Subacute thyroiditis. Autoimmune thyroiditis Symptoms and signs of painless thyroiditis

What's happening?

With all destructive autoimmune thyroiditis, the disease goes through several phases. thyrotoxic phase is the result of an antibody-dependent complement attack on thyrocytes, which results in the release of ready-made thyroid hormones into the bloodstream. If destruction thyroid gland was quite pronounced, the second phase begins - hypothyroid, which usually lasts less than a year. In the future, most often restoration of thyroid function, although in some cases hypothyroidism remains persistent. In all three variants of destructive autoimmune thyroiditis, the process can be monophasic (only thyrotoxic or only hypothyroid phase).

Epidemiology

Postpartum thyroiditis develops in postpartum period in 5-9% of all women, while it is strictly associated with the carriage of AT-TPO. It develops in 50% of carriers of Ab-TPO, while the prevalence of Ab-TPO among women reaches 10%. Postpartum thyroiditis develops in 25% of women with type 1 diabetes.

Prevalence painless(silent) thyroiditis is unknown. Like postpartum thyroiditis, it is associated with the carriage of Ab-TPO and, due to the benign course, most often remains undiagnosed. more often develops in women (4 times) and is associated with the carriage of AT-TPO. The risk of its development in AT-TPO carriers receiving interferon preparations is about 20%. There is no relationship between the start time, duration and regimen of interferon therapy. With the development of cytokine-induced thyroiditis, the abolition or change in the regimen of interferon therapy does not affect the natural course of the disease.

Clinical manifestations

In all three destructive autoimmune thyroiditis, the symptoms of thyroid dysfunction are mild or absent. The thyroid gland is not enlarged, painless on palpation. Endocrine ophthalmopathy never develops. postpartum thyroiditis, usually manifests as mild thyrotoxicosis at about 14 weeks postpartum. In most cases, non-specific symptoms in the form of fatigue, general weakness, some weight loss are associated with recent childbirth. In some cases, thyrotoxicosis is expressed significantly and the situation requires differential diagnosis with diffuse toxic goiter. The hypothyroid phase develops around 19 weeks postpartum. In some cases, the hypothyroid phase of postpartum thyroiditis is associated with postpartum depression.

Painless (silent) thyroiditis is diagnosed with mild, often subclinical thyrotoxicosis, which, in turn, is detected by a non-targeted hormonal study. The diagnosis of the hypothyroid phase of painless thyroiditis can be established retrospectively, with the dynamic observation of patients with subclinical hypothyroidism, which ends with the normalization of thyroid function.

Cytokine-induced thyroiditis also, as a rule, it is not accompanied by severe thyrotoxicosis or hypothyroidism and is most often diagnosed during a planned hormonal study, which is included in the monitoring algorithm for patients receiving interferon preparations.

Diagnostics

The diagnosis is based on anamnestic indications of recent childbirth (abortion) or the patient receiving interferon therapy. In these situations, dysfunction of the thyroid gland is overwhelmingly associated with postpartum and cytokine-induced thyroiditis, respectively. Silent thyroiditis should be suspected in patients with mild, often subclinical thyrotoxicosis who are asymptomatic and have no endocrine ophthalmopathy. The thyrotoxic phase of all three thyroiditis is characterized by a decrease in the accumulation of the radiopharmaceutical according to thyroid scintigraphy. Ultrasound reveals non-specific for all autoimmune disease reduced echogenicity of the parenchyma.

Treatment

In the thyrotoxic phase, the appointment of thyrostatics (thiamazole) is not indicated, since there is no hyperfunction of the thyroid gland in destructive thyrotoxicosis. With severe cardiovascular symptoms, beta-blockers are prescribed. In the hypothyroid phase, replacement therapy with levothyroxine is prescribed. After about a year, an attempt is made to cancel it: if hypothyroidism was transient, the patient will remain euthyroid, with persistent hypothyroidism, an increase will occur. TSH level and decrease in T4.

Forecast

In women with postpartum thyroiditis, the likelihood of its recurrence after the next pregnancy is 70%. Approximately 25-30% of women who have had postpartum thyroiditis later develop a chronic variant of autoimmune thyroiditis with an outcome in persistent hypothyroidism.

