State establishment «dnepropetrovsk medical academy of ministry of health ukraine»

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at methodical meeting

of hospital pediatrics №1 department

Сhief of department professor _____________V. A. Kondratyev

“______” _________________ 2013 y.




Educational discipline


module №


Substantial module №


Theme of the lesson






Dnepropetrovsk, 2013.

  1. Theme urgency:

For the recent years there is significant increase in the amount of children and adults with thyroid hyperplasia. Any physician should be able to identify thyroid disease and evaluate its function. This issue is urgent because untimelydiagnostics and the beginning of treatment of thyroid disorder can cause severe irreversible processes and can form children disability.
2. Specific purposes:

А. Student has to know:

  1. Principles of regulation of human endocrine system.

  2. Characteristics of endocrine system at children

  3. Classification of thyroid disorders at children.

  4. Clinical findings consistent with hypothyroidism, hyperthyroidism.

  5. Contemporary methods of hypothyroidism, hyperthyroidism diagnostics.

  6. Clinical findings consistent with inflammatory processes of thyroid gland.

  7. Clinical and laboratory characteristics of autoimmune thyreoiditis.

  8. Contemporary principles of preventive measures, prophylaxis and treatment of thyroid disorders.

9.Principles of rendering treatment at urgent states at thyroid diseases.
В. Student has to be able to:

  1. Identify thyroid disorder

  2. Formulate diagnosis at thyroid gland diseases according to contemporary classifications.

  3. Conduct treatment of thyroid diseases.

  4. Give emergency medical care to children having thyroid disorders.

  1. Tasks for students` self-dependent work during preparation for the classes.

3.1. List of main terms, parameters, characteristics, which students has to master preparing for the classes.



Diffuse nontoxic goiter

Diffuse enlargement of thyroid gland without disorder of its function.

Diffuse toxic goiter

Disease with increased secretion of thyroid hormones, diffuse enlargement of thyroid gland and ophthalmopathy.


Syndrome, causes by prolonged Т4 and Т3 elevation in blood and tissues with typical clinical findings.


Increased secretion of thyroid hormones by thyroid gland.


Decreased secretion of thyroid hormones by thyroid gland.

Endemic goiter

Enlargement of thyroid gland, which is observed at most of people, who live in geographic areas with insufficient amount of iodine in the environment.

3.2. Theoretical questions for classes:

  1. Features of regulation of endocrine system in childhood.

  2. Functions of thyroid gland hormones.

  3. Classification of thyroid disorders.

  4. Definition of terms «diffuse toxic goiter, hypothyroidism,

autoimmune thyroiditis, endemic goiter».

  1. Clinical findings consistent with hypothyroidism

  2. Clinical findings consistent with hyperthyroidism.

  3. Clinical findings suggesting congenital hypothyroidism.

  4. Clinical findings suggesting diffuse toxic goiter

  5. Clinical findings consistent with autoimmune thyroiditis.

  6. Methods of thyroid disorders diagnostics in childhood.

  7. Principles and methods of treatment of thyroid gland diseases.

  8. Emergency states at thyroid disorders. Providing medical assistance.

  9. Dispensary observation at children having thyroid diseases.

4.3 . Practical works (tasks) which are performed on occupation:

1 To collect complaints, case history and personal (life) history

2. To inspect the child consistently

3. To reveal early symptoms of thyroid disorders

4 .To reveal the signs of the complications of thyroid disorders

5. To evaluate the condition of the child and available clinical symptoms. 6. To evaluate the results of the additional methods of investigation

7. To make the clinical diagnosis according to classification.

8. To make the treatment plan.

9. To make recommendations of dispensary supervision.


  1. Maintenance of the subject:

5.1 . Diffuse toxic goiter ICD 10-X E. 05
1 . Definition: Diffuse toxic goiter (Graves disease, Bazedov's disease – an organ specific autoimmune disease which is characterized by the permanent increased secretion of thyroid hormones, diffuse enlargement of thyroid gland and endocrine ophthalmopathy (50-70% of cases)

2 . Classification of severity of thyrotoxicosis

2.1. Subclinical

- Absence of clinical manifestations of thyrotoxicosis

- Low TTH, normal T3 and T4

2.2. Manifest

- Obvious clinical manifestations

- Low TTG, highT4 and/or T3.

