TSH is a hormone produced by the anterior pituitary gland. Its main task is the regulation of thyroid function in humans. The TSH hormone stimulates the reproduction of T4 and T3 by thyroid cells and their release into the blood. Its increased content in plasma indicates insufficient reproduction of the hormones of the organ, that is, hypothyroidism.

In the early stages of some diseases, T4 and T3 levels may still be normal. Therefore, for patients with various pathologies of the thyroid gland, it is so important to monitor plasma TSH levels for timely diagnosis and appropriate therapy.

The main indications for testing

The level of the hormone in the blood during the analysis is mainly determined in units of the total amount - mcU / ml or mU / l.

An examination may be prescribed by a general practitioner or endocrinologist for the following indications:

• with suspicion of goiter or hyperthyroidism;
• with female and male infertility, problems with erection (libido);
• if the patient is prescribed hormone replacement therapy;
• with heart disease, depression or baldness;
• with damage to muscle tissue (myopathy);
• low temperature, amenorrhea;
• mental retardation, puberty in children.

The thyroid gland is associated with many different systems of the human body, so a malfunction of one of them affects the synthesis of TSH.

The norm of the hormone by age

TSH levels are different in babies, older children, adolescents and adults, below are the normal TSH in children:

• in newborns - 1.1-17;
• in babies up to a year - 1.3-8.5;
• from one year to 6 years - 0.8-6;
• from 7 years to adolescence (14 years), the indicator ranges from 0.28 to 4.3;
• after 14 years - 0.27-3.8.

Plasma TSH levels are influenced by many factors. So, for example, indicators can change depending on the time of day. It reaches the maximum value at night, from 2 to 4 o'clock and in the morning from 6-8 o'clock, the minimum - from 17:00 to 19:00 pm. If a person does not sleep at night, then the process of producing TSH is disrupted. In addition, a reduced rate is observed during childbearing, breastfeeding, which is not considered a violation, since this is the norm of TSH in the blood of women in various physiological states. Certain medications can also interfere with TSH production.

How to pass the analysis?

Before testing TSH blood, you must first prepare for this procedure:

• A few hours before the analysis, you should stop smoking, alcohol, emotional, excessive physical exertion, and also exclude overheating or hypothermia of the body.
• It is advisable not to take medication, if possible (it is worth consulting with the attending physician). First of all, this applies to hormonal drugs, multivitamin complexes, as well as iodine preparations.
• Testing should be done on an empty stomach (12 hours after a meal). Before the analysis, you can drink some plain water.

How is hormone testing done?

When taking blood for TSH, a simple procedure is performed, as in biochemical analysis (plasma is taken from a vein). Testing is done in the morning. The technique for determining hormone levels is called microparticle immunoassay. The object of study is plasma serum.

If the patient has already had problems with the thyroid gland, it is recommended to check the TSH level several times a year. Moreover, it is better to do this in the same clinic at the same time interval, since the research methodology in a single medical institution can be radically different.

Norm T4 and T3: decoding of testing

Thyroxine and triiodothyronine levels are set along with the TSH analysis, and they are closely related, so it is necessary to know the value of all hormones. There is also a TSH norm by age. The acceptable level of T3 in an adult patient ranges from 1.08-3.14 nmol / liter. Regarding T4, this indicator is - 59-135 - this is the norm of TSH in the blood for men, for the fairer sex it is slightly overestimated - 71-142 nmol / liter.

Deviations from these figures indicate the presence of a certain disease in the patient. With elevated T3 hormone, the main causes of disorders are as follows:

• thyroid adenoma;
• hyperthyroidism;
• Pendred's syndrome;
• chronic liver diseases;
• nephrotic abnormalities;
• choriocarcinoma.

Triiodothyronine rises in the presence of pathologies such as:

• hypothyroidism;
• lack of iodine;
• increased physical activity;
• dysfunction of the adrenal glands;
• weight loss.
• Deviations from acceptable T4 values ​​may result from:
• increase: nephrotic disorders, thyrotoxic adenoma, decrease in thyroxin-binding globulin;
• a decrease in the content of T4 is associated with thyroid diseases.

The test results can be affected by the use of hormonal medications, as well as severe prolonged depression.

Norm TTG: decoding of the analysis with overestimated rates

An increased content of the hormone in plasma indicates, first of all, the presence of such pathologies as:

• somatic and mental disorders;
• diseases of the pituitary gland;
• hypothyroidism of various origins;
• unregulated hormone production;
• thyroid resistance;
• adrenal insufficiency;
• inflammation of the thyroid gland;
• malignant tumors of the mammary glands, lungs;
• preeclampsia is a complication during childbearing.

Elevated levels of TSH are often observed after surgery on the gallbladder and other operations, during hemodialysis, after excessive physical exertion, contact with lead and the use of a certain group of drugs.

Hormone norm: low level of TSH

If the test results showed an underestimated level of the hormone in the blood, this indicates the presence of some problems, among which doctors distinguish:

• mental disorders, constant stress;
• thyrotoxicosis of various origins;
• pituitary necrosis, trauma.

The level of the hormone is significantly reduced as a result of fasting, diets and the use of certain medications (cytostatics, anabolics, corticosteroids).

The main symptomatology with low or high TSH

With a high hormone level, the following symptoms are often observed:

• the patient has a goiter;
• there is weakness, fatigue, and low activity;
• lethargy of the psyche, apathy for everything, inattention, irritability, lack of memory;
• violation of normal sleep: during the day - there is constant drowsiness, at night the patient cannot fall asleep;
• swelling, pallor of the skin;
• obesity, practically untreatable;
• low temperature;
• constipation, severe nausea, lack of appetite.

With elevated rates, there are such symptoms as:

• heat;
• tachycardia;
• migraine, pressure;
• tremor of the fingers, trembling throughout the body, mental imbalance;
• excessive appetite;
• constant disorders of the stool, pain.

Hormone therapy in the presence of the symptoms listed above cannot be prescribed to oneself on one's own. If the patient has similar signs, and testing has confirmed a deviation from the norm of TSH, it will not work to be cured with traditional medicine recipes. It requires strict control of specialists and serious medicines.

TSH above or below normal: therapy

If the hormone is overestimated, and is in the range - 7.1-75 μIU / ml, this indicates the presence of hyperthyroidism. Treatment in this case, doctors carry out with the help of artificial thyroxin. Until recently, specialists practiced the dried crushed thyroid gland of various animals, now it is used quite rarely and the patient is transferred to a synthetic medication. Therapy begins with a small dosage of T4, then the amount of the drug is gradually increased until the plasma TSH level reaches normal levels. Since the activity of the natural hormone in each patient is different, the attending physician determines it through diagnostics and prescribes the appropriate drug.

TSH can cause thyroid cancer. Therefore, during therapy, the dosage of the drug can be increased until there is a significant improvement in the patient's health, and hormone levels do not come back to full normal. Usually, doctors recommend preventive examinations for patients with thyroid problems in order to control the levels of hormones in the blood. Low hormone level - 0.01 μIU / ml. To increase it, constant monitoring by an endocrinologist is required to prevent possible relapses.

Timing and cost of testing

A blood test for TSH is carried out in a specialized clinic during the day. The price for the services of specialized laboratories varies depending on the level of the medical institution and the region. The average cost fluctuates around 400 - 600 rubles.

Blood testing for TSH should be carried out in the diagnosis of various diseases of the thyroid gland, which is highly susceptible to negative effects. The pathologies of this organ are quite dangerous, since for many years they do not make themselves felt.

To maintain your health, beauty, it is important to contact an endocrinologist at the first signs of thyroid dysfunction. Analysis of TSH makes it possible to identify diseases at an early stage of its development.

Hyperthyroidism: Symptoms and Diagnosis

Hyperthyroidism is a syndrome that occurs when the thyroid gland produces an excess amount of hormones. Another name for the disorder is thyrotoxicosis.

How does thyrotoxicosis manifest itself?

Symptoms of thyrotoxicosis include the following:

• Constant mood swings, excessive irritability and excessive, previously unusual emotionality;
• Fever and palpitations;
• increased sweating;
• Weight loss.

If a person has these symptoms, he needs to urgently make an appointment with a doctor and take tests that will determine the level of thyroid hormones.

Symptoms and diagnosis of hyperthyroidism

In addition, there are a number of additional symptoms that may indicate the development of thyrotoxicosis in a person:

• Increased blood pressure;
• diarrhea and weakness;
• Menstrual irregularities;
• Weak sexual desire and erectile dysfunction in men;
• Intense hair loss.

Infiltrative ophthalmopathy is another characteristic symptom. It represents visual disturbances, such as a decrease in its sharpness, a feeling of sand in the eyes, photophobia and lacrimation.

How to diagnose thyrotoxicosis?

If a person finds himself with the symptoms listed above, he needs to urgently consult a doctor and pass the appropriate tests. Diagnosis of hyperthyroidism usually takes place in several stages:

1. Carrying out a blood test for hormones: TSH, T3 and T4 free.

This study is decisive, as it proves the fact that thyrotoxicosis is indeed present. TSH is a pituitary hormone that reduces the production of thyroid hormones. If a person is sick with thyrotoxicosis, the concentration of this hormone in the blood will be significantly lower than normal. But the thyroid hormones (T3 and T4 free) will be increased in comparison with the norm.

2. The next step is the determination of antibodies, which will be proof that the disease is of an autoimmune nature.

First, you need to determine the antibodies to TSH receptors (an increase indicates the development of the disease). Next, antibodies to TPO are examined, which will be excessive in autoimmune thyroiditis.

3. Ultrasound examination of the thyroid gland. If a person is sick with thyrotoxicosis, the size of the thyroid gland in a woman will exceed 18 cubic centimeters, and in a man - 25 cubic centimeters.

In addition, accelerated blood flow can be noticed in the thyroid gland. If the blood flow is reduced, we can talk about destructive processes.

4. Sometimes, according to the testimony of a doctor, you will need to undergo a scintigraphy of the organ. This study is designed to determine the ability of the body to capture iodine and technetium. Moreover, with the help of this examination, it is possible to identify the cause that caused thyrotoxicosis.
5. If endocrine ophthalmopathy is present, an MRI of the eye sockets and their ultrasound examination will be necessary.

Decreased TSH level

In medical practice, a low TSH level is much less common than an elevated one. Various conditions of the thyroid gland can lead to this. It immediately becomes more difficult to diagnose the problem, since this condition can occur with increased activity of the thyroid gland, as well as with its insufficient work. This can also be quite an ordinary option, if we consider that TSH is low during pregnancy, the TSH rate during pregnancy should correspond to the gestational age, since at this time there is a natural decrease in the level of the hormone. There is a norm of TSH in pregnant women, corresponding to the trimesters of pregnancy:

Decreased TSH: symptoms

Failure of the hormone level can be tracked not only by a blood test, but also by indirect factors that are observed in such disorders. Symptoms vary according to what exactly caused the disease. If the problem lies in the reduced TSH of the thyroid gland, then the manifestations may be as follows:

• Constant feeling of heat around;
• Increased sweating, which was not previously;
• increased heart rate;
• Frequent shortness of breath even with light exertion;
• Sharp weight loss that continues regardless of lifestyle;
• High heart rate;
• High blood pressure;
• Feeling of sand in the eye area;
• Fussiness, anxiety and irritability.

