How to identify autoimmune thyroiditis. Autoimmune thyroiditis. Changes detected by ultrasound examination

Autoimmune thyroiditis (AIT) or, as it is also called, Hashimoto's thyroiditis, is one of the most common autoimmune diseases of the thyroid gland. It is the most common cause of hypothyroidism - decreased thyroid function.

Most often, AIT is detected in women aged 30–50 years or after pregnancy, and in men aged 40–65 years. The disease does not have pronounced clinical symptoms. For many years, and sometimes decades, it may not manifest itself at all.

There is no pain with this disease. And often the only sign of the presence of sluggish pathological changes in the thyroid gland may be an increased titer of AT-TPO.

What it is?

Autoimmune thyroiditis (AIT) is an inflammatory disease of the thyroid gland that occurs as a result of the body producing antibodies to its own thyroid gland (thyroid gland). It affects 10 people out of a thousand.

Causes

Regardless of the traditionally assumed main cause - hereditary predisposition, thyroiditis requires the occurrence of special conditions and additional reasons for development.

  1. Uncontrolled use of medications, especially hormonal ones or those containing iodine in the active composition;
  2. The presence of foci of chronic diseases of various types in acute form (carious teeth, inflammation in the tonsils or sinuses);
  3. Harmful environment, negative environmental impact, excess of chlorine, iodine, chlorine in water and food, air oversaturated with them;
  4. Hormonal instability is a disruption of the body’s hormonal levels due to other diseases, injuries, pregnancy, after taking medications and in other cases;
  5. The presence of radiation exposure during radiation therapy, or when working with radioactive substances, as well as active exposure to the sun;
  6. Injuries, stressful situations, chemical and thermal burns, in general and directly in the thyroid gland, can also be negatively affected by surgical intervention.

The development of the disease occurs gradually; several factors in combination may become the basis for its acceleration or relapse of active forms.

Classification

What are autoimmune thyroiditis, in terms of type classification? The following types of disease are distinguished:

  1. Postpartum thyroiditis, which becomes a consequence of excessively increased activity of the immune system after suppression during pregnancy.
  2. Chronic thyroiditis of autoimmune origin, in which primary hypothyroidism (thyroid hormone deficiency) develops.
  3. A cytokine-induced variant of the disease that develops with long-term treatment with interferons.
  4. Silent (silent) thyroiditis of the thyroid gland, similar to postpartum, but not caused by pregnancy.

Based on the nature of the course, there are 3 main forms of autoimmune thyroiditis. This:

The development of all types of autoimmune thyroiditis goes through 4 phases:

  • euthyroidism – with preservation of gland function;
  • subclinical phase – with partial disruption of hormone synthesis;
  • thyrotoxicosis – a characteristic symptom of which is a high level of the hormone T4;
  • hypothyroid phase - when, with further damage to the gland, the number of its cells is reduced below a critical threshold.

Symptoms of autoimmune thyroiditis

The manifestations of various forms of the disease have some characteristic features.

Since the pathological significance of chronic autoimmune thyroiditis for the body is practically limited to hypothyroidism developing at the final stage, neither the euthyroid phase nor the phase of subclinical hypothyroidism have clinical manifestations.

The clinical picture of chronic thyroiditis is formed, in fact, by the following multisystem manifestations of hypothyroidism (suppression of thyroid function):

  • intolerance to habitual physical activity;
  • slower reactions to external stimuli;
  • depressive states;
  • apathy, drowsiness;
  • feeling of unmotivated fatigue;
  • decreased memory and concentration;
  • “myxedematous” appearance (puffiness of the face, swelling of the area around the eyes, pallor of the skin with an icteric tint, weakened facial expressions);
  • decreased heart rate;
  • decreased appetite;
  • tendency to constipation;
  • dullness and fragility of hair, increased hair loss;
  • decreased libido;
  • dry skin;
  • tendency to increase body weight;
  • chilliness of the limbs;

A common feature for postpartum, silent and cytokine-induced thyroiditis is a consistent change in the stages of the inflammatory process.

Symptoms characteristic of the thyrotoxic phase:

  • weight loss;
  • intolerance to stuffy rooms;
  • tremor of the limbs, trembling of the fingers;
  • impaired concentration, memory impairment;
  • emotional lability (tearfulness, sudden mood swings);
  • tachycardia, increased blood pressure (blood pressure);
  • feeling of heat, hot flashes, sweating;
  • decreased libido;
  • fatigue, general weakness, followed by episodes of increased activity;
  • menstrual dysfunction in women (from intermenstrual uterine bleeding to complete amenorrhea).

Manifestations of the hypothyroid phase are similar to those of chronic autoimmune thyroiditis.

A characteristic sign of postpartum thyroiditis is the onset of symptoms of thyrotoxicosis by the 14th week, the appearance of signs of hypothyroidism by the 19th or 20th week after birth.

Painless and cytokine-induced thyroiditis, as a rule, does not demonstrate a violent clinical picture, manifesting itself with moderate symptoms, or is asymptomatic and is detected during routine testing of thyroid hormone levels.

Diagnostics

If autoimmune thyroiditis is suspected, the following diagnosis should be performed. Blood sampling to detect hormones:

  1. T4 – free and general;
  2. T3 – free and general.

With an increase in TSH and normal T4 levels, we can talk about the presence of a subclinical stage of the pathology, but if, with an increase in TSH, the T4 level decreases, this means that the first symptoms of the disease are approaching.

The diagnosis is made based on the combination of the following data:

  • the concentration of T4 and T3 is reduced, and the level of TSH is increased;
  • Ultrasound of the thyroid gland determines the hypoechogenicity of the tissue;
  • the level of antibodies to the thyroid enzyme – thyroid peroxidase (AT-TPO) in the venous blood increases.

If there are deviations in only one of the indicators, it is difficult to make a diagnosis. Even in the case of an increase in AT-TPO, we can talk about the patient’s predisposition to autoimmune damage to the thyroid gland.

In the presence of nodular thyroiditis, a biopsy of the node is performed to visualize the pathology, as well as to exclude oncology.

How to treat autoimmune thyroiditis?