2.3. Complicated

- Complications (atrial fibrillation, heart failure, thyroid relative adrenal insufficiency, dystrophic changes of parenchymatous organs, psychosis, the expressed deficiency of weight)

3. Clinical criteria of diagnostics

3.1. Changes of the thyroid gland

As a rule, diffusely enlargement of the both lobes and an isthmus, painless, mobile, elastic consistence. There are could be thyrotoxicosis without enlargement of the thyroid.

Vascular murmure could be heard over gland by auscultation.

3.2. Condition of the skin and its appendages

Velvety, warm, moist. Diffuse sweating. Fragility of nails, hair loss

3.3. Cardiovascular


Tachycardia, increased heart beat, accented tones of the heart, a constant or paroxysmal sinus tachycardia, extrasystoles, paroxysmal or constant atrial fibrillation, predominantly systolic arterial hypertension, increased pulse pressure more than 60 mm hg, myocardiodystrophy, heart failure ("thyrotoxic heart")

3.4. Digestion system

Unstable stool, with tendency to diarrhea, rare isolated abdominal pain . Increased intestinal movement, thyrotoxic hepatosis.

3.5. Nervous system

Increased excitement, irritability, tearfulness, disturbes the concentration of attention, decrease in the school progress, disordered sleep.

Symptom of Mary (tremor of fingers of outstretched arms), tremor of all body ("a symptom of a cable column"), increased reflexes, difficulties in the performance of exact movements

3.6. Muscular system

Muscular weakness, fast fatigue, atrophy, myasthenia, periodic paralysis. Proximal thyrotoxic myopathy.

3.7. Metabolism acceleration

Heat intolerance, weight loss, increased appetite, thirst, • Acceleration of growth, skeleton differentiation • Hypercalcemia, hypercalciuria


3.8. Eye symptoms

Eye symptoms develop as a result of the disorder of autonomic innervation of the eye. Eye fissures are expanded, exophthalmus, blur vision, diplopia

Grefe symptom

Delay in movement of the upper eyelid from iris while looking down

Kokher symptom

Delay in movement of the upper eyelid from iris while looking up

Moebius symptom

Loss of ability to fix a look at a short distance

Shtelvag symptom

Rare blinking

Delrimpl symptom

Widely opened eye fissures

Kraus symptom

Brightness in eyes

It is important to distinguish eye symptoms of a thyrotoxicosis from an isolated endocrine ophthalmopathy (EOP)

3.9. Other endocrine organs

Secondary diabetes mellitus or disordered tolerance to carbohydrates. Thyroidal relative (at normal level of cortisol) adrenal insufficiency (possibility of acute adrenal insufficiency at the stress condition): moderate hyperpegmentation of the skin folds, scars, areolas, genitals, periorbital pigmentation, frequent "poisonings".

3.10. Sexual system

At girls —menarche delay, disorders of menstrual cycle (oligoopsomenorrhea, amenorrhea). At boys - ginecomastiya.

3.11 Diseases accompanying diffuse toxic goiter

Endocrine ophthalmopathy, pretibial micsedema (induration and a hypertrophy of the skin of the anterior surface of the shin), rare - an acropathy: periostal osteopathy of feet and wrists radiographically reminds "soapsuds".

4 . Paraclinical criteria of diagnostics

a. Obligate

- Low TTH, high T4 and/or T3 (at subclinical thyrotoxicosis - normal T4 and T3).

- Ultrasound investigation: diffusion enlargement of thyroid (isn't obligatory criterion of the diagnosis), at color Doppler mapping – increased circulation over thyroid.

