Thyrotoxicosis is a condition caused by excess production of thyroid hormones. It can manifest itself in various forms and degrees, the most common form is diffuse toxic goiter, on the example of which the principles of therapy of a thyrotoxic state can be considered.

The principles of treatment and its schemes are described in detail in various sources of information, including articles, abstracts, books. Now doctors use three approaches to compiling a course of therapy for thyrotoxic syndrome in women and men. Treatment of thyrotoxicosis is according to the following approaches:

• conservative treatment of thyrotoxicosis;
• surgical intervention;
• radioiodine therapy (treatment of a thyrotoxic state with radioactive iodine).

The therapy of hyperthyroidism should be considered on the example of an autoimmune diffuse toxic goiter. When this pathology is detected, conservative methods of treatment with thyreostatics are prescribed to reduce the degree of increase in T3 and T4. It is important to choose the correct dosage so as not to provoke hypothyroidism.In some cases, thyrotoxicosis is treated with surgery.

Autoimmune diffuse toxic goiter is considered a completely curable pathology. As means of pathogenetic treatment of autoimmune diffuse toxic goiter, preparations-derivatives of thiourea are used. These include mercaptoimidazole and propiothiouracil.

Conservative treatment regimen

In the absence of indications for surgery, the duration of the course of therapy with tyrosol, propicil and levothyroxine is from one to one and a half years.

Side effects of therapy for a thyrotoxic state are expressed in inhibition of hematopoiesis until the development of leukopenia up to agranulocytosis. Symptoms of this condition may be sore throat, diarrhea, fever. Allergic skin symptoms and nausea are a complication of treatment. It is important to correctly calculate the dosage so that the therapy does not lead to hypothyroidism.

To correct symptoms, beta-blockers are used, which are necessary to normalize the pulse. They are also able to eliminate sweating, tremors, and reduce the level of anxiety.

As monitoring measures for conservative treatment, the following rules apply:

1. It is necessary to control the concentration of T4 and T3 once a month.
2. Once every three months, the concentration of thyroid-stimulating hormone is measured.
3. An ultrasound examination of the thyroid gland is performed every six months.
4. Control of the level of platelets and leukocytes in the blood - weekly in the first month, then once a month.

In the treatment of hyperthyroidism, mistakes can be made:

• discontinuity in the course of treatment;
• inadequacy of control measures;
• repetition of a long course of thyrostatic treatment after the end of the first course in case of recurrence of the thyrotoxic state.

So far, there are no ideal schemes for the therapeutic correction of hyperthyroidism. Treatment of thyrotoxicosis is quite complicated. It is necessary to establish monitoring, a combination of inpatient and home treatment, approval of minimum doses, prevention of hypothyroidism during correction

Indications for surgery

According to data presented in various sources, such as abstracts, books and articles, there are the following indications for surgery:

1. Formation of nodules against the background of toxic goiter.
2. An increase in the volume of the gland exceeding 45 ml.
3. Compression of surrounding tissues and organs.
4. Retrosternal localization of goiter.
5. Recurrent course of diffuse toxic goiter after a course of treatment.
6. Intolerance to thyrotoxic drugs.
7. Agranulocytosis.

For the operation to be possible, it is necessary to achieve the euthyroid state (T3 and T4 are normal) with the help of thyreostatics. Subtotal removal of the thyroid gland is then performed.

Radioiodine therapy

Radioactive iodine therapy is comparatively safe and highly effective. But in most cases, after treatment with radioactive iodine, hypothyroidism develops, which needs to be corrected.

Therapy of thyrotoxicosis with radioactive iodine is characterized by a direction of action. The method of iodine therapy acts on the tissue of the thyroid gland in a targeted manner. Treatment with radioactive iodine can stop hyperthyroidism. But hypothyroidism becomes a fairly common complication of this technique.

After radioiodine therapy, measures are taken to correct possible hypothyroidism.

Toxic adenoma

Toxic adenoma is the second most common cause of a thyrotoxic condition. It is characterized by symptoms of diffuse toxic goiter in combination with manifestations of damage to the heart and blood vessels, as well as myopathy. In this case, endocrine ophthalmopathy (eye symptoms) is not observed. Treatment in this case is carried out by surgery or radioiodine therapy.

Subclinical thyrotoxicosis

Treatment of subclinical thyrotoxicosis with hormones is not carried out if it does not cause a deterioration in the patient's condition and vivid symptoms of pathology - increased heart rate, ophthalmopathy, fever. Subclinical thyrotoxicosis is not treated in pregnant women, after childbirth. Also, subclinical thyrotoxicosis does not need treatment if it has an autoimmune nature. In case of subacute thyroiditis, hormonal status correction is also not needed. Subclinical thyrotoxicosis, which is also called overt thyrotoxicosis, is mild and may not provoke symptoms. Therapy by any methods, including folk remedies, is not carried out, especially during pregnancy and after childbirth

Thyroiditis

Thyroiditis can be caused by various reasons: autoimmune damage, a viral attack, or a woman's health condition after childbirth. If the thyrotoxic phase of thyroiditis of an autoimmune nature or after childbirth develops, then beta-blocker therapy is performed to eliminate the symptoms. In this case, thyrostatics are not used - after childbirth, they are contraindicated. With thyroiditis of a viral nature, prednisolone therapy is performed according to the scheme. Treatment with folk remedies is prohibited, especially during pregnancy and after childbirth.

Iatrogenic thyrotoxicosis

If some drugs, such as amiodarone (cordarone), enter the human body, then their incorrect intake can provoke a thyrotoxic state. Amiodarone (cordarone) is a drug that contains a lot of iodine. An excess of amiodarone (cordarone) intake provokes the following pathologies:

• amiodarone-induced thyrotoxicity type 1 (caused by an excess of iodine in cordarone);
• amiodarone-induced thyrotoxic condition type 2 (caused by the toxic effect of cordarone on thyroid cells).

If the patient is prescribed amiodarone (cordarone), then the thyroid condition must be diagnosed every six months, even if amiodarone (cordarone) is canceled. To determine the type of pathology caused by an excess of amiodarone (cordarone) intake, diagnostics is carried out by scintigraphy. It is important to choose the right means to replace amiodarone (cordarone).

The iatrogenic form of pathology can be provoked by other reasons, for example, such a biologically active food supplement as Endonorm, which has a thyroid-stimulating effect. An excess of Endonorm can cause an increase in hormone levels, that is, thyrotoxicosis.

Treatment of other forms of thyrotoxicosis

If the condition is caused by an excess of iodine in the body (iodine-induced hyperthyroidism), then the intake of drugs containing this trace element is stopped. The operation is necessary for the nodular form of goiter, in the case of toxic adenoma and thyrotropinoma.

If a highly differentiated cancer is detected, preoperative preparation is performed - the achievement of a euthyroid state with the help of thyreostatics. Next, an operation is performed and radiation therapy is prescribed.

If autosomal dominant non-immunogenic thyrotoxicosis is detected, extirpation of the thyroid gland is prescribed, then replacement therapy with levothyroxine is required.

Treatment of a thyrotoxic condition with folk remedies is not recommended. This can provoke a worsening of the condition, especially if conservative therapy is neglected. Treatment with folk remedies can be carried out extremely rarely and only after consulting a doctor.

An important factor is nutrition for thyrotoxicosis. You should consult your doctor about changing your diet. Diet for thyrotoxicosis is important for all patients, it can reduce the severity of symptoms. If thyrotoxicosis manifests itself in children, then both the nutrition and the main therapy regimens are adjusted - the dosages and the range of indications for surgery differ from those in adults. However, the diet for thyrotoxicosis in adults and children has similar principles. During therapy, it is worth adhering to the prescribed dosages so as not to provoke hypothyroidism.

Care should be taken when correcting hyperthyroidism after childbirth. Drug therapy for increasing hormone levels after childbirth should be minimal.