To date, no effective treatment methods have been developed for autoimmune thyroiditis. If the thyrotoxic phase of the disease occurs (the appearance of thyroid hormones in the blood), the administration of thyrostatics, that is, drugs that suppress the activity of the thyroid gland (thiamazole, carbimazole, propicil), is not recommended.

  • If a patient has problems with the cardiovascular system, beta-blockers are prescribed. If dysfunction of the thyroid gland is detected, a thyroid drug is prescribed - levothyroxine (L-thyroxine) and treatment is necessarily combined with regular monitoring of the clinical picture of the disease and determination of the content of thyroid-stimulating hormone in the blood serum.
  • Often in the autumn-winter period, a patient with AIT experiences the occurrence of subacute thyroiditis, that is, inflammation of the thyroid gland. In such cases, glucocorticoids (prednisolone) are prescribed. To combat the increasing number of antibodies in the patient’s body, non-steroidal anti-inflammatory drugs such as voltaren, indomethacin, and methindole are used.

In case of a sharp increase in the size of the thyroid gland, surgical treatment is recommended.

Forecast

Autoimmune thyroiditis in the vast majority of cases has a favorable prognosis. When persistent hypothyroidism is diagnosed, lifelong therapy with levothyroxine is required. Autoimmune thyrotoxicosis tends to be slow; in some cases, patients can remain in a satisfactory condition for about 18 years, despite minor remissions.

Observation of the dynamics of the disease must be carried out at least once every 6-12 months.

If nodules are detected during an ultrasound examination of the thyroid gland, immediate consultation with an endocrinologist is necessary. If nodes with a diameter of more than 1 cm have been identified and during dynamic observation, comparison of previous ultrasound results, their growth is noted, it is necessary to perform a puncture biopsy of the thyroid gland to exclude a malignant process. Monitoring of the thyroid gland using ultrasound should be carried out once every 6 months. If the diameter of the nodes is less than 1 cm, control ultrasound should be performed once every 6-12 months.

When trying to influence autoimmune processes (in particular, humoral immunity) in the thyroid gland for a long period of time in this pathology, glucocorticosteroids were prescribed in fairly high doses. At the moment, the ineffectiveness of this type of therapy for autoimmune thyroiditis has been clearly proven. The prescription of glucocorticosteroids (prednisolone) is advisable only in the case of a combination of subacute thyroiditis and autoimmune thyroiditis, which usually occurs in the autumn-winter period.

In clinical practice, there have been cases where spontaneous remission occurred in patients with autoimmune thyroiditis with signs of hypothyroidism during pregnancy. There have also been cases when patients with autoimmune thyroiditis, who had a euthyroid state before and during pregnancy, were aggravated by hypothyroidism after childbirth.

In addition to a hereditary predisposition to autoimmune thyroiditis, there are several factors that provoke pathology:

  • disruption of the structure of the thyroid gland as a result of injury or surgery;
  • past infectious and viral diseases (flu, measles);
  • the presence of a focus of chronic infection in the body (tonsillitis, sinusitis);
  • influence of negative environmental conditions;
  • irradiation of organs during radiation therapy or during professional activities;
  • emotional stress can provoke acute thyroiditis;
  • intestinal problems;
  • uncontrolled reception;
  • selenium deficiency;
  • Autoimmune thyroiditis can be caused by diabetes or thyroid disease.

Clinical symptoms

The initial stage of the disease, which can last for several years, is characterized by the absence of symptoms of autoimmune thyroiditis. Antibodies slowly destroy thyroid cells, gradually reducing its function. The development of the disease provokes discomfort in the front of the neck and negative changes in the patient’s appearance. Hashimoto's thyroiditis goes through several stages, successively replacing each other.

First stage

– this stage is characterized by normal functioning of the thyroid gland. Thyroiditis, the symptoms of which are still subjective, is observed in the dynamics of development. Euthyroidism does not have signs of hypo- and hyperthyroidism. This is a borderline condition in which the thyroid gland is enlarged, which is confirmed by palpation during examination, but synthesizes enough hormones. If euthyroidism is caused by iodine deficiency, single or multiple euthyroidism develops. The condition is accompanied by the following symptoms:

  • increasing weakness and fatigue;
  • insomnia or drowsiness;
  • difficulty swallowing, sensation of a foreign object in the throat;
  • weight loss.

Second stage

The subclinical stage is characterized by a massive attack of antibodies on gland cells. Due to their death, areas that are usually at rest are connected to synthesis. The response to the influence of T-lymphocytes is the accelerated production of thyrotropin. Hashimoto's thyroiditis at this stage has a number of symptoms:

  • swelling and painful blush on the face;
  • skin loses elasticity;
  • hoarseness appears in the voice;
  • neuroses.

Third stage

– immune cells do not stop the destruction of the organ, and the damaged gland releases large amounts of T3 and T4 hormones. This condition leads to a sharp deterioration in health, so patients should be observed by an endocrinologist. Manifestations of thyrotoxicosis in autoimmune thyroiditis are:

  • increased sweating;
  • thinning hair and nails;
  • increased blood pressure, tachycardia;
  • shortness of breath when walking;
  • fast fatiguability;
  • decreased bone strength;
  • increased excitability, feeling of anxiety.

Fourth stage

Hypothyroidism - at this stage there is a decrease in thyroid function, causing a persistent lack of hormones. The gland is seriously damaged by antibodies and needs time and treatment to recover. Hormone deficiency is manifested by inhibition of all processes in the body. Characteristic symptoms of thyroiditis in the last stage:

  • apathy, weakness, depression;
  • pale, swollen skin;
  • hair loss on the body and head;
  • rough voice;
  • joint pain;
  • feeling of chilliness;
  • constipation, digestive tract problems.

Acute thyroiditis, especially in purulent form, has intense pain in the neck and jaw. Chills occur and the temperature rises. This condition requires immediate medical attention. Acute non-purulent thyroiditis is characterized by a less pronounced picture of the disease; its signs are:

  • hand tremors;
  • chills;
  • sweating;
  • weight loss.

Acute thyroiditis without adequate treatment turns into hypothyroidism. Inflammation of the thyroid gland gives way to fibrosis. Hashimoto's thyroiditis causes menstrual irregularities in women and sexual dysfunction in men.

