Chronic autoimmune thyroidite code on the ICD 10. E00-E07 thyroid disease. What is affected by the low and high level T4

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 its own cells and tissues. In the IV class of diseases, this pathology (other names - autoimmune chronic thyroiditis, illness or thyroiditis 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 is regulated in the body protein, lipid and carbohydrate metabolism, the work of the cardiovascular system, the tract and the CNS, the 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-RTTG.

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 study of the biopsy is carried out if there is an introduction in the hubs - 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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They cannot cure autoimmune thyroiditis, but, increasing the level of thyroxine, facilitate the symptoms caused by its insufficiency.

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.

Aukimmune thyroiditis code on the ICD 10 is the name of the disease according to the international classification of diseases or ICD. The ICD is a whole system designed specifically for studying diseases and tracking the stage of their development in the world's population.

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 act as part of which thyroid diseases, such as chronic autoimmune thyroiditis. The main purpose of the application of the ICD was the definition of pathologies, analyzing their analysis and comparison of the data obtained in different countries of the 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 the group IV, which includes diseases of the 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 of 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.

To date, all diseases have a specific classification and code on the ICD (10), including autoimmune thyroiditis.

What is MKB 10

International Classification of Diseases (ICD 10) is a system, a grouping diseases and all sorts of health issues. The ICD 10 approved at the World Conference in the capital of France in 1900, where more than 20 states were present. It was found that this classification should be reviewed every 10 years, until today it has been revised 10 times. In Russia, this system entered into force in early 1998. Thanks to the above concept, it improved the ability to systematize diagnoses, organize registration of diseases, to ensure maximum convenience when storing data, keep records of health care. This classification consists of 21 class of diseases that are divided into certain blocks. For convenience, the entire list is located in alphabetical order. On ICD 10 can always be found any illness, including endocrine.

What is an autoimmune thyroiditis and its code on the ICD 10

An autoimmune thyroiditis is classified as endocrine diseases that are characterized by inflammation of the thyroid gland. Inflammation cause certain autoimmune processes in the body. This disease also is the name of the Japanese scientist Hashimoto, since it was studied and described them for more than a century ago. The reasons provoking the development of pathology are quite a lot. First of all, it is a violation of the work of the immune system, which, as a result, produces antibodies that are struggling with their own cells. Secondly, the unfavorable ecological situation, bad habits, etc., adversely affect the work of the gland, develop autoimmune thyroiditis and many other pathologies.

Treatment should be carried out with special care, taking into account all associated features. As a rule, it is carried out using hormone therapy and additional drugs.

Aukimmune thyroiditis on the ICD 10 refers to class 4, diseases of the endocrine system, nutrition disorders and metabolic disorders. It is based on the section of the thyroid gland and has an E06.3 code. This section includes acute, subacute, drug, chronic thyroiditis, as well as a chronic form with turning thyrotoxicosis.

RCRZ (Republican Center for Health Development MD RK)
Version: Clinical Protocols MH RK - 2017

Aukimmune thyroiditis (E06.3)

Endocrinology

general information

Short description


Approved
Joint Commission for Medical Services
Ministry of Health of the Republic of Kazakhstan
from "18" August 2017
Protocol No. 26.


Autimmune thyroiditis - Organo - a specific autoimmune disease, which is the main cause of primary hypothyroidism. Independent clinical value in the absence of violation of the function of the thyroid gland does not have.

Input part

Code (s) μb-10:

MKB-10.
The code Name
E 06.3. Autimmune thyroiditis

Date of development / revision of the Protocol: 2017 year.

Abbreviations used in the protocol:


AIT - autimmune thyroiditis
sv. T4. - free thyroxin
sVT3 - free triiodothyronine
Ttg. - thyroid-stimulating hormone
Tg. - thyroglobulin
TPU - Thyroperoxidase
Schu - thyroid
At to tg. - antibodies to thyroglobulin
AT TO TPU - antibodies to thyroperoxidase

Protocol users: Therapists, general practitioners, endocrinologists.

