Diagnosis of autoimmune thyroiditis, hypertrophic form. Chronic autoimmune thyroiditis

There are only 3 methods of treating autoimmune thyroiditis:

• medicines;
• surgery or radioactive iodine;
• restorative treatment with CRT.

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

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

As a result of such “treatment,” the disease progresses, requiring increasingly larger doses of drugs, 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 uselessness of HRT.

Before making a decision about “treatment” with HRT, we recommend that you search real reviews patients on the Internet or read reviews from our patients who have been trying to be cured in this way for years. For obvious reasons, we do not use HRT in our practice, but rather gradually remove patients’ dependence on taking synthetic hormones.

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

The latter method is of course “safer” than surgical operations, but removal of the thyroid gland any way leads to dangerous disability. Autoimmune processes in the body are not going away and are now controlled lifelong HRT. In addition to disruption of the human digestive, cardiovascular, nervous and reproductive systems, 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 surgery using computer reflex therapy (CRT)

In our medical center held in the city of Samara full recovery function, structure and volume of the thyroid gland without hormones and surgery.

An indicative result of CRT 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 course of CRT 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 coordinated work internal organs Our body is regulated by the coordinated interaction of 3 main control systems: nervous, immune And endocrine. It is on their synchronous and well-coordinated work that the physical state and human health. Any disease progresses and the body cannot cope with it on its own precisely because 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 has proven over 20 years that patients fully recover neuro-immuno-endocrine regulation of the body and, as a consequence, many endocrine and neurological diseases, which were previously not amenable to drug “treatment”.

Efficiency therapy also lies in the fact that the doctor acts on 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 operate a medical device.

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

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

If you do not have the above contraindications, then restore your own hormonal balance and get rid of autoimmune thyroiditis with the help this method This has been a common practice at our center for many years.

Treatment of autoimmune thyroiditis using 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 being restored volume of functioning tissue and structure of the thyroid gland;
• the synthesis of one’s 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 decreases in thyroid gland, 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 it;
• the menstrual cycle is restored;
• women can realize their reproductive function without IVF and give birth healthy child With normal level hormones;
• In addition, the patient’s biological age decreases, health improves, weight decreases, and swelling goes away. That is why the Clinic appeared additional procedures and programs for natural facial rejuvenation.

Leave your contact information and a consulting doctor will contact you

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

What's happening?

With all destructive autoimmune thyroiditis, the disease goes through several phases. Thyrotoxic phase is a consequence of an antibody-dependent complement attack on thyrocytes, which results in the release of ready-made thyroid hormones into the bloodstream. If the destruction of the thyroid gland was sufficiently pronounced, the second phase begins - hypothyroid, which usually lasts no more than a year. What happens most often in the future is restoration of thyroid function, although in some cases hypothyroidism remains persistent. With all three variants of destructive autoimmune thyroiditis, the process can be monophasic (only thyrotoxic or only hypothyroid phase).

Epidemiology

Postpartum thyroiditis develops into postpartum period in 5-9% of all women, while it is strictly associated with carriage of AT-TPO. It develops in 50% of AT-TPO carriers, while the prevalence of AT-TPO carriage 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 carriage of AT-TPO and, due to its benign course, most often remains undiagnosed. develops more often in women (4 times) and is associated with carriage of AT-TPO. The risk of its development in AT-TPO carriers receiving interferon drugs is about 20%. There is no relationship between the time of initiation, duration and regimen of interferon therapy. With the development of cytokine-induced thyroiditis, discontinuation or change of the interferon therapy regimen does not affect the natural course of the disease.

Clinical manifestations

With all three destructive autoimmune thyroiditis, symptoms of thyroid dysfunction are moderate or absent altogether. The thyroid gland is not enlarged and painless on palpation. Endocrine ophthalmopathy never develops. Postpartum thyroiditis, typically manifests with mild thyrotoxicosis at approximately 14 weeks postpartum. In most cases, nonspecific symptoms such as fatigue, general weakness, and some weight loss are associated with recent childbirth. In some cases, thyrotoxicosis is significantly expressed 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 untargeted hormonal testing. Diagnosis of the hypothyroid phase painless thyroiditis can be established retrospectively, during dynamic observation of patients with subclinical hypothyroidism, which ends with 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 routine hormonal study, which is included in the monitoring algorithm for patients receiving interferon drugs.

