Autoimmune thyroiditis and hypothyroidism - what is the difference? Autoimmune thyroiditis Autoimmune thyroiditis of the thyroid gland, subclinical hypothyroidism.

Chronic autoimmune thyroiditis, autoimmune lymphocytic thyroiditis, Hashimoto's thyroiditis, lymphadenomatous goiter, lymphomatous struma.

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Autoimmune thyroiditis (E06.3)

Endocrinology

general information

Short description

Autoimmune thyroiditis- chronic inflammatory disease thyroid gland(thyroid gland) of autoimmune origin, in which, as a result of chronically progressive lymphoid infiltration, gradual destruction of thyroid tissue occurs, most often leading to the development of primary hypothyroidism Hypothyroidism is a thyroid deficiency syndrome characterized by neuropsychiatric disorders, swelling of the face, limbs and trunk, bradycardia
.

The disease was first described by the Japanese surgeon H. Hashimoto in 1912. It develops more often in women after 40 years. There is no doubt about the genetic cause of the disease, which is realized under the influence of factors environment(long-term intake of excess iodine, ionizing radiation, the influence of nicotine, interferon). The hereditary genesis of the disease is confirmed by the fact of its association with certain antigens of the HLA system, most often with HLA DR 3 and DR 5.

Classification

Autoimmune thyroiditis (AIT) is divided into:

1.Hypertrophic AIT(Hashimoto's goiter, classic version) - an increase in the volume of the thyroid gland is characteristic; histologically, massive lymphoid infiltration with the formation of lymphoid follicles, oxyphilic transformation of thyrocytes is revealed in the thyroid tissue.

2. Atrophic AIT- a decrease in the volume of the thyroid gland is characteristic; the histological picture is dominated by signs of fibrosis.

Etiology and pathogenesis

Autoimmune thyroiditis (AIT) develops against the background of a genetically determined defect in the immune response, leading to T-lymphocyte aggression against one’s own thyrocytes, ending in their destruction. The genetic determination of development is confirmed by the fact of the association of AIT with certain antigens of the HLA system, most often with HLA DR 3 and DR 5.
In 50% of cases, relatives of patients with AIT have circulating antibodies to the thyroid gland. In addition, there is a combination of AIT in the same patient or within the same family with other autoimmune diseases - type 1 diabetes, vitiligo Vitiligo is an idiopathic dyschromia of the skin, characterized by the appearance of depigmented spots of various sizes and outlines of a milky white color with a surrounding zone of moderate hyperpigmentation
, pernicious anemia, chronic autoimmune hepatitis, rheumatoid arthritis, etc.
The histological picture is characterized by lymphocytic and plasmacytic infiltration, oncocytic transformation of thyrocytes (formation of Hürthle-Ashkenazi cells), destruction of follicles and proliferation Proliferation - an increase in the number of cells of any tissue due to their reproduction
fibrous (connective) tissue, which replaces the normal structure of the thyroid gland.

Epidemiology

It occurs 4-6 times more often in women than in men. The ratio of people aged 40-60 years suffering from autoimmune thyroiditis between men and women is 10-15:1.
Among the population of various countries, AIT occurs in 0.1-1.2% of cases (in children); in children, there is one boy for every 3 sick girls. AIT is rare in children under 4 years of age; the maximum incidence occurs in the middle of puberty. In 10-25% of practically healthy individuals with euthyroidism Euthyroidism - normal functioning of the thyroid gland, absence of symptoms of hypo- and hyperthyroidism
Antithyroid antibodies may be detected. The incidence is higher in individuals with HLA DR 3 and DR 5.

Risk factors and groups

At-risk groups:
1. Women over 40 years old, with a hereditary predisposition to thyroid diseases or if there are such in close relatives.
2. Persons with HLA DR 3 and DR 5. The atrophic variant of autoimmune thyroiditis is associated with the haplotype Haplotype - a set of alleles at loci of one chromosome (different forms of the same gene located in the same regions), usually inherited together
HLA DR 3, and the hypertrophic variant with DR 5 of the HLA system.

Risk factor: long-term intake of large doses of iodine for sporadic goiter.

Clinical picture

Symptoms, course

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

Euthyroid phase may last for many years or decades, or even throughout life.
Further, as the process progresses, namely, the gradual lymphocytic infiltration of the thyroid gland and the destruction of its follicular epithelium, the number of cells producing thyroid hormones decreases. Under these conditions, in order to provide the body with a sufficient amount of thyroid hormones, the production of TSH (thyroid-stimulating hormone) increases, which hyperstimulates the thyroid gland. Due to this hyperstimulation for an indefinite period of time (sometimes decades), it is possible to maintain T4 production at a normal level. This subclinical hypothyroidism phase, where there are no obvious clinical manifestations, but TSH level elevated with normal T4 values.
With further destruction of the thyroid gland, the number of functioning thyrocytes falls below a critical level, the concentration of T 4 in the blood decreases and hypothyroidism manifests itself, manifesting phase of obvious hypothyroidism.
Quite rarely, AIT can manifest transient thyrotoxic phase (hashi toxicosis). The cause of hashi toxicosis can be both destruction of the thyroid gland and its stimulation due to the transient production of stimulating antibodies to the TSH receptor. Unlike thyrotoxicosis in Graves' disease (diffuse toxic goiter), hashi toxicosis in most cases does not have a pronounced clinical picture of thyrotoxicosis and occurs as subclinical (reduced TSH with normal T3 and T4 values).

The main objective sign of the disease is goiter(enlarged thyroid gland). Thus, the main complaints of patients are associated with an increase in thyroid volume:
- feeling of difficulty when swallowing;
- difficulty breathing;
- often slight pain in the thyroid area.

At hypertrophic form The thyroid gland is visually enlarged, upon palpation it has a dense, heterogeneous (“uneven”) structure, is not fused with the surrounding tissues, and is painless. Sometimes it can be regarded as nodular goiter or thyroid cancer. Tension and slight pain in the thyroid gland may occur with a rapid increase in its size.
At atrophic form the volume of the thyroid gland is reduced, palpation also reveals heterogeneity, moderate density, and the thyroid gland is not fused with the surrounding tissues.

Diagnostics

TO diagnostic criteria Autoimmune thyroiditis includes:

1. Increased level of circulating antibodies to the thyroid gland (antibodies to thyroid peroxidase (more informative) and antibodies to thyroglobulin).

2. Detection of typical ultrasound data of AIT (diffuse decrease in the echogenicity of the thyroid tissue and an increase in its volume in the hypertrophic form, in the atrophic form - a decrease in the volume of the thyroid gland, usually less than 3 ml, with hypoechogenicity).

3. Primary hypothyroidism (manifest or subclinical).

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

A puncture biopsy of the thyroid gland to confirm the diagnosis of AIT is not indicated. It is carried out for differential diagnosis with nodular goiter.
After diagnosis has been established, further study of the dynamics of the level of circulating antibodies to the thyroid gland in order to assess the development and progression of AIT has no diagnostic or prognostic value.
In women planning pregnancy, if antibodies to thyroid tissue are detected and/or ultrasound signs AIT, it is necessary to examine the function of the thyroid gland (determining the level of TSH and T4 in the blood serum) before conception, as well as in each trimester of pregnancy.