The scale of the level of evidence:


BUT High-quality meta-analysis, systematic Overview of RKK or large rock with a very low probability (++) systematic error The results of which can be distributed to the corresponding population.
IN High-quality (++) systematic overview of cohort or studies Case-control or high-quality (++) cohort or studies Case control with a very low risk of systematic error or rock with low (+) risk of systematic error, the results of which can be distributed to the corresponding population .
FROM Cohort or study case-monitoring or controlled study without randomization with a low risk of systematic error (+).
The results of which can be distributed to the appropriate population or rock with a very low or low risk of systematic error (++ or +), the results of which cannot be directly distributed to the corresponding population.
D. A description of a series of cases or uncontrolled research or the opinion of experts.
GPP. Best clinical practice.

Classification


Classification:

· Atrophic form;
· Hypertrophic form.

Clinical options are juvenile thyroiditis and focal (minimum) thyroiditis.

Histologically determined by the lymphoid and plasmocyte infiltration of thyroid tissue, the oncoccitar transformation of thyroidocytes (Gürtle cells), the destruction of follicles, reducing colloid and fibrosis reserves. Juvenile thyroiditis is manifested by moderate lymphoid infiltration and fibrosis. With focal thyroid, parenchymal destruction and lymphoid infiltration are minimal, Gürtle cells are missing.

The course of the disease is long, in the eutyroid phase asymptomatic. AIT, as a rule, is diagnosed at the primary hypothyroidism stage and less frequently (in 10% of cases) debuts transient (no more than 6 months) by thyrotoxicosis.
The manifestic hypothyroidism, which developed in the outcome of the AIT, testifies to the resistant and irreversible degradation of the parenchyma of the thyroid gland and requires lifelong replacement therapy.

Diagnostics

Methods, approaches and diagnostic procedures

Diagnostic criteria

Complaints and history:
During the first years, complaints and symptoms are usually absent. Over time, complaints may appear on the swelling of the face, limbs, drowsiness, depressive state, weakness, fast fatigue, in women - a violation of the menstrual cycle. It is necessary to take into account that hypothyroidism is not developing in all patients, about 30% can only be the carrier of antibodies to the thyroid gland.

Physical examination: With hypertrophic form, the thyroid gland is increased, dense consistency, the surface of its "uneven"; In atrophic shape, the thyroid gland is not increased.

Laboratory research:
Hormonal Profile: Research TSH, SVT3, SVT4, antibodies to thyroperoxidase, antibody to thyroglobulin

Tools:
· Ultrasound of the pin - a cardinal ultrasonic sign - diffuse reduction of tissue echogenic;
· Ton-needle punkey biopsy - according to the testimony.

Indications for consultation of specialists: no.

Diagnostic algorithm

"Large" diagnostic signs, the combination of which allows you to establish AIT, are - primary hypothyroidism (manifest or subclinical), the presence of antibodies to the tissue of the thyroid gland, as well as ultrasound signs of autoimmune pathology.

Differential diagnosis


Differential diagnosisand substantiating additional research


Treatment abroad

Treat treatment in Korea, Israel, Germany, USA

Get advice on medical examination

Treatment

Treatment (ambulatory)


Tactics of treatment on an outpatient level:
Currently, there are no methods for the actual autoimmune process in the thyroid gland. Medical therapy (levothyroxine preparations) are prescribed only when hypothyroidism is detected.

Non-media treatment
Mode: IV.
Table: Diet №15

Medical treatment: The only drug is Levothyroxin sodium in tablets.
Startup daily dose with manifestic hypothyroidism:
· Patients under 60 years old - 1.6-1.8 μg / kg;
· In patients with accompanying diseases of the cardiovascular system and over 60 years old - 12.5-25 μg, followed by an increase of 12.5-25 μg every 6-8 weeks.
Take an empty stomach in the morning no later than 30 minutes before meals. After taking thyroid hormones for 4 hours, avoid reception of antacids, iron and calcium preparations.

The maintenance of the maintenance dose is carried out under the control of the overall state, the pulse rate, dynamic determination of the level of TSH in the blood. The first definition is made not earlier than 6 weeks from the start of therapy, then before reaching the effect - 1 time in 3 months.

