TSH independent thyrotoxicosis. What to do with a low level of TSH

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 I.I. Dedov) THEM. Sechenov

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thyrotoxicosis syndrome

thyrotoxicosis syndrome - 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 (DTG) - Graves-Basedow's disease
• thyrotoxic adenoma
• multinodular toxic goiter
• iodine-induced thyrotoxicosis- (iodine-Basedow)
• highly differentiated cancer thyroid gland
• gestational thyrotoxicosis
• chorioncarcinoma, hydatidiform mole
• autosomal dominant non-immunogenic thyrotoxicosis

TSH dependent

• thyrotropinoma
• syndrome of inappropriate secretion of TSH (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
• artificial
• amiodarone-induced
• iatrogenic

III. due to the production of thyroid hormones outside the thyroid gland.

• struma ovarii
• functionally active thyroid metastases

Due to the most frequent occurrence of DTG (90% of all cases of thyrotoxicosis) among all nosological forms, the diagnosis and treatment of thyrotoxicosis syndrome will be considered using the example this disease with specification of features of a current and therapy of the others. DTG is a hereditary organ-specific autoimmune disease (the pathogenesis is 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 endocrine infiltrative ophthalmopathy.
Clinical Criteria

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

The 1994 WHO classification is recommended for estimating the size of the thyroid gland. This international classification simplified, accessible to physicians 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 thumb examinee's hands.
Grade 2 - goiter is palpable and visible to the eye.

• damage to other organs of internal secretion:

1. development of thyroid adrenal insufficiency;
2. dysfunction of the ovaries menstrual function up to amenorrhea, miscarriage;
3. fibrocystic mastopathy in women, gynecomastia in men;
4. impaired tolerance to carbohydrates, the development of diabetes mellitus;

with DTG 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 treatment for Graves-Basedow disease :

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 examined). Usually it is enough to determine the levels of TSH and free T4;
• 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 according to international standards in adults (over 18 years old), goiter is diagnosed when the volume of the thyroid gland in women is more than 18 ml, in men it is more than 25 ml with a 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, DTG);
  b) "non-classical" - there is an increase in antibodies to the TSH receptor - thyroid-stimulating (with DTG) and blocking the binding of TSH (with AIT);
• thyroid scintigraphy (with retrosternal position of the gland, (multi) nodular toxic goiter to determine the existence of functional autonomy, or the presence of multiple nodes that accumulate radiopharmaceuticals, or the presence of "cold" nodes against the background of increased functioning around the located tissue).

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

• 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 mcg of levothyroxine to therapy (the "block and replace" scheme) to prevent the development of drug-induced hypothyroidism and the strimogenic 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 preoperative preparation).

Among the side effects Special attention should be given 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, b -adrenergic blockers until the heart rate normalizes, after which the dose is gradually reduced until it is canceled. Besides, b blockers eliminate tremor, sweating, anxiety.
Patient monitoring during treatment should be carried out as follows:

• T4 level control once a month;
• control of TSH determined by a highly sensitive method 1 time in 3 months;
• Ultrasound of the thyroid gland to assess the dynamics of the volume of the gland 1 time in 6 months;
• determination of leukocytes and platelets in the blood:

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

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

2. large volume of the gland (more than 45 ml);
3. objective signs of compression of surrounding organs;
4. retrosternal goiter;
5. relapse of DTG after a full course of thyreostatic therapy;
6. intolerance to thyreostatics, development of agranulocytosis.
Surgical treatment is carried out upon reaching euthyroidism with thyreostatics, more often subtotal resection of the thyroid gland is used.
Currently, indications and age limits for therapy are expanding. radioactive iodine given the comparative safety and efficacy 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 there was the tactics of initial administration 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 frequency of hypothyroidism reaches about 80%, recurrence is observed in less than 5% of cases.
Among associated immunopathy the most studied and frequently encountered are endocrine infiltrative ophthalmopathy and pretibial myxedema.
At endocrine infiltrative ophthalmopathy (EOP) there is a lesion of periorbital tissues of autoimmune genesis, which is manifested clinically by disorders of the oculomotor muscles, trophic disorders, and often exophthalmos. Diagnostic criteria are:
-clinically: lacrimation, feeling of "sand", dryness and soreness in the eyes, double vision when looking up, to the sides, limited mobility of the eyeballs, changes in the cornea, exophthalmos, often secondary glaucoma;
-instrumentally: protrusion, signs of thickening of the retrobulbar muscles according to ultrasound, CT, MR orbits.
Treatment endocrine ophthalmopathy presents significant difficulties. A necessary factor is the correction of thyroid status. 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 treatment regimens. A promising avenue for treatment is use of octreotide, human immunoglobulin for which treatment regimens are currently being developed. With severe 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 such an important provoking factor in the progression of EOP as smoking..
Pretibial myxedema occurs in 1-4% of patients with DTG. 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 thyroid status.
Second in frequency cause of thyrotoxicosis - toxic adenoma thyroid gland. The presence of similar DTG clinical symptoms with more pronounced symptoms of the lesion is noted. of cardio-vascular system and myopathy, there is no endocrine ophthalmopathy. On palpation, with ultrasound, a nodular formation is determined (with ultrasound - with a clearly defined capsule and usually increased echogenicity). On scintigraphy, it is a "hot" node with increased accumulation of the radiopharmaceutical (RP) and with a decrease in accumulation in the surrounding tissue. Treatment is surgical or radioiodine therapy.
In the case of the development of thyrotoxic phase of autoimmune and postpartum thyroiditis symptomatic therapy possible b blockers, thyreostatics are not used.
In subacute viral thyroiditis, more often after viral infection, there are complaints of severe pain in the anterior surface of the neck, mostly unilateral, radiating to the ear, fever up to 390C. Carry out treatment with prednisolone 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.
When highly differentiated forms of thyroid cancer are detected, preoperative preparation with thyreostatics is carried out until euthyroidism is achieved, followed by surgical treatment more often in combination with radiation therapy in an oncology hospital.
In autosomal dominant non-immunogenic thyrotoxicosis, extirpation of the thyroid gland is necessary, followed by replacement therapy with levothyroxine.
In the syndrome of inadequate TSH production, a number of authors have proposed the use of TRIAK for the treatment, however, there is a consensus on this issue has not yet developed, and in our country there is no experience in using the drug.