Subacute thyroiditis

Subacute thyroiditis(De Quervain's thyroiditis, granulomatous thyroiditis) is an inflammatory disease of the thyroid gland, presumably of viral etiology, in which destructive thyrotoxicosis is combined with pain syndrome in the neck and symptoms of acute infectious disease.

Etiology

Presumably viral, since during the illness some patients show an increase in the level of antibodies to influenza viruses, mumps, adenoviruses. In addition, subacute thyroiditis often develops after infections of the upper respiratory tract, influenza, mumps, measles. A genetic predisposition to the development of the disease has been proven. Among patients with subacute thyroiditis, carriers of the HLA-Bw35 antigen are 30 times more common.

Pathogenesis

If we adhere to the viral theory of the pathogenesis of subacute thyroiditis, it is most likely that the introduction of the virus into the thyrocyte causes the destruction of the latter with the entry of follicular contents into the bloodstream (destructive thyrotoxicosis). At the end viral infection there is a restoration of thyroid function, in some cases after a short hypothyroid phase.

Epidemiology

Mostly people aged 30 to 60 get sick, while women are 5 or more times more likely than men; the disease is rare in children. In the structure of diseases occurring with thyrotoxicosis, subacute thyroiditis occurs 10-20 times less often than diffuse toxic goiter. We can assume a slightly higher incidence, given the fact that subacute thyroiditis can have a very mild course, masquerading as another pathology (tonsillitis, SARS) with subsequent spontaneous remission.

Clinical manifestations

The clinical picture is presented three groups of symptoms: pain in the neck, thyrotoxicosis (mild or moderate) and symptoms of an acute infectious disease (intoxication, sweating, subfebrile condition). Typical for subacute thyroiditis is a fairly sudden onset of diffuse pain in the neck. Neck movements, swallowing and various irritations of the thyroid gland are very unpleasant and painful. The pain often radiates to the back of the head, ears, and lower jaw. On palpation, the thyroid gland is painful, dense, moderately enlarged; soreness can be local or diffuse, depending on the degree of involvement of the gland in inflammatory process. Characterized by variable intensity and passing (wandering) pain from the region of one lobe to another, as well as pronounced general phenomena: tachycardia, asthenia, weight loss.

An increase in temperature (subfebrile or mild fever) occurs in about 40% of patients. Often, pain in the neck is the only clinical manifestation of subacute thyroiditis, while the patient may not have thyrotoxicosis at all.

Diagnostics

ESR increase- one of the most typical manifestations of subacute thyroiditis, while it can be increased significantly (more than 50-70 mm / h). Leukocytosis, characteristic bacterial infections is absent, moderate lymphocytosis can be determined. As in other diseases that occur with destructive thyrotoxicosis, the level of thyroid hormones is moderately elevated; often there is subclinical thyrotoxicosis, often a euthyroid course of the disease.

According to ultrasound, subacute thyroiditis is characterized by indistinctly limited hypoechoic areas, less often diffuse hypoechoicity. When scintigraphy revealed a decrease in the capture of 99m Tc.

- a disease of the thyroid gland, which is characterized by excessive synthesis of hormones by the gland.

The tactics of treating thyrotoxicosis depends primarily on the cause of this pathological condition.

Causes of thyrotoxicosis

• Graves' disease is also known as diffuse toxic goiter and is characterized by an increase in the secretion of hormones as a result of an increase in the level of antibodies to the gland's own cells.
• The presence of one or many thyroid nodules is accompanied by an increase in the production and release of hormones into the blood. At the same time, the "work" of the goiter cells is not subject to thyroid-stimulating hormone - the hormone of the pituitary gland, which controls the work of the thyroid gland.
• Destructive thyroiditis is characterized by the destruction of thyroid tissue and the release of hormones into the blood from the destroyed thyroid follicles.
• In some cases, thyrotoxicosis can be induced by prolonged or uncontrolled use of iodine-containing drugs (for example, antiarrhythmic drugs that contain iodine). Separately, it is worth noting the thyretoxic conditions that occur with an overdose of drugs that contain thyroid hormones and are used in the treatment of hypothyroidism.

Treatment of thyrotoxicosis

Since thyrotoxicosis most often occurs as a manifestation of Basedow's disease, we will consider the tactics of treatment for this disease.