Laboratory diagnostics

1. General analysis blood: normal or hypochromic anemia.

2. Biochemical analysis blood: changes characteristic of hypothyroidism (increased levels of total cholesterol, triglycerides, moderate increase in creatinine, aspartate transaminase).

3. Hormonal study: various options for thyroid dysfunction are possible:
- increased TSH level, T4 content within normal limits (subclinical hypothyroidism);
- increased TSH levels, decreased T4 (manifest hypothyroidism);
- decrease in TSH level, T4 concentration within normal limits (subclinical thyrotoxicosis).
Without hormonal changes in thyroid function, the diagnosis of AIT is not valid.

4. Detection of antibodies to thyroid tissue: as a rule, there is an increase in the level of antibodies to thyroid peroxidase (TPO) or thyroglobulin (TG). A simultaneous increase in the titer of antibodies to TPO and TG indicates the presence or high risk of autoimmune pathology.

Differential diagnosis

A differential diagnostic search for autoimmune thyroiditis must be carried out depending on the functional state of the thyroid gland and the characteristics of the goiter.

The hyperthyroid phase (hashi toxicosis) should be differentiated from diffuse toxic goiter.
Evidence in favor of autoimmune thyroiditis is:
- the presence of an autoimmune disease (in particular AIT) in close relatives;
- subclinical hyperthyroidism;
- moderate severity of clinical symptoms;
- short period of thyrotoxicosis (less than six months);
- no increase in the titer of antibodies to the TSH receptor;
- characteristic ultrasound picture;
- rapid achievement of euthyroidism when prescribing small doses of thyreostatics.

The euthyroid phase should be differentiated from diffuse nontoxic (endemic) goiter(especially in areas with iodine deficiency).

The pseudonodular form of autoimmune thyroiditis is differentiated from nodular goiter, thyroid cancer. In this case, a puncture biopsy is informative. A typical morphological sign for AIT is local or widespread infiltration of thyroid tissue by lymphocytes (the lesions consist of lymphocytes, plasma cells and macrophages, penetration of lymphocytes into the cytoplasm of acinar cells is observed, which is not typical for the normal structure of the thyroid gland), as well as the presence of large oxyphilic Hurthle cells. Ashkenazi.

Complications

The only clinically significant problem that AIT can lead to is hypothyroidism.

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Treatment

Treatment goals:
1. Compensation of thyroid function (maintaining TSH concentration within 0.5 - 1.5 mIU/l).
2. Correction of disorders associated with an increase in the volume of the thyroid gland (if any).

Currently, the use of sodium levothyroxine in the absence of disturbances in the functional state of the thyroid gland, as well as glucocorticoids, immunosuppressants, plasmapheresis/hemosorption, laser therapy for the purpose of correcting antithyroid antibodies is recognized as ineffective and inappropriate.

The dose of levothyroxine sodium required for replacement therapy for hypothyroidism against the background of AIT is on average 1.6 mcg/kg body weight per day or 100-150 mcg/day. Traditionally, when selecting individual therapy, L-thyroxine is prescribed starting with relatively small doses (12.5-25 mcg/day), gradually increasing them until a euthyroid state is achieved.
Levothyroxine sodium orally in the morning on an empty stomach, 30 minutes before. before breakfast, 12.5-50 mcg/day, followed by increasing the dose by 25-50 mcg/day. up to 100-150 mcg/day. - for life (under control of TSH levels).
A year later, an attempt is made to discontinue the drug in order to exclude the transient nature of thyroid dysfunction.
The effectiveness of therapy is assessed by the level of TSH: when prescribing a full replacement dosage - after 2-3 months, then once every 6 months, then once a year.

According to the clinical recommendations of the Russian Association of Endocrinologists, physiological doses of iodine (about 200 mcg/day) do not have a negative effect on thyroid function in pre-existing hypothyroidism caused by AIT. When prescribing drugs containing iodine, one should be aware of the possible increase in the need for thyroid hormones.

In the hyperthyroid phase of AIT, thyreostatics should not be prescribed; it is better to use symptomatic therapy (ß-blockers): propronolol 20-40 mg orally 3-4 times a day, until clinical symptoms are eliminated.

Surgical treatment is indicated for significant enlargement of the thyroid gland with signs of compression of surrounding organs and tissues, as well as for rapid growth size of the thyroid gland against the background of long-term moderate enlargement of the thyroid gland.

Forecast

The natural course of autoimmune thyroiditis is the development of persistent hypothyroidism, with the appointment of lifelong hormone replacement therapy levothyroxine sodium.

The probability of developing hypothyroidism in a woman with an elevated AT-TPO level and a normal TSH level is about 2% per year, the probability of developing overt hypothyroidism in a woman with subclinical hypothyroidism (TSH is elevated, T 4 is normal) and an elevated AT-TPO level is 4.5 % in year.

In women who are carriers of AT-TPO without thyroid dysfunction, when pregnancy occurs, the risk of developing hypothyroidism and so-called gestational hypothyroxinemia increases. In this regard, in such women it is necessary to monitor thyroid function early stages pregnancy, and, if necessary, at a later stage.

Hospitalization

Term inpatient treatment and examinations for hypothyroidism - 21 days.

Prevention

There is no prevention.

Information

Sources and literature

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

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2 years ago

Diseases of the endocrine system in women occur with the same frequency as gynecological ones, but much less is known about them. In particular, few people understand what autoimmune thyroiditis is, treatment of which should begin as early as possible. Otherwise, the chances of completely getting rid of the problem tend to zero. Who is at risk for this disease, what is its danger?

Clinical picture of autoimmune thyroiditis of the thyroid gland

In official medicine, this disease is also called Hashimoto's thyroiditis (Hashimoto - in different transcriptions), after the Japanese doctor who first described it at the beginning of the 20th century. According to statistics, it is observed in only 4% of the world's population, while obvious symptoms of autoimmune thyroiditis can be observed in only 1%. Women get sick much more often than men - 8 times, while the main risk group consists of elderly patients: over 60 years old, which is partly explained by their level hormonal levels.

Autoimmune thyroiditis is characterized by a chronic inflammatory process in the thyroid gland, in which there is also a failure of the body’s defenses, as a result of which the antibodies of the endocrine system react aggressively to the cells of the thyroid gland, perceiving them as an “enemy”.

In most cases, this disease is inherited from close relatives and is often accompanied by other autoimmune disorders: diffuse goiter, alopecia, myasthenia gravis, collagenosis, etc. may be observed. Moreover, autoimmune thyroiditis often requires factors that provoke its development - these include any situations in which the integrity of the thyroid gland structure is disrupted:

• inflammatory process;
• penetration of infection;
• damage to the thyroid gland due to injury or during surgery.

Also, doctors do not rule out a significant role for such factors as fluctuations in iodine levels - from a serious deficiency to an excess, a person entering an area of ​​radioactive radiation or staying in a place with unfavorable environmental conditions.