Hypothyroidism Syndrome

Hypothyroidism Syndrome- a clinical syndrome caused by a prolonged, 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 - 7-10% among women and 2-3% among men.
According to the level of damage, hypothyroidism is :

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

According to the severity are distinguished:

1. Subclinical (latent)

2. Manifest

• compensated
• decompensated

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

• anomalies in the development of the thyroid gland (dysgenesis, ectopia)
• congenital enzymopathies, accompanied by a violation of the biosynthesis of thyroid hormones

acquired forms

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

Causes secondary hypothyroidism are:

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

Tertiary hypothyroidism:

• violation of the synthesis and secretion of thyroliberin

Peripheral hypothyroidism:

• thyroid resistance syndromes
• hypothyroidism in nephrotic syndrome

Clinical Criteria

Early symptoms hypothyroidism are not very specific, so 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 reduced appetite, lethargy, depression, daytime sleepiness, dry skin, yellowness of the skin caused by hypercarotenemia, swelling, hypothermia, a tendency to bradycardia, constipation, progressive memory loss, hair loss on head, eyebrows.
In women, there is a violation of menstrual function - 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 study blood - definition TSH levels. An increase in the level of TSH is a very sensitive marker of primary hypothyroidism, and therefore the level of TSH 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; Decreased TSH when taking dopamine.

Differential Diagnosis

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

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

• puncture biopsy (according to indications).

In secondary hypothyroidism, the level of TSH is normal or reduced, T4 is reduced. When conducting a test with thyroliberin, the level of TSH is examined initially and 30 minutes after intravenous administration drug. In the primary, TSH increases by more than 25 mIU / l, in the secondary, it remains at the same level.
Principles of treatment
Regardless of the level of damage and the cause that caused the hypothyroidism syndrome, replacement therapy with levothyroxine is prescribed (recently, it has been used much less frequently). combined preparations T3 and T4).
Principles of therapy:

• The initial dose is less, the older the patient and the longer the duration of the course of hypothyroidism. In the elderly and with severe comorbidity, they start with 6.25-12.5 mcg with a gradual increase in dose to a constant maintenance dose. 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 with a manifest form - 0.9 mcg / 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 normalization of the TSH level (which occurs within several months), 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. Assessment of the adequacy of 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, rare complication at the present time - a combination of water-soluble preparations of thyroid hormones and glucocorticoids is used.

Pregnancy and thyrotoxicosis syndrome

The incidence of DTG 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 an increased level of "classic" and "non-classical" antibodies. DTG increases the risk of early pregnancy termination, stillbirth, preterm birth, preeclampsia, low birth weight. Due to the effect 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 thyreostatic therapy. Transition of thyroid-stimulating antibodies (TSH Ab) from mother to fetus is possible, which is unfavorable prognostically due to the possibility of the child developing craniostenosis, hydrocephalus, and severe neonatal thyrotoxicosis syndrome in the future. Fetal thyrotoxicosis may be suspected after 22 weeks of gestation when the fetal heart rate is greater than 160 bpm
For the treatment of DTG during pregnancy, small doses of propylthiouracil (200 mg / day) are used. During pregnancy, only the "block" scheme is used (prescription of thyreostatics without the addition of levothyroxine) and the goal of treatment is to achieve and maintain the level of fT4 at the upper limit of normal.
Radioactive iodine therapy is contraindicated during pregnancy, and surgical treatment is indicated in exceptional cases when medical therapy is not possible, severe drug allergy, very large goiter, associated with malignant thyroid disease, or the need to use high doses of thionamides to maintain euthyroidism. The safest time for subtotal resection of the thyroid gland is the second trimester of pregnancy.
It is necessary to conduct a differential diagnosis of DTG with gestational thyrotoxicosis. The concept of "gestational thyrotoxicosis (GTT)" was introduced by D. Glinoer, according to which GTT is observed in 2-3% of pregnant women and is associated with increased production of chorionic gonadotropin (CG), which has a structural similarity to TSH and stimulates the thyroid gland. Clinically, this condition is accompanied by severe toxicosis of the first half of pregnancy (nausea, sometimes uncontrollable vomiting - hyperemesis gra v idarum). GTT often develops in multiple pregnancies.
In a laboratory study during a normal pregnancy, early dates 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 DTZ in favor of GTT will be evidenced by a decrease in the level of TSH 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. Signs of GTT 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 hydatidiform mole. According to Portl 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 thyroxin-binding globulin or increased iodine excretion. At the same time, with a decrease in the level of TSH in hydatidiform mole (47% of cases) and choriocarcinoma (67% of cases), thyrotoxicosis develops in 1/3 of cases.