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 have no clinical manifestations or endocrine ophthalmopathy. The thyrotoxic phase of all three thyroiditis is characterized by a decrease in the accumulation of radiopharmaceuticals according to thyroid scintigraphy. Ultrasound reveals reduced echogenicity of the parenchyma, nonspecific to all autoimmune diseases.

Treatment

In the thyrotoxic phase, the administration of thyrostatics (thiamazole) is not indicated, since there is no hyperfunction of the thyroid gland in destructive thyrotoxicosis. For 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 the hypothyroidism was transient, the patient will remain euthyroid; with persistent hypothyroidism, the TSH level will increase and T4 will decrease.

Forecast

Women with postpartum thyroiditis have a 70% chance of recurrence after another pregnancy. Approximately 25-30% of women who have suffered postpartum thyroiditis subsequently develop chronic variant autoimmune thyroiditis resulting in persistent hypothyroidism.

Subacute thyroiditis

Subacute thyroiditis(De Quervain's thyroiditis, granulomatous thyroiditis) - inflammatory disease thyroid gland, presumably of viral etiology, in which destructive thyrotoxicosis is combined with pain syndrome in the neck area 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. Proven genetic predisposition to the development of the disease. 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 of the viral infection, thyroid function is restored, in some cases after a short hypothyroid phase.

Epidemiology

The disease mainly affects people aged 30 to 60 years, with women 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 frequently 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 (angina, ARVI) followed by 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, low-grade fever). Typical for subacute thyroiditis is quite sudden appearance diffuse pain in the neck. Cervical movements, swallowing and various irritations of the thyroid gland area 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; pain can be local or diffuse depending on the degree of involvement of the gland in the inflammatory process. Characterized by variable intensity and passing (wandering) pain from one lobe to another, as well as pronounced general phenomena: tachycardia, asthenia, weight loss.

Fever (low-grade fever or mild fever) occurs in approximately 40% of patients. Often, pain in the neck is the only clinical manifestation of subacute thyroiditis, while the patient may have no thyrotoxicosis at all.

Diagnostics

Increase in ESR- one of the most typical manifestations of subacute thyroiditis, and it can be increased significantly (more than 50-70 mm/hour). Leukocytosis characteristic bacterial infections absent, moderate lymphocytosis may be detected. As with other diseases occurring with destructive thyrotoxicosis, the level of thyroid hormones is moderately increased; Subclinical thyrotoxicosis is common, and the euthyroid course of the disease is often observed.

According to ultrasound, subacute thyroiditis is characterized by vaguely limited hypoechoic areas, less often diffuse hypoechogenicity. Scintigraphy reveals a decrease in the uptake of 99m Tc.

Autoimmune thyroiditis is an inflammatory disease of the thyroid gland, which usually has a chronic course. This pathology has an 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, autoimmune thyroiditis affects women over the age of 40, but the development of this disease in 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.

Classification and causes of autoimmune thyroiditis

Autoimmune thyroiditis is collective concept for several types of thyroiditis. Today, there are four main types of thyroiditis that help classify this disease:

• Hashimoto's disease (chronic thyroiditis);
• postpartum thyroiditis;
• silent thyroiditis;
• cytokine-induced thyroiditis.

Hashimoto's thyroiditis

Hashimoto's thyroiditis (lymphocytic, lymphomatous) is accompanied by disruption of the structure and function of the thyroid gland and can cause primary hypothyroidism (decreased thyroid hormonal levels). This type of thyroiditis in most cases is transmitted genetically, and is also combined with other autoimmune diseases.