Forms of the disease

The classification of types of autoimmune thyroiditis includes several diseases united by a common nature:

  • – this form appears in most cases. The disease progresses slowly, without active changes in the condition, and can last for years. Chronic thyroiditis is characterized by a negative effect of T lymphocytes on thyroid cells. The destruction of its structure causes primary hypothyroidism. There are often no obvious signs of thyroiditis, making diagnosis difficult.
  • Postpartum AIT appears 14 weeks after the birth of the child in 5-6% of women. It is caused by the reactivation of the immune system, which was depressed during pregnancy. Symptoms of autoimmune thyroiditis are often attributed to postpartum depression. If the problem is left untreated, destructive autoimmune Hashimoto's thyroiditis develops.
  • Painless thyroiditis has symptoms similar to postpartum thyroiditis: fatigue, sweating, weakness, rapid heartbeat. The mechanism of the disease has not been studied.
  • Cytokine-induced thyroiditis occurs due to the use of interferon for the treatment of blood diseases and hepatitis C.

In chronic thyroiditis of the thyroid gland and other types of disease, there are three main forms. The basis for the classification was clinical manifestations and changes in organ size:

  • Latent form - signs of autoimmune thyroiditis are weakly expressed, there are no compactions in the organ. The size of the gland is slightly increased, hormone synthesis is normal.
  • Hypertrophic form - accompanied by the formation of goiter and nodes. In the diffuse form, the thyroid gland increases evenly. Symptoms of thyroiditis with nodulation or a combination of the two forms may be observed. Organ function in this condition is moderately impaired, but progressive autoimmune attacks lead to its decline.
  • Atrophic form - characterized by a decrease in the size of the gland and hormone deficiency. This condition occurs in older people or after exposure to radiation. This is the most severe form of autoimmune thyroiditis of the thyroid gland.

Diagnostics

Symptoms and treatment of the disease are the function of the endocrinologist, but before making a diagnosis, he must conduct a complex examination. Diagnosis of autoimmune thyroiditis is carried out during laboratory tests and an ultrasound procedure of the thyroid gland. The clinical picture of the disease is also a significant factor for an experienced doctor.

What tests does the examination include:

  • it is necessary to take a general blood test to count lymphocytes;
  • tests for hormones, T4,;
  • immunogram to determine the level of antibodies;
  • allows you to determine the size and structural changes of the thyroid gland;
  • identifies cells characteristic of Hashimoto's autoimmune thyroiditis.

The presence of relatives with disorders of autoimmune processes confirms the diagnosis.

Features of treatment and drugs

Knowing what autoimmune thyroiditis is, patients wonder whether it is possible to cure the thyroid gland? Treatment of the disease depends on its stage. Euthyroidism does not require treatment, but it is necessary to conduct an examination every six months with a blood test. Chronic thyroiditis is kept from progressing to hypothyroidism by taking synthetic hormones. The use of thyroid drugs is the basis for the treatment of autoimmune thyroiditis. They have a positive therapeutic effect on patients. The mechanism is due to several factors:

  • exclusion of clinical manifestations of hypothyroidism;
  • an increase in the concentration of thyroxine, which slows down the release and growth of the thyroid gland;
  • decrease in the amount of antithyroid antibodies.

The diagnosis of Hashimoto's thyroiditis requires long-term use of thyroid medications:

  • L-thyroxine;
  • Thyrotome;
  • Triiodothyronine.

Treatment of autoimmune thyroiditis in the subacute stage is performed with glucocorticoids, which suppress autoimmune reactions. They are an effective replacement for thyroid drugs at high titers of autoantibodies. Treatment of thyroiditis with glucocorticoid drugs is indicated for severe pain syndromes. Therapy with Prednisolone may cause side effects: stomach ulcers, hypertension,

Surgery

The main indicator for surgical intervention is the suspicion of malignant degeneration of the tumor. In addition, surgical treatment is prescribed for the following list of indications:

  • goiter growth that cannot be stopped by conservative treatment;
  • acute thyroiditis, threatening compression of the trachea;
  • node discovery;
  • visual disfigurement of the neck.

Surgery for autoimmune thyroiditis is more technically complex than for other pathological changes in the thyroid gland. There is a high incidence of surgical complications.

Forecast

If treatment for autoimmune thyroiditis is started in a timely manner, the prognosis is favorable. Competent therapy causes stable remission for 15 years. The risk of recurrence of postpartum thyroiditis is 70%, so women should be aware of the risk before becoming pregnant. Doctors have not learned how to completely cure inflammation of the gland, but restoring its functions is a feasible task for medicine.

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

Autoimmune thyroiditis (AIT, Hashimoto's thyroiditis, Hashimoto's goiter, Hashimoto's disease) is an inflammation of the thyroid tissue caused by autoimmune causes, very common in Russia. This disease was discovered exactly 100 years ago by a Japanese scientist named Hashimoto, and since then has been named after him (Hashimoto's thyroiditis). In 2012, the world endocrinological community widely celebrated the anniversary of the discovery of this disease, since from that moment endocrinologists had the opportunity to effectively help millions of patients around the planet.

Autoimmune thyroiditis - causes

Cause of autoimmune thyroiditis lies in the malfunction of the patient’s immune system. With autoimmune thyroiditis, which occurs most often in women, the immune system, which normally provides “police” functions in the body and is engaged in the destruction of foreign cells and organisms, begins to show aggression towards its own organ – the thyroid gland. The thyroid tissue becomes saturated with leukocytes, the activity of which leads to the development of inflammation of the gland - thyroiditis (it is called autoimmune thyroiditis to emphasize that the cause of the disease is a malfunction of the body's own immune system). Over time, due to inflammation, some of the thyroid cells die, and the survivors begin to lack enough to produce the required amount of hormones. Hormonal deficiency develops - hypothyroidism.

Symptoms of autoimmune thyroiditis (AIT)

Symptoms of autoimmune thyroiditis easily confused with the everyday condition of so many of our compatriots: the patient is worried about weakness, drowsiness, fatigue, depression, worsening mood, and sometimes swelling. Figuratively speaking, life begins to lose its colors. Many patients with autoimmune thyroiditis are also bothered by a slowdown in mental activity (“can’t gather their thoughts”), and hair often falls out actively.

