out if there are nodes in the gland - to determine oncological pathologies. In addition, a cytogram of autoimmune thyroiditis helps 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 pathologies of the thyroid gland. In addition, hypothyroidism can be a symptom of other diseases, in particular those associated with dysfunction of the pituitary gland.

, , [

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 have been 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 carried out only in case of its hyperplasia, which interferes with normal breathing, compression of the larynx, and also when malignant neoplasms are detected.

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

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

RCHR (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 Healthcare Quality
Ministry of Health of the Republic of Kazakhstan
dated August 18, 2017
Protocol No. 26

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

INTRODUCTORY PART

ICD-10 code(s):

ICD-10
Code	Name
E 06.3	Autoimmune thyroiditis

Date of protocol development/revision: 2017

Abbreviations used in the protocol:

AIT	-	autoimmune thyroiditis
St. T4	-	free thyroxine
svT3	-	free triiodothyronine
TSH	-	thyroid-stimulating hormone
TG	-	thyroglobulin
TPO	-	Thyroid peroxidase
thyroid gland	-	thyroid
AT to TG	-	antibodies to thyroglobulin
AT to TPO	-	antibodies to thyroid peroxidase

Protocol users: therapists, general practitioners, endocrinologists.

Level of evidence scale:

A	A high-quality meta-analysis, systematic review of RCTs, or large RCTs with a very low probability (++) of bias, the results of which can be generalized to an appropriate population.
IN	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 an appropriate population .
WITH	Cohort or case-control study or controlled trial without randomization with low risk of bias (+). The results of which can be generalized to the relevant population or RCTs with very low or low risk of bias (++ or +), the results of which cannot be directly generalized to the relevant population.
D	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 thyroid tissue, oncocytic transformation of thyrocytes (Hurthle 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 and asymptomatic in the euthyroid phase. 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, which developed as a result of AIT, indicates persistent and irreversible destruction of the thyroid parenchyma and requires lifelong replacement therapy.

Diagnostics

DIAGNOSTIC METHODS, APPROACHES AND PROCEDURES

Diagnostic criteria

Complaints and anamnesis:
During the first years, complaints and symptoms are usually absent. Over time, complaints may appear of swelling of the face and limbs, drowsiness, depression, weakness, fatigue, and in women - menstrual irregularities. It must be taken into account that not all patients develop hypothyroidism; approximately 30% may only be carriers of antibodies to the thyroid gland.

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

Laboratory research:
Hormonal profile: TSH study, fT3, fT4, antibodies to thyroid peroxidase, antibodies to thyroglobulin

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

Indications for specialist consultation: no.

Diagnostic algorithm

“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

Get treatment in Korea, Israel, Germany, USA

Get advice on medical tourism

Treatment

Treatment (outpatient clinic)

OUTPATIENT TREATMENT TACTICS:
Currently, there are no methods of influencing the autoimmune process itself in the thyroid gland. Drug therapy (levothyroxine drugs) is prescribed only if hypothyroidism is detected.

Non-drug treatment
Mode: IV
Table: diet No. 15

Drug treatment: The only medicine is levothyroxine sodium tablets.
Starting daily dose for manifest hypothyroidism:
· in patients under 60 years of age - 1.6-1.8 mcg/kg;
· in patients with concomitant diseases of the cardiovascular system and over 60 years of age - 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 meals. After taking thyroid hormones, avoid taking antacids, iron and calcium supplements for 4 hours.

The maintenance dose is selected under the control of general condition, pulse rate, and dynamic determination of the TSH level in the blood. The first determination is made no earlier than 6 weeks from the start of therapy, then once every 3 months until the effect is achieved.

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

List of essential medicines(having a 100% probability of application):

List of additional medications: no.

Surgical intervention: no.

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

It is advisable to treat patients with concomitant diseases of the cardiovascular system and over 60 years of age on doses of levothyroxine that maintain a state of subclinical hypothyroidism.

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

Indicators of treatment effectiveness: complete elimination of clinical and laboratory signs of hypothyroidism in young people, reduction in its severity in older people.

Hospitalization

Indications for planned hospitalization: none.
Indications for emergency hospitalization: none.

Information

Sources and literature

Minutes of 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. Thyroid diseases. - M.: Medicine. 2000. - 417 p. 3) Kotova G.A. Diseases of the endocrine system. Edited by 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  Doctor. - 2004. - No. 3. - pp. 26-28. 7) Fadeev V.V. Iodine deficiency and autoimmune diseases in the region of mild iodine deficiency: abstract. ... doc. honey. Sci. - Moscow. - 2004. - 26 p. 8) Paltsev M.A., Zairatyants O.V., Vetshev P.S. and others. Autoimmune thyroiditis: pathogenesis, morphogenesis and classification // Pathology Archives. – 1993. - No. 6 – P. 7-13. 9) Khmelnitsky O.K., Eliseeva N.A. Hashimoto's and De Quervain's thyroiditis // Pathology Archives. – M.: Medicine. – 2003. - No. 6. – P. 44-49. 10) Kalinin A.P., Kiseleva T.P. Autoimmune thyroiditis. Guidelines. - Moscow. -1999. - 19 s. 11) Petunina N.A. Clinic, diagnosis and treatment of autoimmune thyroiditis // Problems endocrinol. - 2002. –T48, No. 6. – pp. 16-21. 12) Kaminsky A.V. Chronic autoimmune thyroiditis (etiology, pathogenesis, radiation aspects) // Med. clock-writer Ukraine. -1999. - No. 1(9). - P.16-22. 13) Kandror V.I., Kryukova I.V., Krainova S.I. and others. Antithyroid antibodies and autoimmune diseases of the thyroid gland // Problems of endocrinology. – 1997. - T.43, No. 3. – P. 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 information:
1) Taubaldieva Zhannat Satybaevna - Candidate of Medical Sciences, Head of the Department of Endocrinology, JSC National Scientific Medical Center;
2) Madiyarova Meruert Shayzindinovna - Candidate of Medical Sciences, Head of the Department of Endocrinology of the KF "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 West Kazakhstan State Medical University named after M.O. Ospanova."

Indication of no conflict of interest: No.

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

Indication of the conditions for reviewing the protocol: review of the protocol 5 years after its publication and from the date of its entry into force or if new methods with a level of evidence are available.

Attached files

Attention!

By self-medicating, you can cause irreparable harm to your health.
The information posted on the MedElement website and in the mobile applications "MedElement", "Lekar Pro", "Dariger Pro", "Diseases: Therapist's Guide" cannot and should not replace a face-to-face consultation with a doctor. Be sure to contact a medical facility if you have any illnesses or symptoms that concern you.
The choice of medications and their dosage must be discussed with a specialist. Only a doctor can prescribe the right medicine and its dosage, taking into account the disease and condition of the patient’s body.
The MedElement website and mobile applications "MedElement", "Lekar Pro", "Dariger Pro", "Diseases: Therapist's Directory" are exclusively information and reference resources. The information posted on this site should not be used to unauthorizedly change doctor's orders.
The editors of MedElement are not responsible for any personal injury or property damage resulting from the use of this site.