If we consider the tests of a patient who has been diagnosed with autoimmune thyroiditis, then they will notice a reduced synthesis of thyroid hormones, which causes an increase in TSH levels. In this case, the doctor may see thyrotoxicosis, but it will be temporary: hypothyroidism is a chronic condition in autoimmune thyroiditis. In addition, antibodies to the thyroid gland will be present in the patient's blood.

If we talk about the symptoms of autoimmune thyroiditis of the thyroid gland, it is easiest to identify the problem by palpation: the thyroid area is characterized by increased density, both on one side and on both. The size of the organ can either increase or decrease, depending on the form of the disease: hypertrophic or atrophic. Due to changes in the structure of the thyroid gland, the patient may experience discomfort during swallowing, as well as pain or inability to breathe fully.

How is autoimmune thyroiditis treated?

This disease develops slowly, therefore, according to doctors, there is always a chance to stop it at an early stage, and therefore do without drastic measures - in particular, without surgical intervention. Often, symptoms of thyrotoxicosis are first observed: increased levels of certain thyroid hormones, including T3 and T4. As such, there is no specific therapy regimen today: doctors do not even exclude the treatment of autoimmune thyroiditis of the thyroid gland folk remedies, although the following medications are often used:

• Thyroid drugs are prescribed in case of deficiency of the hormones T3 and T4, and the dosage of such drugs must be determined by a doctor: they depend on blood test results. Since autoimmune thyroiditis is chronic, the duration of treatment with thyroid drugs can be a year or more with mandatory monitoring of hormonal levels every 2 months or more often.
• Glucocorticoids make sense when granulomas form in the thyroid tissue against the background of inflammation, which often occurs due to the activity of viruses. Doctors often prescribe medications based on prednisolone, and the dosage is gradually reduced during the course of treatment - abrupt withdrawal of glucocorticoids is prohibited.
• Selenium-based drugs are mainly prescribed as an additional measure to regulate antibody levels, as well as to make the patient feel better. The course of treatment with such medications cannot be less than 3 months, since the effect occurs only after this period.

If we consider traditional methods treatment of the thyroid gland with autoimmune thyroiditis, the most popular is wearing amber beads close to the neck. However, the effectiveness of this method is in doubt. Among the more understandable methods, the following should be highlighted:

• Preparation of honey-nut tincture: 30 cut green walnuts, 200 g of honey and 1 liter of vodka are mixed in a bottle and left for 2 weeks in a dark room. Drink, filtered, 1 tbsp. l. in the morning on an empty stomach, having breakfast half an hour later. When the entire bottle is drunk, take a break for 10 days and repeat the course 2 more times.
• Ground ginger is consumed 1 tsp. before breakfast and dinner, washed down with warm milk (200 ml) or water. The course lasts a month and can be repeated after six months.
• Cabbage-lemon juice also has a beneficial effect on the thyroid gland: after spinning white cabbage leaves through a juicer, 120 ml of the resulting juice is mixed with 20 ml lemon juice and drink before breakfast. Similar action repeat in the morning. Treatment lasts 90 days.

Traditional methods show the best effect in combination with conservative therapy. In addition, you should remember about preventive measures: support normal level physical activity, but do not engage in professional sports, give up bad habits, try not to take antibiotics and treat all infections.

Special attention in case of problems with the endocrine system requires correction of the diet: this is especially important during periods of exacerbation or active development diseases. The menu must contain protein obtained from fatty fish and white meat, as well as porridge cooked in water - cereals will be the basis of the entire diet. In addition, plant foods are introduced into the diet, but at the same time:

• try to avoid soy sources;
• abstain from flax, millet, horseradish, peanuts;
• do not overuse strawberries, peaches, pears;
• remove spices (limit quantity);
• Avoid alcohol if possible.

Among plant foods, cabbage (heat-treated) and lemon are of particular value for thyroiditis, and it also makes sense to eat foods rich in iodine if tests do not show an excess of this element in the body. The general rules of nutrition are classic: small portions, frequent appointments food, plenty of water, limiting fatty and fried foods, as well as caffeine.

The main factor in the occurrence of autoimmune thyroiditis- violation immune system. It appears as a family disease. There are other autoimmune pathologies in the families of patients. May occur after childbirth.

Provoking factors include: chronic infections of the nasopharynx, caries; infections; yersiniosis (transmitted from livestock, dogs, rodents); pollution of soil, air and water with chlorine, fluorine, nitrates; radiation and solar exposure; stressful situations; long-term, uncontrolled use of iodine-containing drugs or hormones; treatment of blood diseases with interferon drugs; injuries and operations on the thyroid gland.

Iodine intake is important in quantities exceeding the physiological norm. This applies to food products (red food dyes, preservatives, iodine additives in flour, salt), but more often to medicines and dietary supplements.

Classification of forms of Hashimoto's goiter includes latent, hypertrophic, atrophic.

The disease progresses several stages– euthyroid, subclinical, thyrotoxic, .

Signs of the disease found with significant destruction of the gland. In addition to the clinical manifestations of hypothyroidism (weakness, impaired thermoregulation, drowsiness, low blood pressure), its consequence can be infertility. If conception does occur, then during pregnancy it has an adverse effect on the mother and child.

Most patients are at the subclinical and euthyroid stage have no idea that they have thyroiditis. At this time, the thyroid gland retains its size, is not painful, and the hormonal balance is not disturbed. In the first years of the disease, autoimmune thyroiditis usually manifests itself as hyperthyroidism. More often found in children as: tendency to tearfulness, anxiety, agitation; increased irritability, aggressiveness; accelerated heartbeat; increasing the upper pressure indicator; sweating, poor heat tolerance; trembling of eyelids, fingers; weight loss.

In hypertrophic form signs of compression of adjacent tissues come to the fore. Patients experience difficulty breathing, swallowing, possible hoarseness, short-term attacks of dizziness or fainting.

Autoimmune thyroiditis is difficult to identify before the onset of hypothyroidism. Diagnostics includes: general blood test, blood immunology; blood hormones; Ultrasound; . To confirm Hashimoto's chronic autoimmune thyroiditis, the simultaneous presence of the most important signs is necessary: ​​antibodies to thyroid peroxidase exceeding 34 IU/l, hypoechogenicity on ultrasound and symptoms of hypothyroidism.

Treatment is limited to compensating for disturbances in the formation of hormones. Thyrostatics (Mercazolil, Espa-carb) are not used for hashitoxicosis, since hyperthyroidism is associated with the destruction of the thyroid gland, and not with increased synthesis of thyroxine. For palpitations, tachycardia, increased blood pressure, and hand tremors, the beta-blocker Anaprilin is indicated.

With the development of hypothyroidism appointed replacement therapy levothyroxine (L-thyroxine, ). To reduce the antibody titer, selenium (Cefasel) is added to the treatment for three months. Glucocorticoids (Prednisolone, Dexamethasone) are used for exacerbation of inflammation. With a mild inflammatory process, use non-steroidal drugs(Voltaren, Indomethacin). For large sizes, an operation is performed to remove the gland.