If the cause lies in the work of the hypothalamus and pituitary gland, then the symptoms will be as follows:

• chilliness;
• Decreased heart rate;
• low blood pressure;
• Sharp weight gain;
• The appearance of edema of the extremities;
• Hair loss;
• Dry skin;
• High irritability;
• The occurrence of depression;
• Drowsiness;
• General weakness;
• Hoarse voice.

TSH lowered: causes

Many people find it strange when the function of the gland is increased, and the TSH hormone is lowered, which experts can explain what this means. The fact is that it is produced by the pituitary gland, therefore, there is no direct dependence. But he is engaged in regulating the activity of the thyroid gland, lowering and increasing the intensity, depending on the need. Adjustment occurs depending on the analysis of the content of hormones T3 and T4 inside the body. If they are less than the desired level, TSH provokes an increase in the work of the thyroid gland, thereby increasing its level. If T3 and T4 increase, as occurs with thyrotoxicosis, then TSH is produced in a smaller amount. This saves the thyroid gland from additional stimulation.

Considering the case when TSH is below normal and what this means, one can find a negative feedback between thyroid and pituitary hormones. This is all relevant while maintaining the connection of these organs, since in some cases it can be broken and then there are completely strange indicators that need to be considered in the context of specific diseases.

A decrease in the level in thyrotoxicosis is a fairly common occurrence. Almost all forms of this disease, which can be caused by various diseases, lead to such a hormonal shift. The occurrence of diffuse goiter, certain phases of thyroiditis, subacute thyroiditis and other options lead to hormonal disruptions. For each of the cases, an additional examination is needed to more accurately determine what will help in solving this problem.

Removal of the thyroid gland can also lead to these consequences. When the operation takes place, the body needs to replenish TSH and other hormones. In order for this to pass as soon as possible and not entail any consequences, synthetic analogues of the missing substances, including TSH, are prescribed. Here you need to look at the analysis data for all hormones in order to fully recover.

Hormone levels can also decrease with secondary hypothyroidism. This is due to damage to the hypothalamus and pituitary gland. Thus, the organs responsible for regulating the production of TSH simply do not fulfill their function. Due to the affected cells responsible for the secretion of the hormone, it is simply not produced. At the same time, the thyroid gland remains healthy. Because of all this situation, secondary hypothyroidism appears.

If the TSH analysis is lowered, what this means in women, only a doctor can tell, based on the level of increase and other tests. There are also a number of brain diseases that lead to a decrease in TSH. There is also the concept of normal TSH in hypothyroidism, in which the level of serum thyroid-stimulating hormone is increased by 10-12 times, slightly lower rates are recorded less often. Among them are the following:

• Operations that were carried out on the brain, in areas close to those responsible for the production of the hormone;
• Hematomas and other injuries of the skull, especially in the area of ​​the corresponding areas;
• tumor of the hypothalamus;
• pituitary tumor;
• Tumors in neighboring areas that can affect and pressure them;
• Craniopharyngioma;
• Infectious lesions of the brain;
• Autoimmune damage to the pituitary gland;
• Turkish saddle syndrome.

During the syndrome of euthyroid pathology, which can occur with somatic diseases. It can also be caused by conditions that are not related to the thyroid gland. In this case, the pituitary gland reduces the production of TSH during stressful situations. Myocardial infarction can also be attributed to the reasons, since then the level of this hormone often decreases, while T3 and T4 remain normal.

TSH is lowered: treatment

To get rid of a low level of the hormone, you need to know exactly what led to this. After an accurate diagnosis is made, treatment can begin with the method that is most suitable for this. If T3 and T4, thyroid hormones are lowered, and TSH is lowered, then a replacement therapy method is chosen when artificially synthesized hormones in various preparations enter the body. It can be Euthyroc or Thyroxin. If T3 and T4 are low, then drugs should be taken that would suppress the activity of the thyroid gland. Thus, they will be able to increase the level of TSH content in a completely natural way. The main thing here is to ensure that after the end of the course of taking the drugs, everything is preserved at the stage that was achieved.

Many are interested in alternative medicine methods. For example, they are looking for folk remedies that would help in this problem. There are no drugs that directly affect the content of this hormone, so experts always insist on taking medication. Also, there are no foods, the use of which could increase the content of TSH in the body.

Thyrotoxicosis (hyperthyroidism)- symptoms and treatment

What is thyrotoxicosis (hyperthyroidism)? We will analyze the causes of occurrence, diagnosis and methods of treatment in the article of Dr. O. N. Kurashov, an endocrinologist with an experience of 26 years.

Definition of disease. Causes of the disease

Thyrotoxicosis(hyperthyroidism) is a hypermetabolic process caused by an excess of thyroid hormones in the body and their toxic effects on various organs and tissues. It is clinically characterized by an increase in the thyroid gland and damage to other systems and organs.

The first descriptions of this pathology were found in the works of the Persian physician Jurjani, created in 1100.

This syndrome occurs both in women (up to 2%) and in men (up to 0.2%). Most often it occurs in people aged 20-45 years.

There are many causes for thyrotoxicosis. The main ones include:

• increased production of thyroid hormones due to various diseases (, and others);
• excessive intake of drugs containing thyroid hormones (violation of the prescribed treatment regimen).

The provoking factor of the syndrome is the additional amount of iodine that enters the body with the independent use of iodine supplements.

The state of thyrotoxicosis in diffuse toxic goiter is an autoimmune disease. It usually develops as a result of overproduction of antibodies to the thyroid stimulating hormone (TSH) receptor produced by the pituitary gland.

The occurrence of a thyrotoxic state is possible when the functional autonomy of an already existing thyroid node occurs - a single- and multi-nodular goiter. This disease develops for a long time, mainly in people over 45 years of age. So, in the absence of exposure to TSH - the main physiological stimulant - the nodes synthesize the amount of thyreohormones that exceeds the body's need.

If you experience similar symptoms, consult your doctor. Do not self-medicate - it is dangerous for your health!

Symptoms of thyrotoxicosis (hyperthyroidism)

When questioning patients with suspected elevated thyroid function, the following are revealed:

• unpredictable excitability, emotional instability, causeless tearfulness;
• anxiety and impaired concentration of attention that occurs when being in society;
• daily sleep disturbance
• fussiness when doing any work;
• weakness while walking;
• increased sweating of a diffuse nature, not dependent on physical or emotional stress, a feeling of "heat";
• periodic heartbeats;
• trembling in the body and increasing weight loss (rarely observed).

Emotional disorders are combined with motor-volitional disorders: there is a need for constant movement and choreo-like twitches. Moreover, tremor of the limbs and body is a typical symptom of thyrotoxicosis.

An increased amount of thyroid hormones affects cardiac activity

effects thyroid hormones			Change cardiac activity
inotropic		+	heart rate	gain
chronotropic		+	heart rate	increase
dromotropic		+	conduction of excitation in the heart	improvement
bathmotropic		+	excitability of the heart muscle	promotion

Among the characteristic changes that are detected in people with thyrotoxicosis during an examination by an ophthalmologist, there is a lesion of the soft tissues of the orbit. This pathology occurs in 40-50% of patients with involvement of the optic nerve and disease of the auxiliary apparatus of the eye (eyelids, conjunctiva and lacrimal gland). This does not exclude the development of neuropathy of the optic nerve and corneal lesions with the formation of a walleye.

The main syndromes of thyrotoxicosis in diffuse toxic goiter include:

1. a set of symptoms of the central nervous system: astheno-neurotic and anxiety-depressive syndromes;
2. one of the cardiovascular manifestations: persistent sinus tachycardia, paroxysmal or persistent atrial fibrillation, absence of tachycardia, thyrotoxic myocardial dystrophy;
3. gastrointestinal syndromes: increased peristalsis and accelerated evacuation, insufficient digestion of food, periodic abdominal pain up to the simulation of an "acute abdomen", toxic effects on hepatocytes;
4. disorders associated with the endocrine glands: thyroid adrenal insufficiency in women, gynecomastia in men, impaired carbohydrate tolerance, development of osteoporosis.

The pathogenesis of thyrotoxicosis (hyperthyroidism)

The thyroid gland is an organ that produces thyroid hormones such as triiodothyronine (T3) and thyroxine (T4). TSH, a pituitary hormone, has a stimulating effect on them.

With diffuse toxic goiter, thyroid-stimulating antibodies (G) are formed that compete with TSH, a natural stimulator of the thymus gland (an important organ of the immune system).

With the onset of TSH deficiency, the immune process begins to progress. Thyroid-stimulating antibodies stimulate the C-cells of the thyroid gland, activating the secretion of thyrocalcitonin (TKT), which affects the enhancement of immunogenesis and thyrotoxicosis and leads to the progression of the autoimmune process. This effect of antibodies helps to reduce calcium in the blood and increase the excitation of thyrocytes (thyroid cells). A decrease in TSH is accompanied by an increase in thyroliberin and an increase in prolactin.

Significant influence on the progression of thyrotoxicosis has emotional stress and "psychotrauma" due to the active release of adaptation hormones (adrenaline and norepinephrine), which increase the synthesis and secretion of T3 and T4. This leads to atrophy of the thymus gland, a decrease in the concentration of interferon and an increase in the predisposition to infectious diseases and cancer.

A separate role in the pathogenesis of thyrotoxicosis is assigned to the influence of various viruses (triggers of an autoimmune reaction) through thyrocytes.

Classification and stages of development of thyrotoxicosis (hyperthyroidism)

According to ICD 10, there is the following classification of the syndrome:

• E05.0 - thyrotoxicosis with diffuse goiter;
• E05.1 - thyrotoxicosis with toxic single-nodular goiter;
• E05.2 - thyrotoxicosis with toxic multinodular goiter;
• E05.3 - thyrotoxicosis with ectopic thyroid tissue;
• E05.4 - artificial thyrotoxicosis;
• E05.5 - thyroid crisis or coma;
• E05.6 - other forms of thyrotoxicosis;
• E05.7 Thyrotoxicosis, unspecified.