Hypothyroidism and pregnancy

With untreated hypothyroidism, pregnancy is unlikely.
At the same time, if pregnancy has occurred and before the 6-8th week the fetus receives at least enough triiodothyronine, then in the future 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 the subsequent development of gross violations in the intellectual sphere of the unborn child.
In the US, 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 the 4th-5th day of life (in preterm infants on the 7th-14th day): the TSH level is considered to be the norm below 20 mcU/ml.
Treatment of hypothyroidism is carried out with levothyroxine, the dose of which is calculated based on the increased need for the drug during pregnancy up to 1.9-2.3 mcg/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 recommended to prescribe iodine in the form of potassium iodide 200 mcg or as part of special multivitamin preparations, even if they have 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-Chaikoff effect, cause blockade of the thyroid gland in the fetus.

Literature:
1. Hostalek U. Diseases of the thyroid gland and the possibility of their effective treatment. - Thyroid Russia. - Collection of lectures. M. 1997; 6-12.
2. Melnichenko G.A. Hypothyroidism. Rus. honey. journal, 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.

2. What is subclinical thyrotoxicosis?
Subclinical thyrotoxicosis means that the rise in T 3 and/or T 4 levels occurs within the normal range, which nevertheless leads to suppression of TSH secretion by the pituitary gland to a sub normal values. Clinical signs and symptoms are often absent or nonspecific.

3. What are the long-term consequences of subclinical thyrotoxicosis?
Some studies have shown an association of subclinical thyrotoxicosis with accelerated bone loss in postmenopausal women and an increased incidence of atrial arrhythmias, including atrial flutter.

4. List the three main causes of hyperthyroidism.
1.Graves' disease- an autoimmune pathology in which antibodies are produced directed against the TSH receptor, which leads to constant stimulation of the thyroid gland to secrete thyroid hormones. It is often associated with such extrathyroid pathology as ophthalmopathy, pretibial myxedema, and thyroid acropachy.
2. Toxic multinodular goiter (TMUS) usually occurs in the presence of a long multinodular goiter, when individual nodes begin to function autonomously. Patients with mild or overt TMUS also have an increased risk of developing iodine-induced thyrotoxicosis (iodine-based effect) after intravenous contrast or treatment with iodine-containing drugs, such as amiodarone.
3. Toxic adenoma or autonomously functioning thyroid nodes (AFTU) - benign tumors leading to excessive activation of the TSH receptor or its signal transduction apparatus. These tumors often lead to subclinical thyrotoxicosis and tend to bleed spontaneously. APTU must be more than 3 cm in diameter to achieve sufficient secretory capacity to achieve overt hyperthyroidism.

5. What are other rarer causes of hyperthyroidism?
Rarer causes of hyperthyroidism include TSH-secreting pituitary adenomas; stimulation of the TSH receptor by human chorionic gonadotropin (hCG) at extremely high concentrations, observed in the case of choriocarcinomas in women or germ cell tumors in men; struma ovarii (ectopic production of thyroid hormones by teratomas containing thyroid tissue); resistance of thyroid hormones to TSH. Thyroiditis and the administration of excessive amounts of exogenous thyroid hormones (iatrogenic, unintentional or covert) are causes of thyrotoxicosis, but not hyperthyroidism (see question 1).

6. What is clinical picture thyrotoxicosis?
The main symptoms include palpitations, tremors, insomnia, difficulty concentrating, irritability or emotional lability, weight loss, heat intolerance, shortness of breath on exertion, fatigue, frequent stools, shortened menses, hair breakage. On rare occasions, patients gain weight instead, mainly due to the polyphagia needed to cover the accelerated metabolism.

7. What is apathetic (in the Russian-language literature - marantic form of thyrotoxicosis - Ed.) hyperthyroidism?
Elderly patients may lack typical adrenergic features, and conversely, depression and apathy, weight loss, atrial fibrillation, and congestive heart failure may occur.

8. Describe the signs of thyrotoxicosis on physical examination?
In patients with hyperthyroidism, tremors, tachycardia, heart murmurs, warm, moist skin, hyperreflexia with a rapid relaxation phase, and goiter (in Graves' disease) can be noted. Clinical symptoms from the side of the eyes are discussed in question 9.

9. What effect does hyperparathyroidism have on the eyes?
Retraction of the eyelids and an "angry" look are noted for various causes of thyrotoxicosis due to increased adrenergic tone. True ophthalmopathy is characteristic only for Graves' disease and occurs in response to a cross-reaction of thyroid antibodies with antigens on fibroblasts, adipocytes, and myocytes of the retrobulbar eye. The most common manifestations of ophthalmopathy include proptosis, diplopia, and inflammatory changes such as conjunctival injection and periorbital edema.

10. What laboratory tests confirm the diagnosis of thyrotoxicosis?
Determination of TSH using methods of the second or third generation is the most sensitive test for the detection of thyrotoxicosis. Since low TSH can also occur in secondary hypothyroidism, free T4 should be determined. At a normal level of T 4, it is necessary to determine the level of T 3 to exclude T 3 -thyrotoxicosis. Other associated laboratory changes may include mild leukopenia, normocytic anemia, increased hepatic transaminases and alkaline phosphatase, mild hypercalcemia, and low albumin and cholesterol levels.

11. In what cases is antithyroid antibodies determined for the diagnosis of hyperthyroidism?
The cause of hyperthyroidism can usually be identified by history taking, physical examination, and radionuclide studies. Determination of antibodies to the TSH receptor is advisable for pregnant women with Graves' disease to identify the risk of neonatal thyroid dysfunction due to transplacental transfer of stimulating or blocking antibodies. It may also be recommended in euthyroid patients with suspected euthyroid ophthalmopathy and in patients with intermittent periods of hyper- and hypothyroidism due to fluctuating levels of TSH-blocking and TSH-stimulatory antibodies.