- Glucose tolerance test - can be diabetic sugar curve, disordered glucose tolerance or diabetes.

a. Additional

- Increased stimulating antibodies to the receptor of TTH (TSAb)

- Increased ATPO or AMF titers

- For the confirmation of adrenal insufficiency - free cortisol in blood (morning) or in daily urine, blood electrolytes (K, Na)

- In case of endocrine ophthalmopathy - signs of hickening of retrobulbar muscles (Ultrasound investigation, CT, MRI of orbits)

5. Differential diagnostics

Classification of the thyrotoxicosis at children. ICD 10 code

Е 05.0

Diffuse toxic goiter

Е 05.1

Thyrotoxicosis with a toxic one-nodal goiter

Е 05.2

Thyrotoxicosis with a toxic multinodal goiter

Е 05.4

Artificial, yatrogennous thyrotoxicosis

Е 05.5

Thyrotoxic crisis, coma

Е 05.8

TTH-secreting adenoma of pituitary

Е 05.8

Iodine-induced thyrotoxicosis

Е 05.9

Not specified thyrotoxicosis

Р 72.1

Transient neonatal thyrotoxicosis

Е 06.1

Subacute thyroiditis (thyrotoxic phase)

Е 06.2

Chronic thyroiditis with transient thyrotoxicosis (but not AIT)

Е 06.3

Chronic lymphocytic thyroiditis with transient thyrotoxicosis


The thyrotoxicosis is the syndrome caused by prolonged increase of the T4 and T3 level in blood and tissues with characteristic clinical manifestations.

Hyperthyroidism – increase of secretion of thyroid hormones by the thyroid gland.

Causes of thyrotoxicosis:

1 . Thyrotoxicosis which is caused by increased production of thyroid hormones by thyroid gland:


- Diffusion toxic goiter (DTG)

- Thyrotoxic adenoma

- Multinodal toxic goiter

- Iodine-induced thyrotoxicosis (iodine-bazedov)

- Highly differentiated cancer of the thyroid gland

- Gestational thyrotoxicosis

- Horion carcinoma, hydatid mole

- autosom-dominant not immune thyrotoxicosis

B. TTH-dependent

- thyrotropinoma

- syndrome of inadequate secretion of TTH (resistance of thyrotrophs to thyroid hormones)

2 . Thyrotoxicosis isn't caused by increased production of thyroid hormones:

- thyrotoxic phase of autoimmune (AIT), subacute viral and postpartum thyroiditis.

- artifitial

- amiodaron-induced

- yatrogeny

3 . Thyrotoxicosis which is caused by production of thyroid hormones outside the thyroid gland.

- struma ovarii

- functionally active metastases of the thyroid cancer

The hyperthyroidism at adolescents is caused by the diffusion toxic goiter (DTG) in more than 90% of cases.
5. Treatment

1.Thyrostatic medications- methimazole, propylthiouracil.

- Initial dose - 0,3-0,5 mg/kg/day - depending on severity of a hyperthyroidism. The dose is divided into 2-3 intakes. At clinical improvement of the condition (normal pulse, absence of clinical manifestations of a hyperthyroidism) - on the average in 14-21 days - further each 10-16 days the dose should be decreased by 2,5-5 mg to the supporting dose.

- Mean supporting dose - 2,5-7,5 mg/day (about 50% from initial) - 1 time per day.

- Side effects of methimazole: skin allergic itching rash; blood count disorders: leucopenia up to agranulocytosis with fever, sore throat, diarrhea, thrombocytopenia.

- In case of hyperthyroidism owing to the destruction of thyrocytes (hyperthyroid phase of AIT or subacute thyroiditis) antithyroid drugs should not be administered. Symptomatic treatment (β-adrenoblockers, sedative) should be prescribed.

- In case of an allergy to antithyroid drugs or their side effects - preparations of lithium carbonatis in a dose of 30-50 mg/kg/day

2.Beta-adrenoblockers (anaprilin, propranolol) – for the first 4 weeks, combined with antithyroid drugs - 1-2 mg/kg/day in 3-4 intakes. When the heart rate normalizes - gradual decrease in a dose to the full cancellation of a preparation (acute termination of the intake of the drug can cause "a cancellation syndrome", with condition deterioration).