Depending on the influence of TSH, there are three main types of thyrotoxicosis:

Criteria for assessing the severity of thyrotoxicosis

Criteria gravity	Severity
	light	average	heavy
Frequency cardiac cuts (bpm)	80-100	100-120	over 120
Loss body weight (from original)	up to 10-15%	up to 15-30%	over 30%
Availability complications	No	⠀ transient disorders Rhythm ⠀ Disorders of carbohydrate ⠀⠀exchange ⠀ Gastrointestinal ⠀⠀ Disorders	⠀ transient disorders Rhythm ⠀ Disorders of carbohydrate ⠀⠀exchange ⠀ Gastrointestinal ⠀⠀ Disorders ⠀ osteoporosis The secondary adrenal ⠀⠀ Insufficiency

The classification of thyrotoxicosis proposed by professors V.V. Fadeev and G.A. Melnichenko, suggests the division of the syndrome into three types:

Options	manifest type of syndrome	subclinical type of syndrome
TSH level	short	short
Level T3 and T4	elevated or T3 or T4	fine
Clinical manifestations	characteristic clinic and shifts in level thyroid hormones	absent

The subclinical type of thyrotoxicosis may occur as a result of the formation of functional autonomy of the thyroid gland, an overdose of thyroid hormones in thyroid cancer or hypothyroidism, painless thyroiditis.

Complications of thyrotoxicosis (hyperthyroidism)

The long course of the disease affects the formation of bones: there is a decrease in bone density and an increased risk of bone fractures (primarily tubular) in awkward situations. Women with increased thyroid function at menopause have an increased risk of these complications.

Also, cardiovascular disorders pose a serious danger: paroxysmal atrial fibrillation may occur, turning into a permanent form with the risk of thromboembolic complications.

With an increase in adverse environmental factors (for example, stressful situations, various diseases, surgical interventions, etc.), a thyrotoxic crisis may occur. Its characteristic features are:

• sudden excitability;
• an increase in body temperature up to 40 ° C;
• increase in heart rate up to 200 beats / min;
• atrial fibrillation (not always);
• increased nausea, (possibly to the point of vomiting) and diarrhea;
• increased thirst;
• increase in pulse blood pressure;
• the appearance of signs of adrenal insufficiency (occurs later).

The condition worsens after a few hours, so a thyrotoxic crisis requires emergency medical care.

Diagnosis of thyrotoxicosis (hyperthyroidism)

Diagnosing the syndrome involves interviewing the patient, identifying clinical signs and laboratory tests.

At history taking in patients with thyrotoxicosis

Laboratory research is indicated for all patients with thyroid pathology (especially those who have pronounced clinical manifestations of reduced or increased thyroid function), as well as during conservative treatment to control the adequacy of therapy and in the presence of concomitant pathology. The determination of total T3 is important in toxicosis, especially in cases of T3 toxicosis. Laboratory diagnostic indicators for thyrotoxicosis are a high level of free T3 and T4, as well as a low level of TSH in the blood.

Due to the fact that most of T3 and T4 are associated with blood proteins, a study of the free fractions of these hormones is carried out in combination with the determination of the level of TSH. In this case, the free fraction determines the biological effect of thyroid hormones.

⠀ Normal concentration of thyroid hormones and TSH⠀
total T3⠀ free T3⠀ total T4⠀ free T4⠀ TSH⠀	⠀1.2 - 2.08 nmol/l ⠀2.5 - 5.8 pg/ml ⠀64 - 146 nmol/l ⠀11-25 pg/ml ⠀0.24-3.4 mg/ml

Since the content of T3 and T4 is affected by a number of factors (for example, a low-calorie diet, liver disease, long-term medication), it is more expedient to study free fractions of thyroid hormones in combination with TSH.

The main attention should be paid to the level of TSH in the following cases:

• acute mental illness requiring hospitalization;
• diseases of the pituitary gland or hypothalamus;
• rapid changes in thyroid status.

In these cases, this study may lead to an erroneous diagnosis.

If thyroid dysfunction is suspected in severe patients with intact ("uninvolved") hypothalamic-pituitary function, a "panel" approach should be used - simultaneous determination of TSH and free T4.

In hyperthyroidism, the synthesis and secretion of TSH are suppressed, so the determination of very low concentrations of TSH is of fundamental importance in the diagnosis of its various forms. The exception is rare cases of TSH-induced thyrotoxicosis (when TSH secretion is increased), which include a TSH-producing pituitary adenoma and a syndrome of inappropriate TSH secretion due to the resistance of this pituitary hormone to the effects of T3 and T4.

Additional diagnostic methods:

The size of the thyroid gland according to the results of palpation is determined according to the 1994 WHO classification.

Degree increase thyroid gland	Description of the thyroid gland
	Dimensions each share	State on palpation
no goiter	less distal phalanx (tip) patient's thumb	not palpable
I	more distal phalanx	palpable but not visible to the eye
II	more distal phalanx	palpated and visible to the eye

In the event that a patient is palpated with an increase in size or a suspicion of a nodular formation in the thyroid gland, ultrasound diagnostics (ultrasound) is performed with the calculation of the volume of the thyroid gland - the formula (I. Brunn, 1986):

Volume = [(WxDxL) right + (WxDxL) left] x 0.479;

W, D, L are the width, thickness and length of the thyroid gland, and 0.479 is the correction factor for the ellipsoid shape of the organ.

Ultrasound of the thyroid gland is usually performed using a high-frequency transducer with a frequency of 7.5 MHz. The use of color Doppler mapping allows visualization of small vessels in the organ under study and provides information on the direction and average flow velocity.

In some cases, a thyroid scintigraphy can be performed, which shows the ability of the organ to capture iodine and other substances (technetium).

Differential Diagnosis held:

Treatment of thyrotoxicosis (hyperthyroidism)

In the treatment of thyrotoxicosis, the main methods are usually used:

The fight against the syndrome involves the elimination of clinical manifestations of thyrotoxicosis with the normalization of T3, T4 and TSH values ​​and the achievement of a stable remission of the disease.

Conservative therapy

In the conservative treatment of diffuse toxic goiter in patients with a moderately enlarged thyroid gland (up to 40 ml), propylthiouracil (PTU) or thiamazole (Tirozol or Mercazolil) is prescribed. This contributes to the normal functioning of the affected organ. In diagnosed cases of diffuse toxic goiter in the first trimester of pregnancy and the occurrence of side effects while taking thiamazole, PTU is prescribed. As a result of treatment, after 4-6 weeks, an improvement is noted - the level of free T4 normalizes. Additionally, according to indications, beta-blockers are prescribed (for example, 2.5-5 mg of Concor per day).

In severe cases of the process, it is recommended to take glucocorticoids - up to 10-15 mg of prednisolone per day. Then, within 2-3 weeks, the thyreostatic dose is reduced to maintenance (no more than 10 mg per day). In parallel, the patient is usually prescribed 50 micrograms of levothyroxine per day. This treatment regimen is called "Block and replace". Stable maintenance of the level of free T4 and TSH in the norm will indicate the adequacy of the prescribed therapy.

In the presence of persistent side effects of the prescribed treatment, thyreostatic drugs are canceled, radioactive iodine therapy or surgery is prescribed. In the event of a recurrence of thyrotoxicosis, the question arises of the need for radioiodine therapy or thyroidectomy - complete or partial removal of the thyroid gland.

Treatment with radioactive iodine

Radioiodine therapy for diffuse toxic goiter is carried out in case of persistent recurrence of thyrotoxicosis at the end of properly conducted conservative therapy (within 12-18 months) and difficulties in taking thyreostatic drugs (decrease in the number of leukocytes in the blood or the occurrence of allergic reactions).

Treatment with radioactive iodine is carried out in specialized centers with radiation and environmental safety for people and nature. The only contraindications for this therapy are pregnancy and lactation.

The goal of radioiodine therapy in the destruction of hyperfunctioning thyroid tissue is to achieve a stable hypothyroid state.

Surgical treatment

Surgical intervention for diffuse toxic goiter is necessary if the goiter is located behind the sternum, with diffuse and nodular forms of goiter with compression and the patient refuses other methods of therapy. Total and subtotal thyroidectomy are the treatment of choice. In the presence of a nodular formation in the thyroid gland, it is necessary to conduct a puncture biopsy and diagnostic cytological examination. To complicate the course and prognosis of the disease, especially in relation to the ability to work and the state of health in general, may develop atrial fibrillation and severe manifestations of heart failure in thyrotoxicosis.

When a favorable outcome of the disease occurs, patients with thyrotoxicosis should take preventive measures against the occurrence of relapse in the form of:

• compliance with a sparing lifestyle regimen for 3-6 months;
• restrictions on physical activity;
• creation by relatives of psychological peace, and at work - reduction of hours of intensive loads, incl. night shifts (if any).

Such prevention of recurrence of the disease is extremely important, because the thyroid gland is a fragile and at the same time strong organ, with its own "character".

Long-term stable remission of thyrotoxicosis is an indication for sanatorium-and-spa therapy in conditions of low altitude and periodic out-of-town rest in a comfortable environment. At the same time, it is undesirable to stay in the open sun; sunscreen should be used at sea.

Treatment and preventive measures include balneological procedures using native radon waters. Their effectiveness and positive effect on the body have been proven by many years of research conducted at resorts with mineral waters.

Thus, in the treatment of patients with thyrotoxicosis at the Belokurikha resort, the effectiveness of radon procedures in conjunction with drug therapy (mercasolil, microiodine and reserpine) was confirmed. Radon-free nitrogen baths have a preventive effect through thermal and mechanical stimulation of nerve receptors with nitrogen bubbles.

There are three ways to eliminate hyperthyroidism - to reduce the level of thyroid hormones in the blood:

1. destroy excess thyroid hormones medicines

2. destroy the thyroid gland so that it does not produce excess hormones (surgical treatment and radioactive iodine therapy)

3. restore thyroid function

Drug therapy in the "treatment" of hyperthyroidism

Destroy thyroid hormones drug thyreostatic drugs. Drug treatment - for a long time - up to 3 years. Treatment begins with large doses of these drugs, as soon as free T4 normalizes, the thyreostatic dose is gradually reduced to maintenance (10-15 mg per day). This blocks the production of thyroid hormones. In parallel, hormone-replacing drugs are prescribed 50-75 mcg per day to replace the destroyed own hormones. The principle of this treatment: block and replace! The therapy is called hormone replacement therapy (HRT).

Drug "treatment" has many side effects:

• goiter effect (an increase in the size of the thyroid gland while taking thyreostatics);
• complications from the blood (the number of leukocytes, platelets decreases);
• allergic reactions;
• abnormal liver function (ALT, AST increase);
• diarrhea, headache, menstrual disorders, etc.
After discontinuation of thyreostatic drugs, the frequency of relapses of hyperthyroidism reaches 75%.

• Surgical treatment and radioactive iodine therapy in the treatment of hyperthyroidism

  Surgical treatment - surgical removal of the thyroid gland, and radioactive iodine therapy - slow radiation destruction of the thyroid gland, eliminates any possibility of recurrence of hyperthyroidism - a recurrence rate of 0%. But at what cost!