12. What is the difference between thyroid scintigraphy and iodine uptake?
Determination of the capture of iodine with isotopes I-131 or 1-123 is used to quantify the functional state of the thyroid gland. Small doses of radioactive iodine are administered orally, followed by evaluation of distribution in the thyroid gland after 6-24 hours. High capture confirms hyperthyroidism. Scintigraphy is a two-dimensional image of the distribution of activity in the thyroid gland. A uniform distribution in patients with hyperthyroidism confirms Graves' disease, a patchy distribution is characteristic of TMUS, and a unifocal distribution of activity corresponding to the position of the node is indicative of a toxic adenoma.

13. How to treat hyperthyroidism?
The three main treatment options include antithyroid drugs (ATPs) like methimazole and propylthiouracil; radioactive iodine (I-131); surgical intervention. In the absence of contraindications, most patients should receive beta-blockers for heart rate control and symptomatic treatment. Most thyroidologists prefer to prescribe I-131 surgery or long-term treatment ATP (In Russia they prefer conservative treatment, with its ineffectiveness or a tendency to relapse of the disease - surgical treatment, and in third place - treatment with radioactive iodine. - Approx. ed.). Patients receiving I-131 treatment should avoid pregnancy and should be warned that oral contraceptives may not provide reliable protection in hyperthyroidism due to elevated levels of sex hormone-binding globulin and accelerated elimination of contraceptives.

14. In what cases is surgical intervention indicated for hyperthyroidism?
Surgery is rarely the treatment of choice for hyperthyroidism. It is most commonly performed in patients with a "cold" nodule due to Graves' disease, when treatment with I-131 is contraindicated, as in the case of pregnancy, or in patients with very large goiters. Before surgery, patients should achieve a euthyroid state in order to reduce the risk of arrhythmias during induction of anesthesia and the risk of postoperative thyroid crisis.

15. Are there other interventions used to lower thyroid hormone levels?
Yes. Inorganic iodine rapidly reduces the synthesis and release of T 4 and T 3 - Suppression of thyroid hormone synthesis by iodine is known as the Wolff-Chaikoff effect. However, since "escape" from this effect usually occurs after 10-14 days, the drug is used only for quick preparation for surgery or as additional measure in the treatment of thyroid crisis. The usual doses of Lugol's solution are 3-5 drops 3 times a day or diluted potassium iodide solution 1 drop 3 times a day. Ipodate, an oral radiographic contrast agent, has been shown to inhibit T 4 -5" deiodinase activity, thereby reducing T 3 and T 4 levels. The usual doses of ipodate are 1 g per day. Other drugs rarely used to treat hyperthyroidism, include lithium, which reduces the release of thyroid hormones, and potassium perchlorate, which inhibits the uptake of iodine by the thyroid gland.

16. What drugs block the conversion of T4 to T3?
Propylthiouracil, propranolol, glucocorticoids, ipodate and amiodarone inhibit peripheral conversion of T 4 to T 3

17. How effective are ATPs?
Ninety percent of patients treated with ATP achieve a euthyroid state without significant side effects. About half of patients achieve remission after a full course of treatment for 12-18 months. However, only 30% maintain long-term remission; as experience shows, relapse usually occurs in the first two years after discontinuation of drugs. Usual starting doses of methimazole are 30 mg/day or propylthiouracil 100 mg 3 times a day.

18. What side effects noted in the treatment of ATP?
1. Agranulocytosis - rare, but life threatening A complication of ATP therapy occurs in approximately one case per 200-500 people. Patients should be advised to seek immediate treatment for fever, mouth ulcers, and minor infections that do not resolve quickly.
2. Hepatotoxic effect leading to fulminant hepatitis with necrosis during therapy with propylthiouracil and cholestatic jaundice during therapy with methimazole. Patients should report pain in the right hypochondrium, anorexia, nausea, and itching.
3. Skin rash, from limited erythema to exfoliative dermatitis. The reaction to one drug is not eliminated when changing to another, although cross-sensitivity occurs in approximately 50% of cases.

19. What laboratory parameters should be monitored in patients receiving ATP?
Thyroid hormone levels should be investigated when initial high doses of ATP should be reduced to maintenance doses (typically 25-50% of baseline). TSH may remain suppressed for several months; in this situation, the definition of free T 4 is more important for assessing thyroid status. Control of liver enzymes and general analysis blood tests with the formula should be carried out every 1-3 months. Since elevated transaminases and mild granulocytopenia also occur in untreated Graves' disease, it is important to check these parameters before initiating ATP therapy. Many cases of agranulocytosis occur without prior granulocytopenia; thus, a high risk exists even if recent tests were normal. (In Russia, at the initial stages of treatment at a dose of Metizol 20-30 mg, a complete blood count with the formula is monitored every 10 days. - Approx. ed.)

20. How does radioactive iodine work?
Thyroid cells capture and concentrate iodine and use it to synthesize thyroid hormones. The organization of I-131 occurs in the same way as natural iodine. Since I-131 produces locally destructive beta particles, cell damage and death are noted for several months after treatment. Doses of I-131 should be high enough to cause permanent hypothyroidism to reduce relapse rates. Usual doses for Graves' disease are 8-15 mCi; with TMUS, higher doses are used - 25-30 mCi. Such doses are effective in 90-95% of patients.