You should not treat a thyrotoxic condition with folk remedies, especially without recommendations. Treatment of thyrotoxicosis with folk remedies can lead to a worsening of the condition and an increase in symptoms, especially in childhood, during pregnancy and after childbirth. All methods of treatment, including radioactive iodine therapy, should be started only after a detailed consultation with a doctor, diagnosis and determination of a therapeutic course. Treatment of thyrotoxicosis is complex, so you need to strictly adhere to the recommendations.

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

1. destroy excess thyroid hormones medicines

2. destroy the thyroid itself so that it does not produce excess hormones (surgery and radioactive iodine therapy)

3. restore thyroid function

Drug therapy in the "treatment" of hyperthyroidism

Thyroid medications destroy thyroid hormones. Long-term drug treatment - up to 3 years. Treatment begins with large doses of these drugs, as soon as free T4 is normalized, the dose of thyreostatic is gradually reduced to a maintenance dose (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 hormones of their own. The principle of this treatment is: block and replace! And therapy is called hormone replacement therapy (HRT).

Medication "treatment" has many side effects:

• goitrogenic 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;
• dysfunction of the liver (increase in ALT, AST);
• diarrhea, headache, menstrual irregularities, etc.
After discontinuation of thyrostatic drugs, the frequency of recurrence 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, exclude any possibility of recurrence of hyperthyroidism - the recurrence rate is 0%. But at what cost!

  Removal of the thyroid gland any in a way leads to dangerous disability. Autoimmune processes in the body do not disappear anywhere and are now controlled costly life HRT. In addition to disruption of the human digestive, cardiovascular, nervous and reproductive systems, you get life-long hypothyroidism and other chronic diseases. On the danger and therapeutic futility surgery or irradiation radioactive iodine more details can be found at the indicated links.

  Safe treatment hyperthyroidism without hormones and surgeries by the 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.

  Reboot the three main regulatory systems of the body to the state active struggle with harmful external influences of the environment, internal diseases, is the main task of therapy focused on the effect on the body through the autonomic nervous system.

  There are many methods of influencing the nervous system, but, today, only computer reflex therapy acts through the nervous system so that in 93% cases in patients, the neuro-immuno-endocrine regulation of the body is fully 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 acts on the patient's body not "blindly", but, thanks to special sensors and a computer system, sees in what points nervous system and how requires action with a medical device.

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

  FULL NAME - Faizullina Irina Igorevna

  Laboratory research BEFORE treatment M20161216-0003 from 16.12.2016 ()

  Thyroid stimulating hormone (TSH) - 8,22 μIU / ml

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

  Thyroid stimulating hormone (TSH) - 2,05 μIU / ml

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

  

  

  Before each procedure, the doctor diagnoses the patient, based on the results of which he draws up an individual recipe for 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 absent when using any other methods.

  Of course, this method of treatment, like any other, has restrictions and contraindications- this is oncological diseases and mental disorders, disorders of the heart (presence pacemaker, atrial arrhythmia and myacardial 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 has been a common practice in our clinic for many years.

  For a good 20 years, the Gavrilova Clinic in the city of Samara has been carrying out thyroid reconstructive lesions without hormones and surgeries. The author and developer of the method is Natalia Alekseevna Gavrilova. Associate Professor, Ph.D. with general medical experience since 1968, awarded the Order of Medical Merit. If you wish, you can familiarize yourself with bioelectrophysical the basics of the therapeutic effects of reflex therapy and specific examples of treatment.

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

  Hyperthyroidism treatmentby the method of computer reflex therapy without side effects leads to the following results:

  • Are being restored functioning tissue and structure of the thyroid gland;
  • The level of your own thyroid hormones T4 (thyroxine) and T3 (triiodine-thyronine), as well as the level of TSH (pituitary hormone), is normalized, 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;
  • Have getting better aboutgeneral state of health 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.

Standard approaches to the treatment of thyrotoxicosis and hypothyroidism syndromes

G.A. Melnichenko, S.V. Lesnikova

Department of Endocrinology (Head - Academician of the Russian Academy of Medical Sciences II Dedov) MMA named after THEM. Sechenov

Url

Thyrotoxicosis syndrome

Thyrotoxicosis syndrome- a clinical syndrome caused by an excess of thyroid hormones.
Thyrotoxicosis syndrome is:
I. due to increased production of thyroid hormones by the thyroid gland:
TSH-independent

• diffuse toxic goiter (DTZ) - Graves' disease - Basedow
• thyrotoxic adenoma
• many (nodular) toxic goiter
• iodine-induced thyrotoxicosis- (iodine-Basedow)
• highly differentiated thyroid cancer
• gestational thyrotoxicosis
• chorionic carcinoma, cystic drift
• autosomal dominant non-immunogenic thyrotoxicosis

TSH-dependent

• thyrotropinoma
• syndrome of inappropriate TSH secretion (resistance of thyrotrophs to thyroid hormones)

II. not associated with increased production of thyroid hormones:

• thyrotoxic phase of autoimmune (AIT), subacute viral and postpartum thyroiditis
• artifactual
• amiodarone-induced
• iatrogenic

III. caused by the production of thyroid hormones outside the thyroid gland.

• struma ovarii
• functionally active thyroid metastases

In connection with the most frequent occurrence of thyrotoxicosis (90% of all cases of thyrotoxicosis) among all nosoforms, the diagnosis and treatment of thyrotoxicosis syndrome will be considered using the example of this disease, specifying the characteristics of the course and therapy of the rest. DTG is a hereditary organ-specific autoimmune disease (the pathogenesis is based on the production of specific thyroid-stimulating antibodies), characterized by prolonged excessive production of thyroid hormones by the thyroid gland, clinically manifested by thyrotoxicosis syndrome and combined in at least 50% of patients with ophthalmic infarction.
Clinical criteria

• increased excitability, general weakness, fatigue, tearfulness;
• shortness of breath with little physical exertion;
• tremors of the body and limbs, increased sweating;
• weight loss against the background of increased appetite (but there may also be a fat-Basedov variant, i.e. a variant of the disease with an increase in body weight);
• subfebrile condition;
• fragility and hair loss;
• hyperdefecation;
• cardiac arrhythmias: constant sinus tachycardia, paroxysms and constant atrial fibrillation, paroxysms against the background of normal sinus rhythm;
• there is an increase in systolic with a decrease in diastolic pressure;
• on examination - eye symptoms of thyrotoxicosis associated with a violation of the autonomic innervation of the oculomotor muscles. Endocrine infiltrative ophthalmopathy occurs in at least 50% of cases;
• on palpation: diffuse enlargement of the thyroid gland (which is not an obligatory criterion - there may be a normal size of the gland); "buzzing" (due to abundant vascularization of the gland).

To assess the size of the thyroid gland, the WHO 1994 classification is recommended. This international classification is simplified, available to doctors of all specialties and allows comparison of data from different countries.

Grade 0 - no goiter.
Grade 1 - the goiter is not visible, but palpable, while the size of its lobes is larger than the distal phalanx of the subject's thumb.
Grade 2 - the goiter is palpable and visible to the eye.

• damage to other organs of internal secretion:

1. development of thyrogenic adrenal insufficiency;
2. ovarian dysfunction with menstrual dysfunction up to amenorrhea, miscarriage;
3. fibrocystic breast disease in women, gynecomastia in men;
4. violation of tolerance to carbohydrates, the development of diabetes mellitus;

with DTZ often occur associated immunopathies , the most studied are endocrine infiltrative ophthalmopathy, pretibial myxedema, which will be described below.

Long-term results (5 years or more) of Graves-Basedow disease treatment :

Outcomes of conservative thyreostatic therapy with thiamazole ( n = 80)	Thyroid function	Outcomes of surgical treatment ( n = 52)
34.69% (n = 34)	Euthyroidism	28.85% (n = 16)
2.04% (n = 2)	Hypothyroidism	34.54% (n = 18)
63.27% (n = 62)	Relapse	34.62% (n = 19)

Laboratory and instrumental diagnostics as a first-order study includes:

• hormonal blood test: decrease in TSH, determined by a highly sensitive method (with TSH-dependent thyrotoxicosis, TSH is increased); increased levels of T3, T4 (during pregnancy, only free fractions of T4, T3 are studied). Determination of TSH and free T4 levels is usually sufficient;
• Ultrasound of the thyroid gland with determination of the volume and position of the gland (normal, partially retrosternal); there is an increase in the thyroid gland, a decrease in the echogenicity of the parenchyma.