There are 3 treatment options for thyrotoxicosis:

1. Medical correction of hormone levels.
2. Treatment with radioactive iodine.
3. Surgery.

Medical therapy

• The drug is most often used to treat thyrotoxicosis. It prevents the structural formation of hormone molecules, as well as iodination of thyroglobulin molecules.
• Preparations are also used, the molecules of which are absorbed instead of iodine molecules, thereby reducing its content in the colloid. An example of such preparations is Potassium Perchlorate.
• In some cases, microiodine preparations are effective, which can reduce the blood supply to the thyroid gland and reduce the iodine content in thyroid hormones.

Treatment with radioactive iodine

Treatment with radioactive iodine is based on the ingestion of drugs containing radioactive iodine. They enter the tissue of the thyroid gland, cause the death of active thyrocytes, due to which there is a decrease in the synthesis of gland hormones. The most common complication this method is the excessive destruction of thyrocytes and their replacement connective tissue, as a result of which the patient develops hypothyroidism - a condition opposite to hypertoxicosis.

Surgery

If conservative therapy fails, surgery. Also, the doctor can offer this method of treatment to the patient with a significant increase in the gland with compression of the nearby organs of the neck.

With destructive thyroiditis The mainstay of treatment is glucocorticoids. These drugs are able to stop the processes of tissue destruction, but the dosage and duration of the drug should always be selected individually.

There are only 3 methods of treatment of autoimmune thyroiditis:

• medicines;
• surgery or radioactive iodine;
• rehabilitation treatment of CRT.

Learn from the mistakes of others: hormones and surgery do not eliminate the cause of autoimmune thyroiditis

The first method is HRT (replacement hormone therapy) (or drug therapy drugs). This is a regular intake or replacement of hormones that the body lacks. synthetic analogues. HRT does not eliminate the development of autoimmune thyroiditis, but only reduces its manifestations in the analyzes for some time.

As a result of such “treatment”, the disease progresses, increasing doses of drugs are required, which, coupled with the lack of recovery, leads to numerous side effects and disorders of the human digestive, cardiovascular, nervous and reproductive systems. You can learn more about the dangers and therapeutic futility of HRT.

Before deciding to "treat" with HRT, we recommend that you search for real patient reviews on the Internet or read the reviews of our patients who have tried to be cured in this way for years. For obvious reasons, we do not use HRT in our practice, but on the contrary, we gradually remove the dependence of patients on taking synthetic hormones.

surgery with autoimmune thyroiditis, it is prescribed in advanced cases or with large volumes of the thyroid gland to stop excess production immune system antibodies. Those. instead of eliminating the cause of the disease, the thyroid gland is offered to be partially or completely removed with a scalpel or laser. As an alternative to completely stop the thyroid gland without surgery, it is proposed to irradiate it with radioactive iodine.

The latter method is of course "safer" surgical operations but removal of the thyroid gland any way leads to a dangerous disability. Autoimmune processes in the body do not disappear and are now controlled lifelong HRT. In addition to the violation of the digestive, cardiovascular, nervous and reproductive systems of a person, you get lifelong hypothyroidism and other chronic diseases.

For more than 20 years, there has been a safe treatment of autoimmune thyroiditis without hormones and operations using computer reflex therapy (CRT)

In our medical center in the city of Samara, they carry out a complete restoration of the function, structure and volume of the thyroid gland without hormones and operations.

An indicative CRT result for one of our patients, who once again double-checked the results for hormones in her regional clinic:

FULL NAME - Fayzullina Irina Igorevna

Laboratory research BEFORE treatment M20161216-0003 from 16.12.2016 ()

Thyroid Stimulating Hormone (TSH) - 8,22 μIU/ml

Laboratory research AFTER 1 CRT course M20170410-0039 from 10.04.2017 ()

Thyroid Stimulating Hormone (TSH) - 2,05 μIU/ml

Free thyroxine (T4) - 1,05 ng/dl

What is the secret of such results?

The reason for recovery is the restoration of the patient's own neuro-immuno-endocrine regulation

The point is that the coordinated work internal organs Our body is regulated by the coordinated interaction of 3 main control systems: nervous, immune and endocrine. It is from their synchronous and well-coordinated work that the physical condition and health of a person depends. Any disease progresses and the body cannot cope with it on its own precisely because of failure in the synchronous operation of these systems.

CRT through the autonomic nervous system "reboots" the work of the three main regulatory systems of the body to the state active struggle with current diseases.