21. In what cases is it indicated to prescribe ATP before treatment with I-131?
In elderly patients and patients with systemic diseases, ATP is often used to reduce the synthesis of thyroid hormones by the thyroid gland, thereby reducing the risk of I-131-induced thyroid crisis. The preparation of ATP is also used for severe thyrotoxicosis, the impossibility of permanent treatment or the risk of pregnancy. Preparation may reduce the success rate of radioactive iodine treatment by inhibiting I-131 organization. When used for the preparation of ATPs, they must be canceled 4-7 days prior to the application of I-131.

22. How long after treatment with I-131 should pregnancy or breastfeeding be avoided?
Pregnancy should be avoided for at least 6 months after treatment with I-131. In addition, it is necessary to achieve stable doses replacement therapy thyroid hormones and the absence of active ophthalmopathy. Radioactivity breast milk, as determined in one study following a therapeutic dose of I-131 of 8.3 mCi, remained high for 45 days. If 99 tons of technetium is used for diagnostic purposes, feeding can be resumed after 2-3 days.

23. Can I-131 cause or exacerbate ophthalmopathy in Graves' disease?
This is an area of ​​discussion. In the natural course of the disease, 15-20% of patients develop overt ophthalmopathy. In most cases, it occurs in the period from 18 months before the onset of clinical manifestation to 18 months from the onset of thyroid otosycosis. Thus, new cases can be expected to coincide with I-131 treatment. Some studies, however, have shown that ophthalmopathy is more likely to worsen with I-131 treatment than with surgery or ATP treatment. As a result, patients with active moderate or severe ophthalmopathy, it is recommended to avoid treatment with I-131.

24. How to manage thyrotoxicosis during pregnancy?
It is necessary to interpret the results of laboratory studies with caution during pregnancy, since low TSH values ​​\u200b\u200bare not typical for the first trimester, and the total T 4 is increased due to an increase in the level of thyroxine-binding globulin (TSG). The best indicator of thyroid function during pregnancy is free T 4 . Nuclear tests such as iodine uptake or scintigraphy are contraindicated during pregnancy due to the effect of isotopes on the fetus. Since the use of I-131 is also contraindicated in pregnancy, the choice of treatment is limited to ATP or surgery in the second trimester. Propylthiouracil is usually preferred as it passes the placental barrier to a lesser extent than methimazole. Pregnant women with Graves' disease need close monitoring to achieve adequate control and prevention of hypothyroidism, as the course of the disease often improves during pregnancy. It is necessary to determine antibodies to the TSH receptor that can cross the placenta after 26 weeks, in the third trimester to assess the risk of neonatal thyroid dysfunction.

TSH or thyroid-stimulating hormone stimulates thyroid function. It activates the absorption of iodine entering the body by the gland, stimulates the synthesis of T3 and T4 thyroids.

Determining the concentration of thyroid-stimulating hormone in the blood is the most important diagnostic method study of thyroid function. Its deviation from normal values ​​indicates the development of thyroid pathology associated with an excess or deficiency of T3 and T4. And any dysfunction of the thyroid gland, as a rule, leads to a systemic failure in the body.

Decreased levels of thyroid-stimulating hormone indicate an excess of thyroid or hyperfunction of the thyroid gland.

In adults normal TSH defined in the range from 0.4 to 4.0 mU/l. If the thyroid-stimulating hormone is low, then, according to the feedback rule, the thyroid hormones T3 and T4 are above normal.

To clarify the diagnosis in a patient with low TSH, the next step is to determine the concentration of thyroids.

Thyrotoxicosis syndrome occurs when the following diseases thyroid gland:

• Basedow's disease;
• Autoimmune thyroiditis or inflammation of the thyroid gland (in the thyrotoxic phase);
• Multinodular toxic goiter;
• Toxic adenoma of the thyroid gland.

The above conditions are mainly autoimmune nature, that is, they develop against the background of pathological production of autoantibodies by the body. Therefore, with diagnosed thyrotoxicosis, it is also important to determine the presence of antibodies in the blood to thyroid hormone receptors. In Basedow's disease, autoimmune antibodies to the TSH receptor are elevated.

There are cases when, together with reduced thyrotropin, on the contrary, the concentration of T3 and T4 decreases. This picture indicates the development of hypothyroidism (thyroid insufficiency), not associated with the function of the thyroid gland, but caused by disorders of the hypothalamus or pituitary gland.

Main symptoms

Unlike a condition caused by thyroid deficiency (hypothyroidism), thyrotoxicosis, as a rule, has pronounced clinical symptoms:

• Availability goiter, soft to the touch;
• Endocrine ophthalmopathy is a condition in which eyeballs go beyond the boundaries of the orbits;
• Emotional instability: nervousness, tearfulness, irritability, vanity;
• Tachycardia;
• Unreasonable weight loss with increased appetite;
• feeling of heat;
• sweating;
• Warm extremities.

By the severity of the symptoms, you can determine the stage of the disease. The brighter the symptoms, the longer the disease proceeds.

Causes of pathology

The reasons for the occurrence of thyrotoxicosis associated with Basedow's disease have not been identified. However, according to statistics women get sick more often than men, and more patients are registered in iodine-deficient regions.

Thyrotoxicosis is divided into three types:

• Hyperthyroidism is a condition caused by hyperfunction of the thyroid gland (Graves' disease, toxic goiter).
• Thyrotoxicosis destructive - a condition that occurs when the thyroid follicles are destroyed.
• Thyrotoxicosis arising from other causes not related to thyroid hyperfunction is a drug-induced, thyrotoxic phase of subacute and postpartum thyroiditis.