With ultrasound in accordance with international standards in adults (over 18 years old), a goiter is diagnosed when the volume of the thyroid gland in women is more than 18 ml, in men more than 25 ml with the lower limit of the norm of 9 ml;
In rare cases, the following studies are carried out as a differential diagnosis:

• determination of the level of antibodies to thyroid tissue:
  a) "classic" - there is an increase in antibodies to thyroglobulin (TG) and thyroid peroxidase (TPO) (with AIT, DTZ);
  b) "non-classical" - there is an increase in antibodies to the TSH receptor - thyroid-stimulating (with DTZ) and blocking the binding of TSH (with AIT);
• scintigraphy of the thyroid gland (with the retrosternal position of the gland, (many) nodular toxic goiter to determine the existence of functional autonomy, or the presence of multiple nodes accumulating RP, or the presence of "cold" nodes against the background of increased functioning around the tissue located).

Treatment principles
Currently, there are three main approaches to the treatment of thyrotoxicosis syndrome (for example, DTZ):
1. conservative therapy;
2. Surgical treatment (subtotal resection of the thyroid gland);
3. radiological method - therapy with radioactive iodine - (131I).
With the newly diagnosed DTZ in Russia, the tactics of long-term conservative therapy with thyreostatics is chosen; in the presence of certain indications, which will be described below, surgical treatment is recommended. Recently, more attention has been paid to radiological treatment.
It should be noted that thyrotoxicosis is absolutely curable due to thyrotoxicosis syndrome. The means of pathogenetic therapy in this case are thiourea derivatives, which include mercaptoimidazole and propylthiouracil.
Conservative therapy scheme

• The initial dose of thiamazole is 20-40 mg / day, propicil 200-400 mg / day until euthyroidism is achieved (on average, this stage takes 3-8 weeks).
• Gradually reduce the dose of thiamazole by 5 mg (propicil 50 mg) over 5-7 days to a maintenance dose of 5-10 mg of thiamazole (propicil 50-100 mg).
• At the stage of euthyroidism - the addition of 50-100 μg levothyroxine to the therapy (the "block and replace" scheme) to prevent the development of drug hypothyroidism and the strumogenic effect of thyreostatics.
• The duration of treatment is 12-18 months (if there are no indications for surgical treatment and thyreostatics are not used as a preoperative preparation).

Among the side effects, special attention should be paid to the state of bone marrow hematopoiesis due to the possibility of developing leukopenic reactions up to agranulocytosis (in 1% of cases), the symptoms of which are the appearance of fever, sore throat, diarrhea. 1-5% have allergic reactions in the form of a skin rash accompanied by itching, nausea.
As symptomatic therapy, it is prescribed b - adrenergic blockers until the heart rate is normalized, after which the dose is gradually reduced until it is canceled. Besides, b -blockers eliminate tremors, sweating, anxiety.
Patient monitoring in the course of treatment should be carried out as follows:

• control of the T4 level once a month;
• control of TSH, determined by a highly sensitive method, once every 3 months;
• Ultrasound of the thyroid gland to assess the dynamics of the volume of the gland once every 6 months;
• determination of leukocytes and platelets in the blood:

• 1 time per week in the 1st month of thyreostatic therapy;
• Once a month when switching to maintenance doses.

Typical errors encountered in the treatment of thyrotoxicosis are:
a) intermittent courses;
b) inadequate control of treatment;
c) reappointment of long-term thyrostatic therapy in case of recurrence of thyrotoxicosis after a full course of 12-18 months.
Currently, the problems of the lack of "ideal" and etiotropic treatment, standard monitoring recommendations, continuity of inpatient and outpatient treatment, and minimum effective maintenance doses remain unresolved.
The question of the need surgical treatment for thyroid disease occurs in the following situations:
1.the emergence or detection of nodes against the background of DTZ;

2. large volume of the gland (more than 45 ml);
3. objective signs of compression of the surrounding organs;
4. retrosternal goiter;
5. relapse of DTG after a full course of thyreostatic therapy;
6. intolerance to thyreostatics, the development of agranulocytosis.
Surgical treatment is carried out upon reaching euthyroidism with thyreostatics; subtotal resection of the thyroid gland is often used.
Currently, the indications and age range for therapy are expanding. radioactive iodine given the comparative safety and effectiveness of this method. According to D. Glinoer, 1987 and B. Solomon, 1990 (questionnaire of the European Thyroid Association), with newly diagnosed uncomplicated Graves-Basedow disease in a 40-year-old woman with children and not planning a pregnancy, in Europe and Japan was the tactics of the initial prescription of 131I therapy would be chosen in 20%, in the USA - in 70% of similar cases. In Russia, less than 1% of patients would receive 131I treatment.
With radioiodine therapy, the incidence of hypothyroidism reaches about 80%, relapse is observed in less than 5% of cases.
Among associated immunopathies the most studied and common are endocrine infiltrative ophthalmopathy and pretibial myxedema.
At endocrine infiltrative ophthalmopathy (EOP) damage to the periorbital tissues of autoimmune genesis occurs, manifested clinically by disorders of the oculomotor muscles, trophic disorders and often exophthalmos. The diagnostic criteria are:
-clinically: lacrimation, feeling of "sand", dryness and soreness in the eyes, double vision when looking up, to the sides, limitation of the mobility of the eyeballs, changes in the cornea, exophthalmos, often secondary glaucoma;
- instrumental: protrusion, signs of thickening of retrobulbar muscles according to ultrasound, CT, MR of the orbits.
Treatment endocrine ophthalmopathy presents significant difficulties. Correction of thyroid status is a necessary factor. In the presence of double vision when looking up and to the sides, thickening of the retrobulbar muscles and tissues of the orbit, glucocorticoids are prescribed, there are various therapy regimens. A promising treatment trend is the use of octreotide, a human immunoglobulin, treatment regimens for which are currently being developed. With pronounced symptoms of ophthalmopathy, the absence of the effect of steroid therapy and the presence of fibrosis of the tissues of the orbit with the threat of loss of vision, surgical correction is performed. In addition, it is necessary to remember about such an important provoking factor in the progression of EOP, such as smoking.
Pretibial myxedema occurs in 1-4% of patients with DTZ. The skin of the anterior surface of the lower leg thickens, becomes edematous, hyperemic, disorders are accompanied by itching. For treatment, dressings with dimethyl sulfoxide are used in combination with steroid therapy, also against the background of correction of the thyroid status.
Second in frequency the cause of thyrotoxicosis is a toxic adenoma thyroid gland. The presence of similar DTG clinical symptoms with more pronounced symptoms of damage to the cardiovascular system and myopathy is noted, endocrine ophthalmopathy is absent. On palpation, with ultrasound, a nodular formation is determined (with ultrasound - with a pronounced capsule and usually increased echogenicity). In scintigraphy, it is a "hot" nodule with increased accumulation of radiopharmaceutical (RP) and a decrease in accumulation in the surrounding tissue. Treatment is surgery or radioiodine therapy.
In the case of the development of the thyrotoxic phase of the autoimmune and postpartum thyroiditis possible symptomatic therapy b -blockers, thyreostatics are not used.
With subacute viral thyroiditis, more often after a viral infection, there are complaints of severe pain in the anterior surface of the neck, mainly one-sided, radiating to the ear, an increase in body temperature up to 390C. Treatment with prednisolone is carried out according to the scheme.
With iodine-induced thyrotoxicosis, it is recommended to stop taking iodine-containing drugs.
Surgical treatment is carried out with multinodular toxic goiter, toxic adenoma, thyrotropinoma.
If highly differentiated forms of thyroid cancer are detected, preoperative preparation with thyreostatics is performed until euthyroidism is achieved, followed by surgical treatment more often in combination with radiation therapy in an oncological hospital.
With autosomal dominant non-immunogenic thyrotoxicosis, extirpation of the thyroid gland is required, followed by replacement therapy with levothyroxine.
With the syndrome of inadequate TSH production, a number of authors suggested using TRIAK for treatment, however, there is no consensus on this issue yet, and in our country there is no experience of using the drug.

