Thyrotoxicosis syndrome: causes, diagnosis, treatment. Standard approaches to the treatment of thyrotoxicosis and hypothyroidism syndromes Main indications for testing
Hello, Svetlana Mikhailovna! Sorry, it seemed to us that that information was enough. The disease manifested itself at the institute at the 1st year, she studies in Tomsk. We live in Kazakhstan. 05/12/05 T3 3.8 norm 1.2-3.0; T4 300 norm 40-120; TSH 0.1 norm 0.23-3.4. Ultrasound: location and shape b / o; contours of moderate tuberosity, uneven. Volumetric formations were not detected. Prv share thickness 17.5 width 19.2 length 54 volume 8.70 cm3; left lobe thickness 17.4 width 17.0 length 54.5 cm3. Isthmus 7.1. DTZ 1 st thyrotoxicosis was first detected. mercazolol 5mg 2t*3 times for 5 days, then 2t*3 times for 10 days, then 1t*3 times; Atenolol (I don’t understand exactly what the name is) 50 mg 1/2 * 2 times for 10 days, then 1/2t 1 time for 10 days; valerian 2t * 3 times 10 days. 6.06.05 Mercazolil 5 mg 1t*3 times until 18.06.05, then 1t*2 times until 1.07.05; L-thyroxine 100mg 1/4t*1 time, atenolol; valerian 10 days of each month 10.08.05 T4 104.5 norm 53-158. Ultrasound: the contours are not even, moderately bumpy, volumetric formations are not detected; dimensions right lobe thickness 17.2 width 16.3 length 48.0 volume 6.45 cm3; left lobe thickness 15.1 width 17.6 length 49.8 volume 6.35 cm3; isthmus thickness 5.8. Mercazolil 1t * 2 times, L-thyroxine cancel. 11.08.05 Mercazolil 5mg 1t * 2 times until 20.08.05, then switch to 1t * 1 time up to 12 months, valerian 1t * 3 times 10 days. 24.08.05 Z-6.0*10b grade 9 L, ESR 5,nv 130 Mercazolil 5mg 1t*1time, iodamarin 200 1t*1time 3 months 0.23-3.4; T4 freedom 65.7 norm 11-24; T3 free 6.7 norm 2.5-5.8 Mercazolil 5 mg t * 3 times, valerian 2 t * 3 times; glycine 2 t * 3 times , taktivin after 10 days on 27.08.06, on the recommendation of the attending physician, they switched to another, more experienced doctor. left lobe 1.7 * 2.16 * 5.3 cm, volume 9.3 cm3, isthmus 0.63 volume 19.0 cm3 norm 9-18, contour uneven, bumpy; echo density is reduced, echostructure is extremely heterogeneous; focal changes were not revealed, in both lobes hypoechoic areas merge with each other; regional lymph nodes are not enlarged. tests 8.08.06 TSH 0.17 norm 0.23-3.4; T3 3.42 norm 0.8-2.8; T4 freedom 16.9 norm 10-35, ATkTPO 25.1 (the norm is not indicated) Tyrozol 30, 10 mg * 3 times (until the symptoms of thyrotoxicosis decrease for about a month, then gradually reduce by 5 mg in 10-14 days until the dose is maintained at 10 mg for 1.5 years)? 20. Reduce the dose of tyrosol by 10 mg in 2 weeks. leave the dose of 10 mg for a year. I called the doctor and consulted. T3 1.0 norm 1.0-2.8; T4 freedom 19.6 norm 10-35. tyrosol 10mg, take off euthyrox 25.08.07 euthyrox was taken again for the last week due to the fact that heaviness appeared in the whole body, now the heaviness disappears, but swelling of the hands appeared unexpressed. TSH 3.1 T3 1.0 T4 free 19.6 against the background of tyrosol 10 mg. To prescribe tyrosol 5 mg 2-3 months tyrosol stopped taking since November 2007, due to the deterioration of her health, she began to take tyrosol again from the end of December 2007. Her condition improved. tyrosol 15 mg-1m EC, then 10 mg (Session started). 01/26/08 T3 3.4 norm 1-2.8; Т4 Free 32.1 norm 10-23.2; TSH 0.08 norm 0.23-3.4. reception was 4.02.08: Tirrzol stopped taking in November 2007. complaints: unexpressed general weakness, weight loss of 4 kg within a month. Shields of iron - diffuse increased to 2 tbsp (before that it was 1 tbsp.). Tyrozol 15 mg, then 10 mg long-term. This was the last visit to Tamara Ilyinichna (our doctor died), treatment began in Tomsk. 07/30/08 TSH 0.1 norm 0.23-3.4; T4 free 18.7 norm 10-23.2. Ultrasound: 7.08.08 iron shields are in a typical position; contours are fuzzy; horseshoe shape; diameter: 57.9 mm; isthmus thickness 6.4mm; melt dimensions length 50.2 width 22.7 thickness 16.8; lion length 50, width 22.4 thickness 17.2; the echostructure is heterogeneous with alternating hyper and hypoexogenous zones; mixed density. Nodular formations were found. tyrosol 15 mg The answer to your question: from November 2009 to January 2010, she took only tyrosol 15 mg without L-thyroxine AT to the TSH receptor was not prescribed. Thank you in advance.