It is possible to differentiate the above conditions through such studies as determining the level autoantibodies to rTG if the concentration is higher than normal, then we are talking about Basedow's disease or multinodular toxic goiter.

Thyrotoxicosis with autoimmune thyroiditis(AIT) most often has a temporary manifestation and quickly passes into the phase of hypothyroidism as the disease progresses. However, in some cases, AIT can occur in only one phase - thyrotoxic or hypothyroidism. AIT is diagnosed through the analysis of AT-TPO, which determines the concentration of antibodies to thyroperoxidase.

Drug-induced thyrotoxicosis can occur against the background of long-term use of thyroid hormone preparations for the treatment of hypothyroidism.

Decreased TSH during pregnancy

Decreased TSH during pregnancy may be due to the condition itself and is observed in 30% of pregnant women. In 4%, a reduced level of thyrotropin is accompanied by T4 - given state called hyperthyroidism of pregnant women. It occurs in the first trimester of gestation and passes by the middle of the second.

In very rare cases (0.5%), the picture of thyrotoxicosis can manifest itself with an excess of iodine in the body or, conversely, with its deficiency.

A pregnant woman should take 200 mcg of iodine in tablets daily in addition - these are the preparations "Iodomarin", "Iodbalance", "Iodine-active" and others.

After childbirth

In 50% of women whose blood contains antibodies to TPO, there is a risk of developing postpartum thyroiditis, which turns into chronic AIT, and then into persistent hypothyroidism. Postpartum thyroiditis develops approximately 3 months after childbirth and begins with a thyrotoxicosis phase, which is diagnosed by an increase in T3 and T4 and a decrease in TSH. The woman has symptoms such as pathological weight loss, weakness and fatigue. After 1.5 - 2 months, the thyrotoxicosis phase usually turns into hypothyroidism.

Methods of treatment

The most common cause of thyrotoxicosis is Basedow's disease or diffuse toxic goiter. Treatment is carried out in 3 ways: therapeutic, surgical and radioactive iodine therapy.

The main therapeutic methods include taking drugs that suppress the synthesis of thyroid hormones - these are antithyroid drugs. thiamazole("Tiamazol", "Tirozol", "Merkazolil") and propylthiouracil("Propicil"). Treatment is prescribed for a period of 1 - 1.5 years. Patients are examined at least once a month. For relieve symptoms of hyperthyroidism(tachycardia, tremor, sweating) therapy with beta-blockers is indicated - Propranolol, Anaprilin, Metoprolol.

Treatment with radioactive iodine gives good results and has been successfully used for more than 40 years. The therapy is performed by a radiologist. This method contraindicated in pregnancy and lactation.

Thyroid surgery in order to remove its tissues has been successfully used for more than 50 years and is effective method treatment of thyrotoxicosis. The operation is performed only against the background of a general improvement in the patient's well-being and normalization of his body weight, therefore, a few months before the procedure, the patient is prescribed antithyroid therapy.

The main treatment for thyrotoxicosis is radioactive iodine therapy, as it most often helps to achieve a full recovery. Its only drawback is the possible development of hypothyroidism.

Thyrotoxicosis is a condition associated with an excess of thyroid hormones in the body. This condition is also called hyperthyroidism. This is not a diagnosis, but a consequence of certain thyroid diseases or exposure to external factors.

The root "toxicosis" characterizes these changes well. With thyrotoxicosis, intoxication occurs with an excess of one's own thyroid hormones. An excess of hormones in the body leads to various physical changes and emotional changes.

Causes of thyrotoxicosis

There are many reasons for thyrotoxicosis. Conventionally, they can be divided into several groups:

1. Diseases accompanied by excessive production of thyroid hormones.

These include:

A) Diffuse toxic goiter (Graves' disease, Graves' disease). This disease in 80-85% of cases is the cause of thyrotoxicosis.

For some reason, the immune system fails. Leukocytes (white blood cells) begin to produce so-called antibodies - proteins that bind to thyroid cells and cause it to produce more hormones. Often these antibodies also attack the cells of the orbit - there is a so-called endocrine ophthalmopathy. Such diseases, when cells immune system begin to produce substances that attack their own organs are called autoimmune. Graves' disease is an autoimmune disease.

The disease can occur at any age, but most often occurs in young people from 20-40 years old.

B) Toxic adenoma and multinodular toxic goiter.

Presence of a thyroid nodule(s) that overproduces thyroid hormones. Normally, excess production of thyroid hormones is suppressed by pituitary hormones (TSH). Toxic adenoma and multinodular toxic goiter function autonomously, that is, excess thyroid hormones are not suppressed by pituitary hormone (TSH). This disease is more common in older people.

C) Thyrotropinoma is a formation of the pituitary gland, which in excess synthesizes thyroid-stimulating hormone (TSH), which stimulates the thyroid gland. A very rare disease. It proceeds with the clinic of thyrotoxicosis.

2. Diseases associated with the destruction (destruction) of thyroid tissue and the release of thyroid hormones into the blood.

These diseases include destructive thyroiditis (subacute thyroiditis, thyrotoxicosis with autoimmune thyroiditis, postpartum thyroiditis, painless thyroiditis).

Cordarone-induced (amiodarone-induced) thyrotoxicosis can also be attributed to this group of diseases. This is thyrotoxicosis, which occurs as a result of treatment with iodine-containing antiarrhythmic drugs (Amiodarone, Kordaron). Taking drugs causes destruction (destruction) of thyroid cells and the release of hormones into the blood.