  Thyroid removal any way leads to a dangerous disability. Autoimmune processes in the body do not disappear and are now controlled expensive life 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. On danger and therapeutic futility surgery or exposure radioactive iodine More details can be found at the links provided.

  Safe treatment hyperthyroidism without hormones and operations method of computer reflex therapy, which is aimed precisely at eliminating the malfunction of not only the human immune system, but also for restoration and coordinated work human nervous and endocrine systems.

  The coordinated work of the internal organs of 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.

  Rebooting the body's three major regulatory systems to a state of active struggle with harmful external environmental influences, internal diseases, is the main task of therapy focused on the impact on the body through the autonomic nervous system.

  There are many methods of influencing the nervous system, but, to date, only computer reflex therapy acts through the nervous system in such a way that 93% cases in patients, the neuro-immuno-endocrine regulation of the body is completely restored and, as a result, many endocrine and neurological diseases that previously did not respond to drug "treatment" recede and completely disappear.

  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.

  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

  

  

  Before each procedure, the doctor conducts a diagnosis of the patient, based on the results of which he makes an individual prescription of points for the procedure in accordance with the treatment plan. During the procedure itself, every second scanning of the current state of the patient allows you to accurately dose the effect, which in principle is not available when exposed to any other methods.

  Of course, this method of treatment, like any other, has restrictions and contraindications- This oncological diseases and mental disorders, disorders of the heart (presence pacemaker, flickering arrhythmia and myocardial infarction in the acute period) HIV-infection and congenital hypothyroidism. If you do not have the above contraindications, then getting rid of hyperthyroidism using this method in our clinic has been a common practice for many years.

  For a good 20 years now, the Gavrilova Clinic in the city of Samara has been carrying out thyroid gland restoration without hormones and operations. The author and developer of the method is Gavrilova Natalya Alekseevna. Associate Professor, Ph.D. with general medical experience since 1968, awarded the Order of Medical Merit. If you wish, you can learn more about bioelectrophysical the basics of the therapeutic effect of reflex therapy and specific treatment examples.

  Using the method of computer reflex therapy, the doctor restores the neuro-immuno-endocrine regulation of the entire patient's body. Restoration of the structure and function of the thyroid gland is a manifestation of how the body, using its internal reserves and capabilities, self-regenerates in a natural way for it.

  Treatment of hyperthyroidismcomputer reflex therapy method without side effects leads to the following results:

  • are recovering functioning tissue and structure of the thyroid gland;
  • Normalizes the level of own thyroid hormones T4 (thyroxine) and T3 (triiodothyronine), as well as the level of TSH (pituitary hormone), which is confirmed by blood tests;
  • If the patient takes hormone replacement drugs, it is possible to reduce their dosage and completely cancel at the end of treatment;
  • At getting better aboutgeneral well-being to the state of a healthy person;
  • Often, after a course of treatment, diseases associated with the work of the nervous system, allergic and other autoimmune diseases disappear..

  Leave your contact and the consulting doctor will contact you

  

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

Thyrotoxicosis is a syndrome that occurs in various pathological conditions of the human body. The frequency of thyrotoxicosis in Europe and Russia is 1.2% (Fadeev V.V., 2004). But the problem of thyrotoxicosis is determined not so much by its prevalence as by the severity of the consequences: affecting metabolic processes, it leads to the development of severe changes in many body systems (cardiovascular, nervous, digestive, reproductive, etc.).

Thyrotoxicosis syndrome, which consists in the excessive action of the hormones thyroxine and triiodothyronine (T4 and T3) on target organs, in most clinical cases is a consequence of thyroid pathology.

The thyroid gland is located on the anterior surface of the neck, covering the front and sides of the upper tracheal rings. Being horseshoe-shaped, it consists of two lateral lobes connected by an isthmus. The laying of the thyroid gland occurs at 3-5 weeks of embryonic development, and from 10-12 weeks it acquires the ability to capture iodine. As the largest endocrine gland in the body, it produces thyroid hormones (TH) and calcitonin. The morphofunctional unit of the thyroid gland is the follicle, the wall of which is formed by a single layer of epithelial cells - thyrocytes, and the lumen contains their secretory product - colloid.

Thyrocytes capture iodine anions from the blood and, by attaching it to tyrosine, remove the resulting compounds in the form of tri- and tetraiodothyronines into the lumen of the follicle. Most of triiodothyronine is formed not in the thyroid gland itself, but in other organs and tissues, by splitting off an iodine atom from thyroxine. The part of iodine remaining after splitting off is again captured by the thyroid gland to participate in the synthesis of hormones.

The regulation of thyroid function is under the control of the hypothalamus, which produces thyrotropin-releasing factor (thyreoliberin), under the influence of which the pituitary thyroid-stimulating hormone (TSH) is released, which stimulates the production of T3 and T4 by the thyroid gland. There is a negative feedback between the level of thyroid hormones in the blood and TSH, due to which their optimal concentration in the blood is maintained.

The role of thyroid hormones:

Increase the sensitivity of adrenergic receptors, increasing the heart rate (HR), blood pressure;

At the intrauterine stage, they contribute to the differentiation of tissues (nervous, cardiovascular, musculoskeletal systems), during childhood - the formation of mental activity;

Increase oxygen consumption and basal metabolic rate:

• By activating the synthesis of proteins (including enzymes);

  Increasing the uptake of calcium ions from the blood;

  Activating the processes of glycogenolysis, lipolysis, proteolysis;

  Facilitating the transport of glucose and amino acids into the cell;

  Increasing heat production.

Causes of thyrotoxicosis

An excess of thyroid hormones in the blood may be the result of diseases manifested by hyperfunction of the thyroid gland or its destruction - in this case, thyrotoxicosis is due to the passive intake of T4 and T3 into the blood. In addition, there may be causes independent of the thyroid gland, such as an overdose of thyroid hormones, T4- and T3-secreting ovarian teratoma, and metastases of thyroid cancer (Table 1).

Hyperthyroidism. The first place among diseases accompanied by increased formation and secretion of thyroid hormones is occupied by diffuse toxic goiter and multinodular toxic goiter.

Diffuse toxic goiter (DTG) (Basedow-Graves' disease, Pari's disease) is a systemic autoimmune disease with a hereditary predisposition, which is based on the production of stimulating autoantibodies to TSH receptors located on thyrocytes. The detection of circulating autoantibodies in 50% of relatives of DTG, the frequent detection of the HLA DR3 haplotype in patients, and a frequent combination with other autoimmune diseases indicate a genetic predisposition. The combination of DTG with autoimmune chronic adrenal insufficiency, type 1 diabetes mellitus, and other autoimmune endocrinopathies is referred to as type 2 autoimmune polyglandular syndrome. It is noteworthy that women get sick 5-10 times more often than men, the manifestation of the disease occurs in young and middle age. Hereditary predisposition under the action of trigger factors (viral infection, stress, etc.) leads to the appearance in the body of thyroid-stimulating immunoglobulins - LATS-factors (long action thyreoid stimulator, long-acting thyroid stimulator). By interacting with thyroid-stimulating hormone receptors on thyrocytes, thyroid-stimulating antibodies cause an increase in the synthesis of the hormones T4 and T3, which leads to the onset of a state of thyrotoxicosis.

Multinodular toxic goiter - develops with a long-term chronic lack of iodine in food. In fact, this is one of the links in the chain of successive pathological conditions of the thyroid gland, which are formed in conditions of mild to moderate iodine deficiency. Diffuse non-toxic goiter (DNZ) turns into nodular (multinodular) non-toxic goiter, then the functional autonomy of the thyroid gland develops, which is the pathophysiological basis of multinodular toxic goiter. In conditions of iodine deficiency, the thyroid gland is exposed to the stimulating effect of TSH and local growth factors, causing hypertrophy and hyperplasia of the follicular cells of the thyroid gland, which leads to the formation of a struma (DNC stage). The basis for the development of nodes in the thyroid gland is the microheterogeneity of thyrocytes - different functional and proliferative activity of thyroid cells.

If iodine deficiency persists for many years, then thyroid stimulation, becoming chronic, causes hyperplasia and hypertrophy in thyrocytes, which have the most pronounced proliferative activity. Which leads over time to the emergence of focal accumulations of thyrocytes with the same high sensitivity to stimulating effects. Under conditions of ongoing chronic hyperstimulation, the active division of thyrocytes and the delay against this background of reparative processes leads to the development of activating mutations in the genetic apparatus of thyrocytes, leading to their autonomous functioning. Over time, the activity of autonomous thyrocytes leads to a decrease in the level of TSH and an increase in the content of T3 and T4 (the phase of clinically obvious thyrotoxicosis). Since the process of formation of the functional autonomy of the thyroid gland is extended in time, iodine-induced thyrotoxicosis manifests itself in older age groups - after 50 years.

Thyrotoxicosis during pregnancy. The frequency of thyrotoxicosis in pregnant women reaches 0.1%. Its main cause is diffuse toxic goiter. Since thyrotoxicosis reduces fertility, pregnant women rarely have a severe form of the disease. It is not uncommon for pregnancy to occur during or after medical treatment for thyrotoxicosis (because this treatment restores fertility). Contraception is recommended for young women with thyrotoxicosis receiving thionamides to avoid unwanted pregnancies.

Toxic thyroid adenoma (Plummer's disease) is a benign tumor of the thyroid gland that develops from the follicular apparatus and autonomically hyperproduces thyroid hormones. Toxic adenoma may occur in a pre-existing non-toxic nodule, in connection with this nodular euthyroid goiter is considered as a risk factor for the development of toxic adenoma. The pathogenesis of the disease is based on the autonomous hyperproduction of thyroid hormones by adenoma, which is not regulated by thyroid-stimulating hormone. The adenoma secretes predominantly triiodothyronine in large quantities, which leads to suppression of the production of thyroid-stimulating hormone. This reduces the activity of the rest of the thyroid tissue surrounding the adenoma.

TSH-secreting pituitary adenomas are rare; they account for less than 1% of all pituitary tumors. In typical cases, thyrotoxicosis develops against the background of a normal or elevated TSH level.

Selective resistance of the pituitary gland to thyroid hormones - a condition in which there is no negative feedback between the level of thyroid hormones of the thyroid gland and the level of pituitary TSH, characterized by normal TSH levels, a significant increase in T4 and T3 levels and thyrotoxicosis (because the sensitivity of other target tissues to thyroid hormones is not violated). A pituitary tumor in such patients is not visualized.