Thyrotoxicosis (hyperthyroidism)- symptoms and treatment
What is thyrotoxicosis (hyperthyroidism)? We will analyze the causes of occurrence, diagnosis and methods of treatment in the article of Dr. O. N. Kurashov, an endocrinologist with an experience of 26 years.
Definition of illness. Causes of the disease
Thyrotoxicosis(hyperthyroidism) is a hypermetabolic process caused by an excess of thyroid hormones in the body and their toxic effects on various organs and tissues. It is clinically characterized by an increase in the thyroid gland and damage to other systems and organs.
The first descriptions of this pathology were found in the works of the Persian physician Jurjani, created in 1100.
This syndrome occurs both in women (up to 2%) and in men (up to 0.2%). Most often it occurs in people aged 20-45 years.
There are many causes for thyrotoxicosis. The main ones include:
- increased production of thyroid hormones due to various diseases (, and others);
- excessive intake of drugs containing thyroid hormones (violation of the prescribed treatment regimen).
The provoking factor of the syndrome is the additional amount of iodine that enters the body with the independent use of iodine supplements.
The state of thyrotoxicosis in diffuse toxic goiter is an autoimmune disease. It usually develops as a result of overproduction of antibodies to the thyroid stimulating hormone (TSH) receptor produced by the pituitary gland.
The occurrence of a thyrotoxic state is possible when the functional autonomy of an already existing thyroid node occurs - a single- and multi-nodular goiter. This disease develops for a long time, mainly in people over 45 years of age. So, in the absence of exposure to TSH - the main physiological stimulant - the nodes synthesize the amount of thyreohormones that exceeds the body's need.
If you experience similar symptoms, consult your doctor. Do not self-medicate - it is dangerous for your health!
Symptoms of thyrotoxicosis (hyperthyroidism)
When questioning patients with suspected elevated thyroid function, the following are revealed:
- unpredictable excitability, emotional instability, causeless tearfulness;
- anxiety and impaired concentration of attention that occurs when being in society;
- daily sleep disturbance
- fussiness when doing any work;
- weakness while walking;
- increased sweating of a diffuse nature, not dependent on physical or emotional stress, a feeling of "heat";
- periodic heartbeats;
- trembling in the body and increasing weight loss (rarely observed).
Emotional disorders are combined with motor-volitional disorders: there is a need for constant movement and choreo-like twitches. Moreover, tremor of the limbs and body is a typical symptom of thyrotoxicosis.
An increased amount of thyroid hormones affects cardiac activity
Among the characteristic changes that are detected in people with thyrotoxicosis during an examination by an ophthalmologist, there is a lesion of the soft tissues of the orbit. This pathology occurs in 40-50% of patients with involvement of the optic nerve and disease of the auxiliary apparatus of the eye (eyelids, conjunctiva and lacrimal gland). This does not exclude the development of neuropathy of the optic nerve and corneal lesions with the formation of a walleye.