Postpartum thyroiditis

Postpartum thyroiditis is the best studied and considered the most common. Main etiological factor Predisposing to its development is an excessive reaction of the body's immune system during pregnancy. If there is a predisposition, destructive autoimmune thyroiditis may develop, which is considered more dangerous.

Silent thyroiditis

The causes of painless thyroiditis have not yet been thoroughly elucidated. According to clinical data, it is very similar to postpartum thyroiditis, only its development is not associated with pregnancy.

Cytokine-induced thyroiditis

Cytokine-induced thyroiditis occurs as a result of treatment with interferon-containing drugs, in patients diagnosed with hepatitis C, as well as in certain blood diseases.

In addition to differentiation into clinical types, autoimmune hypothyroidism has three main forms:

• latent form;
• hypertrophic form;
• atrophic form.

Latent form

The latent form is characterized by immunological signs and the absence of clinical manifestations. In most cases, the gland practically does not increase in size or its increase is insignificant, the functions are not impaired, there are no seals, and sometimes symptoms of thyrotoxicosis or hypothyroidism are observed.

Hypertrophic form

In the hypertrophic form, an increase in the size of the thyroid gland is visualized, with frequent cases of thyrotoxicosis and hypothyroidism. Hyperplasia of the thyroid gland can be diffuse, evenly distributed throughout the entire volume or with the formation of nodes (nodular form); there are also rare cases of a combination of both forms.

Atrophic form

For the atrophic form characteristic feature is the absence of enlargement of the thyroid gland, and in some cases even its reduction. The main clinical symptom of this form is hypothyroidism. The risk group for this pathology includes elderly people and young people who have been exposed to radiation. The atrophic form is the most severe because there is massive destruction of thyrocytes, as well as a sharp decline functions of the thyroid gland.

Causes of autoimmune thyroiditis

There is a proven fact that autoimmune thyroiditis does not occur through the fault of the patient and his attitude to his health. The main reason for the manifestation of this disease is genetic predisposition. As a result of numerous studies, scientists have discovered genes that cause the development of autoimmune thyroiditis. Therefore, if there was such a disease in the family, the patient is at risk of developing this pathology.

Also, the cause of autoimmune thyroiditis can be stress suffered the day before.

According to statistics, the occurrence of this disease is related to the age and gender of the patient. In most cases (4-10 times more often), women are affected by autoimmune thyroiditis than men. As for the age range, the majority of patients are people aged 40-50 years. But, unfortunately, this disease has become younger and has begun to occur periodically in adolescents and children.

Poor ecology and living in a polluted environment can also trigger the development of autoimmune thyroiditis.

Triggering factors for the manifestation of this disease can be various viral and bacterial infections.

The human immune system is one of the most important systems of the body. This system is responsible for recognizing and identifying foreign agents, in particular microorganisms, and preventing their penetration into human body and further development therein. Due to stress, in the presence of a genetic predisposition, as well as a combination of other factors, a failure occurs in this protective system organism, it begins to confuse “self” and “foreign”. After which he begins to attack “his own”. These dysfunctions are called autoimmune and include large group diseases. In the process of autoimmune diseases, the body produces antibodies, which are proteins (lymphocytes) and which are directed against their organ.

In autoimmune thyroiditis, antibodies are produced against thyroid cells, called antithyroid autoantibodies. Such antibodies contribute to the destruction of thyroid cells, as a result of which hypothyroidism (decreased efficiency of the thyroid gland) can develop. Based on the mechanism of development of this disease, autoimmune thyroiditis is also called chronic lymphocytic thyroiditis.

Symptoms of autoimmune thyroiditis

The majority of cases of autoimmune thyroiditis are asymptomatic. The absence of symptoms is due to the absence of dysfunction of the thyroid gland. This condition is known as euthyroidism. In some cases, patients complain of slight discomfort in the front of the neck, and also prefer clothing without high collars and scarves.

When this disease is complicated by hypothyroidism, the clinical picture changes significantly. At severe symptoms At this stage of autoimmune thyroiditis, an experienced specialist needs only a visual examination of the patient to determine the diagnosis.