Molar mole and choriocarcinoma secrete large amounts of human chorionic gonadotropin (CG). Chorionic gonadotropin, similar in structure to TSH, causes transient suppression of the thyroid-stimulating activity of the adenohypophysis and an increase in the level of free T4. This hormone is a weak stimulator of TSH receptors on thyrocytes. When the concentration of hCG exceeds 300,000 units / l (which is several times the maximum concentration of hCG during normal pregnancy), thyrotoxicosis may occur. Removal of the hydatidiform mole or chemotherapy of choriocarcinoma eliminates thyrotoxicosis. The level of hCG can also increase significantly with toxicosis of pregnant women and cause thyrotoxicosis.

Destruction of the thyroid gland

The destruction of thyrocytes, in which thyroid hormones enter the bloodstream and, as a result, the development of thyrotoxicosis, is accompanied by inflammatory diseases of the thyroid gland - thyroiditis. These are mainly transient autoimmune thyroiditis (AIT), which include painless ("silent") AIT, postpartum AIT, cytokine-induced AIT. With all these variants, phase changes occur in the thyroid gland associated with autoimmune aggression: in the most typical course, the phase of destructive thyrotoxicosis is replaced by a phase of transient hypothyroidism, after which, in most cases, restoration of thyroid function occurs.

Postpartum thyroiditis occurs against the background of excessive reactivation of the immune system after natural gestational immunosuppression (rebound phenomenon). The painless (“silent”) form of thyroiditis passes in the same way as the postpartum one, but only the provoking factor is unknown, it proceeds without connection with pregnancy. Cytokine-induced thyroiditis develops after the appointment of interferon drugs for various diseases.

The development of thyrotoxicosis is possible not only with autoimmune inflammation in the thyroid gland, but also with its infectious damage, when subacute granulomatous thyroiditis develops. A viral infection is thought to be the cause of subacute granulomatous thyroiditis. The causative agents are thought to be Coxsackievirus, adenoviruses, mumps virus, ECHO viruses, influenza viruses, and Epstein-Barr virus. There is a genetic predisposition to subacute granulomatous thyroiditis as the incidence is higher in individuals with HLA-Bw35 antigen. The prodromal period (lasting several weeks) is characterized by myalgia, subfebrile temperature, general malaise, laryngitis, and sometimes dysphagia. Thyrotoxicosis syndrome occurs in 50% of patients and appears in the stage of severe clinical manifestations, which include pain on one side of the anterior surface of the neck, usually radiating to the ear or lower jaw on the same side.

Other causes of thyrotoxicosis

Drug-induced thyrotoxicosis is a common cause of thyrotoxicosis. Often, the doctor prescribes excessive doses of hormones; in other cases, patients secretly take excessive amounts of hormones, sometimes with the aim of losing weight.

T 4 - and T 3 -secreting ovarian teratoma (ovarian struma) and large hormone-active metastases of follicular thyroid cancer are very rare causes of thyrotoxicosis.

Clinical picture in thyrotoxicosis syndrome

The cardiovascular system. The most important target organ for thyroid disorders is the heart. In 1899, R. Kraus introduced the term "thyrotoxic heart", which refers to a symptom complex of disorders of the cardiovascular system caused by the toxic effect of excess thyroid hormones, characterized by the development of hyperfunction, hypertrophy, dystrophy, cardiosclerosis and heart failure.

The pathogenesis of cardiovascular disorders in thyrotoxicosis is associated with the ability of TG to bind directly to cardiomyocytes, providing a positive inotropic effect. In addition, by increasing the sensitivity and expression of adrenergic receptors, thyroid hormones cause significant changes in hemodynamics and the development of acute heart disease, especially in patients with coronary heart disease. There is an increase in heart rate, an increase in stroke volume (SV) and minute volume (MO), acceleration of blood flow, a decrease in total and peripheral vascular resistance (OPVR), a change in blood pressure. Systolic pressure increases moderately, diastolic pressure remains normal or low, as a result of which the pulse pressure increases. In addition to all of the above, thyrotoxicosis is accompanied by an increase in circulating blood volume (CBV) and erythrocyte mass. The reason for the increase in BCC is a change in the serum level of erythropoietin in accordance with a change in the serum level of thyroxine, which leads to an increase in the mass of red blood cells. As a result of an increase in the minute volume and mass of circulating blood, on the one hand, and a decrease in peripheral resistance, on the other, pulse pressure and the load on the heart in diastole increase.

The main clinical manifestations of heart pathology in thyrotoxicosis are sinus tachycardia, atrial fibrillation (AF), heart failure and the metabolic form of angina pectoris. If the patient has coronary heart disease (CHD), hypertension, heart defects, thyrotoxicosis will only accelerate the occurrence of arrhythmias. There is a direct dependence of MP on the severity and duration of the disease.

The main feature of sinus tachycardia is that it does not disappear during sleep and slight physical activity increases the heart rate dramatically. In rare cases, sinus bradycardia occurs. This may be due to congenital changes or to the depletion of the function of the sinus node with the development of its weakness syndrome.

Atrial fibrillation occurs in 10-22% of cases, and the frequency of this pathology increases with age. At the beginning of the disease, atrial fibrillation is paroxysmal in nature, and with the progression of thyrotoxicosis, it can become permanent. In young patients without concomitant cardiovascular pathology, after subtotal resection of the thyroid gland or successful thyrostatic therapy, sinus rhythm is restored. In the pathogenesis of atrial fibrillation, an important role is played by electrolyte imbalance, more precisely, a decrease in the level of intracellular potassium in the myocardium, as well as depletion of the nomotropic function of the sinus node, which leads to its depletion and transition to a pathological rhythm.

For thyrotoxicosis, atrial arrhythmias are more characteristic, and the appearance of ventricular arrhythmias is characteristic only of a severe form. This may be due to the higher sensitivity of the atria to the arrhythmogenic effect of TSH compared to the ventricles, since the density of beta-adrenergic receptors in the atrial tissue prevails. As a rule, ventricular arrhythmias occur when thyrotoxicosis is combined with cardiovascular diseases. With the onset of persistent euthyroidism, they persist.

The musculoskeletal system. Increased catabolism leads to muscle weakness and atrophy (thyrotoxic myopathy). The patients look emaciated. Muscle weakness is manifested when walking, climbing a mountain, getting up from your knees, or lifting weights. In rare cases, transient thyrotoxic paralysis occurs, lasting from several minutes to several days.

Elevated levels of thyroid hormones lead to a negative mineral balance with loss of calcium, which is manifested by increased bone resorption and reduced intestinal absorption of this mineral. Bone resorption prevails over its formation, so the concentration of calcium in the urine is increased.

Patients with hyperthyroidism have low levels of the vitamin D-1,25(OH)2D metabolite, sometimes hypercalcemia, and decreased serum parathyroid hormone levels. Clinically, all these disorders lead to the development of diffuse osteoporosis. Pain in the bones, pathological fractures, collapse of the vertebrae, the formation of kyphosis are possible. Arthropathy in thyrotoxicosis develops rarely, according to the type of hypertrophic osteoarthropathy with thickening of the phalanges of the fingers and periosteal reactions.

Nervous system. Damage to the nervous system in thyrotoxicosis almost always occurs, so it was previously called "neurothyroidism" or "thyroid neurosis". The pathological process involves the central nervous system, peripheral nerves and muscles.

Exposure to excess thyroid hormones primarily leads to the development of symptoms of a neurasthenic nature. Complaints of increased excitability, anxiety, irritability, obsessive fears, insomnia are typical, there is a change in behavior - fussiness, tearfulness, excessive motor activity, loss of the ability to concentrate (the patient abruptly switches from one thought to another), emotional instability with a quick change in mood from agitation to depression. True psychoses are rare. A syndrome of lethargy and depression, called "apathetic thyrotoxicosis", usually occurs in elderly patients.

Phobic manifestations are very characteristic of thyrotoxicosis. Often there is cardiophobia, claustrophobia, social phobia.

In response to physical and emotional stress, panic attacks occur, manifested by a sharp increase in heart rate, increased blood pressure, blanching of the skin, dry mouth, chill-like trembling, and fear of death.

Neurotic symptoms in thyrotoxicosis are nonspecific, and as the disease develops and worsens, they fade away, giving way to severe organ damage.

Tremor is an early symptom of thyrotoxicosis. This hyperkinesis persists both at rest and during movements, and emotional provocation enhances its severity. The tremor affects the hands (Marie's symptom is a tremor of the fingers of outstretched hands), the eyelids, the tongue, and sometimes the whole body (the "telegraph pole symptom").

As the disease worsens, fatigue, muscle weakness, diffuse weight loss, and muscle atrophy progress. In some patients, muscle weakness reaches extreme severity and even leads to death. Extremely rarely, with severe thyrotoxicosis, attacks of generalized muscle weakness (periodic thyrotoxic hypokalemic paralysis) can suddenly occur, affecting the muscles of the trunk and extremities, including the respiratory muscles. In some cases, paralysis is preceded by bouts of weakness in the legs, paresthesia, and pathological muscle fatigue. Paralysis develops rapidly. Such attacks can sometimes be the only manifestation of thyrotoxicosis. Electromyography in patients with periodic paralysis reveals polyphasia, a decrease in action potentials, the presence of spontaneous activity of muscle fibers and fasciculations.

Chronic thyrotoxic myopathy occurs with a long course of thyrotoxicosis, characterized by progressive weakness and fatigue in the proximal muscle groups of the extremities, more often the legs. Difficulties are noted when climbing stairs, getting up from a chair, combing hair. Symmetrical hypotrophy of the muscles of the proximal limbs gradually develops.

Thyrotoxic exophthalmos. Thyrotoxic exophthalmos always occurs against the background of thyrotoxicosis, more often in women. The palpebral fissure in such patients is wide open, although there is no exophthalmos, or it does not exceed 2 mm. An increase in the palpebral fissure occurs due to the retraction of the upper eyelid. Other symptoms can also be detected: when looking directly, a strip of sclera is sometimes visible between the upper eyelid and the iris (Dalrymple's symptom). When looking down, the lowering of the upper eyelid lags behind the movement of the eyeball (Graefe's symptom). These symptoms are due to an increase in the tone of the smooth muscles that lift the upper eyelid. Characterized by rare blinking (Stellvag's symptom), gentle tremor of the eyelids when they close, but the eyelids close completely. The range of motion of the extraocular muscles is not disturbed, the fundus of the eye remains normal, and the functions of the eye do not suffer. Reposition of the eye is not difficult. The use of instrumental research methods, including computed tomography and nuclear magnetic resonance, proves the absence of changes in the soft tissues of the orbit. The described symptoms disappear on the background of drug correction of thyroid dysfunction.

Eye symptoms of thyrotoxicosis must be distinguished from an independent disease of endocrine ophthalmopathy.