The main syndromes of thyrotoxicosis in diffuse toxic goiter include:
- a set of symptoms of the central nervous system: astheno-neurotic and anxiety-depressive syndromes;
- one of the cardiovascular manifestations: persistent sinus tachycardia, paroxysmal or persistent atrial fibrillation, absence of tachycardia, thyrotoxic myocardial dystrophy;
- gastrointestinal syndromes: increased peristalsis and accelerated evacuation, insufficient digestion of food, periodic pain in the abdomen until the simulation of an "acute abdomen", toxic effects on hepatocytes;
- disorders associated with the endocrine glands: thyroid adrenal insufficiency in women, gynecomastia in men, impaired carbohydrate tolerance, development of osteoporosis.
The pathogenesis of thyrotoxicosis (hyperthyroidism)
The thyroid gland is an organ that produces thyroid hormones such as triiodothyronine (T3) and thyroxine (T4). TSH, a pituitary hormone, has a stimulating effect on them.
With diffuse toxic goiter, thyroid-stimulating antibodies (G) are formed that compete with TSH, a natural stimulator of the thymus gland (an important organ of the immune system).
With the onset of TSH deficiency, the immune process begins to progress. Thyroid-stimulating antibodies stimulate the C-cells of the thyroid gland, activating the secretion of thyrocalcitonin (TKT), which affects the enhancement of immunogenesis and thyrotoxicosis and leads to the progression of the autoimmune process. This effect of antibodies helps to reduce calcium in the blood and increase the excitation of thyrocytes (thyroid cells). A decrease in TSH is accompanied by an increase in thyroliberin and an increase in prolactin.
Significant influence on the progression of thyrotoxicosis has emotional stress and "psychotrauma" due to the active release of adaptation hormones (adrenaline and norepinephrine), which increase the synthesis and secretion of T3 and T4. This leads to atrophy of the thymus gland, a decrease in the concentration of interferon and an increase in the predisposition to infectious diseases and cancer.
A separate role in the pathogenesis of thyrotoxicosis is assigned to the influence of various viruses (triggers of an autoimmune reaction) through thyrocytes.
Classification and stages of development of thyrotoxicosis (hyperthyroidism)
According to ICD 10, there is the following classification of the syndrome:
- E05.0 - thyrotoxicosis with diffuse goiter;
- E05.1 - thyrotoxicosis with toxic single-nodular goiter;
- E05.2 - thyrotoxicosis with toxic multinodular goiter;
- E05.3 - thyrotoxicosis with ectopic thyroid tissue;
- E05.4 - artificial thyrotoxicosis;
- E05.5 - thyroid crisis or coma;
- E05.6 - other forms of thyrotoxicosis;
- E05.7 Thyrotoxicosis, unspecified.
Depending on the influence of TSH, there are three main types of thyrotoxicosis:
Criteria for assessing the severity of thyrotoxicosis
The classification of thyrotoxicosis proposed by professors V.V. Fadeev and G.A. Melnichenko, suggests the division of the syndrome into three types:
The subclinical type of thyrotoxicosis may occur as a result of the formation of functional autonomy of the thyroid gland, an overdose of thyroid hormones in thyroid cancer or hypothyroidism, painless thyroiditis.
Complications of thyrotoxicosis (hyperthyroidism)
The long course of the disease affects the formation of bones: there is a decrease in bone density and an increased risk of bone fractures (primarily tubular) in awkward situations. Women with increased thyroid function at menopause have an increased risk of these complications.
Also, cardiovascular disorders pose a serious danger: paroxysmal atrial fibrillation may occur, turning into a permanent form with the risk of thromboembolic complications.
With an increase in adverse environmental factors (for example, stressful situations, various diseases, surgical interventions, etc.), a thyrotoxic crisis may occur. Its characteristic features are:
- sudden excitability;
- an increase in body temperature up to 40 ° C;
- increase in heart rate up to 200 beats / min;
- atrial fibrillation (not always);
- increased nausea, (possibly to the point of vomiting) and diarrhea;
- increased thirst;
- increase in pulse blood pressure;
- the appearance of signs of adrenal insufficiency (occurs later).
The condition worsens after a few hours, so a thyrotoxic crisis requires emergency medical care.
Diagnosis of thyrotoxicosis (hyperthyroidism)
Diagnosing the syndrome involves interviewing the patient, identifying clinical signs and laboratory tests.