Diagnosis of AIT

Diagnosis of autoimmune thyroiditis(its name is often shortened to three letters - AIT) is established if the patient has three so-called “major” signs: characteristic changes in the structure of the thyroid tissue during ultrasound examination, an increase in the blood titer of antibodies to the thyroid tissue (antibodies to thyroid peroxidase, antibodies to thyroglobulin), as well as an increase in the level of the hormone TSH and a decrease in the level of the hormones T4 and T3 in the blood. It is important to note that the diagnosis of Autoimmune Thyroiditis should not be made in cases where hormone levels are within normal limits. If there is no increase in the level of TSH in the blood (at least) or an increase in the level of TSH in combination with a decrease in the level of T3, T4 (in the most severe cases), it is impossible to make a diagnosis of autoimmune thyroiditis (AIT). The fairly common conclusions “Autoimmune thyroiditis, euthyroidism” are incorrect because they confuse doctors and often lead to the unreasonable prescription of thyroid hormones to the patient.

Autoimmune thyroiditis on ultrasound of the thyroid gland

Ultrasound examination of AIT usually reveals a decrease in the echogenicity of the gland and the appearance of pronounced diffuse changes. Translating into “human” language, we can say that with autoimmune thyroiditis, the thyroid gland looks dark on the ultrasound machine screen and has a very heterogeneous structure - in some places the tissue is lighter, in others it is darker. Ultrasound doctors often detect nodes in the thyroid tissue in cases of Hashimoto's disease. It should be noted that often these seals are not real nodes and are simply foci with a pronounced inflammatory process; they are also called “pseudo-nodes”. Most often, a qualified ultrasound physician can distinguish a pseudonodule in autoimmune thyroiditis from a nodule, but in some cases this is not easy to do. That is why doctors often write a conclusion something like this: “Signs of AIT. Nodes (pseudonodules?) of the thyroid gland” to emphasize his uncertainty in assessing the nature of the changes. If formations with a diameter of 1 cm or more are detected in the thyroid tissue against the background of autoimmune thyroiditis, the patient is recommended to undergo a biopsy to clarify their nature. In some cases, after receiving the results of the study, it becomes clear that the examined node is a pseudonodule against the background of AIT (the cytologist’s answer in such cases is usually short: “Autoimmune thyroiditis” or “Hashimoto’s thyroiditis”). At the same time, against the background of autoimmune thyroiditis, it is possible to identify both nodes of a colloid (benign) structure and malignant neoplasms.

Treatment of autoimmune thyroiditis

Treatment of the cause of autoimmune thyroiditis– improper functioning of the immune system – is currently impossible, since suppression of the immune system leads to a decrease in the body’s defense against viruses and bacteria, which can be dangerous. That is why doctors have to treat not the cause of autoimmune thyroiditis, but its consequence - a lack of hormones, or rather one hormone - thyroxine, which is produced by the thyroid gland from iodine supplied with food. A revolution in the treatment of AIT occurred when doctors were able to use thyroid hormones freely. Luckily for us, pharmacists have synthesized an exact copy of the human hormone thyroxine, which is completely indistinguishable from the original. If AIT and the associated lack of hormones are detected, the endocrinologist prescribes artificial thyroxine to the patient, which allows the hormone levels to return to normal. When administered correctly, thyroxine does not cause any side effects. The only inconvenience of such treatment is that it should be continued throughout the patient’s life, since once it begins, autoimmune thyroiditis (AIT) never goes away, and the patient constantly requires drug support.

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Chronic autoimmune thyroiditis (CAIT, AIT, lymphomatous thyroiditis, obsolete - Hashimoto's disease) - all these are names for one pathology, namely: chronic inflammation of the thyroid gland, which is based on autoimmune processes.

When it occurs, antibodies to the cells of your own thyroid gland begin to circulate in the blood and damage them. The immune system fails and it begins to mistake its own proteins for foreign ones.

Among thyroid pathologies, chronic autoimmune thyroiditis occupies a leading place among thyroid pathologies - 35%; and thyroid lesions themselves are immediately after diabetes in terms of prevalence.

AIT of the thyroid gland is present in 3-4% of the world's population. In general, endocrine pathologies are in 2nd place in frequency of occurrence after CVD.

AIT of the thyroid gland occurs more often in women - 10-20 times. The peak of cases occurs at the age of 40-50 years. When thyroiditis appears in children, intelligence definitely suffers - it begins to lag behind. In recent years, there has been a tendency towards rejuvenation of this pathology.

Causes of AIT

Chronic autoimmune thyroiditis (lymphomatous thyroiditis) always has only a hereditary nature. It is often accompanied by additional autoimmune pathologies: diabetes, lupus erythematosus, rheumatism, diarrhea, myasthenia, Sjogren's syndrome, vitiligo, collagenosis, etc. But to get sick, heredity alone is not enough; it needs to work. Then provoking factors called triggers come to the rescue.

The most significant of them is chronic infections of the ENT organs. Next come carious teeth; infections (flu, mumps, measles); uncontrolled use of iodine-containing drugs and hormones; the effects of radiation, dangerous in any dose; poor ecology with excess fluorine and chlorine in the external environment; lack of selenium and zinc; insolation; psychotrauma and stress.

With poor genetics, such patients have a tendency from birth to acquire thyroiditis. They have a defect in the genes that code for the activity of the immune system. This is bad because it complicates treatment; facilitates the task of prevention.

Poor ecology gives increased access to various toxins and pesticides into the body, and the thyroid gland becomes the first in their path. Therefore, in any hazardous production, do not forget about protection and compliance with safety regulations.

Negative effects of drugs. These may recently include interferons, iodine, lithium preparations, hormones, and estrogens.

When treated with interferons, cytokines enter the blood en masse, which literally bombard the thyroid gland, disrupting its functioning and causing inflammation with a picture of chronic thyroiditis.

Pathogenesis

The process of development of autoimmunization is very complex and multifaceted. For a general idea, it happens like this: any cells of the body - both microbial and “native” - are always required to “introduce themselves”.