Endocrine ophthalmopathy (Graves) is a disease associated with damage to periorbital tissues of autoimmune origin, which in 95% of cases is combined with autoimmune thyroid diseases. It is based on lymphocytic infiltration of all eye socket formations and retroorbital edema. The main symptom of Graves' ophthalmopathy is exophthalmos. Edema and fibrosis of the oculomotor muscles lead to limited mobility of the eyeball and diplopia. Patients complain of pain in the eyes, photophobia, lacrimation. Due to non-closure of the eyelids, the cornea dries up and may ulcerate. Optic nerve compression and keratitis can lead to blindness.

Digestive system. Food intake increases, some patients have an insatiable appetite. Despite this, patients are usually thin. Due to increased peristalsis, stools are frequent, but diarrhea is rare.

Sexual system. Thyrotoxicosis in women reduces fertility and can cause oligomenorrhea. In men, spermatogenesis is suppressed, potency occasionally decreases. Sometimes there is gynecomastia, due to the accelerated peripheral conversion of androgens to estrogens (despite the high level of testosterone). Thyroid hormones increase the concentration of sex hormone-binding globulin, and thereby increase the total content of testosterone and estradiol; however, serum levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) may be elevated or normal.

Metabolism. Patients are usually thin. Anorexia is common in the elderly. On the contrary, in some young patients, the appetite is increased, so they put on weight. Since thyroid hormones increase heat production, heat loss through sweating also increases, resulting in mild polydipsia. Many do not tolerate heat well. In patients with insulin-dependent diabetes mellitus with thyrotoxicosis, the need for insulin increases.

The thyroid gland is usually enlarged. The size and consistency of the goiter depend on the cause of thyrotoxicosis. In a hyperfunctioning gland, blood flow increases, which causes the appearance of local vascular noise.

Thyrotoxic crisis is a sharp exacerbation of all symptoms of thyrotoxicosis, being a severe complication of the underlying disease, accompanied by hyperfunction of the thyroid gland (in clinical practice, this is usually toxic goiter). The following factors contribute to the development of the crisis:

Prolonged lack of treatment for thyrotoxicosis;

Intercurrent infectious and inflammatory processes;

Severe mental trauma;

Surgical treatment of any nature;

Treatment of toxic goiter with radioactive iodine, as well as surgical treatment of the disease, if a euthyroid state has not been previously achieved; in this case, as a result of massive destruction of the thyroid gland, a large amount of thyroid hormones is released into the blood.

The pathogenesis of the crisis is an excessive intake of thyroid hormones into the blood and severe toxic damage to the cardiovascular system, liver, nervous system and adrenal glands. The clinical picture is characterized by a sharp excitement (up to psychosis with delusions and hallucinations), which is then replaced by adynamia, drowsiness, muscle weakness, apathy. On examination: the face is sharply hyperemic; eyes wide open (pronounced exophthalmos), rare blinking; profuse sweating, later replaced by dry skin due to severe dehydration; the skin is hot, hyperemic; high body temperature (up to 41-42 ° C).

High systolic blood pressure (BP), diastolic blood pressure is significantly reduced, with a far advanced crisis, systolic blood pressure drops sharply, acute cardiovascular failure may develop; tachycardia up to 200 beats per minute turns into atrial fibrillation; dyspeptic disorders intensify: thirst, nausea, vomiting, loose stools. Liver enlargement and jaundice may develop. Further progression of the crisis leads to loss of orientation, symptoms of acute adrenal insufficiency. Clinical symptoms of a crisis often increase within a few hours. In the blood, TSH may not be determined, while the level of T4 and T3 is very high. Hyperglycemia is observed, the values ​​of urea, nitrogen increase, the acid-base state and the electrolyte composition of the blood change - the level of potassium is increased, sodium - falls. Leukocytosis with a neutrophilic shift to the left is characteristic.

Diagnostics

If thyrotoxicosis is suspected, the examination includes two stages: an assessment of the function of the thyroid gland and finding out the cause of the increase in thyroid hormones.

Thyroid Function Assessment

1. Total T4 and free T4 are elevated in almost all patients with thyrotoxicosis.

2. Total T3 and free T3 are also increased. In less than 5% of patients, only total T3 is elevated, while total T4 remains normal; such conditions are called T3 thyrotoxicosis.

3. The basal level of TSH is greatly reduced, or TSH is not detected. Test with thyreoliberin is optional. Basal TSH levels are reduced in 2% of euthyroid older adults. A normal or elevated basal TSH level in the presence of elevated total T4 or total T3 indicates thyrotoxicosis caused by an excess of TSH.

4. Thyroglobulin. An increase in the level of thyroglobulin in the blood serum is detected in various forms of thyrotoxicosis: diffuse toxic goiter, subacute and autoimmune thyroiditis, multinodular toxic and non-toxic goiter, endemic goiter, thyroid cancer and its metastases. Medullary thyroid cancer is characterized by a normal or even reduced serum thyroglobulin content. In thyroiditis, the concentration of thyroglobulin in the blood serum may not correspond to the degree of clinical symptoms of thyrotoxicosis.

Modern laboratory methods make it possible to diagnose two variants of thyrotoxicosis, which very often are stages of one process:

Subclinical thyrotoxicosis: characterized by a decrease in TSH levels in combination with normal levels of free T4 and free T3.

Manifest (explicit) thyrotoxicosis is characterized by a decrease in the level of TSH and an increase in the level of free T4 and free T3.

5. Absorption of radioactive iodine (I123 or I131) by the thyroid gland. A small dose of radioactive iodine uptake test within 24 hours is important for assessing thyroid function. Twenty-four hours after an oral dose of I123 or I131, uptake of the isotope by the thyroid is measured and then expressed as a percentage. It should be taken into account that the absorption of radioactive iodine significantly depends on the content of iodine in food and in the environment.

The state of the patient's iodine pool is reflected differently in the results of measuring the absorption of radioactive iodine in various diseases of the thyroid gland. Hyperthyroxinemia with high uptake of radioactive iodine is characteristic of toxic goiter. There are many reasons for hyperthyroxinemia against the background of low radioactive iodine uptake: excess iodine in the body, thyroiditis, thyroid hormone intake, ectopic production of thyroid hormone. Therefore, when a high content of thyroid hormones in the blood is detected against the background of a low capture of I123 or I131, it is necessary to carry out a differential diagnosis of diseases (Table 2).

6. Radionuclide scanning. The functional state of the thyroid gland can be determined in the test with the capture of a radiopharmaceutical (radioactive iodine or technetium pertechnetate). When using an iodine isotope, the areas of the gland that capture iodine are visible on the scintigram. Non-functioning areas are not visualized and are called "cold".

7. Suppression tests with T3 or T4. In thyrotoxicosis, the absorption of radioactive iodine by the thyroid gland under the influence of exogenous thyroid hormones (3 mg of levothyroxine once orally or 75 μg/day of liothyronine orally for 8 days) does not decrease. Recently, this test is rarely used, since highly sensitive methods for determining TSH and methods for thyroid scintigraphy have been developed. The test is contraindicated in heart disease and elderly patients.

8. Ultrasound examination (ultrasound), or echography, or ultrasonography. This method is informative and significantly helps in the diagnosis of autoimmune thyroiditis, to a lesser extent - diffuse toxic goiter.

Establishing the cause of thyrotoxicosis

Thyroid-stimulating autoantibodies are markers of diffuse toxic goiter. Kits are available for the determination of these autoantibodies by enzyme-linked immunosorbent assay (ELISA).

All autoantibodies to TSH receptors (including thyroid-stimulating and thyroid-blocking autoantibodies) are determined by measuring the binding of IgG from patient serum to TSH receptors. These autoantibodies are detected in approximately 75% of patients with diffuse toxic goiter. A test for all TSH receptor autoantibodies is simpler and cheaper than a test for thyroid-stimulating autoantibodies.

Antibodies to myeloperoxidase are specific for diffuse toxic goiter (as well as for chronic lymphocytic thyroiditis), so their determination helps to distinguish diffuse toxic goiter from other causes of thyrotoxicosis.

Thyroid scintigraphy is performed in patients with thyrotoxicosis and nodular goiter to find out:

• Whether there is an autonomous hyperfunctioning node that accumulates all radioactive iodine and suppresses the function of normal thyroid tissue.

  Are there multiple nodes that accumulate iodine.

  Whether the palpable nodes are cold (hyperfunctioning tissue is located between the nodes).

Differential diagnosis of diseases accompanied by thyrotoxicosis

Of all the causes leading to the development of thyrotoxicosis, the most relevant (due to their prevalence) are diffuse toxic goiter and multinodular toxic goiter. Very often, the cause of unsuccessful treatment of toxic goiter is just errors in the differential diagnosis of Graves' disease and multinodular toxic goiter, due to the fact that the methods of treatment for these two diseases differ. Therefore, in the event that the presence of thyrotoxicosis in a patient was confirmed by a hormonal study, in most cases it is necessary to differentiate Graves' disease and functional autonomy of the thyroid gland (nodular and multinodular toxic goiter).

In both variants of toxic goiter, the clinic is primarily determined by thyrotoxicosis syndrome. When making a differential diagnosis, it is necessary to take into account the age peculiarity: in young people, who, as a rule, we are talking about Graves' disease, in most cases there is a detailed classical clinical picture of thyrotoxicosis, while in older patients, in whom multinodular disease is more common in our region. toxic goiter, often there is an oligo- and even monosymptomatic course of thyrotoxicosis. For example, its only manifestation may be supraventricular arrhythmias, which are associated with coronary artery disease for a long time, or unexplained subfebrile condition. In most cases, it is already possible to make a correct diagnosis based on the anamnesis, examination and clinical picture. The young age of the patient, a relatively short history of the disease (up to a year), diffuse enlargement of the thyroid gland and severe endocrine ophthalmopathy are characteristic signs of Graves' disease. In contrast, patients with multinodular toxic goiter may indicate that many years or even decades ago they had a nodular or diffuse goiter without thyroid dysfunction.

Thyroid scintigraphy: Graves' disease is characterized by a diffuse increase in the uptake of the radiopharmaceutical, with functional autonomy, "hot" nodes or alternation of zones of increased and decreased accumulation are detected. It often turns out that in a multinodular goiter, the largest nodes detected by ultrasound, according to scintigraphy, turn out to be “cold” or “warm”, and thyrotoxicosis develops as a result of hyperfunctioning of the tissue surrounding the nodes.

Differential diagnosis of toxic goiter and thyroiditis does not cause any particular difficulties. In subacute granulomatous thyroiditis, the leading symptoms are: malaise, fever, pain in the thyroid gland. The pain radiates to the ears, when swallowing or turning the head intensifies. The thyroid gland is extremely painful on palpation, very dense, nodular. The inflammatory process usually begins in one of the lobes of the thyroid gland and gradually captures the other lobe. The erythrocyte sedimentation rate (ESR) is increased, antithyroid autoantibodies, as a rule, are not detected, and the absorption of radioactive iodine by the thyroid gland is sharply reduced.