1. In such patients, the eyelids and face appear pasty, the patient’s movements are slow, the face has a pale color with a yellow tint, while the cheekbones have a pronounced blush, which is especially noticeable on a pale face.
2. Patients with autoimmune thyroiditis, complicated by hypothyroidism, suffer from hair loss, up to the formation of balding areas. Moreover, hair loss can occur not only on the head, but also under the arms, on the pubis and eyebrows near the upper corner of the eye.
3. During a conversation, the patient has a particular expression of facial expressions, while his speech is leisurely in nature, because he needs some time and effort to remember the right words. Due to swelling of the tongue, the speech of such patients becomes difficult to understand. Due to swelling of the nasal mucosa, the patient has to breathe through the mouth.
4. Among subjective feelings the patient notes weakness, fatigue, drowsiness, decreased memory and performance.
5. The pulse in such patients is usually rare (bradycardia). Women with thyroiditis often have dysfunction menstrual cycle, which can cause infertility.

With autoimmune thyroiditis complicated by hyperthyroidism (increased production of hormones), patients experience:

• tachycardia;
• sweating;
• tremor (shaking) of the fingers;
• decreased attention;
• memory impairment;
• hypertension;
• frequent mood changes;
• increased fatigue.

Diagnosis of autoimmune thyroiditis

Diagnosis of autoimmune thyroiditis is based on identifying the main symptoms of this disease and laboratory tests. The patient's medical history reveals the presence of this disease in his close relatives; this can help determine the patient's predisposition to autoimmune thyroiditis. According to the results laboratory research you can determine the presence of antibodies to certain components of the thyroid gland (peroxidase, thyroglobulin, second colloid antigen, thyroid hormones, thyroid-inhibiting, thyroid-stimulating antibodies, etc.). At the stage of absence of clinical symptoms, laboratory diagnostics helps determine thyroid-stimulating hormone in blood serum.

With a sharp change in the clinical course of the disease, the risk of malignant degeneration of the thyroid gland (nodule) increases. To exclude this option, a fine-needle biopsy is necessary. Patients with symptoms of thyrotoxicosis may also be at risk for malignant changes in the thyroid gland. But most often, autoimmune thyroiditis is benign in nature and thyroid lymphomas are extremely rare. To control the size of the thyroid gland, the patient is recommended to undergo sonography or ultrasound examination. But it is impossible to make a diagnosis based on ultrasound examinations alone, because similar symptoms are characteristic of diffuse toxic goiter and differential diagnosis is important.

Treatment of autoimmune thyroiditis

There is no specific treatment regimen for autoimmune thyroiditis. Treatment tactics depend on the form of the disease. The main task in the treatment of this disease is to maintain the required amount of thyroid hormones in the blood.

Euthyroidism does not require treatment, but regular examination (once a year) is required. The examination includes TSH control and hormonal examination.

For hypothyroidism, it is recommended to prescribe thyroid hormones (Levothyroxine, L-thyroxine, Eutyroxine). Such treatment is necessary to normalize the level of thyroid hormones, which the body lacks. The treatment regimen is selected by an endocrinologist individually for each patient.

At the stage of thyrotoxicosis, thyreostatics are not prescribed; instead, it is advisable to prescribe symptomatic treatment. The goal of symptomatic treatment in this case is to reduce and eliminate the symptoms of the disease (regulation of the cardiovascular system, etc.). Each specific case requires individual selection of therapy.

Prognosis for autoimmune thyroiditis

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 long period For this pathology, glucocorticosteroids were prescribed in fairly high doses. On this 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.

Prevention of autoimmune thyroiditis

The main principle of preventing autoimmune thyroiditis is regular visit preventive examinations. If there is an established diagnosis of autoimmune thyroiditis, without significant thyroid dysfunction, the patient must be constantly monitored by an endocrinologist for timely detection and treatment of manifestations of hypothyroidism.