At history taking in patients with thyrotoxicosis
Laboratory research is indicated for all patients with thyroid pathology (especially those who have pronounced clinical manifestations of reduced or increased thyroid function), as well as during conservative treatment to control the adequacy of therapy and in the presence of concomitant pathology. The determination of total T3 is important in toxicosis, especially in cases of T3 toxicosis. Laboratory diagnostic indicators for thyrotoxicosis are a high level of free T3 and T4, as well as a low level of TSH in the blood.
Due to the fact that most of T3 and T4 are associated with blood proteins, a study of the free fractions of these hormones is carried out in combination with the determination of the level of TSH. In this case, the free fraction determines the biological effect of thyroid hormones.
Since the content of T3 and T4 is affected by a number of factors (for example, a low-calorie diet, liver disease, long-term medication), it is more expedient to study free fractions of thyroid hormones in combination with TSH.
The main attention should be paid to the level of TSH in the following cases:
- acute mental illness requiring hospitalization;
- diseases of the pituitary gland or hypothalamus;
- rapid changes in thyroid status.
In these cases, this study may lead to an erroneous diagnosis.
If thyroid dysfunction is suspected in severe patients with intact ("uninvolved") hypothalamic-pituitary function, a "panel" approach should be used - simultaneous determination of TSH and free T4.
In hyperthyroidism, the synthesis and secretion of TSH are suppressed, so the determination of very low concentrations of TSH is of fundamental importance in the diagnosis of its various forms. The exceptions are rare cases of TSH-induced thyrotoxicosis (when TSH secretion is increased), which include TSH-producing pituitary adenoma and the syndrome of inappropriate TSH secretion, due to the resistance of this pituitary hormone to the effects of T3 and T4.
Additional diagnostic methods:
The size of the thyroid gland according to the results of palpation is determined according to the 1994 WHO classification.
In the event that a patient is palpated with an increase in size or a suspicion of a nodular formation in the thyroid gland, ultrasound diagnostics (ultrasound) is performed with the calculation of the volume of the thyroid gland - the formula (I. Brunn, 1986):
Volume = [(WxDxL) right + (WxDxL) left] x 0.479;
W, D, L are the width, thickness and length of the thyroid gland, and 0.479 is the correction factor for the ellipsoid shape of the organ.
Ultrasound of the thyroid gland is usually performed using a high-frequency transducer with a frequency of 7.5 MHz. The use of color Doppler mapping allows visualization of small vessels in the organ under study and provides information on the direction and average flow velocity.
In some cases, a thyroid scintigraphy can be performed, which shows the ability of the organ to capture iodine and other substances (technetium).
Differential Diagnosis held:
Treatment of thyrotoxicosis (hyperthyroidism)
In the treatment of thyrotoxicosis, the main methods are usually used:
The fight against the syndrome involves the elimination of clinical manifestations of thyrotoxicosis with the normalization of T3, T4 and TSH values and the achievement of a stable remission of the disease.
Conservative therapy
In the conservative treatment of diffuse toxic goiter in patients with a moderately enlarged thyroid gland (up to 40 ml), propylthiouracil (PTU) or thiamazole (Tirozol or Mercazolil) is prescribed. This contributes to the normal functioning of the affected organ. In diagnosed cases of diffuse toxic goiter in the first trimester of pregnancy and the occurrence of side effects while taking thiamazole, PTU is prescribed. As a result of treatment, after 4-6 weeks, an improvement is noted - the level of free T4 normalizes. Additionally, according to indications, beta-blockers are prescribed (for example, 2.5-5 mg of Concor per day).
In severe cases of the process, it is recommended to take glucocorticoids - up to 10-15 mg of prednisolone per day. Then, within 2-3 weeks, the thyreostatic dose is reduced to maintenance (no more than 10 mg per day). In parallel, the patient is usually prescribed 50 micrograms of levothyroxine per day. This treatment regimen is called "Block and replace". Stable maintenance of the level of free T4 and TSH in the norm will indicate the adequacy of the prescribed therapy.
In the presence of persistent side effects of the prescribed treatment, thyreostatic drugs are canceled, radioactive iodine therapy or surgery is prescribed. In the event of a recurrence of thyrotoxicosis, the question arises of the need for radioiodine therapy or thyroidectomy - complete or partial removal of the thyroid gland.