Transient autoimmune thyroiditis (subacute lymphocytic thyroiditis) - clarification in the anamnesis of childbirth, abortion, use of interferon preparations. Thyrotoxic (initial) stage of subacute postpartum thyroiditis lasts 4-12 weeks, followed by a hypothyroid stage lasting several months. Thyroid scintigraphy: for the thyrotoxic stage of all three types of transient thyroiditis, a decrease in the accumulation of the radiopharmaceutical is characteristic. Ultrasound examination reveals a decrease in the echogenicity of the parenchyma.

Acute psychosis. In general, psychosis is a painful mental disorder, manifested entirely or mainly by an inadequate reflection of the real world with a violation of behavior, a change in various aspects of mental activity, usually with the appearance of phenomena that are not characteristic of the normal psyche (hallucinations, delusions, psychomotor, affective disorders, etc.). The toxic effect of thyroid hormones can cause acute symptomatic psychosis (i.e., as one of the manifestations of a general non-communicable disease, infection and intoxication). In almost a third of patients hospitalized with acute psychosis, total T4 and free T4 are elevated. In half of patients with elevated T4 levels, T3 levels are also increased. After 1-2 weeks, these indicators are normalized without treatment with antithyroid drugs. It is believed that the increase in thyroid hormone levels is caused by the release of TSH. However, the level of TSH at the initial examination of hospitalized patients with psychosis is usually low or is at the lower limit of the norm. It is likely that TSH levels may rise in the early stages of psychosis (before hospitalization). Indeed, some patients with amphetamine addiction who are hospitalized with acute psychosis find insufficient reduction in TSH levels against the background of elevated T4 levels.

Treatment for thyrotoxicosis syndrome

Treatment of thyrotoxicosis depends on the causes that caused it.

toxic goiter

The methods of treatment of Graves' disease and various clinical variants of the functional autonomy of the thyroid gland differ. The main difference is that in the case of functional autonomy of the thyroid gland against the background of thyrostatic therapy, it is impossible to achieve a stable remission of thyrotoxicosis; after the abolition of thyreostatics, it naturally develops again. Thus, the treatment of functional autonomy consists in the surgical removal of the thyroid gland or its destruction with the help of radioactive iodine-131. This is due to the fact that thyrostatic therapy cannot achieve complete remission of thyrotoxicosis; after the drug is discontinued, all symptoms return. In the case of Graves' disease in certain groups of patients, stable remission is possible with conservative therapy.

Long-term (18-24 months) thyrostatic therapy, as the basic treatment for Graves' disease, can be planned only in patients with a slight enlargement of the thyroid gland, in the absence of clinically significant nodules in it. In the event of a relapse after one course of thyreostatic therapy, the appointment of a second course is futile.

Thyrostatic therapy

Thiamazole (Tyrozol®). An antithyroid drug that disrupts the synthesis of thyroid hormones by blocking peroxidase, which is involved in tyrosine iodination, reduces the internal secretion of T4. Thiamazole preparations are the most popular in our country and in European countries. Thiamazole reduces the basal metabolism, accelerates the excretion of iodides from the thyroid gland, increases the reciprocal activation of the synthesis and release of TSH by the pituitary gland, which is accompanied by some hyperplasia of the thyroid gland. It does not affect thyrotoxicosis, which has developed due to the release of hormones after the destruction of thyroid cells (with thyroiditis).

The duration of action of a single dose of Tyrozol® is almost 24 hours, so the entire daily dose is prescribed in one dose or divided into two or three single doses. Tyrozol® is presented in two dosages - 10 mg and 5 mg of thiamazole in one tablet. The dosage of Tyrozol® 10 mg allows to halve the number of tablets taken by the patient, and, accordingly, increase the level of patient compliance.

Propylthiouracil. It blocks thyroid peroxidase and inhibits the conversion of ionized iodine into its active form (elemental iodine). Violates the iodination of tyrosine residues of the thyroglobulin molecule with the formation of mono- and diiodothyrosine and, further, tri- and tetraiodothyronine (thyroxine). Extrathyroid action is to inhibit the peripheral transformation of tetraiodothyronine into triiodothyronine. Eliminates or weakens thyrotoxicosis. It has a goiter effect (an increase in the size of the thyroid gland), due to an increase in the secretion of thyroid-stimulating hormone from the pituitary gland in response to a decrease in the concentration of thyroid hormones in the blood. The average daily dosage of propylthiouracil is 300-600 mg/day. The drug is taken fractionally, every 8 hours. PTU accumulates in the thyroid gland. It has been shown that fractional intake of PTU is much more effective than a single intake of the entire daily dose. PTU has a shorter duration of action than thiamazole.

For long-term therapy of Graves' disease, the most commonly used scheme is "block and replace" (an antithyroid drug blocks the activity of the thyroid gland, levothyroxine prevents the development of hypothyroidism). It has no advantages over thiamazole monotherapy in terms of the frequency of relapses, but due to the use of large doses of thyrostatics, it allows more reliable maintenance of euthyroidism; in the case of monotherapy, the dose of the drug very often has to be changed in one direction or the other.

With moderate thyrotoxicosis, about 30 mg of thiamazole (Tyrozol®) is usually prescribed first. Against this background (after about 4 weeks), in most cases it is possible to achieve euthyroidism, as evidenced by the normalization of the level of free T4 in the blood (the level of TSH will remain low for a long time). Starting from this moment, the dose of thiamazole is gradually reduced to maintenance (10-15 mg) and levothyroxine (Eutirox®) is added to the treatment at a dose of 50-75 mcg per day. The patient receives this therapy under periodic monitoring of the level of TSH and free T4 for 18-24 months, after which it is canceled. In the event of a relapse after a course of thyrostatic therapy, the patient is shown a radical treatment: surgery or radioactive iodine therapy.

Beta blockers

Propranolol quickly improves the condition of patients by blocking beta-adrenergic receptors. Propranolol also slightly reduces the level of T3, inhibiting the peripheral conversion of T4 to T3. This effect of propranolol does not appear to be mediated by beta-adrenergic blockade. The usual dose of propranolol is 20-40 mg orally every 4-8 hours. The dose is adjusted to reduce resting heart rate to 70-90 min-1. As the symptoms of thyrotoxicosis disappear, the dose of propranolol is reduced, and when euthyroidism is reached, the drug is canceled.

Beta-blockers eliminate tachycardia, sweating, tremor and anxiety. Therefore, taking beta-blockers makes it difficult to diagnose thyrotoxicosis.

Other beta-blockers are no more effective than propranolol. Selective beta1-blockers (metoprolol) do not reduce T3 levels.

Beta-blockers are especially indicated for tachycardia, even against the background of heart failure, provided that tachycardia is due to thyrotoxicosis, and heart failure is due to tachycardia. A relative contraindication to the use of propranolol is chronic obstructive pulmonary disease.

iodides

A saturated solution of potassium iodide at a dose of 250 mg 2 times a day has a therapeutic effect in most patients, but after about 10 days the treatment usually becomes ineffective (the "escape" phenomenon). Potassium iodide is mainly used to prepare patients for operations on the thyroid gland, since iodine causes hardening of the gland and reduces its blood supply. Potassium iodide is very rarely used as the drug of choice in the long-term treatment of thyrotoxicosis.

Currently, more and more specialists around the world are inclined to believe that the goal of radical treatment of Graves' disease is persistent hypothyroidism, which is achieved by almost complete surgical removal of the thyroid gland (extremely subtotal resection) or by introducing sufficient doses of I131 for this, after which the patient is prescribed replacement therapy. levothyroxine. An extremely undesirable consequence of more economical resections of the thyroid gland are numerous cases of postoperative recurrences of thyrotoxicosis.

In this regard, it is important to understand that the pathogenesis of thyrotoxicosis in Graves' disease is predominantly associated not with a large volume of hyperfunctioning thyroid tissue (it may not be increased at all), but with the circulation of thyroid-stimulating antibodies that are produced by lymphocytes. Thus, when not the entire thyroid gland is removed during surgery for Graves' disease, a “target” for antibodies to the TSH receptor is left in the body, which, even after complete removal of the thyroid gland, can continue to circulate in the patient throughout life. The same applies to the treatment of Graves' disease with radioactive I131.

Along with this, modern preparations of levothyroxine make it possible to maintain a quality of life in patients with hypothyroidism, which differs little from that in healthy people. Thus, the preparation of levothyroxine Euthyrox® is presented in the six most necessary dosages: 25, 50, 75, 100, 125 and 150 mcg of levothyroxine. A wide range of dosages allows you to simplify the selection of the required dose of levothyroxine and avoid the need to crush the tablet to obtain the required dosage. Thus, a high dosing accuracy and, as a result, an optimal level of hypothyroidism compensation is achieved. Also, the absence of the need to crush tablets can improve patient compliance and their quality of life. This is confirmed not only by clinical practice, but also by the data of many studies that have specifically studied this issue.

Subject to the daily intake of a replacement dose of levothyroxine, there are practically no restrictions for the patient; women can plan pregnancy and give birth without fear of recurrence of thyrotoxicosis during pregnancy or (quite often) after childbirth. It is obvious that in the past, when approaches to the treatment of Graves' disease were actually developed, involving more economical resections of the thyroid gland, hypothyroidism was naturally considered as an unfavorable outcome of the operation, since therapy with animal thyroid extracts (thyroidin) could not provide adequate compensation for hypothyroidism.

Obvious benefits of radioactive iodine therapy include:

Security;

The cost is cheaper than with surgical treatment;

Does not require preparation with thyreostatics;

Hospitalization for only a few days (in the US, treatment is carried out on an outpatient basis);

If necessary, you can repeat;

There are no restrictions for elderly patients and in relation to the presence of any concomitant pathology.

The only contraindications: pregnancy and breastfeeding.

Treatment of thyrotoxic crisis. It begins with the introduction of thyreostatic drugs. The initial dose of thiamazole is 30-40 mg per os. If it is impossible to swallow the drug - the introduction through the probe. Effective is the intravenous drip of 1% Lugol's solution based on sodium iodide (100-150 drops in 1000 ml of 5% glucose solution), or 10-15 drops every 8 hours inside.

To combat adrenal insufficiency, glucocorticoid drugs are used. Hydrocortisone is administered intravenously at a dose of 50-100 mg 3-4 times a day in combination with large doses of ascorbic acid. It is recommended to prescribe beta-blockers in a large dose (10-30 mg 4 times a day orally) or intravenously 0.1% propranolol solution, starting with 1.0 ml under the control of pulse and blood pressure. They are being phased out gradually. Inside, reserpine is prescribed 0.1-0.25 mg 3-4 times a day. With severe microcirculatory disorders - Reopoliglyukin, Gemodez, Plasma. To combat dehydration, 1-2 liters of 5% glucose solution, physiological solutions are prescribed. Vitamins (C, B1, B2, B6) are added to the dropper.