3. Iatrogenic thyrotoxicosis - thyrotoxicosis caused by an overdose of thyroid hormone preparations (L-thyroxine, Euthyrox - drugs for the treatment of hypothyroidism - a condition associated with a decrease in the production of thyroid hormones).

These are the main causes of thyrotoxicosis.

If you have been feeling irritable, emotional lately, notice frequent mood swings, tearfulness, increased sweating, a feeling of heat, palpitations, a feeling of interruptions in the work of the heart, lost weight - this is a reason to see a doctor and get tested for thyroid hormones. These are symptoms of thyrotoxicosis.

Other symptoms of thyrotoxicosis include: blood pressure, loose stools, weakness, the presence of fractures, intolerance to a hot climate, increased hair loss, menstrual irregularities, decreased libido (sexual desire), erectile dysfunction.

With an increase in the size of the thyroid gland, complaints of swallowing disorders, an increase in the volume of the neck may appear.

Diffuse toxic goiter (Graves' disease) is also characterized by the presence of infiltrative ophthalmopathy - lacrimation, photophobia, a feeling of pressure and "sand" in the eyes, there may be double vision, vision loss is possible. Noteworthy is exophthalmos - "protrusion" of the eyeballs.

exophthalmos

Diagnosis of thyrotoxicosis

If you notice these symptoms in yourself, you need to take hormonal tests to rule out or confirm the presence of thyrotoxicosis.

Diagnosis of thyrotoxicosis:

1. Hormonal blood test:

Blood on TSH, T3 free, T4 free.

The main study proving the presence of thyrotoxicosis.

Thyrotoxicosis is characterized by a decrease in TSH (a pituitary hormone that reduces the production of thyroid hormones) in the blood, an increase in T3, T4, - thyroid hormones.

2. Determination of antibodies - confirmation of the autoimmune nature of the disease.

Definition needed

Antibodies to TSH receptors (an increase in antibodies to the TSH receptor - proves the presence of Graves' disease)

Antibodies to TPO (increased in Graves' disease, autoimmune thyroiditis).

3. Perform an ultrasound of the thyroid gland.

Diffuse toxic goiter (Graves' disease), as the most common cause of thyrotoxicosis, is characterized by:

An increase in the size, volume of the thyroid gland (an increase in the volume of the thyroid gland over 18 cm cube in women and more than 25 cm cube in men is called a goiter),

Acceleration, increased blood flow in the thyroid gland.

For other causes of thyrotoxicosis, these signs are not characteristic. With destructive processes, a decrease in blood flow in the thyroid gland is determined.

4. In some cases, the doctor may prescribe a study - thyroid scintigraphy. This study shows how much iodine and other substances (technetium) can be taken up by the thyroid gland. This study allows you to clarify the cause of thyrotoxicosis.

Graves' disease is characterized by increased intense uptake of the radiopharmaceutical.

Thyrotoxicosis due to destruction (destruction) of thyroid tissue is characterized by a decrease in uptake or lack of uptake of iodine (technetium).

5. In the presence of endocrine ophthalmopathy, exophthalmos, ultrasound of the orbit or magnetic resonance or CT scan eye area.

Treatment of thyrotoxicosis

To determine the tactics of treatment, you must first determine the cause of thyrotoxicosis. The most common cause of thyrotoxicosis is Graves' disease.

There are three treatments for Graves' disease: medical treatment, surgical treatment, and radioactive iodine therapy. Drug treatment consists in the appointment of thyreostatic drugs (drugs that reduce the production of thyroid hormones). There are two such drugs: Thiamazole (Tyrozol, Mercazolil, Metizol) and propylthiouracil (Propicil). Initially, the drug is prescribed at a dose of about 30 mg per day, after the normalization of thyroid hormones, they switch to a maintenance dose of 5-15 mg per day. The duration of treatment with thyreostatics is usually 1-1.5 years.

Treatment of destructive processes in the thyroid gland (thyrotoxicosis associated with the destruction of thyroid cells and the release of excess thyroid hormones into the blood) is carried out with glucocorticosteroid hormones (Prednisolone). These drugs reduce the process of destruction of thyroid cells. Dosage and duration of treatment are selected individually.

Surgical treatment on the thyroid gland with thyrotoxicosis is performed only after treatment with thyreostatics when the normalization of thyroid hormones is achieved.

What lifestyle should be followed to promote recovery?

To promote recovery, you need to regularly take the drugs prescribed by your doctor and undergo hormonal control tests.

And also, it should be borne in mind that the likelihood of a stable remission is higher in non-smokers. If you smoke, you are more likely to have thyrotoxicosis recurrence after the end of thyreostatic therapy. Therefore, if you smoke, quitting smoking will increase your chances of recovery.

Treatment of thyrotoxicosis with folk remedies

Treatment should be avoided folk remedies. Thyrotoxicosis is a serious condition that, without adequate timely treatment may lead to serious complications, primarily from the cardiovascular system (for example, severe arrhythmias).

Therefore, the identified thyrotoxicosis requires mandatory treatment with medications. Treatment with various folk remedies "from the thyroid gland", which the neighbors will advise you, most likely will not only not help, but will also harm, since thyrotoxicosis without treatment can lead to serious complications.

In addition to the main treatment, you can advise good nutrition, eat more vegetables and fruits. Perhaps the appointment of multivitamin complexes (Vitrum, Centrum and others) or an additional appointment to the main therapy of B vitamins (Milgamma, Neuromultivit).