To do this, they put something like a signal flag on their surface - this is a special specific protein. This protein or proteins are called “antigens”, to eliminate which, if they are foreign, the immune system produces antibodies that destroy them.

The ENT organs, together with the thyroid gland, have one common drain - the lymphatic system, which absorbs all toxins and pathogens. Lymphatic vessels permeate the entire gland, like blood vessels, and when incoming pathogenic agents merge into the lymph, they permanently mark the thyroid gland as infected. And immune cells every second approach any cell and check it for danger using their antigens. They receive a “list” of antigens during the mother’s pregnancy.

Interestingly, some organs do not normally have such permitted antigens. Such organs are surrounded by a cellular barrier that does not allow lymphocytes to pass through for inspection.

ShchZh is just one of those. When this barrier is disrupted due to markings, chronic autoimmune thyroiditis occurs. Moreover, in such patients, gene disruption occurs in terms of making lymphocytes more aggressive. Those. lymphocytes are of poor quality. Therefore, the immune system malfunctions and zealously rushes to protect the body from what it believes is an impostor gland, and sends its killers to it. And they are already destroying all the cells in a row - their own and others. From damaged cells, all their contents enter the blood: organelles - destroyed parts of internal components, hormones. This leads to even greater creation of antibodies to thyrocytes. A vicious circle arises, the process becomes cyclical. This is how autoimmune processes arise.

Why does this occur more in women? Their estrogens directly affect the immune system, but testosterone does not.

Classification of the disease

  1. HAIT or Hashimoto's disease. It is often simply called AIT, as a classic example of thyroiditis; Its course is benign. Chronic autoimmune thyroiditis (Hashimoto's disease or thyroiditis) is also called lymphomatous goiter because it causes swelling of the gland due to its inflammation.
  2. Postpartum thyroiditis– develops 1.5 months after birth, when the thyroid gland becomes inflamed due to increased immune reactivity. This happens because during gestation the thyroid gland was suppressed in order to preserve the fetus, which, in fact, is foreign to the pregnant woman’s body. Upon completion of childbirth, the thyroid gland may overreact - this varies from person to person. The clinical picture consists of manifestations of mild hyperthyroidism: weight loss, asthenia. Sometimes a feeling of heat, tachycardia, mood swings, insomnia, and hand tremors may occur. But gradually, over 4 months, these signs are replaced by hypothyroidism. It can be mistaken for postpartum depression.
  3. Painless form– etiology is not clear. The pathogenesis is similar to postpartum. Signs of mild hyperthyroidism are also present; the symptoms are attributed to overwork.
  4. Cytokine-induced form– appears when treating any pathologies with interferons. Most often this occurs during the treatment of hepatitis C to prevent its progression to cirrhosis.

Symptoms of thyroiditis of the thyroid gland can be either in the direction of hyperthyroidism or in the direction of hypofunction, but the manifestations are usually minor.

Current separation:

  1. Latent form - the thyroid gland works in N, but the volume may be slightly increased.
  2. Hypertrophic variant - an increase in the size of the thyroid gland occurs due to several nodes or diffusely. Then thyroiditis with nodulation is diagnosed.
  3. Atrophic appearance: hormones are less than normal, size is also reduced. This is already hypofunction of the thyroid gland.

Stages and symptoms of AIT

All existing stages smoothly transition into each other.

Euthyroid stage - lymphocytes see enemies in the thyroid cells and decide to attack them. Antibody production begins. Thyrocytes are destroyed. If a small number of cells die, euthyroidism is maintained.

Symptoms may be disturbing due to an increase in the volume of the thyroid gland, when it can be palpated. There may be difficulties in swallowing, performance decreases when the patient quickly gets tired even from usual activities.

Subclinical stage - symptoms may be the same. The number of destroyed cells continues to grow, but for now those thyrocytes that should normally be at rest are included in their work. TSH stimulates them to do this.

Thyrotoxicosis - occurs when there is a large number of antibodies. Symptoms:

  • irritability, anger, fussiness;
  • increasing fatigue;
  • weakness;
  • tearfulness;
  • heat intolerance;
  • hyperhidrosis;
  • tachycardia;
  • diarrhea;
  • decreased libido;
  • MC violations.

Hypothyroidism - most of the cells are destroyed, the gland is reduced and the last stage of AIT begins.

Symptoms:

  • apathy and tendency to low mood;
  • inhibition of speech, movements and thinking;
  • loss of appetite and weight gain;
  • the skin thickens due to constant swelling, acquires a yellowish or waxy tint; it is so dense that it is impossible to fold it;
  • the face is pasty, expressionless;
  • chronic constipation due to slow peristalsis;
  • chilliness;
  • hair loss;
  • brittle nails;
  • hoarseness of voice;
  • oligomenorrhea;
  • arthralgia.

The effect of AIT on fertility

All stages, except for the state of hypothyroidism, do not particularly affect conception; it can occur. The exception is hypothyroidism. Infertility may develop and conception becomes impossible.

The fact is that thyroid hormones are directly related to the ovaries. When there are few thyroid hormones, the ovaries work poorly, and proper processes in the form of ovulation and follicle maturation do not occur.

If a woman takes this into account and is registered with an endocrinologist and receives hormone replacement, pregnancy occurs. But due to the autoimmunity of the process, antibodies will not allow the fetus to carry to term.

Moreover, the dose of Eutirox in such cases does not solve anything. Doctors in such cases may prescribe Progesterone.

Monitoring by a doctor throughout gestation is necessary in any case. Typically, the dose of thyroxine increases by 40%, because there is a need for it in two organisms - the mother and the fetus.

Otherwise, the child in the womb may die or be born with congenital hypothyroidism. And this is equivalent not only to impaired metabolism, but also to congenital dementia.

Symptoms of AIT in general

Despite the variety of forms and stages of AIT, they all have one common manifestation - the presence of an inflammatory process in the thyroid gland. It always requires treatment. The onset of pathology in 90% of cases is asymptomatic.

This gland functions normally for a long time. The period of such a course lasts up to 2-3 years or more. Then the first calls come.

Its early signs are discomfort in the neck, a feeling of squeezing in the throat, a lump in it; This is especially felt when wearing high collars, sweaters, etc.