Treatment of transient autoimmune thyroiditis in the thyrotoxic stage: the appointment of thyreostatics is not indicated, since there is no hyperfunction of the thyroid gland. With severe cardiovascular symptoms, beta-blockers are prescribed.

I131 is never used during pregnancy, as it crosses the placenta, accumulates in the thyroid gland of the fetus (starting from the 10th week of pregnancy) and causes cretinism in the child.

During pregnancy, propylthiouracil is considered the drug of choice, but thiamazole (Tyrozol®) can also be used at the lowest effective dose. Additional intake of levothyroxine (block and replace scheme) is not indicated, since this leads to an increase in the need for thyreostatics.

If a subtotal resection of the thyroid gland is necessary, then it is better to do it in the first or second trimester, since any surgical intervention in the third trimester can cause premature birth.

With proper treatment of thyrotoxicosis, pregnancy ends with the birth of a healthy child in 80-90% of cases. The frequency of preterm birth and spontaneous abortion is the same as in the absence of thyrotoxicosis. ЃЎ

Literature

Lavin N. Endocrinology. Publishing house "Practice", 1999.

Dedov I.I., Melnichenko G.A., Fadeev V.V. Endocrinology. M.: Publishing house "Geotar-media", 2007.

Dedov I. I., Gerasimov G. A., Sviridenko N. Yu., Melnichenko G. A., Fadeev V. V. Iodine deficiency diseases in Russia. A simple solution to a complex problem. M.: Publishing house "Adamant", 2002.

Ametov A.S., Konieva M.Yu., Lukyanova I.V. Cardiovascular system in thyrotoxicosis // Сonsilium Medicum. 2003, Vol. 05 No. 11.

Brovkina A.F., Pavlova T.L. Endocrine ophthalmopathy from the point of view of an ophthalmologist and endocrinologist // Supplement of the Russian Medical Journal "Clinical Ophthalmology" dated January 08, 2000, volume 1, No. 1.

Cattail W. M., Arki R. A. Pathophysiology of the endocrine system. Per. from English, ed. N. A. Smirnova. Moscow: Binom publisher, St. Petersburg: Nevsky dialect. 2001.

V. V. Smirnov,doctor of medical sciences, professor
N. V. Makazan

RSMU, Moscow

Thyrotoxicosis

Asked by: evgeniya

Female gender

Age: 53

Chronic diseases: Toxic diffuse goiter, menopause, depression

Hello! I am 53 years old, 6 years ago I was diagnosed with diffuse toxic goiter, thyrotoxicosis. All these years she drank tyrosol (5-ku), six months ago, the tests and ultrasound were normal, the pills were canceled. Now I have TSH 0.18 μIU / ml and an enlarged thyroid gland + two nodes of 5 mm each (maybe they appeared because I take femoston 1/5 from menopause?) T3 and T4 are normal. Is this possible? How necessary is the operation? Sincerely, Evgenia

20 responses

Don't forget to rate the doctors' answers, help us improve them by asking additional questions on the topic of this question.
Also do not forget to thank the doctors.

Hello Evgeniya.

Yes, this is quite possible, this situation is called "subclinical thyrotoxicosis". Strictly following the letter of the treatment protocol recommended to us by the Ministry of Health, with such a recurrence of thyrotoxicosis, we must immediately refer patients for surgical treatment or treatment with radioactive iodine. In practice, we are still trying to restart treatment with Tyrozole. You need to discuss this individually with your doctor. Additionally, I would recommend that you definitely check the level of antibodies to TSH receptors - they show the likelihood of a relapse of thyrotoxicosis in the future and determine the prognosis of the disease.

As for the nodules in the thyroid gland, I would like to see a complete description of the ultrasound first. Attach a photo of the ultrasound protocol to the message.

Evgeniya 2016-06-03 07:55

Nadezhda Sergeevna, thank you very much for your answer. I am now temporarily in Kyrgyzstan and, unfortunately, they do not take pictures on ultrasound, but only a description: the dimensions of the shields. The glands are enlarged, in the right lobe there are hypoechoic nodes 4 mm and 5 mm in size. A / t to TG 38 (norm 0-100). Here to me suggest most to be defined or determined between khir. Treatment and treatment of radioact. Iodine. What should be considered when choosing a treatment?

The choice of treatment tactics is always a task doctor and not the patient. Do you have the opportunity to consult with another specialist in person, to get an alternative opinion?
I say because personally I would start with the re-appointment of Tyrozol, especially given the normal titer of antibodies to TSH receptors.

If you choose between surgical treatment and radioactive iodine treatment, then I would be inclined in favor of radioactive iodine treatment - so there is no chance of damaging the parathyroid glands, the recurrent nerve and a number of other formations, since the intervention is less invasive.

Sincerely, Nadezhda Sergeevna.

Evgeniya 2016-06-07 07:12

Nadezhda Sergeevna, thank you for the detailed consultations. I had the experience of an unsuccessful operation on the stomach, or rather its consequences, so I was very happy about the opportunity to be treated with pills. Can I start taking Tyrozol on my own (I was in the clinic, the doctor was on vacation) according to the usual scheme - 1 week. -6 tablets, 2 weeks -5, etc., or is 5 Tyrozol enough?
With respect and great gratitude, Evgenia.

Evgenia, unfortunately, there is no "usual" scheme for the drug treatment of thyrotoxicosis; Tyrosol is selected in each case individually.
You definitely need to consult an endocrinologist in person on this matter. Do you have the opportunity to visit another doctor? When does your doctor return from vacation?
Sincerely, Nadezhda Sergeevna.

Hello, Nadezhda Sergeevna! Thank you for your attention. The doctor will be only in July, there is no other. And she still did not offer to be treated with pills. I have a resting heart rate of 90 and I can hardly endure the heat, so I still wanted not to delay the treatment. Based on the available tests and ultrasound, can an appointment be made? While I accept atenolol 5-ku. Sincerely, Evgenia.

To treat thyrotoxicosis without seeing the patient is, frankly, not a good idea. But let's try to come up with something so as not to lose a whole month of treatment before your doctor leaves his vacation.

To get started write to me clearly the results of the latest analyzes for TSH, T3 and T4 with the dates of delivery, units of measurement and norms in your laboratory.

Above you wrote A / t to TG 38 (norm 0-100)."It's still antibodies to thyroglobulin or antibodies to TSH receptors? This is an extremely important point.

I also need to see a fresh clinical blood test (I am interested in leukocytes and hemoglobin) and a biochemical blood test (I am interested in liver and kidney tests).

Are you currently taking any medications other than Atenolol? I truly understand that you canceled Tirozol six months ago?

Sincerely, Nadezhda Sergeevna.

Evgeniya 2016-06-10 12:36

Nadezhda Sergeevna, hello! Yesterday I completed the necessary tests, they are within the normal range. On hormones handed over on May, 30th. TSH 0.18 μMEml (0.30-3.60), T4 free. -1.37 (0.65-1.74), T3-1.41 (0.68-1.89), Ab to TG (antibodies to thyroglobulin) 36.54 (0-100). tyrosol stopped taking since November 2015.
I drink from menopause for half a tab. Femoston 1/5. I now have symptoms of depression, a very serious condition in the morning (for 7 years I took Amitriptyline 1 tablet several times for 1-2 months) now I am trying to do without drugs. I sleep very badly, sleep is not strong and sometimes. Hours of everything, but at the same time I do not want to sleep during the day. With respect and hope for your help, Evgenia.

Good night, Evgeniya.
It's great that you passed the necessary examination so quickly. In this case, the action plan is as follows:

1. You start taking Tyrozol (as an option - Mercazolil, Espa-carb) at a dosage of 5 mg in the morning.
2. Coming soon for a blood test antibodies to TSH receptors(not to be confused with AT-TG, antibodies to thyroglobulin). Send me the results right away.
3. After 10-14 days, re-monitor the level of leukocytes in the blood (mandatory; now it is approaching the lower limit of the norm, while taking the drug, the situation may worsen).
4. After 1-1.5 months, re-check the blood test for TSH and free T4.

Additionally:

1. Continue taking Femoston 1/5.
2. Continue taking Atenolol at a dosage of 5 mg or replace it with Concor at a similar dosage.
3. To improve mood and alleviate other associated symptoms, try taking Fluxen at a dosage of 20 mg 1 time per day, in the morning. The drug is taken regardless of the meal.
4. Be sure to consult a general practitioner about the level of hemoglobin and red blood cells, as well as the level of bilirubin.

Sincerely, Nadezhda Sergeevna.

Today I passed the tests, the ttg is the same 0.18 (0.30-3.6), t4sv. -2.36 (0.65-1.74). Doctor in the lab. He said that such a slight change could not worsen his well-being. And I don't know what else you can think of me terribly bad. Do I need to increase the dose of tyrosol? Sorry for disturbing you so often

Evgenia 2016-06-14 13:28

Nadezhda Sergeevna! Sorry for not answering right away. My health has deteriorated sharply: my blood pressure is 160/100, sweating does not stop, I feel like at a high temperature, my body is constantly sticky, I am so weak that I cannot go to work these days. Abruptly "left" the stomach.

Let's just say that the doctor in the laboratory should fulfill his functional duties - to perform laboratory research, and not to give advice on treatment.
An increase in the level of free T4 just could lead to a deterioration in your condition, especially considering that earlier the result of this analysis was normal.

Evgenia, this is a question for you - did you take the tests both times in the same laboratory? Is there any reason to doubt the quality of the research?
Thyrozol 5mg You've already started taking it, right?

Sincerely, Nadezhda Sergeevna.

Yes, Nadezhda Sergeevna, I have been taking tests in the same laboratory for all 6 years. There was an opportunity to double-check in Russia, the results coincided. Tyrozol before delivery of analyzes last time accepted only 2 days. THANK YOU SO MUCH FOR YOU DON'T LEAVE A SINGLE APPLICATION WITHOUT ANSWER

You are always welcome, Evgenia, the main thing is that the result is good.
In this case, I will slightly change the above recommendations:

1. Increase the dosage of Thyrozol to 10 mg in the morning + 5 mg in the afternoon + 5 mg in the evening. Then decrease by 2.5 mg (half a 5 mg tablet) every 7 days. At the same time, start reducing the morning dosage (up to 5 mg), then remove the tablet at lunchtime.
2. TSH and T4 free will need to be rechecked after 4 weeks.
3. Show yourself in person to at least a general practitioner. The presence of thyrotoxicosis does not negate the fact that any concomitant disease could develop, it is better to play it safe. Moreover, you still need to consult a general practitioner about blood tests.

All other recommendations are unchanged.