Read more in our article about autoimmune thyrotoxicosis, its manifestations and treatment.

Read in this article

Causes of development of autoimmune thyroiditis

The main factor in the occurrence of this disease is a violation of the immune system, which begins to perceive the cells of the thyroid gland as foreign and produce antibodies against them. Autoimmune thyroiditis appears as a familial disease. Patients and their blood relatives have antibodies to the enzymes (thyroid peroxidase) and, which are involved in the formation of the hormones thyroxine and triiodothyronine.

In addition, in the families of patients there are other pathologies of an autoimmune nature - type 1 diabetes mellitus, rheumatoid arthritis, hepatitis, pernicious anemia, vitiligo. The mere presence of antibodies does not guarantee the development of an active process. Therefore, even with a genetic predisposition, exposure to a provoking factor is necessary. The role of the following reasons has been proven:

• chronic infections of the nasopharynx, especially tonsillitis, sinusitis, caries;
• spicy viral infections, especially hepatitis;
• intestinal infectious diseases, yersiniosis (transmitted from livestock, dogs, rodents);
• pollution of soil, air and water with chlorine, fluorine, nitrates (stimulate the activity of T and B lymphocytes responsible for cellular immunity and the formation of antibodies);
• radiation and solar exposure;
• stressful situations;
• long-term, and especially uncontrolled use of iodine-containing drugs or hormones;
• treatment of blood diseases with interferon drugs;
• injuries and operations on the thyroid gland.

Recent studies of the significance of these factors have proven that an important, and perhaps the main one, is the consumption of iodine in quantities exceeding the physiological norm. This applies to food products (red food dyes, preservatives, iodine additives in flour, salt), but more often to medicines and dietary supplements.

It should be noted that self-treatment or prevention of iodine deficiency with iodine or Lugol's solution is extremely dangerous. Similar conditions can also occur when the dose of multivitamins is exceeded or when Cordarone is used for a long time.

Autoimmune thyroiditis can occur after childbirth. Its development is associated with the activation of the body's defenses after a period of oppression during pregnancy. If the patient does not have a hereditary predisposition, then it may spontaneously stop. There is also a painless (“mute, silent”) version of the disease that is not associated with pregnancy or any other known cause.

Classification of Hashimoto's goiter

Depending on the severity of symptoms and changes in the thyroid gland, the disease can have several clinical forms.

Latent

Antibodies are detected in the blood, but there are no signs of changes in the functioning of the thyroid gland. Erased symptoms of a slight increase or decrease in hormone production are possible. During examination, there may be a slight increase in the size of the organ; no seals are detected.

Hypertrophic

With the development of a goiter, there may be a uniform proliferation of tissues - a diffuse increase, or nodes may form against its background (diffuse-nodular form). Sometimes a node is found in unchanged tissue (). In the initial stage, there is excessive synthesis of hormones (hyperthyroidism), but in most patients the function does not change (euthyroidism) or decreases (hypothyroidism).

As autoimmune inflammation progresses, the thyroid tissue is attacked by antibodies and killer lymphocytes, which leads to its destruction. During this period, the patients' condition worsens, and the production of hormones decreases, a hypothyroid state develops with a decrease in metabolic processes in the body.

Atrophic

The most severe form, since the function of the organ is significantly reduced due to massive destruction of thyroid cells. Its size decreases, and hypothyroidism becomes persistent. It is more common in elderly patients and with radiation exposure at a young age.

Stages of the disease

The disease goes through several stages in its development. The patient does not always have all of them. A monophasic course for a long period is possible.

Euthyroid

The thyroid gland is functioning normally. This phase of autoimmune thyroiditis lasts several or decades, and can last a lifetime.

Subclinical

It begins with an exacerbation due to a massive attack of T-lymphocytes. These cells intensively enter the thyroid gland and begin to destroy its tissue. In response, the pituitary gland intensively produces thyroid-stimulating hormone (TSH) and thus stimulates the formation of thyroxine, maintaining its normal level.

Thyrotoxic

With extensive damage to cells, hormones from them enter the bloodstream. This is accompanied by symptoms of thyrotoxicosis (tachycardia, weight loss, sweating, hand tremors). Together with hormones, parts of the follicles also enter the circulatory network. They act as antigens and provoke the formation of antibodies to their own cells.

Hypothyroid

What is terrible autoimmune thyroiditis

In Russia, Ukraine and Belarus, Hashimoto's thyroiditis affects from 4 to 12% of the population, depending on the region. As the environment becomes polluted, its prevalence increases. The difficulty of early detection of the disease is due to the fact that more than one year or even a decade passes from the moment of autoimmune damage to complications. Signs of the disease are detected when the gland is significantly destroyed, when the patient loses the ability to produce hormones.

In addition to the clinical manifestations of hypothyroidism (weakness, impaired thermoregulation, drowsiness, low blood pressure), its consequence can be infertility. Moreover, it occurs not only in the obvious variant of the disease (manifest), but also in the latent (subclinical) variant.

If, with severe manifestations, patients cannot become pregnant due to ovulation disorders, then subclinical hypothyroidism is accompanied by habitual miscarriages. An excessive reaction of the immune system is often explained by infertility in endometriosis.

If conception does occur, then during pregnancy hypothyroidism has an adverse effect on the expectant mother and child. This manifests itself in the following complications:

• threat of premature birth;
• preeclampsia ( high blood pressure, swelling, convulsive syndrome);
• placental abruption;
• slowing of intrauterine development of the fetus;
• bleeding after childbirth;
• cardiac dysfunction;
• anemia.

Placental abruption

The newborn has pathologies of the nervous and skeletal systems and a slow heart rate. The combination of autoimmune thyroiditis and thyroid cancer is not common, but possible.

Symptoms of pathology in adults and children

Most patients at the subclinical and euthyroid stage of the disease do not realize that they have thyroiditis. At this time, the thyroid gland retains its size, is not painful, and the hormonal balance is not disturbed. Some patients may develop nonspecific signs that do not lead them to see a doctor:

• discomfort in the neck area,
• feeling of a lump in the throat,
• fast fatiguability,
• general weakness,
• flying joint pains.

In the first years of the disease, autoimmune thyroiditis usually manifests itself as hyperthyroidism. It is called hashitoxicosis. More often found in children in the form of:

• tendency to tearfulness, anxiety, agitation;
• increased irritability, aggressiveness;
• accelerated and increased heartbeat;
• increase in the upper pressure indicator (high systolic and pulse);
• sweating, poor heat tolerance;
• trembling of eyelids, fingers;
• weight loss.

Autoimmune thyroiditis in children

This stage is short-lived and, unlike toxic goiter, does not lead to the appearance of eye symptoms (bulging eyes, increased shine of the eyes, widening of the palpebral fissure). Subsequently, thyroid function weakens by an average of 5% every year. The phase of relatively normal functioning lasts a long time, and only with the development of hypothyroidism can autoimmune thyroiditis be suspected.