Thyroiditis is usually called an inflammatory process in the thyroid gland. Clinical manifestation thyroiditis is not the same, therefore there are several forms of inflammation of the thyroid gland, one of which is long-lasting and is called chronic thyroiditis. The disease belongs to the group of autoimmune pathologies of the gland. The main patient population for chronic inflammation thyroid glands – older women. However, the disease is not limited only to the choice of this category of humanity; representatives of the male sex, young women, and children are less often registered with autoimmune disorders.

If in family tree cases of autoimmune diseases have not been detected in humans, then worry about the occurrence chronic thyroiditis not worth it. The likelihood of developing an autoimmune thyroid disorder increases if you have a family history. A pathological condition of an autoimmune nature is fraught with its manifestation, which may be absent for a number of years.

Clinical picture

The chronic form of thyroiditis develops without obvious signs, since the pathological state of individual cells is compensated by the doubled work of healthy thyrocytes. The increase in destructive metamorphoses leads to excessive concentrations of thyroid hormones in the blood or the appearance of symptoms of a hypothyroid state. Different shapes autoimmune disease manifest themselves in approximately 85% of cases by a high concentration of autoimmune bodies to the thyroid follicles. A more detailed clinical picture can be described when differentiating autoimmune pathology.

Stages of pathology

The disease develops according to the following scheme:

1. In the euthyroid phase, signs of conflict between antibodies and follicular cells are not detected. A blood test does not reveal changes in the levels of triiodothyronine and thyroxine. With such a pathological condition, a person can live from several months to the end of his life.
2. The subclinical phase is characterized by an increase destructive changes in the thyroid gland. Measuring the level of thyroid hormones from the blood taken shows a noticeable decrease.
3. The thyrotoxicosis phase is noted as the peak stage of the disease. Damage to glandular thyrocytes leads to the release of thyroxine and triiodothyronine into the intercellular environment, from where they enter the blood. Excess thyroid hormones cause a thyrotoxic state. The beginning destruction of the glandular cells of the organ leads to the movement of individual fragments of the destroyed cells into the blood. In response to visible changes, there is an increase in the produced antibodies to thyrocytes. With further progress pathological condition The thyroid gland shows a state of hypothyroidism.
4. The patient usually remains in the hypothyroidism stage for 1-2 years. After the specified period, the functionality of the thyroid gland is restored. The last stage is not always characteristic of the chronic form of thyroiditis. The stage of thyrotoxicosis may be the last in the development of the pathology.

Types of disease

Chronic thyroiditis can develop in several directions depending on the manifestation clinical picture and morphological metamorphoses of the thyroid gland:

1. Hidden or latent form, in which external manifestations no pathology is noted. The course of the disease can only be guessed by immunity disorders. The thyroid gland is within normal limits or slightly enlarged. The functionality of the thyroid gland is not impaired, there are no structural changes in the glandular tissue. In some cases, there is a slight change in the concentration of thyroid hormones in the blood, both in the direction of hypothyroidism and in the thyrotoxic direction.
2. Hypertrophic form, accompanied by multiple formation of nodes or diffuse enlargement of the organ. In this condition, the level of hormones in the blood decreases markedly.
3. Thyroid function is markedly reduced in the atrophic type of autoimmune disease. A similar state of the endocrine organ is characteristic of a shock dose of ionizing radiation or old age. With the total death of thyroid follicles, the functionality of the thyroid gland is consistently low.

Nodular type of pathology

Nodules often accompany chronic thyroiditis. For autoimmune diseases inflammatory reactions follicular thyrocytes are damaged varying degrees gravity. Ultrasound reveals structural change gland tissue and its hyperplasia. Treatment of the disease is prescribed in accordance with the patient’s medical history and the disorders identified during the ultrasound examination.