3. Whet euthyroidism has been achieved (on the average in 6-8 weeks from an initiation of treatment) - the combined therapy: thionamides (methimazole, etc.) 5-10 mg/day and L-thyroxin 25-50 mcg/day.

4. Glucocorticoids:

- At the severe course of the hyperthyroidism, if assosiated with endocrine ophthalmopathy

- If adrenal insufficiency is present

- At poor parameters of complete blood count (leucopenia, thrombocytopenia)

- If there is accompanying disorder, stressfull condotion - for the prevention of acute adrenal failure

- Prednisone at a short course of 0,2-0,3 mg/kg/day for 2-3 intakes, with gradual decrease in 7-10 days at 2,5-5 mg each 5-7 days to full cancellation.

6. Additional methods of treatment

- Sanitation of the centers of an infection.

- Sedative preparations.

- Vitamins.

- Hepatoprotectors

Treatment duration: 2-4 years

Criteria of efficiency of treatment:

- Absence of clinical manifestations of hyperthyroidism

- T4 and TTH normalization

Prevention: Sanitation of the centers of an infection, restriction of sun exposure

Dispensary supervision of 3-4 years after clinical recovery, and also after surgical treatment.

7 . Thyrotoxic crisis:

Thyrotoxic crisis is the complication of diffuse toxic goiter. The disease can occur after stressful condition, exertion, intercurrent disease, most often - after strumectomy if operation is performed without achievement of the compensation of the disease.

Clinical manifestations of thyrotoxic crisis are aggravated clinical manifestations of hyperthyroidism: hyperthermia, vomiting, sweating, acute heart failure, motor anxiety or adinamiya, behavioral disturbances (up to psychosis), hallucinations which change to stupor, unconsciousness, and then - to coma. The death as the resulf of acute heart and adrenal failure. Treatment of thyrotoxic crisis:

  1. Thyonamides (methimazole, etc.) - 40-80 mg/day (orally, through a naso-gastric probe or per rectum)

  2. For the suppression of the secretion of thyroid hormones 1% solution of Lugol is administered in an hour after thyonamides, in which potassium iodine is replaced with sodium iodine (1 g of iodine, 2 g of sodium of iodide, 100 ml of the distilled water) - intravenously or in an enema, 50-100 drops on 0,5 l of 5% of glucose solution or isotonic solution of sodium chloride, further – oral intake of solution at 20-25 drops 3 times in days with milk. It is possible to use intravenous administration of 5-10 ml of 10% of iodide sodiumsolution instead of Lugol solution.

  3. Due to the adrenal hypofunction and for the decrease of peripheral effects of thyroid hormones, beginning from the first hour of crisis resolution - glucocorticoids (2-6 mg/kg by prednisone) intravenously with isotonic solution of sodium chloride, 5% of glucose - to 2-3 l per day.

  4. If blood pressure is low – mineralocorticoides - fludrocortisones: children <1 year-old– 180-300 mcg/sq.m, 1-3 years – 70-100 mcg/sq.m, 3-14 years – 25-50 mcg/sq.m

  5. β-adrenoblockers 2 mg/kg per day orally 3-6 times per day or intravenously slowly 1 mg per minute, to reduce a dose gradually.

  6. Sedative medications (diazepam of 0,5-1,0 mg/kg), at the severe psychomotor excitement - in/m aminazine (1-2 mg/kg) or droperidol (0,5 mg/kg), or chloralhydratis in enemas (by 0,5-1 g in the enema). In complicated cases – therapeutic anesthesia (oxygen, with oxibutiratis sodium, hexenal, sibazone) for 1-3 days.

  7. Desensibilizing preparations are prescribed- suprastin (2% 0,5-1 ml), pipolphen (2,5% 0,5 - 1мл), a Dimedrol (1% 1-2 ml).

  8. To eliminate the expressed hyperthermia the patient is cooled with fans, ward airing, applying of bubbles with ice to reflexive zones (to the head, to feet, to the epigastric region, in the inguinal area), covering with damp sheets. If there is no effect - amidopirin or contrical as the antagonists of proteases (20-40 000 U) intravenously in 250-500 ml of isotonic solution of sodium chloride, at its absence - analginum 50% 1-2 ml intravenously. It is undesirable to administer salycylates through their enhancing of the thyroid hormones.