In the hypertrophic form, signs of compression of adjacent tissues come to the fore. Patients experience difficulty breathing, swallowing, possible hoarseness, short-term attacks of dizziness or fainting. In the case of severe hypothyroidism, patients note:

• apathy, lethargy, drowsiness;
• constant chilliness;
• memory loss;
• swelling of the face, legs;
• steady increase in body weight;
• hair loss, increased brittleness of nails;
• dry skin;
• decreased blood pressure and slowed heart rate.

Watch the video about autoimmune thyroiditis:

Hormone analysis and other diagnostic methods

Autoimmune thyroiditis is difficult to identify before the onset of hypothyroidism. To make a diagnosis, take into account:

• manifestations of the disease;
• data from laboratory and instrumental research methods;
• the presence of similar pathologies in blood relatives.

When examining the patient, they find:

• general blood test – increased lymphocytes;
• blood immunology – antibodies to thyroglobulin, thyroid peroxidase, thyroxine, triioditronine;
• blood hormones - when TSH increases, hypothyroidism is detected. If thyroxine is normal, then it is subclinical, and if it decreases, it is obvious;
• Ultrasound – dimensions are reduced or increased depending on the shape, echogenicity is reduced;

In order to confirm chronic autoimmune Hashimoto's thyroiditis, the simultaneous presence of the most important signs is necessary: ​​antibodies to thyroid peroxidase exceeding 34 IU/l, hypoechogenicity on ultrasound and symptoms of hypothyroidism. None of these criteria alone provides grounds for a definitive diagnosis.

Treatment of acute and chronic forms

There is no specific therapy for the disease that would prevent its further progression. Despite understanding the causes and mechanisms of development of autoimmune thyroiditis, its treatment is limited to compensation for disturbances in the formation of hormones.

Thyrostatics (Mercazolil, Espa-carb) are not used for hashitoxicosis, since hyperthyroidism is associated with the destruction of the thyroid gland, and not with increased synthesis of thyroxine. For palpitations, tachycardia, increased blood pressure, hand tremors and sweating, the beta blocker Anaprilin is indicated.

Taking into account the examination data, hormone intake can be started already at the subclinical stage and during the period of euthyroidism in a minimal dose. This therapy inhibits the formation of TSH and the progression of autoimmune destruction. To reduce the antibody titer, selenium (Cephasel) is added to the treatment for three months.

Glucocorticoids (Prednisolone, Dexamethasone) are used for exacerbation of inflammation, which most often occurs against the background of viral or bacterial infections in the autumn-winter period. For mild inflammatory processes, non-steroidal drugs (Voltaren, Indomethacin) are used. If the goiter reaches a large size, patients undergo surgery to remove the gland.

Prognosis for patients

With timely detection of the disease, it is possible to compensate for dysfunction of the thyroid gland and achieve satisfactory well-being of patients. Despite the fact that antibodies continue to be produced throughout life, in many cases it is possible to reduce their number and prevent massive cell destruction.

It is possible to maintain good performance for 10-15 years, subject to constant monitoring of the state of hormone production.

In women, if antibodies to thyroid peroxidase are detected during pregnancy, hypothyroidism may develop, and postpartum autoimmune thyroiditis may recur in the future. In every third patient, this process leads to persistent low activity of the thyroid gland, requiring the use of levothyroxine.

Autoimmune thyroiditis occurs with a hereditary predisposition. When the immune system is disrupted, antibodies to thyroid cells are formed in the body. They gradually destroy the follicles, leading over time to hypothyroidism.

Clinical manifestations may be absent until there is a persistent decline in organ function. To make a diagnosis, it is necessary to have antibodies in the blood, ultrasound signs and symptoms of thyroid hormone deficiency. For treatment, symptomatic and substitution therapy is used.

Autoimmune hypothyroidism is a deficiency of thyroid hormones caused by immunoinflammatory damage to the thyroid gland. This is the last phase, which is characterized by a slowdown in metabolism in the body. Manifested by rapid weight gain, drowsiness, lethargy, chilliness, and slowness of speech. To diagnose autoimmune thyroiditis (AIT), they resort to hormonal analysis for T3 and T4, and histological examination.

Why do thyroid problems occur?

Autoimmune hypothyroidism is a deficiency of the thyroid gland caused by its atrophy against the background of an autoimmune lesion. Is last stage Hashimoto's thyroiditis. According to statistics, autoimmune inflammation occurs in 20% of cases of all thyroid diseases. AIT is diagnosed 20 times more often in women, which is due to the effect of estrogens on lymphoid tissue and disorders of the X chromosome.

Autoimmune inflammation is caused by genetic defects in the immune system. It starts against thyrocytes - the functional cells of the thyroid gland. Defender cells damage the organ, which leads to disruption of its secretory activity, atrophy (exhaustion) and hypothyroidism.

Factors that provoke autoimmune disorders:

• past infectious diseases;
• excessive consumption of chlorine from food;
• uncontrolled use of hormonal drugs;
• foci of chronic infection;
• abuse of sunbathing;
• radiation exposure;
• pregnancy;
• long-term therapy with interferon drugs;
• poisoning from volatile chemicals;
• chronic stress.

Hypothyroidism is a common form functional disorders thyroid disease, which occurs with prolonged deficiency of thyroid hormones.

With a lack of triiodothyronine (T3) and thyroxine (T4), metabolism slows down, which leads to disturbances in the functioning of the digestive, immune, and cardiovascular systems.

How are AIT and hypothyroidism related?

Hypothyroidism and autoimmune thyroiditis are closely related. The first disease occurs against the background of the second due to depletion of the thyroid gland caused by autoinflammation of thyrocytes. Under the influence of internal and external factors arise in the immune system pathological changes, as a result of which it begins to secrete antibodies to thyroid peroxidase, an enzyme that stimulates the synthesis of thyroid hormones. Their high concentration in the blood indicates aggression of the immune system towards the thyroid gland.

In endocrinology, there are several types of AIT:

• painless;
• chronic;
• cytokine-induced;

All variants of autoimmune thyroiditis are united by the phase nature of the changes that occur in the gland. Initially, all patients exhibit symptoms of thyrotoxicosis. When autoantibodies damage a large number of thyrocytes, the production of T3 and T4 is greatly reduced. Due to a lack of thyroid hormones, thyrotoxicosis gives way to hypothyroidism.

Along the way, there are 3 forms of AIT - latent, hypertrophic and atrophic. Signs of hypothyroidism increase with Hashimoto's atrophic thyroiditis. Due to inflammation, the number of working thyrocytes in the organ decreases. When it is depleted, the production of thyroid hormones decreases, resulting in hypothyroidism. The risk group includes:

• older women;
• patients who have undergone radiotherapy;
• people with congenital autoimmune diseases.

Unlike other types of AIT, the atrophic form of the disease is the worst tolerated. Massive death of thyrocytes leads to persistent deficiency of T3 and T4, which negatively affects the functioning of other organs and systems.

The difference between autoimmune hypothyroidism and AIT is that the first disease is only one of the phases of immunoinflammatory damage to the gland.