Currently, medicine prefers conservative complex treatment of nodular formations to surgical intervention. chronic form thyroiditis. Part complex treatment The following methods are included:

1. preparations with iodine and hormone replacement therapy with Levothyroxine and its analogues;
2. treatment with herbs and other traditional medicine;
3. titration of antibodies shows a lower level if the patient improves his psycho-emotional state. The thyroid gland also begins to restore its structure due to the normalization of mental mood;
4. normalization psycho-emotional state occurs faster and easier if the patient uses art therapy, music therapy and other means of relaxation.

Lymphocytic form

The lymphocytic form of chronic thyroiditis affects a certain type of blood lymphocyte and, for this reason, this type of autoimmune pathology is considered organ-specific. T-suppressors, known as CD8 lymphocytes, as a result of destruction, trigger a chain reaction mechanism, during which T-helpers form pathological complexes with thyrocyte antigens. If a person being examined has a complex of CD4 lymphocytes (T-helper cells) with a local antigen in the thyroid gland, then the autoimmune pathology is hereditary. When lymphocytic thyroiditis is detected, a complex of other disorders of the thyroid gland is detected.

Only one out of twenty patients with lymphocytic chronic thyroiditis is a man, the rest of the patients are women. The disease mainly occurs in women of childbearing age with hyperplasia of the thyroid gland without other noticeable signs. The main complaints of patients with gland hyperplasia are associated with bursting sensations in the neck and the occurrence of pressing pain. Less commonly, patients complain of changes in voice timbre or swallowing disorders.

Changes in the size of the thyroid gland are not always accompanied by noticeable symptoms. The determining factor in the formation of signs of hyperplasia is the state of hormones when the functioning of the gland is disrupted: decrease, increase or normal, euthyroid state.

Signs that appear

Chronic thyroiditis develops in two directions: lymphocytic and fibrous. Within these areas, several options for the development of pathological events are known:

1. autoimmune form;
2. Hashimoto's disease;
3. non-purulent form;
4. lymphomatous form; Riedel's goiter.

Although the autoimmune type of chronic thyroiditis is defined as hereditary disease, its development begins under the influence of provoking factors. These include viral infection upper respiratory tract, dental caries, inflammatory processes in the tonsils, etc. It turns out that hereditary predisposition alone cannot serve as the sole reason for the progression of pathology.

It has become noticed that with a high level of radiation exposure and uncontrolled use of iodine-containing medications for a long time, a failure occurs immune reactions, the result of which is immune aggression towards thyrocytes.

The onset of the disease is asymptomatic, possibly individual symptoms low intensity: pain in the thyroid gland upon palpation, “lump in the throat,” malaise and aching joint pain. An enlarged thyroid gland can have a compressive effect on the throat.

At further development The disease produces symptoms characteristic of a hyperthyroid state: increased heart rate, excessive sweating, increased systolic pressure.

The development of the disease can occur in two directions: the atrophic nature of the gland and its hypertrophy.

With thyroid atrophy, hyperplasia is not observed; in the blood, when analyzed, a decrease in the concentration of thyroid hormones is detected. This form of pathology is typical for the elderly or people who have previously experienced a high dose of radioactive radiation.

With hypertrophic chronic thyroiditis of an autoimmune nature, diffuse hyperplasia or enlargement of the gland is detected due to the formation of nodular forms. In medical practice a nodular form is often detected against the background of a general increase in the size of the thyroid gland. The level of thyroid hormones in the blood is within the normal range or has a slight decrease, although forms with a significant excess of the normal concentration of thyroid hormones are not uncommon.

Diagnosis of thyroid inflammation

Examination of a patient with suspected chronic thyroiditis begins with an examination by an endocrinologist, palpation of the gland and anamnesis. The next stage in differentiating the disease is donating blood for hormonal analysis and determining the concentration of thyroid antibodies.

If there are no antibodies in the blood, a fine-needle aspiration biopsy is performed, followed by cytological analysis.

Ultrasound gives a picture of changes in the structure and size of the gland. No malignant nodes were identified in this form of thyroid dysfunction. An important role in establishing a diagnosis is played by the hereditary pattern of gland conditions among close relatives and in the human family tree.