Hypothyroidism syndrome

Hypothyroidism syndrome- a clinical syndrome caused by a long-term, persistent lack of thyroid hormones in the body or a decrease in their biological effect at the tissue level. The prevalence of overt primary hypothyroidism in the population is 0.2-1%, subclinical primary hypothyroidism is 7-10% among women and 2-3% among men.
According to the lesion level, hypothyroidism is :

• primary thyrogenic
• secondary pituitary
• tertiary hypothalamic
• tissue transport peripheral

According to the severity, there are:

1. Subclinical (latent)

2. Manifest

• compensated
• decompensated

3. Severe course (complicated) - with the development of heart failure, cretinism, effusion in serous cavities, secondary pituitary adenoma.
Most common primary hypothyroidism, the reasons for which are:
congenital forms

• anomalies of the thyroid gland (dysgenesis, ectopia)
• congenital enzymopathies, accompanied by impaired biosynthesis of thyroid hormones

acquired forms

• autoimmune thyroiditis (AIT), including in the framework of the autoimmune polyglandular syndrome, more often type II (Schmidt's syndrome), less often type I.
• thyroid surgery
• thyreostatic therapy (radioactive iodine, thyreostatics, lithium preparations)
• subacute viral, postpartum
• thyroiditis (hypothyroid phase)
• endemic goiter

The reasons secondary hypothyroidism are:

• congenital and acquired panhypopituitarism (Sheien-Simmonds syndrome, large pituitary tumors, adenomectomy, irradiation of the pituitary gland, lymphocytic hypophysitis)
• isolated TSH deficiency
• in the framework of congenital panhypopituitarism syndromes

Tertiary hypothyroidism:

• violation of the synthesis and secretion of thyroliberin

Peripheral hypothyroidism:

• thyroid resistance syndromes
• hypothyroidism with nephrotic syndrome

Clinical criteria

The early symptoms of hypothyroidism are not very specific, therefore, the initial stages of the disease, as a rule, are not recognized and patients are unsuccessfully treated by various specialists.
Patients complain of a feeling of chilliness, an unmotivated increase in body weight against a background of decreased appetite, lethargy, depression, daytime sleepiness, dry skin, yellowness of the skin caused by hypercarotinemia, edema, hypothermia, a tendency to bradycardia, constipation, progressive memory loss, hair loss on head, eyebrows.
In women, menstrual dysfunction is noted - from menometrorrhagia to amenorrhea; in connection with the hyperproduction of thyrotropin-releasing hormone by the hypothalamus against the background of hypothyroxinemia, hyperprolactinemic hypogonadism may develop in primary hypothyroidism, which is manifested by amenorrhea, galactorrhea and secondary polycystic ovaries.
Laboratory diagnostics primary hypothyroidism includes:
Hormonal blood test - determination of the level of TSH. An elevated TSH level is a very sensitive marker of primary hypothyroidism, and therefore the TSH level is the most important diagnostic criterion for hypothyroidism:

• in the subclinical form - an increase in TSH (within 4.01< ТТГ < 10 mU/L) при нормальном уровне Т4 и отсутствии клинической симптоматики;
• with a manifest form - an increase in TSH, a decrease in T4;
• it should be borne in mind that an increase in the level of TSH can occur with uncompensated adrenal insufficiency, taking metoclopramide, sulpiride, which are dopamine antagonists; decrease in TSH-when taking dopamine.

Differential diagnosis

In the presence of AIT as the most common cause of primary hypothyroidism, characteristic markers can be determined:

• "classic" antibodies - to TG and TPO;
• "non-classical" antibodies to the TSH receptor - blocking TSH binding. But for the diagnosis of AIT, it is necessary to additionally conduct:
• Ultrasound of the thyroid gland (presence of linear hyperechoic (fibrous) layers, capsule compaction, heterogeneity of the echo structure with pronounced hypo- and hyperechoic inclusions);

• puncture biopsy (according to indications).

With secondary hypothyroidism, the TSH level is normal or low, T4 is low. When conducting a test with thyroliberin, the TSH level is examined initially and 30 minutes after intravenous administration of the drug. With the primary, TSH increases by more than 25 mMU / L, with the secondary, it remains at the same level.
Treatment principles
Regardless of the level of damage and the cause that caused the syndrome of hypothyroidism, replacement therapy with levothyroxine is prescribed (recently, combined drugs T3 and T4 have been used much less often).
Therapy principles:

• The initial dose is less, the older the patient is and the longer the duration of hypothyroidism. In the elderly and with severe concomitant pathology, they start from 6.25-12.5 μg with a gradual increase in the dose to a constant maintenance one. In young people, it is possible to prescribe a full replacement dose immediately.
• A constant maintenance dose is prescribed at the rate of 1.6 μg of the drug per 1 kg of body weight (75-100 μg for women, 100-150 μg for men);
• - with severe concomitant pathology in the manifest form - 0.9 μg / kg;
• - with severe obesity, the calculation is per 1 kg of "ideal" body weight.
• The dose increase in young patients occurs within 1 month, in the elderly, more slowly, in 2-3 months, in the presence of cardiac pathology - in 4-6 months.
• After the normalization of the TSH level (which occurs within several months), the TSH control is carried out 1 time in 6 months.
• In secondary hypothyroidism in combination with secondary hypocorticism, levothyroxine is prescribed only against the background of corticosteroid therapy. Evaluation of the adequacy of the treatment of secondary hypothyroidism is carried out only on the basis of the T4 level in dynamics.
• In the treatment of hypothyroid coma - an extremely formidable but, fortunately, rarely occurring complication at present - a combination of water-soluble preparations of thyroid hormones and glucocorticoids is used.

Pregnancy and thyrotoxicosis syndrome

The incidence of DTZ is 2 cases per 1000 pregnancies. When making a diagnosis, they are based on a decrease in the level of TSH, an increase in free fractions of T3, T4, and the determination of an increased level of "classical" and "non-classical" antibodies. DTZ increases the risk of early termination of pregnancy, stillbirth, premature birth, preeclampsia, and low birth weight. Due to the action of pregnancy as a factor of immunosuppression by the II-III trimester, remission of DTG is possible, which sometimes makes it possible to temporarily cancel thyrostatic therapy. Transition of thyroid-stimulating antibodies (TSH Ab) from mother to fetus is possible, which is prognostically unfavorable due to the possibility of the child developing craniostenosis, hydrocephalus, and severe neonatal thyrotoxicosis syndrome in the future. Fetal thyrotoxicosis can be suspected at more than 22 weeks of gestation, when the fetal heart rate exceeds 160 beats / min.
For the treatment of DTG during pregnancy, small doses of propylthiouracil (200 mg / day) are used. During pregnancy, only the "block" regimen is used (prescribing thyreostatics without connecting levothyroxine) and the goal of treatment is to achieve and maintain the level of svT4 at the upper limit of the norm.
Radioactive iodine therapy is contraindicated during pregnancy, and surgical treatment is indicated in exceptional cases when drug therapy is impossible, severe drug allergies, a very large goiter, in combination with a malignant process in the thyroid gland, or the need to use large doses of thionamides to support euthyroidism. The safest time for subtotal resection of the thyroid gland is the second trimester of pregnancy.
It is necessary to carry out differential diagnosis of DTG with gestational thyrotoxicosis. The concept of "gestational thyrotoxicosis (HTT)" was introduced by D. Glinoer, according to which HTT is observed in 2-3% of pregnant women and is associated with increased production of chorionic gonadotropin (CG), which is structurally similar to TSH and stimulates the thyroid gland. Clinically, this condition is accompanied by severe toxicosis of the first half of pregnancy (nausea, sometimes indomitable vomiting - hyperemesis gra v idarum). GTT develops more often in multiple pregnancies.
In a laboratory study during normal pregnancy in the early stages, there is a decrease in the level of TSH, sometimes below the standard values, with a normal level of free T4. For differential diagnosis with DTG in favor of GTT will be evidenced by a decrease in TSH levels in combination with an increase in free T4 in early pregnancy; hCG level more than 100,000 units / l; lack of thyroid-stimulating antibodies; no history of DTG, endocrine ophthalmopathy. GTT signs spontaneously regress within 2 months, treatment with thyreostatics is not required; the prognosis of pregnancy does not worsen and DTG does not develop in the postpartum period.
The level of hCG can also increase with choriocarcinoma and cystic drift. According to Poertl et al. (1998), out of 85 pregnant women, 28% have a decrease in TSH, and thyrotoxicosis occurs in only 1%, which can be explained either by an increased level of thyroxine-binding globulin, or by an increased excretion of iodine. At the same time, with a decrease in the level of TSH with cystic drift (47% of cases) and choriocarcinoma (67% of cases), thyrotoxicosis develops in 1/3 of cases.