Treatment with radioactive iodine
Radioiodine therapy for diffuse toxic goiter is carried out in case of persistent recurrence of thyrotoxicosis at the end of properly conducted conservative therapy (within 12-18 months) and difficulties in taking thyreostatic drugs (decrease in the number of leukocytes in the blood or the occurrence of allergic reactions).
Treatment with radioactive iodine is carried out in specialized centers with radiation and environmental safety for people and nature. The only contraindications for this therapy are pregnancy and lactation.
The goal of radioiodine therapy in the destruction of hyperfunctioning thyroid tissue is to achieve a stable hypothyroid state.
Surgical treatment
Surgical intervention for diffuse toxic goiter is necessary if the goiter is located behind the sternum, with diffuse and nodular forms of goiter with compression and the patient refuses other methods of therapy. Total and subtotal thyroidectomy are the treatment of choice. In the presence of a nodular formation in the thyroid gland, it is necessary to conduct a puncture biopsy and diagnostic cytological examination. To complicate the course and prognosis of the disease, especially in relation to the ability to work and the state of health in general, may develop atrial fibrillation and severe manifestations of heart failure in thyrotoxicosis.
When a favorable outcome of the disease occurs, patients with thyrotoxicosis should take preventive measures against the occurrence of relapse in the form of:
- compliance with a sparing lifestyle regimen for 3-6 months;
- restrictions on physical activity;
- creation by relatives of psychological peace, and at work - reduction of hours of intensive loads, incl. night shifts (if any).
Such prevention of recurrence of the disease is extremely important, because the thyroid gland is a fragile and at the same time strong organ, with its own "character".
Long-term stable remission of thyrotoxicosis is an indication for sanatorium-and-spa therapy in conditions of low altitude and periodic out-of-town rest in a comfortable environment. At the same time, it is undesirable to stay in the open sun; sunscreen should be used at sea.
Treatment and preventive measures include balneological procedures using native radon waters. Their effectiveness and positive effect on the body have been proven by many years of research conducted at resorts with mineral waters.
So, in the treatment of patients with thyrotoxicosis at the Belokurikha resort, the effectiveness of radon procedures in conjunction with drug therapy (mercasolil, microiodine and reserpine) was confirmed. Radon-free nitrogen baths have a preventive effect through thermal and mechanical stimulation of nerve receptors with nitrogen bubbles.
There are three ways to eliminate hyperthyroidism - to reduce the level of thyroid hormones in the blood:
1. destroy excess thyroid hormones medicines
2. destroy the thyroid gland so that it does not produce excess hormones (surgical treatment and radioactive iodine therapy)
3. restore thyroid function
- goiter effect (an increase in the size of the thyroid gland while taking thyreostatics);
- complications from the blood (the number of leukocytes, platelets decreases);
- allergic reactions;
- abnormal liver function (ALT, AST increase);
- diarrhea, headache, menstrual disorders, etc.
Surgical treatment and radioactive iodine therapy in the treatment of hyperthyroidism
Surgical treatment - surgical removal of the thyroid gland, and radioactive iodine therapy - slow radiation destruction of the thyroid gland, eliminates any possibility of recurrence of hyperthyroidism - a recurrence rate of 0%. But at what cost!
Thyroid removal any way leads to a dangerous disability. Autoimmune processes in the body do not disappear and are now controlled expensive life HRT. In addition to the violation of the digestive, cardiovascular, nervous and reproductive systems of a person, you get lifelong hypothyroidism and other chronic diseases. On danger and therapeutic futility surgery or exposure radioactive iodine More details can be found at the links provided.
Safe treatment hyperthyroidism without hormones and operations method of computer reflex therapy, which is aimed precisely at eliminating the malfunction of not only the human immune system, but also for restoration and coordinated work human nervous and endocrine systems.
The coordinated work of the internal organs of our body is regulated by the coordinated interaction of 3 main control systems: nervous, immune And endocrine. It is from their synchronous and well-coordinated work that the physical condition and health of a person depends. Any disease progresses and the body cannot cope with it on its own precisely because of failure in the synchronous operation of these systems.
Rebooting the body's three major regulatory systems to a state of active struggle with harmful external environmental influences, internal diseases, is the main task of therapy focused on the impact on the body through the autonomic nervous system.