Features of treatment for chronic thyroiditis

There is no clear treatment plan for the disease. In the case of thyrotoxicosis, it is dangerous to prescribe drugs from the thyreostatic group due to an insufficient increase in the functionality of the thyroid gland. To reduce the thyrotoxic effect are prescribed medicines to relieve symptoms of the disease. Long-term and persistent hypothyroidism is treatable replacement therapy synthetic hormones such as Levothyroxine. Drug analogues begin to be used with a small dosage, gradually increasing it and achieving a normal concentration of thyroid hormones in the blood. Once every 60-70 days, the blood should be tested for thyroid-stimulating hormone levels.

If chronic thyroiditis is accompanied by subacute form inflammation of the thyroid gland; during cold periods, a drug from the group of glucocorticosteroids (Prednisolone) is prescribed.

For hyperthyroidism and thyroid hyperplasia, the doctor may prescribe Thiamazole or its analogues.

When using Indomethacin or Voltaren, which are non-steroidal drugs to relieve inflammation, the symptoms of the disease subside.

Consequences and prognosis of the disease

If Hashimoto's thyroiditis is not treated for a long time, severe hypothyroidism develops in the form of myxedema. Patients must exclude a number of other concomitant diseases ( diabetes, ophthalmopathy, Graves' disease, adrenal insufficiency, etc.).

Disease Prevention

Pregnant women should strictly follow the gynecologist's instructions if a thyroid dysfunction is detected. This form is dangerous in the first trimester, when there is a possibility of toxicosis or the threat of miscarriage.

To prevent thyroiditis, a diet is proposed that excludes animal fats and includes more fish, vegetables, lactic acid products, herbs, vitamins and cereals in the diet.

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. Disease of the thyroid gland, accompanied by its enlargement, usually painless; most common in women, often immediately after childbirth; usually does not require specific treatment; in rare cases (10%) leads to irreversible hypothyroidism.

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14. What are the causes of silent thyroiditis?

Some researchers consider silent thyroiditis to be a variant of subacute thyroiditis, since a small percentage of patients with histologically proven subacute thyroiditis also do not have pain in the thyroid gland. In such cases, fever and weight loss sometimes occur, which is sometimes confused with systemic diseases or malignant tumor. Other authors, due to the similarity of the histological picture, consider silent thyroiditis to be a variant of Hashimoto's thyroiditis. In rare cases, pain in the thyroid gland is observed.

KEY POINTS: THYROIDITIS

1. On early stages subacute thyroiditis absorption radioactive iodine(PRI) the thyroid gland is reduced; ESR is significantly increased.
2. Globular proteins of human blood plasma, as well as warm-blooded animals. The nature of the formation is as follows: 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 serums 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.
   " data-tipmaxwidth="500" data-tiptheme="tipthemeflatdarklight" data-tipdelayclose="1000" data-tipeventout="mouseout" data-tipmouseleave="false" class="jqeasytooltip jqeasytooltip11" id="jqeasytooltip11" title=" Antibodies">Антитела!} to TPO are present in the serum of approximately 10% of premenopausal women; many of them develop thyroid dysfunction after childbirth Specialized organs or groups of cells that synthesize and secrete substances are secretions. Depending on the location of secretion, there are distinguished endocrine glands (endocrine), which do not have special excretory ducts and secrete the substances they produce - hormones - directly into the blood or lymph, and exocrine glands (exocrine), which have excretory ducts through which the secretion is excreted either on the surface of the body (sweat, tear, milk), or into hollow organs (for example, the gastrointestinal tract and genitourinary system).
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3. Amiodarone-induced thyropathies can manifest as iodine hyperthyroidism and destructive thyroiditis.
4. Subacute thyroiditis may require the use of painkillers (or steroids) and β-blockers, and subsequently L-T4, but the disease usually resolves spontaneously.
5. Acute infectious thyroiditis requires rapid opening/drainage of the lesion and the use of antibiotics.

15. What is destructive thyroiditis?

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

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

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