  9. For the rehydration and desintoxication - glucose-salt solutions (1:1) intravenously or per rectum. To introduce no more then 2-3 l per day, at heart failure - 1-1,5 l.

10. Cardiac glycosides are administered in case of persistent tachycardia which isn't decresed by ƅ-adrenoblockators and also for the prevention of side effects of the blockers at the cardiovascular system (for example corglycon 0,06% 0,5-1,0 ml intravenously slowly with 20 ml of 40% glucose or with hydrocortisone, 5% glucose or 0,9% of sodium chloride).

11. High doses of vitamins (C or B, especially B1)

12 . Continuous oxygen therapy.

13 . For microcirculatory improvement - albumine solution, blood plasma, rheopolyglucin.

14 . For the prevention of infection - antibiotics of a wide range of action in high doses.

15 . Treatment of thyrotoxic crisis is carried out to the full resolution of clinical and metabolic manifestations (7-10 days). If within 24-48 hours the condition doesn't improve and if the patient is in comatose condition the plasmapheresis and/or peritoneal dialysis, hemosorbtion are recommended.

5.2 . Hypothyroidism

ICD 10 code:

Е 00 - Syndrome of congenital iodine insufficiency

Е 02. – Subclinical hypothyroidism (minimal thyroid insufficiency)

Е 03.0 - Congenital hypothyroidism with diffuse goiter

Е 03.1 - Congenital hypothyroidism without goiter

Е 03.2 – Medication- induced hypothyroidism

Е 03.3 - After infectious hypothyroidism

Е 03.4 - Atrophy of the thyroid gland (acquired)

Е 03.5 – Hypothyroid coma

Е 03.8 - Other specified hypothyroidism

Е 03.9 - Not specified hypothyroidism

E. 89 - After procedural hypothyroidism

1 . Definition. Hypothyroidism is the clinical syndrome caused by prolong, stable deficiency of thyroidal hormones or decrease in their biological effect at tissue level.

2 . Classification.

A. By the level of damage

1 . Primary (thyroidal)

2 . Secondary (pituitary), tertiary (hypothalamic)

a. Panhypopituitrizm

b. The isolated deficiency of TTH

c. Anomalies of hypothalamo-pituitary system

3 . Fabric (transport, peripheral) - resistance to thyroid hormones; hypothyroidism at a nephrotic syndrome.

B. 1. Congenital:

- anomalies of the development of thyroid gland: dysgenesis (agenesis, hypoplasia, dystopia, ectopy);

- dyshormonogenesis: congenital enzimopathy that are associated with disorders of biosynthesis of thyroid hormones; defect of receptors to TTH;

- congenital panhypopituitarizm;

- transient;

- iatrogenic;

- caused by maternal thyroblocking antibodies;

- idiopathic.

2 . Acquired:

- thyroiditis (autoimmune thyroiditis, hypothyroid phase, subacute viral),

- postprocedural (thyroid gland operations),

- iatrogenic (antithyroid therapy by radioactive iodine, antithyroid drugs)

- endemic goiter.

C. By the course of the disease :

- Tansient

- Subclinical (minimum thyroid insufficiency)

- Manifest

G. By the condition of compensation:

- Compensated

- Decompensated

D. Complications: thyroidal nanizm, encephalopathy, cretinism, polyneuropathy, myopathy, hypothyroid coma, sexual development disoders (delay or premature puberty), and etc.

Example of the formulation of the diagnosis:

- Primary hypothyroidism owing to autoimmune thyroiditis, moderate severety, compensated. Hypothyroid encephalopathy І degree.