With subclinical hypothyroidism (an increase in the level of TSH in combination with a normal level of T4 in the blood and the absence of a clinic of hypothyroidism) is recommended:
· Re-hormonal study after 3 - 6 months to confirm the persistent nature of the function of the thyroid gland; If subclinical hypothyroidism is detected during pregnancy, the treatment with levothyroxin in a complete replacement dose is assigned immediately;

List of basic medicines(having a 100% probability of use):

List of additional drugs: no.

Surgical intervention: no.

Further maintenance:
· After reaching the clinical and laboratory effect to determine the adequacy of the dose of Levothyroxine, a TTG study is carried out 1 time in 6 months. The criterion for the adequacy of substitution therapy of subclinical hypothyroidism is the persistent maintenance of the normal level of TSH in the blood (0.5-2.5 MME / l).

Patients with concomitant diseases of the cardiovascular system and over 60 years old are advisable on the doses of levothyroxine supporting the state of subclinical hypothyroidism.

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

Indicators of the effectiveness of treatment: Full elimination of clinical laboratory signs of hypothyroidism in young, a decrease in its severity - in the elderly.

Hospitalization

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

Information

Sources and literature

  1. Meeting Protocols of the Joint Commission on the Quality of Medical Services MD RK, 2017
    1. 1) Fadeev.R., Melnichenk.A. Hypothyroidism. Guide for doctors. - M., 2002. - 218 p. 2) Brasermann L.I. Diseases of the thyroid gland. - M.: Medicine. 2000. - 417 p. 3) Kotova G.A. Diseases of the organs of the endocrine system. Edited by Dedova 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. - №3. - P. 26-28. 7) Fadeev V.V. Iodicate and autoimmune diseases in the light iodine deficit region: author. ... dot. honey. science - Moscow. - 2004. - 26 p. 8) Finger M.A., Timeyano.R., Nerevp.s. and others. Autoimmune thyroiditis: pathogenesis, morphogenesis and classification // Archive of pathology. - 1993. - №6 - pp. 7-13. 9) Khmelnitsky O.K., Eliseeva N.A. Thiereoiditis Hashimoto and De Kervena // Archive of pathology. - M.: Medicine. - 2003. - № 6. - P. 44-49. 10) Kalinin A.P., Kiseleva TP Aukoimmune thyroiditis. Guidelines. - Moscow. -1999. - 19 s. 11) Petunina N.A. Clinic, diagnosis and treatment of autoimmune thyroiditis // Endocrinol problems. - 2002. -T48, №6. - P. 16-21. 12) Kaminsky A.V. Chronic autoimmune thyroiditis (etiology, pathogenesis, radiation aspects) // Honey. Hourfis. Ukraine. -1999. - №1 (9). - p.16-22. 13) Kandrorv.I., Kryukova I.V., Khrinkov. And. et al. Anti-ramp antibodies and autoimmune thyroid diseases // Problems of endocrinology. - 1997. - T.43, №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 qualifying data:
1) Taubaldiyeva Zhannat Satybaevna - Candidate of Medical Sciences, Head of Endocrinology, JSC "National Scientific Medical Center";
2) Madeyarova Merurt Shayzindinovna - Candidate of Medical Sciences, Head of Endocrinology Department of the UMC, Republican Diagnostic Center;
3) SMARGULOVA Gaziza Azhmagievna - Candidate of Medical Sciences, Associate Professor, Head of the Department of Internal Diseases and Clinical Pharmacology of RGP on PVV "West Kazakhstan State Medical University named after M.O. Ospanova. "

Indication for the lack of conflict of interest: not.

Reviewers:
1) Bazarov Anna Vikentievna - Candidate of Medical Sciences, Associate Professor of the Department of Endocrinology JSC "Medical University of Astana";
2) Temirgaliyeva Gulnare Shahmpsna - Candidate of Medical Sciences, Endocrinologist LLP "Multidisciplinary Medical Center MEYIRIM".

Note Protocol Review Conditions: 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 the level of evidence.

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