Sometimes slight weakness and pain in the joints occurs fleetingly. All symptoms are combined into 3 large groups: asthenic; hormone-forming; behavioral.

Asthenic symptoms manifest themselves in fatigue and general weakness; lethargy appears; muscle tone decreases. Frequent headaches and dizziness; sleep disorders. Asthenia is enhanced by increased production of hormones. There may be weight loss. Then such manifestations as increased heart rate and body tremors appear; increased appetite.

In men, impotence develops, in women, the circulatory cycle goes astray. The gland is enlarged at this time, it changes the size of the neck, which becomes thick and deformed.

Characteristic signs of behavioral disorders: the patient is often anxious, whiny, and constantly fussing. In conversation, he often loses the topic of conversation, becoming verbose but meaningless.

Chronic autoimmune thyroiditis is also different in that it does not manifest itself for a very long time. In the later stages of AIT, the clinical picture is similar to hypothyroidism. The symptoms are due to the inhibition of all processes in the body, which is where most of the symptoms come from.

The mood often gives off a depressive tint;

  • memory decreases;
  • difficulty concentrating and concentrating;
  • the patient is apathetic, drowsy or complains of fatigue;
  • weight is gained steadily, at different rates, against the background of decreased appetite;
  • bradycardia and decreased blood pressure;
  • chilliness;
  • weakness, despite good nutrition;
  • cannot perform normal amount of work;
  • inhibited in reactions, thoughts, movements, speech;
  • the skin is lifelessly dry, yellowish, dry;
  • peeling of the skin; facial pastiness;
  • inexpressiveness of facial expressions; hair loss and brittle nails;
  • loss of libido;
  • chronic constipation;
  • oligomenorrhea or intermenstrual bleeding.

Diagnostics

  1. In the UAC – leukopenia and increased lymphocytes. The hormonal profile changes depending on the stage of the pathology.
  2. Ultrasound of the thyroid gland - changes in the size of the gland also depend on the stage. If there are nodes, there is uneven magnification.
  3. FNA - fine-needle aspiration biopsy - reveals an increased number of lymphocytes and cells characteristic of AIT.
  4. Rarely, lymphomas may occur.
  5. AIT is most often a benign process. From time to time it causes exacerbations, which can be kept under control by a doctor.
  6. HRT becomes mandatory. With age, the risk of developing AIT increases.

Patients retain their ability to work for many years – up to 15-20 years.

Complications

Consequences arise from improper or lack of treatment. Among them: the appearance of a goiter - occurs because inflammation constantly irritates the tissue of the gland, causing swelling of its tissues. It begins to produce hormones in increased quantities and increases in volume.

If it is large in size, compartment syndrome may occur. Deterioration of heart function - with thyroiditis, metabolism is disrupted and LDL increases.

What is LDL? These are low density lipoproteins, i.e. bad cholesterol, which always increases the load on the myocardium and affects the walls of blood vessels, which cannot but affect cardiac activity.

Deterioration of mental health. Decreased libido is the same for both sexes.

Myxedematous coma - can appear during a long course of the disease against the background of improper treatment or its sudden cancellation. This is acute thyroiditis, which requires the most urgent measures. Hypothermia, stress, and sedatives predispose to coma.

There is an exacerbation of all the symptoms of hypothyroidism under the influence of a number of factors. Lethargy, drowsiness and weakness appear, up to loss of consciousness. Urgent assistance and calling an ambulance are required.

Congenital defects in the fetus - they usually occur in mothers with AIT without treatment. Such children, as a rule, have mental retardation, physical deformities, and congenital kidney pathologies.

Therefore, when planning a child, the mother should check. First of all, the condition of your thyroid gland. Today it is impossible to completely cure chronic thyroiditis of the thyroid gland, but it can be corrected with the help of hormone replacement therapy for many years.

Treatment of HAIT

Chronic autoimmune thyroiditis (Hashimoto's thyroiditis) and its treatment do not require any specific therapy. During the thyrotoxicosis phase, treatment is symptomatic and with thyreostatics. Prescribe Mercazolil, Thiamazole, beta-blockers.

For hypothyroidism - treatment with L-thyroxine. In the presence of coronary artery disease in elderly patients, the dose at the beginning is minimal. Monitoring of hormone levels and treatment is carried out every 2 months. In the cold season (autumn and winter), AIT can worsen and turn into subacute thyroiditis, then glucocorticosteroids are prescribed (most often Prednisolone). There are often cases when a potential mother suffered from euthyroidism during pregnancy, and with the completion of childbirth, the thyroid gland began to reduce its functions until the onset of hypothyroidism.

In any case, to influence the inflammatory process, NSAIDs are prescribed - Voltaren, Metindol, Indomethacin, Ibuprofen, Nimesil, etc. They also reduce the production of antibodies. Treatment is supplemented with vitamins and adaptogens. Decreased immunity is treated with immunocorrectors. The presence of CVD requires the prescription of adrenergic blockers.

When a goiter appears as a result of hyperthyroidism and if compartment syndrome occurs, treatment is usually surgical.

Forecast

The progression of the disease occurs very gradually. With adequate HRT, long-term remission is achieved.

At the same time, patients maintain their normal functioning for more than 15-18 years, even taking into account exacerbations. They are usually short-term and may be associated with hypothermia in the cold season against the background of provoking moments.

Prevention

There is no special prophylaxis, but in endemic areas with iodine deficiency, mass iodine prophylaxis is carried out. In addition, timely administration of therapy for chronic infections of the nasopharynx is required, sanitization of the oral cavity and hardening of the body are carried out.

Autoimmune thyroiditis is a pathology that mainly affects older women (45-60 years old). The pathology is characterized by the development of a strong inflammatory process in the thyroid gland. It occurs due to serious disruptions in the functioning of the immune system, as a result of which it begins to destroy thyroid cells.

The susceptibility of older women to pathology is explained by X-chromosomal disorders and the negative effect of estrogen hormones on the cells that form the lymphoid system. Sometimes the disease can develop in both young people and small children. In some cases, pathology is also found in pregnant women.

What can cause AIT, and can it be recognized independently? Let's try to figure it out.

What it is?