- Congenital hypothyroidism, severe form, decompensated. Cretinism. Thyroidal nanizm

3Criteria of diagnostics:

1 . Clinical:

In the neonatal period:

  • Big weight of the newborn child (more than 3 500 g)

  • Pale, dry skin

  • Dense edema on back surfaces of the hands, a foot, in supraclavicular regions

  • Edematous face

  • Increased in a size tongue and lips

  • Rough, a low timbre a voice when crying

  • Signs of immaturity of the newborn at full-term pregnancy

  • Late disappearing of the umbilical cord, poor healing of the umbilical wound

  • Weak sucking reflex

  • Slow movements, diminished reflexes

  • Late mekonium taking off

At children older then 3 month:

- Delay of psychomotor development

- Late closing of a fontanel

- Meteorism, constipations,

- Dryness, pallor of skin

- Brittle, dry hair

- Cold hands, feet

- Widely sunk down nose bridge

- Late teeth eruption and replacement of permanent teeth

- Muscles: hypotonia, hypertrophy, possible seizures

- Growth delay (thyroidal nanizm)

At adolescents:

- Decrease in intelligence of different degree

- Growth delay (thyroidal nanizm)

- Delay or advancing of sexual development

- Dryness, pallor of skin

- Brittle, dry hair

- Face, extremities, tongue edema

- Bradycardia

Paraclinical investigation:


- Complete blood count: anemia, sometimes accelerated ESR

- High cholesterol, ƅ-lipoproteins

- Electrocardiogram: sinus bradycardia (in the first months of life pulse can be within normal range), decrease voltage, delay of conduction, systole prolongation

- Visualization of a thyroid gland – ultrasound investigation

Hormonal diagnostics (has to be carried out by highly sensitive devices):

- At the subclinical hypothyroidism: high thyrotropic hormone (TTH) (higher then 2,5 mU/l, but no more then 10 mU/l), normal T4, absence of clinical manifestations.

- At the manifest hypothyroidism - TTH is higher then 10 mU/l, T4 decreased;

- At the secondary hypothyroidism - TTH normal or decreased, T4 decreased.

- For the differential diagnostics of primary and secondary hypothyroidism - test with thyrooliberin: evaluation of the TTH level before and 30 minutes after intravenous administration of the medication. At primary hypothyroidism - TTH increases more than 25 U/l, at secondary - remains at the previous level.

B. Adiitional investigations

- X-ray of hands: delay of "bone" age, epiphyseal dysgenesis

- For the diagnostics of AIT: antibodies to thyroperoxidase (ATPO) or to the microsomal fraction (AMF) - above the upper limit by 2-3 times.

- The blood analysis on toxoplasmosis

4 . Treatment of hypothyroidism

It is carried out for life.

a. Replacement therapy by thyroid hormones (L-tiroxine) is administered irrespectively of the level of affection and the reasons which caused hypothyroidism.

- The full replacement dose is administered at once.

- TTH control (at primary hypothyroidism) or T4 (at secondary hypothyroidism) is carried out: while shoosing individuale dose - 1 time per 1 month, further, at achievement of compensation (TTH 0,5-2,0 mU/l) - 1 time per 6 months.

L-thyroxin doses:


Daily dose, mcg/kg



0-3 months.


3-6 m.


6-12 m.


1-3 m.


3-10 m.


10-15 m.


> 15 m.


b. Symptomatic treatment of anemia, encephalopathy, polyneuropathy, etc.

Indications to hospitalization: severe decompensation of the disease

Criteria of efficiency of treatment:

- Absence of clinical symptoms of the disease

- Normal growth rates and pubertal development

- TTH 0,4-2,0 mU/ml.

5 . Prevention:

Elimination of the causes which lead to hypothyroidism

6 . Dispensary supervision – lifelong
3. Autoimmune тиреоидит (AIT)

ICD X code - Е 06.3

1. DEFINITION: Autoimmune thyroiditis (AIT) – a chronic disease which at children and adolescents has specific clinical manifestations and the course, caused by a recent debut of the disease and therefore the minimal morphofunctional changes of the thyroid gland (TG) at initial stages of immunopathological process.