There are many methods of influencing the nervous system, but only computer reflex therapy for 20 years has proven that patients fully recover neuro-immuno-endocrine regulation of the body and, as a result, recede and completely disappear many endocrine and neurological diseases that previously did not respond to drug "treatment".

Efficiency therapy also lies in the fact that the doctor affects the patient’s body not “blindly”, but, thanks to special sensors and a computer system, sees what points nervous system and how many required to use a medical device.

CRT may look like acupuncture, but it is not, because. works without the use of needles and on other principles.

CRT, like any treatment method, has its own contraindications for use: oncological diseases and mental disorders , Availability pacemaker, flickering arrhythmia and myocardial infarction in acute period, HIV-infection and congenital hypothyroidism.

If you do not have the above contraindications, then restoring your own hormonal balance and getting rid of autoimmune thyroiditis using this method in our center has been a common practice for many years.

Treatment of autoimmune thyroiditis by computer reflex therapy without side effects leads to the following results:

• the growth of nodes and cysts stops, they gradually decrease in size and, most often, completely resolve;
• are recovering the volume of functioning tissue and the structure of the thyroid gland;
• synthesis of own thyroid hormones is restored, which is confirmed by ultrasound data and normalization of the level of thyroid hormones TSH and T4;
• the activity of autoimmune processes in the thyroid gland decreases,which is confirmed by a decrease in the titer of antibodies AT-TPO, AT-TG and AT to TSH receptors;
• if the patient takes hormone replacement drugs, it is possible to reduce their dosage and eventually completely cancel;
• the menstrual cycle is restored;
• women can realize childbearing function without IVF and give birth healthy child with normal hormone levels;
• in addition, the biological age of the patient decreases, health improves, weight decreases, and edema disappears. That is why the Clinic has additional procedures and programs for natural facial rejuvenation.

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Head of the department, endocrinologist, reflexologist, candidate of medical sciences.

Both men and women (regardless of pregnancy) sometimes experience transient symptoms of thyrotoxicosis. As with subacute thyroiditis, these symptoms are often replaced by manifestations of hypothyroidism, but without pain in the thyroid gland. This condition is called differently: hyperthyroiditis, silent thyroiditis; transient painless thyroiditis with hyperthyroidism and lymphocytic thyroiditis. Thyroid disease, accompanied by its enlargement, is usually painless; most common in women, often immediately after childbirth; usually does not require specific treatment; in rare cases (10%) leads to irreversible hypothyroidism.

14. What are the causes of painless thyroiditis?

Some researchers consider silent thyroiditis a variant of subacute thyroiditis because a small percentage of patients with histologically proven subacute thyroiditis also have no thyroid pain. In such cases, fever and weight loss sometimes occur, which is sometimes confused with systemic diseases or malignant tumor. Other authors consider painless thyroiditis a variant of Hashimoto's thyroiditis due to the similarity of the histological pattern. In rare cases, pain in the thyroid gland is noted.

KEY MESSAGES: THYROIDITIS

1. On the early stages subacute thyroiditis radioactive iodine(ATN) thyroid gland is reduced; ESR is significantly increased.
2. Globular proteins of human blood plasma, as well as warm-blooded animals. The nature of education is such a response to the penetration of antigens (viruses, bacteria, toxins, etc.) into the body and having the ability to bind to them in a special way; used as part of immune sera in the treatment and prevention of infectious diseases; A.'s reaction with antigens is used in the diagnosis of various diseases (serological reactions) and in forensic medicine.
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3. Amiodarone-induced thyroiditis can be manifested by iodine hyperthyroidism and destructive thyroiditis.
4. In subacute thyroiditis, it may be necessary to prescribe painkillers (or steroids) and β-blockers, and later L-T 4 , but usually the disease resolves spontaneously.
5. Acute infectious thyroiditis requires rapid opening/drainage of the focus and the use of antibiotics.

15. What is destructive thyroiditis?

Inflammatory Infiltration, -i; well. Excessive penetration and deposition in the tissues of metabolic products, various cells, etc., observed during inflammation, dystrophy or tumors.

16. What test is indicated for a patient with symptoms of hyperthyroidism, elevated T4 levels and reduced serum TSH levels?