Autoimmune thyroiditis is an inflammation that occurs in the tissues of the thyroid gland, the main cause of which is a serious malfunction in the immune system. Against this background, the body begins to produce an abnormally large amount of antibodies, which gradually destroy healthy thyroid cells. Pathology develops in women almost 8 times more often than in men.

Reasons for the development of AIT

Hashimoto's thyroiditis (the pathology got its name in honor of the doctor who first described its symptoms) develops for a number of reasons. The primary role in this issue is given to:

  • regular stressful situations;
  • emotional overstrain;
  • excess iodine in the body;
  • unfavorable heredity;
  • the presence of endocrine diseases;
  • uncontrolled intake;
  • negative influence of the external environment (this could be poor ecology and many other similar factors);
  • unhealthy diet, etc.

However, do not panic - autoimmune thyroiditis is a reversible pathological process, and the patient has every chance to improve the functioning of the thyroid gland. To do this, it is necessary to ensure a reduction in the load on its cells, which will help reduce the level of antibodies in the patient’s blood. For this reason, timely diagnosis of the disease is very important.

Classification

Autoimmune thyroiditis has its own classification, according to which it occurs:

  1. Painless, the reasons for its development have not been fully established.
  2. Postpartum. During pregnancy, a woman’s immunity weakens significantly, and after the birth of a baby, on the contrary, it becomes more active. Moreover, its activation is sometimes abnormal, since it begins to produce an excessive amount of antibodies. Often the consequence of this is the destruction of “native” cells of various organs and systems. If a woman has a genetic predisposition to AIT, she needs to be extremely careful and carefully monitor her health after childbirth.
  3. Chronic. In this case, we are talking about a genetic predisposition to the development of the disease. It is preceded by a decrease in the production of hormones in organisms. This condition is called primary.
  4. Cytokine-induced. This thyroiditis is a consequence of taking interferon-based medications used in the treatment of hematogenous diseases and.

All types of AIT, except the first, are manifested by the same symptoms. The initial stage of development of the disease is characterized by the occurrence of thyrotoxicosis, which, if diagnosed and treated untimely, can develop into hypothyroidism.

Stages of development

If the disease was not detected in a timely manner, or for some reason it was not treated, this may cause its progression. The stage of AIT depends on how long ago it developed. Hashimoto's disease is divided into 4 stages.

  1. Eutheroid phase. Each patient has its own duration. Sometimes a few months may be enough for the disease to enter the second stage of development, while in other cases several years may pass between phases. During this period, the patient does not notice any special changes in his well-being and does not consult a doctor. Secretory function is not impaired.
  2. At the second, subclinical stage, T lymphocytes begin to actively attack follicular cells, leading to their destruction. As a result, the body begins to produce significantly less St. hormone. T4. Eutheriosis persists due to a sharp increase in TSH levels.
  3. The third phase is thyrotoxic. It is characterized by a strong surge in the hormones T3 and T4, which is explained by their release from destroyed follicular cells. Their entry into the blood becomes a powerful stress for the body, as a result of which the immune system begins to rapidly produce antibodies. When the level of functioning cells drops, hypothyroidism develops.
  4. The fourth stage is hypothyroid. Thyroid function can recover on its own, but not in all cases. It depends on the form in which the disease occurs. For example, chronic hypothyroidism can last for quite a long time, moving into an active stage followed by a phase of remission.

The disease can be in one phase or go through all the stages described above. It is extremely difficult to predict exactly how the pathology will progress.

Symptoms of autoimmune thyroiditis

Each form of the disease has its own characteristics of manifestation. Since AIT does not pose a serious danger to the body, and its final phase is characterized by the development of hypothyroidism, neither the first nor the second stages have any clinical signs. That is, the symptoms of the pathology are, in fact, a combination of those anomalies that are characteristic of hypothyroidism.

We list the symptoms characteristic of autoimmune thyroiditis of the thyroid gland:

  • periodic or constant depressive state (a purely individual symptom);
  • memory impairment;
  • problems with concentration;
  • apathy;
  • constant drowsiness or feeling tired;
  • a sharp jump in weight, or a gradual increase in body weight;
  • deterioration or complete loss of appetite;
  • slow heart rate;
  • chilliness of hands and feet;
  • loss of strength even with adequate nutrition;
  • difficulty performing ordinary physical work;
  • inhibition of reaction in response to the influence of various external stimuli;
  • dullness of hair, its fragility;
  • dryness, irritation and peeling of the epidermis;
  • constipation;
  • decreased sexual desire or its complete loss;
  • menstrual irregularities (development of intermenstrual bleeding, or complete cessation of menstruation);
  • swelling of the face;
  • yellowness of the skin;
  • problems with facial expressions, etc.

Postpartum, silent (asymptomatic) and cytokine-induced AIT are characterized by alternating phases of the inflammatory process. In the thyrotoxic stage of the disease, the manifestation of the clinical picture occurs due to:

  • sudden weight loss;
  • sensations of heat;
  • increased sweating intensity;
  • feeling unwell in stuffy or small rooms;
  • trembling in fingers;
  • sudden changes in the patient’s psycho-emotional state;
  • increased heart rate;
  • seizures;
  • deterioration of attention and memory;
  • loss or decrease in libido;
  • fatigue;
  • general weakness, which even proper rest does not help get rid of;
  • sudden attacks of increased activity;
  • problems with the menstrual cycle.

The hypothyroid stage is accompanied by the same symptoms as the chronic stage. Postpartum AIT is characterized by the manifestation of symptoms of thyrotoxicosis in the middle of the 4th month, and the detection of symptoms of hypothyroidism at the end of the 5th - early 6th month of the postpartum period.

In painless and cytokine-induced AIT, no special clinical signs are observed. If ailments do appear, they have an extremely low degree of severity. If they are asymptomatic, they are detected only during a preventive examination in a medical institution.

What does autoimmune thyroiditis look like: photo

The photo below shows how the disease manifests itself in women:

Diagnostics

It is almost impossible to detect its presence before the first warning signs of pathology appear. If there are no ailments, the patient does not consider it advisable to go to the hospital, but even if he does, it will be almost impossible to identify the pathology using tests. However, when the first adverse changes in the functioning of the thyroid gland begin to occur, a clinical study of a biological sample will immediately identify them.