2 . Classification of autoimmune thyroiditis

1 . By functional condition of the thyroid gland:

- Hypothyroidism

- Euthyroidism

- Hyperthyroidism

2 . According to the size of thyroid gland:

- Hypertrophic form

- Atrophic form

3 . . According to the clinical course:



4. According to the nosological form:

- AIT as independent disease

- AIT in combination with other thyroid diseases (subacute thyroiditis, nodal goiter, hyperthyroidism)

- As the component of the autoimmune polyendocrine syndrome

3. Criteria of diagnostics

There is no way of the establishment of the diagnosis of AIT based on application of any uniform diagnostic criterion. The main diagnostic principle is an application of an integrated approach:

  • At the first stage all children with diffuse nontoxic goiter (DNC) (according to clinical manifestations and data of palpation), ultrasound of thyroid, antithyroidal antibodies (ATPO or AMF) should bt carried out.

  • For the specification of the thyroidal function and definition of the phase of the course of AIT – serum TTH, fТ3, fТ4.

- By specific indications - morphological verification with biopsy of the goiter.

5 . Hypertrophic form (Hashimoto's goiter)

Hypertrophic form of AIT (Hashimoto's goiter) at children and teenagers is diagnosed in case of existence of the following obligatory signs:

- Increase in volume of thyroid gland of more than 97 percentiles of standard gender values, depending upon the body surface area (determined by the nomogram)

- High titer of antibodies to the thyroidal peroxidase – ATPO (or to microsomal fraction of thyrocites – AMF) in blood serum – above the maximum threshold of "a gray zone" (if it is specified) or in 2 and more times above the upper limit of "norm" (according to reference values of the used set of reactants).

- Ultrasonic changes of structure of thyroid: diffuse heterogeneity - decreased echogenity with – hyperechogenic and isoechogenic regions.

- Decrease in function of thyroid at AIT isn't an obligate symptom of the disease and isn't its main diagnostic criterion. However existence of the acquired primary hypothyroidism at children and adolescents should be regarded as the result of AIT (an atrophic or hypertrophic form).

6 . Treatment.

It is carried out on an outpatient basis.

1 . Sanitation of the centers of an infection

2 . Administration of any preparations and methods for the purpose of influencing on autoimmune process should not be used due to the lack of proofs of their efficiency on autoimmune process in thyroid (immunodepresants, immunomodulators, glucocorticoids, plasma exchange, preparations of thyroid hormones, etc.)

3 . Indications to the L-thyroxin treatment:

- obvious hypothyroidism (high TTG, low fТ4);

- subclinical hypothyroidism (normal T4, high TTH levels that confirmed by double investigation);

- significant increase in volume of thyroid (more than for 30% from the upper limit of norm) if level of T4 is normal and the TTH level is higher than 2 mU/l:

- for the elimination and/or prevention of progressing of the growth of the goiter;

- for the prevention of the syndrome of a compression and (pseudo) nodal formation;

- for the preparation for the reproductive period and for pregnancy.

Achievement of the normal TTH level and its permanent preservation at an optimum level (0,5-2,0 mU/l) are criteria of adequacy of L-thyroxin treatment.

4 . Potassium iodide in a dose of 200 mcg/day for 6 - 12 months is recommended to children who have diffuse goiter with geterogenous structure in the absence of antibodies to TPO. At a positive effect of the therapy (the goiter decreases or disappears) the goiter is treated as endemic (iodine-deficient) and intake of potassium iodide of should be continued. In the absence of effect (the goiter progresses) therapy with L-thyroxin is appointed.

Patients with AIT which live in regions of iodine deficiency, can receive physiological doses of iodine (100-200 mcg/day)

Criteria of the efficacy of treatment

normalization of structure and size of thyroid gland

In case of hypothyroidism - normal TTH

7 . Prevention:

Elimination of risk factors. Specific prevention doesn't exist.

8 . Dispensary supervision: all children with the confirmed or probable diagnosis of AIT need in constant, lifelong dispensary supervision

4 . Endemic goiter

ICD X-E 01.0 code

1 . Definition: Endemic goiter is the enlargement of thyroid gland, which is observed at significant number people, who live in geographic areas with insufficient amount of iodine in the environment.

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