Symptoms at different stages

Signs depend on the stage of autoimmune inflammation and changes in the thyroid gland. All forms of AIT, without exception, have several phases that successively replace each other:

• Euthyroid. The amount of antibodies to thyroid cells is insignificant, so inflammation occurs in a latent (hidden) form. There are no local or general symptoms of AIT. Depending on the provoking factors, this phase lasts from 1-2 years to decades.
• Subclinical. As autoimmune disorders progress, T lymphocytes begin to bombard thyroid cells. Its performance gradually decreases, so the amount of T3 and T4 in the blood decreases. To stabilize hormonal levels, the adenohypophysis secretes more (TSH), which stimulates the functioning of the gland and the synthesis of iodine-containing substances.
• Thyrotoxic. When thyrocytes are damaged by antibodies, large amounts of T3 and T4 are released into the blood. When their concentration exceeds normal values, thyrotoxicosis occurs.
• Hypothyroid. With further autoimmune inflammation, the number of hormonally active cells in the gland is greatly reduced. In the hypothyroid phase, the metabolism of lipids, minerals, proteins and carbohydrates sharply slows down.

The clinical picture becomes clear only in the last two phases of AIT. When there is an excess of T3 and T4 in the blood, complaints arise about:

• weight loss;
• mood swings;
• increased appetite;
• feeling of heat;
• sweating;
• temperature increase;
• insomnia;
• accelerated speech;
• unstable chair;
• aggressiveness;
• decreased libido.

Primary hypothyroidism against the background of autoimmune thyroiditis is manifested by the following symptoms:

• dry skin;
• drowsiness;
• weight gain;
• frequent constipation;
• decreased performance;
• slow speech;
• memory impairment;
• chilliness;
• gynecomastia (breast growth in men according to the female type);
• cardiopalmus;
• apathy;

In 15% of patients, AIT is monophasic, that is, symptoms of only the thyrotoxic or hypothyroid phase appear.

Possible dangerous consequences

Autoimmune thyroiditis resulting in hypothyroidism is dangerous due to irreversible changes in the gland. With a deficiency of T3 and T4 in the body, all metabolic processes slow down, which negatively affects the functioning of the cardiovascular, digestive, respiratory and other systems.

Possible consequences of AIT with hypothyroidism:

• arrhythmia;
• atherosclerosis;
• gynecomastia in men;
• dysphagia (impaired swallowing);
• myocardial infarction;
• decrease in intellectual activity;
• increasing drowsiness;
• abdominal dropsy;
• hypothermia (lower temperature).

Atrophy of the thyroid gland leads to increasing drowsiness, depression of consciousness up to. In case of comatose state the risk of death increases several times.

What tests need to be taken

It is difficult to diagnose AIT before the hypothyroid phase. Gland dysfunction is indicated characteristic symptoms– mood swings, dry skin, weight gain or loss. If other family members have autoimmune disorders, the likelihood of an endocrine disease is confirmed.

To diagnose autoimmune thyroiditis and hypothyroidism, the endocrinologist prescribes a comprehensive examination:

• Clinical blood test. Autoimmune damage to the gland is indicated by a high concentration of leukocytes.
• . High thyrotropin with normal thyroxine is a sign of latent hypothyroidism. With gland atrophy, the content of T3 and T4 in the blood decreases.
• ultrasound. Depending on the phase of AIT, or is detected.
• Immunogram. In patients with AIT, antibodies to thyroid hormones and thyroid peroxidase are detected.

Hyperechogenicity of the thyroid gland on ultrasound and high level antibodies to thyroid peroxidase cannot be considered evidence of autoimmune thyroiditis.

If necessary, prescribe. After the tissue is collected, it is sent to histological examination. With autoimmune inflammation, an increased content of T-lymphocytes and dysfunctional thyrocytes is detected.

Basic rules of treatment

Specific treatment for the thyroid gland in AIT has not been developed. So far, endocrinologists do not have effective methods to relieve autoimmune inflammation.

Principles of therapy for hypothyroidism against the background of AIT:

• Replenishment of T3 and T4 deficiency. To normalize hormonal levels, they are prescribed with levothyroxine - Eutirox, L-Thyrox euro. Medicines stimulate metabolism, which reduces the risk of complications from the gastrointestinal tract, hematopoietic and cardiovascular systems.
• Relieving inflammation in the gland. To reduce the severity of autoimmune reactions in thyrocytes, glucocorticosteroids are used - Dexamethasone, Prednisolone, Betaspan. The drugs are recommended only for the combined course of autoimmune and.
• Decrease in the number of antibodies to gland cells. To reduce the content of autoantibody titers in the blood, take non-steroidal anti-inflammatory drugs - Metindol retard, Bioran, Diklak.

Lifestyle with autoimmune hypothyroidism

People with hypothyroidism have a very slow metabolism, so they quickly gain weight. Due to disturbances in mineral metabolism, lesions of the limbs and face are common. Therefore, when treating the thyroid gland, you need to make lifestyle changes.

During periods of acute inflammation, the glands refuse to consume salt, as it retains fluid in the body. Limit fast food, processed foods and canned vegetables.

To eliminate the symptoms of AIT, you should:

• exercise;
• observe ;
• to refuse from bad habits.

To stimulate the synthesis of T3 and T4, saltwater fish, shrimp, kelp, apples, pork, and greens are introduced into the diet.

Is the disease curable?

With timely initiation of therapy, it is possible to prevent the destruction of the gland by autoantibodies. Satisfactory performance of patients is maintained for 10-15 years. Under the influence of provoking factors, relapses of AIT cannot be excluded.

If Hashimoto's thyroiditis was caused by pregnancy, the risk of exacerbation in the next pregnancy will be 70-75%. In 25% of patients the disease progresses to chronic form. As a result of massive death of thyroid cells, AIT is complicated by persistent hypothyroidism.

Prevention of hypothyroidism as a consequence of AIT

Thyroid insufficiency due to AIT occurs due to an unbalanced diet and ignoring the doctor’s recommendations. To avoid hypothyroidism, it is recommended:

• consume iodized salt;
• accept ;
• Get tested for T3 and T4 once every six months.

During pregnancy and after childbirth, women should monitor the function of the gland. Endocrinologists recommend early registration with the antenatal clinic. Timely detection of hormonal imbalance and hormone replacement therapy prevents serious complications.

Autoimmune thyroiditis is an inflammatory disease of the thyroid gland, which usually has a chronic course.

This pathology is of autoimmune origin and is associated with damage and destruction of follicular cells and follicles of the thyroid gland under the influence of antithyroid autoantibodies. Typically, autoimmune theroiditis does not have any manifestations on initial stages, only in rare cases is there an enlargement of the thyroid gland.

This disease is the most common among all thyroid pathologies. Most often, women over the age of 40 suffer from autoimmune thyroiditis, but the development of this disease is more early age also possible, in rare cases Clinical signs Autoimmune thyroiditis occurs even in childhood.