If other family members suffer or have previously suffered from similar disorders, this means that you are at risk. In this case, it is necessary to visit a doctor and undergo preventive examinations as often as possible.

Laboratory tests for suspected AIT include:

  • general blood test, which determines the level of lymphocytes;
  • a hormone test required to measure serum TSH;
  • immunogram, which establishes the presence of antibodies to AT-TG, thyroid peroxidase, as well as to thyroid hormones of the thyroid gland;
  • fine-needle biopsy, necessary to determine the size of lymphocytes or other cells (their increase indicates the presence of autoimmune thyroiditis);
  • Ultrasound diagnosis of the thyroid gland helps to determine its increase or decrease in size; with AIT, a change in the structure of the thyroid gland occurs, which can also be detected during ultrasound.

If the results of an ultrasound examination indicate AIT, but clinical tests refute its development, then the diagnosis is considered doubtful and does not fit into the patient’s medical history.

What will happen if left untreated?

Thyroiditis can have unpleasant consequences, which vary for each stage of the disease. For example, during the hyperthyroid stage, the patient may have an abnormal heart rhythm (arrhythmia) or heart failure, and this is fraught with the development of such a dangerous pathology as myocardial infarction.

Hypothyroidism can lead to the following complications:

  • dementia;
  • infertility;
  • premature termination of pregnancy;
  • inability to bear fruit;
  • congenital hypothyroidism in children;
  • deep and prolonged depression;
  • myxedema.

With myxedema, a person becomes hypersensitive to any downward changes in temperature. Even a common flu, or another infectious disease suffered during this pathological condition, can cause a hypothyroid coma.

However, there is no need to worry too much - such a deviation is a reversible process and can be easily treated. If you choose the right dosage of the drug (it is prescribed depending on the level of hormones and AT-TPO), then the disease may not appear for a long period of time.

Treatment of autoimmune thyroiditis

Treatment of AIT is carried out only at the last stage of its development - at. However, in this case, certain nuances are taken into account.

Thus, therapy is carried out exclusively for manifest hypothyroidism, when the TSH level is less than 10 mIU/l, and St. T4 is reduced. If the patient suffers from a subclinical form of the pathology with a TSH of 4-10 mIU/1 l and normal values ​​of St. T4, then in this case treatment is carried out only in the presence of symptoms of hypothyroidism, as well as during pregnancy.

Today, the most effective medications for treating hypothyroidism are levothyroxine-based medications. The peculiarity of such drugs is that their active substance is as close as possible to the human hormone T4. Such drugs are absolutely harmless, so they are allowed to be taken even during pregnancy and breastfeeding. The drugs cause virtually no side effects, and, despite the fact that they are based on a hormonal element, they do not lead to weight gain.

Levothyroxine-based drugs should be taken “isolated” from other medications, since they are extremely sensitive to any “foreign” substances. The dose is taken on an empty stomach (half an hour before meals or other medications) with plenty of liquid.

Calcium supplements, multivitamins, iron supplements, sucralfate, etc. should be taken no earlier than 4 hours after taking levothyroxine. The most effective drugs based on it are L-thyroxine and Eutirox.

Today there are many analogues of these drugs, but it is better to give preference to the originals. The fact is that they have the most positive effect on the patient’s body, while analogues can only bring a temporary improvement in the patient’s health.

If from time to time you switch from originals to generics, then you must remember that in this case you will need to adjust the dosage of the active substance - levothyroxine. For this reason, every 2-3 months it is necessary to take a blood test to determine the TSH level.

Nutrition for AIT

Treating the disease (or significantly slowing its progression) will have better results if the patient avoids foods that harm the thyroid gland. In this case, it is necessary to minimize the frequency of consumption of products containing gluten. The following are prohibited:

  • cereals;
  • flour dishes;
  • bakery products;
  • chocolate;
  • sweets;
  • fast food, etc.

At the same time, you should try to eat foods fortified with iodine. They are especially useful in the fight against the hypothyroid form of autoimmune thyroiditis.

In case of AIT, it is necessary to take the issue of protecting the body from the penetration of pathogenic microflora with the utmost seriousness. You should also try to clean it of pathogenic bacteria that are already in it. First of all, you need to take care of cleansing the intestines, because this is where harmful microorganisms actively multiply. To do this, the patient’s diet should include:

  • fermented milk products;
  • Coconut oil;
  • fresh fruits and vegetables;
  • lean meat and meat broths;
  • different types of fish;
  • seaweed and other seaweed;
  • sprouted grains.

All products from the above list help strengthen the immune system, enrich the body with vitamins and minerals, which, in turn, improves the functioning of the thyroid gland and intestines.

Important! If there is a hyperthyroid form of AIT, it is necessary to completely exclude from the diet all foods that contain iodine, since this element stimulates the production of hormones T3 and T4.

For AIT, it is important to give preference to the following substances:

  • selenium, which is important for hypothyroidism, as it improves the secretion of hormones T3 and T4;
  • B vitamins, which help improve metabolic processes and help keep the body in good shape;
  • probiotics, important for maintaining intestinal microflora and preventing dysbiosis;
  • adaptogen plants that stimulate the production of hormones T3 and T4 in hypothyroidism (Rhodiola rosea, Reishi mushroom, ginseng root and fruit).

Treatment prognosis

What's the worst thing you can expect? The prognosis for treatment of AIT is, in general, quite favorable. If persistent hypothyroidism occurs, the patient will have to take levothyroxine-based medications for the rest of his life.

It is very important to monitor the level of hormones in the patient’s body, so once every six months it is necessary to take a clinical blood test and ultrasound. If during an ultrasound examination a nodular compaction is noticed in the thyroid area, this should be a good reason to consult an endocrinologist.

If, during an ultrasound, an increase in nodules was noticed, or their intensive growth is observed, the patient is prescribed a puncture biopsy. The resulting tissue sample is examined in the laboratory in order to confirm or refute the presence of a carcinogenic process. In this case, ultrasound is recommended to be performed every six months. If the node does not tend to increase, then ultrasound diagnostics can be performed once a year.