Hypothyroidism and pregnancy

Pregnancy is unlikely if hypothyroidism is untreated.
At the same time, if pregnancy has begun and before the 6-8th week, the fetus receives at least a sufficient amount of triiodothyronine, then later the fetal thyroid gland already begins to function independently.
Of course, if there is an iodine deficiency and no correction is carried out, then there is a high probability of subsequent development of gross violations in the intellectual sphere of the unborn child.
In the United States, subclinical hypothyroidism (TSH within 4.01< ТТГ < 10,0 mU/l) регистрируется у 2% беременных. Это состояние встречается и в регионах с йоддефицитом, и в регионах с достаточным поступлением йода, где это, вероятно, связано с аутоиммунным процессом.
Serious complications of decompensated primary hypothyroidism are arterial hypertension in the mother, fetal malformations, premature birth, miscarriage.
Over the past 15 years, mass screening of newborns for neonatal hypothyroidism has been introduced, which includes the determination of plasma TSH (from the heel) not earlier than 4-5 days of life (in premature infants on the 7-14th day): the norm is considered to be the level of TSH below 20 μU / ml.
Hypothyroidism is treated with levothyroxine, the dose of which is calculated based on the increased need for the drug during pregnancy up to 1.9-2.3 μg / kg under the mandatory control of TSH once a month. In subclinical forms of hypothyroidism during pregnancy, levothyroxine is also prescribed.
In addition, in iodine-deficient regions, pregnant women are advised to prescribe iodine in the form of potassium iodide 200 mcg or as part of special multivitamin preparations, even in the presence of autoimmune thyroiditis, which does not lead to aggravation of AIT during pregnancy, but compensates for iodine deficiency in the fetus. It is extremely dangerous for pregnant women to use in one form or another any iodine preparations exceeding 500 mcg / day, since such doses, according to the Wolff-Chaikov effect, cause a blockade of the thyroid gland in the fetus.

Literature:
1. Hostalek U. Diseases of the thyroid gland and the possibility of their effective treatment. - Tyroid Russia. - Collection of lectures. M. 1997; 6-12.
2. Melnichenko G.A. Hypothyroidism Rus. honey. zhurn., 1999; 7, 7 (89 ).
3. Michaud P. Consensus proposal on the use of 131I in the treatment of thyrotoxicosis. Sociedad Chilena de Endocrinologia y Metabolismo, Hospital Dr Sotero del Rio, Santiago, Chile. Rev Med Chil. 1998 Jul; 126 (7): 855-65.
4. Glinoer D., Kinthaert J., Lemone M. Risk / benefit of thyroid hormone supplementation during pregnancy. Merck European Thyroid Symposium "The Thyroid and Tissues" - Strasburg. 1994; 194-8.
5. Kimura et al. Gestational thyrotoxicosis and hyperemesis gravidarum: possible role of hCG with higher stimulating activity. Japa Clin. Endocr. 1993; 38: 345-50.

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: influencing 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 front of the neck, covering the front and sides of the upper tracheal rings. Being a horseshoe shape, 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 (TG) and calcitonin. The morphofunctional unit of the thyroid gland is a follicle, the wall of which is formed by one layer of epithelial cells - thyrocytes, and the lumen contains their secretory product - a 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 the iodine atom from thyroxine. The part of iodine remaining after cleavage is again captured by the thyroid gland to participate in the synthesis of hormones.

Regulation of thyroid function is under the control of the hypothalamus, which produces thyrotropin-releasing factor (thyroliberin), under the influence of which the release of thyroid-stimulating hormone of the pituitary gland (TSH), which stimulates the production of the thyroid gland T3 and T4. 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 prenatal 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;

  By 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 can be a consequence of diseases manifested by hyperfunction of the thyroid gland or its destruction - in this case, thyrotoxicosis is caused by the passive entry of T4 and T3 into the blood. In addition, there may be causes independent of the thyroid gland - overdose of thyroid hormones, T4- and T3-secreting ovarian teratoma, metastases of thyroid cancer (Table 1).

Hyperfunction of the thyroid gland. The first place among diseases accompanied by increased education and secretion of thyroid hormones is occupied by diffuse toxic goiter and multinodular toxic goiter.

Diffuse toxic goiter (DTG) (Graves-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. Genetic predisposition is evidenced by the detection of circulating autoantibodies in 50% of DTG relatives, the frequent detection of the HLA DR3 haplotype in patients, and a frequent combination with other autoimmune diseases. 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 at a 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). Interacting with thyroid-stimulating hormone receptors on thyrocytes, thyroid-stimulating antibodies cause an increase in the synthesis of hormones T4 and T3, which leads to the appearance of a state of thyrotoxicosis.

Multinodular toxic goiter - develops with prolonged 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 and moderate iodine deficiency. Diffuse non-toxic goiter (DNZ) turns into nodular (multinodular) non-toxic goiter, then 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 that cause hypertrophy and hyperplasia of the follicular cells of the thyroid gland, which leads to the formation of a struma (DNZ stage). The basis for the development of nodes in the thyroid gland is the microheterogeneity of thyrocytes - various functional and proliferative activities of thyroid cells.

If iodine deficiency persists for many years, then stimulation of the thyroid gland, becoming chronic, causes hyperplasia and hypertrophy in thyrocytes, which have the most pronounced proliferative activity. This eventually leads to the emergence of focal accumulations of thyrocytes with the same high sensitivity to stimulating effects. Under the conditions of ongoing chronic hyperstimulation, active division of thyrocytes and a 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 autonomic thyrocytes leads to a decrease in the level of TSH and an increase in the content of T3 and T4 (the phase of clinically apparent thyrotoxicosis). Since the process of forming the functional autonomy of the thyroid gland is extended over 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, a severe form of the disease is rarely observed in pregnant women. Often, pregnancy occurs during or after drug treatment of thyrotoxicosis (since this treatment restores fertility). Contraceptives are recommended for young women with thyrotoxicosis receiving thionamides to avoid unwanted pregnancies.

Toxic adenoma of the thyroid gland (Plummer's disease) is a benign tumor of the thyroid gland that develops from the follicular apparatus and autonomously hyperproduces thyroid hormones. Toxic adenoma can occur in a pre-existing non-toxic nodule; therefore, nodular euthyroid goiter is considered a risk factor for the development of toxic adenoma. The pathogenesis of the disease is based on the autonomous hyperproduction of thyroid hormones by the adenoma, which is not regulated by thyroid-stimulating hormone. The adenoma secretes in large quantities mainly triiodothyronine, which leads to suppression of the production of thyroid-stimulating hormone. At the same time, the activity of the rest of the thyroid tissue surrounding the adenoma decreases.

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

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 TSH of the pituitary gland, characterized by a normal level of TSH, a significant increase in the levels of T4 and T3 and thyrotoxicosis (since the sensitivity of other target tissues to thyroid hormones violated). A pituitary tumor in such patients is not visualized.