Complications of thyrotoxicosis

With untimely, inadequate treatment, complications of thyrotoxicosis develop, such as atrial fibrillation, arterial hypertension (increased blood pressure), thyrotoxicosis contributes to the development and deterioration of the course coronary disease heart, damage to the central nervous system in severe cases, it can lead to thyrotoxic psychosis. These complications are associated with the cardiotoxic effect of excess thyroid hormones (that is, an increased amount of thyroid hormones worsens the state of the cardiovascular system: it leads to an accelerated metabolism in myocardial cells, increases the heart rate, as a result of which complications develop).

An acute complication is thyrotoxic crisis - a serious complication that occurs after stress, during surgery on the thyroid gland against the background of thyrotoxicosis. This is a life threatening condition. The main symptoms are fever up to 38-40°, pronounced heartbeat up to 120-200 beats per minute, cardiac arrhythmias, disorders of the central nervous system.

To prevent these complications, timely diagnosis and treatment of thyrotoxicosis is necessary. Therefore, when signs of thyrotoxicosis appear, it is necessary to consult a doctor and undergo a hormonal examination.

Prevention of thyrotoxicosis

It should be remembered that there is a genetic predisposition to thyroid diseases. If your close relatives have thyroid diseases, then you are also recommended to periodically perform an ultrasound of the thyroid gland, hormonal studies.

If you notice symptoms of thyrotoxicosis in yourself, you need to perform a study of thyroid hormones.

If hypothyroidism has already been detected, it is necessary to start treatment in a timely manner to prevent complications of thyrotoxicosis.

Thyrotoxicosis doctor's consultation

Question: When treating with thyreostatics, how often do you need to undergo hormonal studies?
Answer: If there is a course drug treatment thyrotoxicosis, then the first study of thyroid hormones (T3 free, T4 free) after the start of thyreostatic therapy should be performed one month after the start of therapy. Further, against the background of a decrease in the dose of thyreostatics, it is necessary to perform the study several more times with an interval of 1 month. The study of TSH should be performed no earlier than 3 months after the start of thyreostatic therapy, since it remains low for a long time. After selecting a maintenance dose of thyreostatics, a hormonal study can be carried out once every 2-3 months.

Question: What are the restrictions while taking thyreostatics?
Answer: Until the level of thyroid hormones normalizes, it is recommended to reduce physical activity. After the normalization of hormones (achieving euthyroidism), it is possible to increase the level of physical activity.

Question: What is the probability of remission after a course of thyreostatic therapy?
Answer: The course of thyreostatic therapy usually lasts 12-18 months. After that, studies are carried out in order to make sure of the possibility of remission (ultrasound of the thyroid gland is performed, the study of antibodies to the TSH receptor). After that, therapy is stopped. However, the probability of recurrence of the disease sometimes exceeds 50%. Usually, a relapse occurs within the first year after discontinuation of thyreostatic therapy. In case of treatment failure, surgical removal of the thyroid gland or treatment with radioactive iodine is indicated.

Doctor endocrinologist Artemyeva Marina Sergeevna

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

If you have the following symptoms: feeling of inner trembling, anxiety, nervousness, cardiopalmus, increased sweating, slight spontaneous weight loss, soreness in the thyroid gland, fever - an endocrinologist, general practitioner or other doctor may send you to take a hormone test.

Next picture: in the analyzes, a reduced TSH below 0.4 mIU / ml (below the lower laboratory limit!) with a normal level of free T4 and / or a normal level of free T3 is the 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 when normal levels free T3 and T4"(according to V. Fadeyev).

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

Subclinical thyrotoxicosis (official abbreviation STyr) may or may not have noticeable symptoms. But 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 - you need to find out the reason for the appearance of STyr.

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

Naturally, the doctor determines the cause, you can only help him by 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, is typical for the first trimester of pregnancy, but when twins are conceived, the TSH level can drop to 0.005 mIU/ml- and this is not a pathology. Therefore, before starting diagnosis and treatment, young women, and sometimes women after 45 years of age, need to be determined using a test or blood test for hCG - are you pregnant?

To clarify the diagnosis, a detailed blood test for thyroid hormones is given: TSH, T4 free, T3 free, 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.

In order to determine the treatment, consider:
- the reason that caused STir
- 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.

Severity of STyr. 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, subclinical thyrotoxicosis can be persistent (permanent) or transient (transient)- therapy will also depend on this.

Treatment of STI is mandatory for the following groups of patients:

1. patients younger than 65 years of age with symptoms of thyrotoxicosis, especially if antibodies to the TSH receptor are elevated or iodine uptake is increased when performing an 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, Pritzmetall's angina, previous stroke or transient ischemic attack

3. Patients with a proven cause of STIr - toxic adenoma or multinodular toxic goiter, treatment 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 STyr increases the risk of fractures in elderly patients at times (especially those older than 65 years)

Thyrostatic drugs (Thyrozol, Mercazolil, Propicil) are the first choice in the treatment of young patients with Graves' disease (diffuse toxic goiter) with STI 2, and in patients older than 65 years with Graves' disease with STI 1- th degree, since the probability of remission after 12–18 months of therapy with thyreostatics is high and can reach 40–50%.

Therapy with radioactive iodine is indicated in a situation of poor tolerance of thyreostatics, as well as in the recurrence of thyrotoxicosis and in patients with concomitant cardiac pathology.

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

In other cases, it is shown to monitor the state of the thyroid gland, primarily the state of the hormonal background, first control TSH, T4 free, T3 free after 3 months, and in the absence of symptoms and changes in hormone levels, control tests every 6-12 months.