The second name for this disease is often heard - Hashimoto's thyroiditis (in honor of the Japanese scientist Hashimoto, who first described this pathology). But in reality, Hashimoto's thyroiditis is just a type of autoimmune thyroiditis, which includes several types.

Statistics

The incidence of the disease, according to various sources, varies from 1 to 4%; in the structure of thyroid pathology, autoimmune damage accounts for every 5–6th case. Women are much more likely (4–15 times) to suffer from autoimmune thyroiditis.

The average age of onset of a detailed clinical picture, indicated in the sources, varies significantly: according to some sources, it is 40–50 years, according to others – 60 and older, some authors indicate the age of 25–35 years. It is reliably known that in children the disease occurs extremely rarely, in 0.1–1% of cases.

Reasons for development

The main cause of this type of thyroiditis, as was established by the Japanese scientist Hakaru Hashimoto, is the body’s specific immune response. Most often, the immune system protects the human body from negative external factors, viruses and infections, producing special antibodies for these purposes. In some cases, due to an autoimmune failure, the immune system can attack the cells of its own body, including thyroid cells, which leads to their destruction.

According to experts, the main reason for this type of immune response is genetic predisposition, but there are other risk factors that can lead to the development of thyroiditis:

• infectious diseases: it is during this period that the body’s immunity may fail, so in a child, for example, chronic autoimmune thyroiditis can be observed against the background of a previous infectious disease;
• other autoimmune diseases: it is assumed that the patient’s body is characterized by this kind of reaction to its own cells;
• Stressful situations can also cause problems with the immune system;
• poor ecology in the place of permanent residence, including radioactive radiation: contributes to a general weakening of the body, its susceptibility to infections, which again can trigger a reaction of the immune system to its own tissues;
• taking a certain set of medications that can affect the production of thyroid hormones;
• lack or, on the contrary, excess of iodine in food, and therefore in the patient’s body;
• smoking;
• possible previous operations on the thyroid gland or chronic inflammatory processes in the nasopharynx.

Among other things, another risk factor is considered to be the patient’s gender and age: for example, women suffer from autoimmune thyroiditis several times more often than men, and average age Patients range from 30 to 60 years of age, although in some cases the disease can be diagnosed in women under 30 years of age, as well as in children and adolescents.

Classification

Autoimmune thyroiditis can be divided into several diseases, although they all have the same nature:

1. Chronic thyroiditis (also known as lymphomatous thyroiditis, previously called autoimmune Hashimoto's thyroiditis or Hashimoto's goiter) develops due to a sharp increase in antibodies and a special form of lymphocytes (T-lymphocytes), which begin to destroy thyroid cells. As a result, the thyroid gland sharply reduces the amount of hormones produced. This phenomenon is called hypothyroidism by doctors. The disease has a clearly expressed genetic form, and the disease is very common in relatives of the patient diabetes mellitus and various forms of damage to the thyroid gland.

2. Postpartum thyroiditis is the best studied due to the fact that this disease occurs more often than others. Illness occurs due to overload female body during pregnancy, as well as in case of existing predisposition. It is this relationship that leads to the fact that postpartum thyroiditis turns into destructive autoimmune thyroiditis.

3. Painless (silent) thyroiditis is similar to postpartum thyroiditis, but the reason for its appearance in patients has not yet been identified.

4. Cytokine-induced thyroiditis can occur in patients with hepatitis C or with a blood disorder if these diseases are treated with interferon.

By clinical manifestations and depending on changes in the size of the thyroid gland, autoimmune thyroiditis is divided into the following forms:

• Latent - when clinical symptoms absent, but immunological signs appear. In this form of the disease, the thyroid gland is either normal size or slightly enlarged. Its functions are not impaired and no compaction is observed in the body of the gland;
• Hypertrophic – when the functions of the thyroid gland are disrupted, and its size increases, forming a goiter. If the increase in the size of the gland is uniform throughout the entire volume, then this is a diffuse form of the disease. If nodules form in the body of the gland, the disease is called a nodular form. However, there are frequent cases of simultaneous combination of both of these forms;
• Atrophic – when the size of the thyroid gland is normal or even reduced, but the amount of hormones produced is sharply reduced. This picture of the disease is common for older people, and for young people - only in case of their radiation exposure.

Symptoms of autoimmune thyroiditis

It should be noted right away that autoimmune thyroiditis often occurs without pronounced symptoms and is detected only during an examination of the thyroid gland.

At the onset of the disease, in some cases throughout life, normal thyroid function may be maintained, the so-called state when the thyroid gland produces a normal amount of hormones. This condition is not dangerous and is normal; it only requires further dynamic monitoring.

Symptoms of the disease occur if, as a result of the destruction of thyroid cells, a decrease in its function occurs -. Often, at the very beginning of autoimmune thyroiditis, there is an increase in the function of the thyroid gland; it produces more hormones than normal. This condition is called thyrotoxicosis. Thyrotoxicosis may persist or may develop into hypothyroidism.

The symptoms of hypothyroidism vary.

Symptoms of hypothyroidism are:

Weakness, memory loss, apathy, depression, low mood, pale, dry and cold skin, rough skin on the palms and elbows, slow speech, swelling of the face, eyelids, overweight or obesity, chilliness, cold intolerance, decreased sweating, increased, swelling of the tongue, increased hair loss, brittle nails, swelling in the legs, hoarseness, nervousness, menstrual irregularities, constipation, joint pain.

Symptoms are often nonspecific, occur in a large number of people, and may not be associated with thyroid dysfunction. However, if you have most of the following symptoms, your thyroid hormones may need to be tested.

Symptoms of thyrotoxicosis are:

Increased irritability, weight loss, mood swings, tearfulness, rapid heartbeat, feeling of interruptions in heart function, increased blood pressure, diarrhea ( liquid stool), weakness, tendency to fractures (bone tissue strength decreases), feeling of heat, intolerance to hot climates, sweating, increased hair loss, menstrual irregularities, decreased libido (sexual desire).

Diagnostics

It is quite difficult to diagnose AIT before the onset of hypothyroidism. The diagnosis of autoimmune thyroiditis is made by endocrinologists according to clinical picture, data laboratory research. The presence of autoimmune disorders in other family members confirms the likelihood of autoimmune thyroiditis.

Laboratory tests for autoimmune thyroiditis include:

• general blood test - an increase in the number of lymphocytes is determined
• immunogram - characterized by the presence of antibodies to thyroglobulin, thyroid peroxidase, second colloid antigen, antibodies to thyroid hormones of the thyroid gland
• determination of T3 and T4 (total and free), TSH level in blood serum. An increase in TSH levels with normal T4 levels indicates subclinical hypothyroidism, increased level TSH with a reduced concentration of T4 – about clinical hypothyroidism
• Ultrasound of the thyroid gland - shows an increase or decrease in the size of the gland, changes in structure. The results of this study serve to complement the clinical picture and other laboratory results.
• fine-needle biopsy of the thyroid gland - allows you to identify a large number of lymphocytes and other cells characteristic of autoimmune thyroiditis. It is used when there is evidence of possible malignant degeneration of a thyroid nodule.