Vesicular drift and choriocarcinoma secrete large amounts of chorionic gonadotropin (CG). Chorionic gonadotropin, similar in structure to TSH, causes a transient suppression of the thyrotropic activity of the adenohypophysis and an increase in the level of free T4. This hormone is a weak stimulant of TSH receptors on thyrocytes. When the concentration of HCG exceeds 300,000 U / L (which is several times higher than the maximum concentration of HCG in normal pregnancy), thyrotoxicosis may occur. Removal of the cystic mole or chemotherapy of choriocarcinoma eliminates thyrotoxicosis. The level of hCG can significantly increase with toxicosis of pregnant women and cause thyrotoxicosis.

Destruction of the thyroid gland

The destruction of thyrocytes, in which the flow of thyroid hormones into the blood occurs and, as a consequence, 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 options, phase changes occur in the thyroid gland associated with autoimmune aggression: in the most typical course, the phase of destructive thyrotoxicosis is replaced by the phase of transient hypothyroidism, after which, in most cases, the function of the thyroid gland is restored.

Postpartum thyroiditis occurs on 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 postpartum, but only the provoking factor is unknown, proceeds outside of connection with pregnancy. Cytokine-induced thyroiditis develops after prescribing interferon preparations for various diseases.

The development of thyrotoxicosis is possible not only with autoimmune inflammation in the thyroid gland, but also with infectious damage to it, when subacute granulomatous thyroiditis develops. Subacute granulomatous thyroiditis is thought to be caused by a viral infection. It is believed that the causative agents may be Coxsackie virus, 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 (lasts several weeks) is characterized by myalgia, low-grade fever, general ill health, 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 front surface of the neck, usually radiating to the ear or lower jaw from the same side.

Other causes of thyrotoxicosis

Medication thyrotoxicosis- a common cause of thyrotoxicosis. Often, the doctor prescribes excessive doses of hormones; in other cases, patients secretly take excessive amounts of hormones, sometimes in order to lose 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.

The clinical picture of 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 is understood as a symptom complex of cardiovascular disorders 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 ischemic heart disease. There is an increase in heart rate, an increase in stroke volume (SV) and minute volume (MV), an acceleration of blood flow, a decrease in total and peripheral vascular resistance (OPSR), and a change in blood pressure. Systolic pressure increases moderately, diastolic pressure remains normal or low, as a result of which pulse pressure increases. In addition to all of the above, thyrotoxicosis is accompanied by an increase in the volume of circulating blood (BCC) and erythrocyte mass. The reason for the increase in BCC is a change in the serum level of erythropoietin in accordance with the change in the serum level of thyroxine, which leads to an increase in the mass of erythrocytes. 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 load on the heart in diastole increase.

The main clinical manifestations of cardiac pathology in thyrotoxicosis are sinus tachycardia, atrial fibrillation (MP), heart failure and the metabolic form of angina pectoris. If the patient has coronary heart disease (IHD), hypertension, heart defects, thyrotoxicosis will only accelerate the onset 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 minor physical activity dramatically increases the heart rate. In rare cases, sinus bradycardia occurs. This may be due to congenital changes or to the depletion of the sinus node function with the development of a syndrome of its weakness.

Atrial fibrillation occurs in 10-22% of cases, and the frequency of this pathology increases with age. At the onset of the disease, atrial fibrillation is paroxysmal, 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 thyreostatic therapy, the 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 for severe forms. This may be due to the higher sensitivity of the atria to the arrhythmogenic action of TSH in comparison with the ventricles, since the density of beta-adrenergic receptors in the atrial tissue predominates. 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 occurs when walking, climbing a hill, getting up from your knees, or lifting weights. In rare cases, transient thyrotoxic paralysis occurs, lasting from several minutes to several days.

Elevated thyroid hormone levels result in a negative mineral balance with a loss of calcium, which is manifested by increased bone resorption and decreased intestinal absorption of this mineral. Resorption of bone tissue predominates over its formation, therefore, the concentration of calcium in the urine is increased.

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

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

Exposure to excess thyroid hormones primarily leads to the development of neurasthenic symptoms. Complaints of increased excitability, anxiety, irritability, obsessive fears, insomnia are typical, a change in behavior is noted - fussiness, tearfulness, excessive motor activity, loss of the ability to concentrate (the patient abruptly switches from one thought to another), emotional instability with a rapid change in mood from agitation before depression. True psychoses are rare. The 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, pale skin, dry mouth, chill-like tremors, fear of death.

Neurotic symptoms in thyrotoxicosis are nonspecific, and as the disease develops and aggravates, they fade away, being replaced by severe organ lesions.

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

As the disease progresses, fatigue, muscle weakness, diffuse weight loss, and muscle atrophy progress. In some patients, muscle weakness reaches an extreme degree and even leads to death. Exceptionally rarely, with severe thyrotoxicosis, attacks of generalized muscle weakness (periodic thyrotoxic hypokalemic paralysis) may suddenly occur, involving the muscles of the trunk and limbs, including the respiratory muscles. In some cases, paralysis is preceded by attacks 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 prolonged 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, brushing hair. Symmetrical muscle hypotrophy of the proximal extremities gradually develops.

Thyrotoxic exophthalmos. Thyrotoxic exophthalmos always occurs against the background of thyrotoxicosis, more often in women. The eye gap in such patients is wide open, although there is no exophthalmos, or it does not exceed 2 mm. The enlargement of the palpebral fissure occurs due to the retraction of the upper eyelid. Other symptoms can also be found: when looking directly, a strip of sclera between the upper eyelid and the iris is sometimes visible (Dahlrymple symptom). When looking down, the drooping of the upper eyelid lags behind the movement of the eyeball (Grefe's symptom). These symptoms are caused by an increase in the tone of the smooth muscles that lift the upper eyelid. Characterized by rare blinking (Stellwag symptom), gentle tremor of the eyelids when they are closed, but the eyelids close completely. The range of movements of the extraocular muscles is not disturbed, the fundus of the eye remains normal, and the functions of the eye are not affected. Eye repositioning 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 against the background of drug correction of thyroid dysfunction.

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

Endocrine ophthalmopathy (Graves') is a disease associated with damage to the periorbital tissues of autoimmune genesis, which in 95% of cases is combined with autoimmune diseases of the thyroid gland. It is based on lymphocytic infiltration of all orbital 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 the non-closing of the eyelids, the cornea dries out and can ulcerate. Compression of the optic nerve and keratitis can lead to blindness.

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

The reproductive system. Thyrotoxicosis in women reduces fertility and can cause oligomenorrhea. In men, spermatogenesis is suppressed, and sometimes potency decreases. Gynecomastia is sometimes noted, due to the accelerated peripheral conversion of androgens to estrogens (despite high testosterone levels). 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) can be either elevated or normal.

Metabolism. Patients are usually thin. The elderly are characterized by anorexia. On the contrary, some young patients have an increased appetite, so they put on weight. Since thyroid hormones increase heat production, heat loss due to sweating also increases, which leads to 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 the hyperfunctioning gland, blood flow increases, which leads to 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 a toxic goiter). The following factors contribute to the development of a crisis:

Long-term absence of treatment for thyrotoxicosis;

Intercurrent infectious and inflammatory processes;

Severe mental trauma;

Surgical treatment of any kind;

Treatment of toxic goiter with radioactive iodine, as well as surgical treatment of the disease, if the 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 are released into the blood.

The pathogenesis of the crisis consists in excessive intake of thyroid hormones into the bloodstream and severe toxic damage to the cardiovascular system, liver, nervous system and adrenal glands. The clinical picture is characterized by sharp excitement (up to psychosis with delusions and hallucinations), which is then replaced by adynamia, drowsiness, muscle weakness, and 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-reaching crisis, systolic blood pressure drops sharply, the development of acute cardiovascular failure is possible; tachycardia up to 200 beats per minute turns into atrial fibrillation; dyspeptic disorders intensify: thirst, nausea, vomiting, loose stools. Possible enlargement of the liver and the development of jaundice. Further progression of the crisis leads to loss of orientation, symptoms of acute adrenal insufficiency. The clinical symptoms of a crisis often increase within a few hours. In the blood, TSH may not be detected, while the levels of T4 and T3 are very high. Hyperglycemia is observed, the values ​​of urea, nitrogen increase, the acid-base state and electrolyte composition of the blood change - the level of potassium is increased, sodium - decreases. Characterized by leukocytosis with a neutrophilic shift to the left.