PRI should be determined within 24 hours. At increased activity thyroid gland (as in Graves' disease or toxic nodular goiter) is increased, and in destructive thyroiditis it is reduced. This is due to both a decrease in TSH levels (due to an acute increase in serum T4) and a loss способности!} damaged thyroid follicles absorb and organize iodine. (antithyroid drugs, radioiodine therapy or thyroidectomy) is absolutely contraindicated Painkillers (salicylates or prednisone) quickly eliminate pain in the thyroid gland. The symptoms of hypothyroidism are eliminated by thyroid hormones, the treatment of which, depending on the severity of the disease, should last 6-12 months. Many patients do not need treatment at all.

Autoimmune thyroiditis - a concept that unites a heterogeneous group inflammatory diseases thyroid gland, developing as a result of immune autoaggression and manifested by destructive changes in the tissue of the gland varying degrees expressiveness.

Despite the wide distribution, the problem of autoimmune thyroiditis has been little studied, due to the lack of specific clinical manifestations that make it possible to detect the disease at an early stage. Often for a long time (sometimes throughout life) patients do not know that they are carriers of the disease.

The frequency of occurrence of the disease, according to various sources, varies from 1 to 4%; in the structure of the pathology of the thyroid gland, its autoimmune damage accounts for every 5–6th case. Much more often (4–15 times) women are exposed to autoimmune thyroiditis. Average age of onset of deployed clinical picture, indicated in the sources, varies significantly: according to some data, it is 40-50 years old, according to others - 60 and older, some authors indicate the age of 25-35 years. It is reliably known that in children the disease is extremely rare, in 0.1–1% of cases.

Causes and risk factors

The main cause of the disease is a malfunction of the immune system, when it recognizes thyroid cells as foreign and begins to produce antibodies (autoantibodies) against them.

The disease develops against the background of a genetically programmed defect in the immune response, which leads to the aggression of T-lymphocytes against their own cells (thyrocytes) with their subsequent destruction. This theory is supported by a clear trend towards the diagnosis in patients with autoimmune thyroiditis or their genetic relatives of other immune diseases: chronic autoimmune hepatitis, diabetes type I, pernicious anemia, rheumatoid arthritis etc.

Autoimmune thyroiditis often manifests itself in members of the same family (in half of the patients, the next of kin are also carriers of antibodies to thyroid cells), in this case, genetic analysis reveals haplotypes HLA-DR3, DR4, DR5, R8.

The main consequence of autoimmune thyroiditis is the development of persistent overt hypothyroidism, the pharmacological correction of which does not cause significant difficulties.

Risk factors that can provoke a breakdown in immune tolerance:

• excess intake of iodine;
• exposure to ionizing radiation;
• taking interferons;
• transferred viral or bacterial infections;
• unfavorable ecological situation;
• concomitant allergopathology;
• exposure to chemicals, toxins, prohibited substances;
• chronic stress or acute excessive psycho-emotional stress;
• trauma or surgery on the thyroid gland.

Forms of the disease

There are 4 main forms of the disease:

1. Chronic autoimmune thyroiditis, or Hashimoto's thyroiditis (disease), or lymphocytic thyroiditis.
2. Postpartum thyroiditis.
3. Painless thyroiditis, or "silent" ("silent") thyroiditis.
4. Cytokine-induced thyroiditis.

Chronic autoimmune thyroiditis also has several clinical forms:

• hypertrophic, in which the gland is enlarged to varying degrees;
• atrophic, accompanied by a sharp decrease in the volume of the thyroid gland;
• focal (focal);
• latent, characterized by the absence of changes in the tissues of the gland.

Stages of the disease

During chronic autoimmune thyroiditis, 3 consecutive phases are distinguished:

1. euthyroid phase. There are no dysfunctions of the thyroid gland, the duration is several years.
2. The phase of subclinical hypothyroidism is the progressive destruction of gland cells, which is compensated by the stress of its functions. There are no clinical manifestations, the duration is individual (possibly lifelong).
3. The phase of overt hypothyroidism is a clinically pronounced decrease in the function of the gland.

In postpartum, silent and cytokine-induced thyroiditis, the phase of the autoimmune process is somewhat different:

I. Thyrotoxic phase - a massive release into the systemic circulation of thyroid hormones from cells destroyed during an autoimmune attack.

II. Hypothyroid phase - a decrease in the level of thyroid hormones in the blood against the background of massive immune damage to gland cells (usually lasts no more than a year, in rare cases - for life).

III. Recovery phase of thyroid function.

Rarely, a monophasic process is observed, the course of which is characterized by stuck in one of the phases: toxic or hypothyroid.