The diagnostic criteria for autoimmune thyroiditis are:

• increased levels of circulating antibodies to the thyroid gland (AT-TPO);
• detection of hypoechogenicity of the thyroid gland by ultrasound;
• signs of primary hypothyroidism.

In the absence of at least one of these criteria, the diagnosis of autoimmune thyroiditis is only probabilistic. Since an increase in the level of AT-TPO, or the hypoechogenicity of the thyroid gland by itself does not prove autoimmune thyroiditis, this does not allow establishing an accurate diagnosis. Treatment is indicated for the patient only in the hypothyroid phase, therefore, as a rule, there is no urgent need to make a diagnosis in the euthyroid phase.

The worst thing you can expect: possible complications of thyroiditis

Different stages of thyroiditis have different complications. Thus, the hyperthyroid stage can be complicated by arrhythmia, heart failure, and even provoke myocardial infarction.

Hypothyroidism can cause:

• infertility;
• recurrent miscarriage;
• congenital hypothyroidism in a newborn child;
• dementia;
• atherosclerosis;
• depression;
• myxedema, which looks like intolerance to the slightest cold, constant drowsiness. If you are given sedatives in this state, experience severe stress, or become ill infectious disease, you can provoke a hypothyroid coma.

Fortunately, this condition responds well to treatment and, if you take drugs in a dose adjusted to the level of hormones and AT-TPO, you can not feel the presence of the disease for a long time.

Why is thyroiditis dangerous during pregnancy?

The thyroid gland weighs only fifteen grams, but its influence on the processes occurring in the body is enormous. Hormones produced by the thyroid gland are involved in metabolism, the production of certain vitamins, and many vital processes.

Autoimmune thyroiditis provokes disruption of the thyroid gland in two thirds of cases. And pregnancy very often gives impetus to the worsening of the disease. With thyroiditis, the thyroid gland produces less hormones than it should. This disease belongs to autoimmune diseases. Thyroiditis differs from other diseases of the thyroid gland in that even the use medicines most often does not help increase hormone production. And these hormones are absolutely necessary for both the mother’s body and the baby’s developing body. Thyroiditis can cause disturbances in the formation nervous system in the unborn child.

During pregnancy, do not be negligent about a disease such as thyroiditis. The fact is that it is especially dangerous in the first trimester, when thyroiditis can provoke a miscarriage. According to research, forty-eight percent of women suffering from thyroiditis had a threatened miscarriage during pregnancy, and twelve and a half percent suffered from severe forms of toxicosis in the early stages.

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How to treat thyroiditis?

Treatment of the pathology is completely medicinal and depends on the stage at which autoimmune thyroiditis is. Treatment is prescribed regardless of age and does not stop even in case of pregnancy, of course, if there are necessary indications. The goal of therapy is to maintain thyroid hormones at their physiological level (monitoring indicators every six months, the first control should be carried out after 1.5-2 months).

At the stage of euthyroidism drug treatment is not carried out.

Regarding the treatment tactics of the thyrotoxic stage, the decision is left to the doctor. Typically, thyreostatics like Mercazolil are not prescribed. Therapy is symptomatic: beta blockers are used (Anaprilin, Nebivolol, Atenolol); in case of severe psycho-emotional excitability, sedatives are prescribed. In the case of a thyrotoxic crisis, treatment in a hospital is carried out using injections of glucocorticoid hormones (Prednisolone, Dexamethasone). The same drugs are used when autoimmune thyroiditis is combined with subacute thyroiditis, but therapy is performed on an outpatient basis.

In the stage of hypothyroidism, synthetic T4 (thyroxine) called “L-thyroxine” or “Euthyrox” and, if there is a lack of triiodothyronine, its laboratory-created analogues are prescribed. The dosage of thyroxine for adults is 1.4-1.7 mcg/kg of weight, for children – up to 4 mcg/kg.

Thyroxine is prescribed to children if there is an increase in TSH and normal or reduced level T4 if the gland is enlarged by 30 percent or more of normal for age. If it is enlarged, its structure is heterogeneous, and AT-TPO is absent, iodine is prescribed in the form of potassium iodide at a dosage of 200 mcg/day.

When a diagnosis of autoimmune thyroiditis is made to a person living in an area with iodine deficiency, physiological doses of iodine are used: 100-200 mcg/day.

L-thyroxine is prescribed to pregnant women if TSH is more than 4 mU/l. If they only have AT-TPO and TSH is less than 2 mU/L, thyroxine is not used, but TSH levels are monitored every trimester. In the presence of AT-TPO and TSH 2-4 mU/l, L-thyroxine is needed in prophylactic doses.

If the thyroiditis is nodular, in which cancer cannot be excluded, or if the thyroid gland compresses the organs of the neck, significantly complicating breathing, surgical treatment is performed.

Nutrition

The diet should be normal in caloric content ( energy value at least 1500 kcal), or better if you calculate it according to Mary Chaumont: (weight * 25) minus 200 kcal.

The amount of protein should be increased to 3 g per kg of body weight, and saturated fats and easily digestible carbohydrates should be limited. You need to eat every 3 hours.

What you can eat:

• vegetable dishes;
• baked red fish;
• fish fat;
• liver: cod, pork, beef;
• pasta;
• dairy products;
• legumes;
• eggs;
• butter;
• porridge;
• bread.

Salted, fried, spicy and smoked foods, alcohol and seasonings are excluded. Water – no more than 1.5 l/day.

You need fasting - once a week or 10 days - days on juices and fruits.

Folk remedies

Treatment with folk remedies for autoimmune thyroiditis is contraindicated. With this disease, you should generally refrain from any self-medication. Only an experienced doctor can prescribe adequate treatment in this case, and it must be carried out under the mandatory systematic supervision of tests.

Immunomodulators and immunostimulants are not recommended for use in autoimmune thyroiditis. It is very important to follow some principles of correct healthy eating, namely: eat more fruits and vegetables. During illness, as well as during periods of stress, emotional and physical activity, it is recommended to take microelements and vitamins necessary for the body (such vitamin preparations like Supradin, Centrum, Vitrum, etc.)

Forecast for life

Normal health and performance in patients can sometimes be maintained for 15 years or more, despite short-term exacerbations of the disease.

Autoimmune thyroiditis and elevated antibody levels may be considered a factor increased risk the occurrence of hypothyroidism in the future, that is, a decrease in the amount of hormones produced by the gland.

In the case of postpartum thyroiditis, the risk of recurrence after another pregnancy is 70%. However, about 25–30% of women subsequently develop chronic autoimmune thyroiditis with the transition to persistent hypothyroidism.

Prevention

It is currently impossible to prevent the manifestation of acute or subacute thyroiditis using specific preventive measures.

Experts advise to comply general rules, helping to avoid a number of diseases. Regular hardening, timely therapy for diseases of the ears, throat, nose, teeth, and the use of sufficient vitamins are important. A person who has had cases of autoimmune thyroiditis in his family should be very careful about his own health and consult a doctor at the first suspicion.

To avoid relapse of the disease, it is important to carefully follow all doctor’s instructions.