Diagnostics

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

Assessment of thyroid function

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

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

3. The basal level of TSH is greatly reduced, or TSH is not detected. Thyroliberin test is optional. The basal TSH level is reduced in 2% of elderly people with euthyroidism. A normal or increased basal TSH level against a background of increased total T4 or total T3 levels indicates thyrotoxicosis caused by excess 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 normal or even reduced serum thyroglobulin levels. With 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 are very often stages of one process:

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

Manifest (overt) thyrotoxicosis is characterized by a decrease in TSH levels and an increase in free T4 and free T3 levels.

5. Absorption of radioactive iodine (I123 or I131) by the thyroid gland. To assess the function of the thyroid gland, a test for the absorption of a small dose of radioactive iodine over 24 hours is important. 24 hours after ingestion of a dose of I123 or I131, the uptake of the isotope by the thyroid gland is measured and then expressed as a percentage. It should be borne in mind that the absorption of radioactive iodine significantly depends on the iodine content in food and in the environment.

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

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

7. Suppressive tests with T3 or T4. With 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 of thyroid scintigraphy have been developed. The test is contraindicated in heart disease and in 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 the serum of patients with TSH receptors. These autoantibodies are detected in about 75% of patients with diffuse toxic goiter. The test for all autoantibodies to TSH receptors is simpler and cheaper than the test for thyroid-stimulating autoantibodies.

Antibodies to myeloperoxidase are specific for diffuse toxic goiter (as well as for chronic lymphocytic thyroiditis), therefore, 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:

• Is there an autonomous hyperfunctioning node that accumulates all radioactive iodine and suppresses the function of normal thyroid tissue?

  Are there multiple sites that accumulate iodine?

  Are palpable nodules cold (hyperfunctioning tissue is located between nodules).

Differential diagnosis of diseases accompanied by thyrotoxicosis

Of all the reasons leading to the development of thyrotoxicosis, the most relevant (due to their prevalence) are diffuse toxic goiter and multinodular toxic goiter. Very often, the reason for the failure of the treatment of toxic goiter is precisely the errors in the differential diagnosis of Graves' disease and multinodular toxic goiter, due to the fact that the methods of treatment of 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 between Graves' disease and the functional autonomy of the thyroid gland (nodular and multinodular toxic goiter).

In both cases of toxic goiter, the clinic is primarily determined by the thyrotoxicosis syndrome. When carrying out a differential diagnosis, it is necessary to take into account the age peculiarity: in young people, who, as a rule, have Graves' disease, in most cases there is a detailed classical clinical picture of thyrotoxicosis, while in elderly patients, who in our region more often have multinodular 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 heart disease for a long time, or unexplained subfebrile condition. In most cases, already according to the history, examination and clinical picture, it is possible to make the correct diagnosis. The patient's young age, 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 they had a nodular or diffuse goiter many years or even decades ago without compromising thyroid function.

Thyroid scintigraphy: Graves' disease is characterized by a diffuse increase in the uptake of the radiopharmaceutical; functional autonomy reveals "hot" nodes or alternation of zones of increased and decreased accumulation. 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. With subacute granulomatous thyroiditis, the leading symptoms are: malaise, fever, pain in the thyroid gland. The pain radiates to the ears, increases with swallowing or turning the head. The thyroid gland on palpation is extremely painful, 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, the absorption of radioactive iodine by the thyroid gland is sharply reduced.

Transient autoimmune thyroiditis (subacute lymphocytic thyroiditis) - finding out a history of childbirth, abortion, use of interferon drugs. The thyrotoxic (initial) stage of subacute postpartum thyroiditis lasts 4-12 weeks, giving way to the hypothyroid stage lasting several months. Thyroid scintigraphy: the thyrotoxic stage of all three types of transient thyroiditis is characterized by a decrease in the accumulation of the radiopharmaceutical. Ultrasound examination reveals a decrease in the echogenicity of the parenchyma.

Acute psychosis. In general, psychosis is a painful mental disorder that manifests itself entirely or predominantly in an inadequate reflection of the real world with behavioral disturbances, changes 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-infectious disease, infection and intoxication). In almost one third of patients hospitalized with acute psychosis, total T4 and free T4 are elevated. In half of patients with elevated T4 levels, the T3 level is 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, TSH levels in the initial examination of hospitalized patients with psychosis are usually low or lower than normal. It is likely that TSH levels may rise in the early stages of psychosis (before hospitalization). Indeed, in some patients with an addiction to amphetamines hospitalized with acute psychosis, an insufficient decrease in the level of TSH is found against the background of an increased level of T4.

Treatment for thyrotoxicosis syndrome

Treatment of thyrotoxicosis depends on the reasons that caused it.

Toxic goiter

Treatments for Graves' disease and different clinical options for thyroid functional autonomy 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 thyrostatics, it develops again naturally. Thus, the treatment of functional autonomy consists in the surgical removal of the thyroid gland or its destruction using radioactive iodine-131. This is due to the fact that thyrostatic therapy cannot achieve complete remission of thyrotoxicosis; after discontinuation of the drug, all symptoms return. In the case of Graves' disease in certain groups of patients, persistent remission is possible during conservative therapy.

Long-term (18-24 months) thyrostatic therapy, as the basic method of treating 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. If a relapse develops after one course of thyreostatic therapy, the appointment of a second course is futile.

Thyrostatic therapy

Tiamazole (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. In our country and in European countries, thiamazole preparations are the most popular. Thiamazole reduces basal metabolism, accelerates the excretion of iodides from the thyroid gland, increases reciprocal activation of 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 develops as a result of 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, therefore 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 you to halve the number of tablets taken by the patient, and, accordingly, increase the level of patient compliance.

Propylthiouracil. Blocks thyroid peroxidase and inhibits the conversion of ionized iodine to its active form (elemental iodine). Violates the iodination of tyrosine residues of the thyroglobulin molecule with the formation of mono- and diiodotyrosine and, further, tri- and tetraiodothyronine (thyroxine). The extrathyroid action is to inhibit the peripheral transformation of tetraiodothyronine into triiodothyronine. Eliminates or weakens thyrotoxicosis. It has a goitrogenic effect (an increase in the size of the thyroid gland), due to an increase in the secretion of thyroid-stimulating hormone of 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 the 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 monotherapy with thiamazole in terms of the incidence of relapses, but due to the use of large doses of thyrostatic it allows more reliably to maintain 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). From this moment on, the dose of thiamazole is gradually reduced to a maintenance dose (10-15 mg) and levothyroxine (Eutirox®) is added to the treatment at a dose of 50-75 mcg per day. The specified therapy under periodic control of the level of TSH and free T4, the patient receives 18-24 months, after which it is canceled. If a relapse develops after a course of thyrostatic therapy, the patient is shown radical treatment: surgery or radioactive iodine therapy.

Beta-blockers

Propranolol quickly improves the condition of patients by blocking beta-adrenergic receptors. Propranolol also slightly lowers T3 levels by inhibiting the peripheral conversion of T4 to T3. This effect of propranolol, apparently, is not mediated by the blockade of beta-adrenergic receptors. The usual dose of propranolol is 20-40 mg orally every 4-8 hours. The dose is selected so as to reduce the 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, tremors and anxiety. Therefore, taking beta-blockers complicates the diagnosis of thyrotoxicosis.

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

Beta-blockers are especially indicated for tachycardia, even against the background of heart failure, provided that the 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.

Yodides

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, treatment usually becomes ineffective (the phenomenon of "escape"). Potassium iodide is used mainly to prepare patients for operations on the thyroid gland, since iodine causes the gland to thicken and reduces its blood supply. Potassium iodide is very rarely used as a drug of choice for 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 the introduction of sufficient doses of I131, after which the patient is prescribed substitution therapy levothyroxine. An extremely undesirable consequence of more economical resections of the thyroid gland are numerous cases of postoperative recurrence of thyrotoxicosis.