Due to the acute onset, due to the massive destruction of thyrocytes, postpartum, silent and cytokine-induced forms are combined into a group of so-called destructive autoimmune thyroiditis.

Postpartum thyroiditis can degenerate into chronic autoimmune (with a further outcome in overt hypothyroidism) in 20-30% of women.

Symptoms

Manifestations various forms diseases 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 polysystemic manifestations of hypothyroidism (depression of thyroid function):

• lethargy, drowsiness;
• feeling of unmotivated fatigue;
• intolerance to habitual physical activity;
• slowing down reactions to external stimuli;
• depressive states;
• decreased memory and concentration;
• "myxedematous" appearance(puffiness of the face, puffiness of the area around the eyes, pallor skin with an icteric tint, weakening of facial expressions);
• dullness and fragility of hair, their increased loss;
• dry skin;
• tendency to increase body weight;
• chilliness of the limbs;
• slowing of the pulse;
• loss of appetite;
• tendency to constipation;
• decreased libido;

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

Much more often (4–15 times) women are exposed to autoimmune thyroiditis.

Symptoms characteristic of the thyrotoxic phase:

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

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

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

Painless and cytokine-induced thyroiditis usually do not show a violent clinical picture, manifesting itself with symptoms of moderate severity, or are asymptomatic and are detected during a routine study of thyroid hormone levels.

Diagnostics

Diagnosis of autoimmune thyroiditis involves a series of laboratory and instrumental research to confirm the fact of autoaggression of the immune system:

• determination of antibodies to thyroid peroxidase (AT-TPO) in the blood (an elevated level is established);
• determination of the concentration of T3 (triiodothyronine) and free T4 (thyroxine) in the blood (an increase is detected);
• level detection thyroid-stimulating hormone(TSH) in the blood (with hyperthyroidism - a decrease against the background of an increase in T3 and T4, with hypothyroidism - the opposite ratio, a lot of TSH, little T3 and T4);
• Ultrasound of the thyroid gland (hypoechogenicity is detected);
• definition clinical signs primary hypothyroidism.

Autoimmune thyroiditis often occurs in members of the same family (in half of the patients, the next of kin are also carriers of antibodies to thyroid cells).

The diagnosis of "chronic autoimmune thyroiditis" is considered legitimate when there is a combination of changes in the level of microsomal antibodies, TSH and thyroid hormones in the blood with a characteristic ultrasound picture. In the presence of specific symptoms of the disease and an increase in the level of antibodies in the absence of changes on ultrasound or instrumentally confirmed changes in the thyroid tissue with normal level AT-TPO diagnosis is considered probable.

For the diagnosis of destructive thyroiditis, the connection with previous pregnancy, childbirth or abortion and the use of interferons is extremely important.

Treatment

There is no specific treatment for autoimmune inflammation of the thyroid gland; symptomatic therapy is carried out.

With the development of hypothyroidism (both in chronic and destructive thyroiditis), it is indicated replacement therapy thyroid hormone preparations based on levothyroxine.

In thyrotoxicosis against the background of destructive thyroiditis, the appointment of antithyroid drugs (thyrostatics) is not indicated, since there is no hyperfunction of the thyroid gland. Treatment is carried out symptomatically, more often with beta-blockers with severe cardiac complaints in order to reduce heart rate and blood pressure.

Surgical removal of the thyroid gland is indicated only with a rapidly growing goiter that compresses Airways or vessels of the neck.

Possible complications and consequences

Complications of autoimmune processes in the thyroid gland are not typical. The main consequence is the development of persistent overt hypothyroidism, the pharmacological correction of which does not cause significant difficulties.

Forecast

Carriage of Ab-TPO (both asymptomatic and accompanied by clinical manifestations) is a risk factor for the development of persistent hypothyroidism (suppression of thyroid function) in the long term.

The probability of developing hypothyroidism in women with elevated levels of antibodies to thyroid peroxidase against the background of unchanged levels of thyroid-stimulating hormone is 2% per year. In the presence of advanced level AT-TPO and laboratory signs of subclinical hypothyroidism, the probability of its transformation into overt hypothyroidism is 4.5% per year.

Postpartum thyroiditis can degenerate into chronic autoimmune (with a further outcome in overt hypothyroidism) in 20-30% of women.

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