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

Along with this, modern preparations of levothyroxine allow maintaining the quality of life in patients with hypothyroidism, which differs little from that of healthy people. Thus, the drug levothyroxine Eutirox® is presented in the six most necessary dosages: 25, 50, 75, 100, 125 and 150 μg of levothyroxine. A wide range of dosages makes it possible to simplify the selection of the required dose of levothyroxine and to avoid the need to crush the tablet to obtain the required dosage. Thus, a high dosing accuracy is achieved and, as a result, an optimal level of compensation for hypothyroidism. Also, the absence of the need to crush tablets allows you to increase the compliance of patients 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 for the patient, there are practically no restrictions; women can plan pregnancy and give birth without fear of developing recurrence of thyrotoxicosis during pregnancy or (quite often) after childbirth. Obviously, in the past, when, in fact, there were approaches to the treatment of Graves' disease, implying 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.

The obvious benefits of radioactive iodine therapy include:

Security;

Cost - cheaper than surgical treatment;

Does not require preparation with thyrostatics;

Hospitalization for just a few days (in the United States, treatment is carried out on an outpatient basis);

Repeat if necessary;

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

The only contraindications are pregnancy and breastfeeding.

Treatment of a thyrotoxic crisis. It begins with the introduction of thyrostatic drugs. The initial dose of thiamazole is 30-40 mg orally. If it is impossible to swallow the drug - introduction through a tube. Intravenous drip administration 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, is effective.

To combat adrenal insufficiency, glucocorticoid drugs are used. Hydrocortisone is injected intravenously, 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 by mouth) or intravenously 0.1% propranolol solution, starting from 1.0 ml under the control of pulse and blood pressure. They are canceled gradually. Inside, reserpine 0.1-0.25 mg is prescribed 3-4 times a day. With pronounced microcirculatory disorders - Reopolyglyukin, 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.

During pregnancy, I131 is never used, since it passes through 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 in the minimum effective dose. Additional administration of levothyroxine (“block and replace” scheme) is not indicated, since this leads to an increase in the need for thyrostatics.

If a subtotal resection of the thyroid gland is required, then it is better to do it in the first or second trimester, since any surgical interventions 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 incidence of premature birth and spontaneous abortion is the same as in the absence of thyrotoxicosis. ЃЎ

Literature

Lavigne N. Endocrinology. Praktika Publishing House, 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 // Consilium Medicum. 2003, v. 05 no. 11.

Brovkina A.F., Pavlova T.L.

Cattail W. M., Arki R. A. Pathophysiology of the endocrine system. Per. from English, ed. N. A. Smirnova. M .: Publishing house Binom publisher, S.-Pb .: Nevsky dialect. 2001.

V. V. Smirnov,Doctor of Medical Sciences, Professor
N. V. Makazan

Russian State Medical University, Moscow

We continue the theme of erased, "disguised" states in endocrinology. First you need to define the concepts.

If you have any of the following symptoms: feeling of inner tremors, anxiety, nervousness, rapid heartbeat, increasing sweating, slight spontaneous weight loss, soreness in the thyroid gland, fever - an endocrinologist, therapist or other doctor may send you to get tested for hormones.

Next picture: in the analyzes, a reduced TSH below 0.4 mIU / ml (below the lower limit in the laboratory!) with a normal level of free T4 and / or a normal level of free T3 is a concept subclinical thyrotoxicosis.

Most specialists have adopted the definition of subclinical thyrotoxicosis (STyr) - "This is a phenomenon in which a reduced level of TSH is determined with normal levels of free T3 and T4"(by V. Fadeyev).

Determining the level of TSH is the most frequent hormonal test in the world! Its reduced or suppressed level requires interpretation quite often.
If everything is clear with the true thyrotoxicosis syndrome, then with its erased form - "subclinical thyrotoxicosis", the endocrinologist will still have to smash his head.

Subclinical thyrotoxicosis (the official abbreviation is STyr) may or may not have noticeable symptoms. But for that, this symptom is both "subclinical", and the main questions here will be: is it dangerous? And should this condition be treated? To clarify the first question, it is necessary to find out the reason for the appearance of STyr.

The reasons may be:
- multinodular toxic goiter
- single-node goiter with transformation into a toxic adenoma (if the node size is more than 2.5 cm)
- Hashi-toxicosis with AIT
- debut of DTZ (diffuse toxic goiter) in the erased version,
- STyr as a symptom of a tumor, localization outside the thyroid gland (
e.g. lung tumors)
- overdose of L-thyroxine
- the effect of other drugs (for example, after an X-ray contrast study using a large dose of iodine)
- syndrome of euthyroid pathology, etc.

Naturally, the doctor determines the cause, you can only help him - telling in detail about the change in well-being over the next 3-6 months.

Interesting fact: it happens - physiological decrease in TSH from 0.1 - 0.39, typical for the first trimester of pregnancy, but with the conception of twins, the TSH level can drop to 0.005 mIU / ml- and this is not a pathology. Therefore, before starting diagnostics and treatment, young women, and sometimes women after 45 years old, need to determine with the help of a test or blood test for hCG - are you pregnant?

To clarify the diagnosis, a detailed blood test is taken for thyroid hormones: TSH, free T4, free T3, antibodies to TPO, antibodies to TG, antibodies to the TSH receptor. The doctor decides whether to do a thyroid scintigraphy or an iodine uptake curve, less often an MRI of the neck organs.

In order to determine the treatment, take into account:
- the reason that caused STyr
- patient's age
- concomitant diseases, especially cardiovascular, stroke, the presence of atrial fibrillation or atrial fibrillation, heart failure and some others
- the severity of the condition.

STyr severity... There are only two of them
Grade 1 - with a TSH level of 0.1-0.39 mIU / ml
Grade 2 - with a TSH level below 0.1 mIU / ml.

In addition, sublinic thyrotoxicosis can be persistent (permanent) or transient (transient)- therapy will also depend on this.

STyr treatment is mandatory for the following groups of patients:

1.patients under 65 years of age, with symptoms of thyrotoxicosis, especially if antibodies to the TSH receptor are elevated or the uptake of iodine is increased during the iodine uptake curve / signs of thyrotoxicosis on thyroid scintigraphy

2.patients over 65 years of age with / without signs of TTZ, with ischemic heart disease, angina pectoris, atrial fibrillation, Pritzmetal's angina, stroke or transient ischemic attack

3.patients with a proven cause of STIR - toxic adenoma or multinodular toxic goiter, treatment is more often with radioiodine

5.In addition, the treatment of subclinical thyrotoxicosis is indicated for severe osteoporosis with or without a history of fractures, since STIR increases the risk of fractures in elderly patients at times (especially over 65 years of age)

Thyrostatic drugs (Tyrozol, Mercazolil, Propicil) are the first choice in the treatment of young patients with Graves 'disease (diffuse-toxic goiter), occurring with STyr 2, and in patients over 65 years of age with Graves' disease, proceeding with STyr 1- degree, since the likelihood of remission after 12-18 months of therapy with thyreostatics is high and can reach 40-50%.

Radioactive iodine therapy is indicated in a situation of poor tolerance of thyreostatics, as well as in case of recurrence of thyrotoxicosis and in patients with concomitant cardiac pathology.

If the decision is made for lifelong therapy with thyrostatics, such cases also happen (when it is impossible to operate on the thyroid gland) - it must be remembered that these drugs can cause a sharp drop in the level of leukocytes - leukopenia with the transition to agranulocytosis, angina, that is, it is necessary periodically (1 time in 3 months .) control the clinical blood test and, preferably, liver biochemistry - ALT, AST, GGTP.

In other cases, monitoring the state of the thyroid gland is shown, primarily the state of the hormonal background, first monitoring TSH, free T4, free T3 after 3 months, and in the absence of symptoms and hormone level dynamics - monitoring tests every 6-12 months.