There are many methods of influencing the nervous system, but, to date, only computer reflex therapy acts through the nervous system in such a way that 93% cases in patients, the neuro-immuno-endocrine regulation of the body is completely restored and, as a result, many endocrine and neurological diseases that previously did not respond to drug "treatment" recede and completely disappear.
Efficiency therapy also lies in the fact that the doctor affects the patient’s body not “blindly”, but, thanks to special sensors and a computer system, sees what points nervous system and How many required to use a medical device.
An indicative CRT result for one of our patients, who once again double-checked the results for hormones in her regional clinic:
FULL NAME - Fayzullina Irina Igorevna
Laboratory research BEFORE treatment M20161216-0003 from 16.12.2016 ()
Thyroid Stimulating Hormone (TSH) - 8,22 μIU/ml
Laboratory research AFTER 1 CRT course M20170410-0039 from 10.04.2017 ()
Thyroid Stimulating Hormone (TSH) - 2,05 μIU/ml
Free thyroxine (T4) - 1,05 ng/dl
Before each procedure, the doctor conducts a diagnosis of the patient, based on the results of which he makes an individual prescription of points for the procedure in accordance with the treatment plan. During the procedure itself, every second scanning of the current state of the patient allows you to accurately dose the effect, which, in principle, is not available when exposed to any other methods.
Of course, this method of treatment, like any other, has restrictions and contraindications- This oncological diseases And mental disorders, disorders of the heart (presence pacemaker, flickering arrhythmia And myocardial infarction in the acute period) HIV-infection and congenital hypothyroidism. If you do not have the above contraindications, then getting rid of hyperthyroidism using this method in our clinic has been a common practice for many years.
For a good 20 years now, the Gavrilova Clinic in the city of Samara has been carrying out thyroid gland restoration without hormones and operations. The author and developer of the method is Gavrilova Natalya Alekseevna. Associate Professor, Ph.D. with general medical experience since 1968, awarded the Order of Medical Merit. If you wish, you can learn more about bioelectrophysical the basics of the therapeutic effect of reflex therapy and specific treatment examples.
Using the method of computer reflex therapy, the doctor restores the neuro-immuno-endocrine regulation of the entire patient's body. Restoration of the structure and function of the thyroid gland is a manifestation of how the body, using its internal reserves and capabilities, self-regenerates in a natural way for it.
Treatment of hyperthyroidismcomputer reflex therapy without side effects leads to the following results:
- are recovering functioning tissue and structure of the thyroid gland;
- Normalizes the level of own thyroid hormones T4 (thyroxine) and T3 (triiodothyronine), as well as the level of TSH (pituitary hormone), which is confirmed by blood tests;
- If the patient takes hormone replacement drugs, it is possible to reduce their dosage and completely cancel at the end of treatment;
- At getting better aboutgeneral well-being to the state of a healthy person;
- Often, after a course of treatment, diseases associated with the work of the nervous system, allergic and other autoimmune diseases disappear..
Leave your contact and the consulting doctor will contact you
Head of the department, endocrinologist, reflexologist, candidate of medical sciences.
Drug therapy in the "treatment" of hyperthyroidism
Destroy thyroid hormones drug thyreostatic drugs. Drug treatment - for a long time - up to 3 years. Treatment begins with large doses of these drugs, as soon as free T4 normalizes, the thyreostatic dose is gradually reduced to maintenance (10-15 mg per day). This blocks the production of thyroid hormones. In parallel, hormone-replacing drugs are prescribed 50-75 mcg per day to replace the destroyed own hormones. The principle of this treatment: block and replace! The therapy is called hormone replacement therapy (HRT).
Drug "treatment" has many side effects:
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 amount of hormones in the body leads to various physical changes and changes in the emotional sphere.
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 the cells of the 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 heart failure, have lost weight - this is a reason to see a doctor and get tested for thyroid hormones. These are symptoms of thyrotoxicosis.
Also, the symptoms of thyrotoxicosis include: increased 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 computed tomography of the orbit area is performed.
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
It should be warned against treatment with folk remedies. Thyrotoxicosis is a serious condition that, without adequate timely treatment, can 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 of coronary heart disease, damage to the central nervous system in severe cases 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 severe 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 a course of drug treatment of thyrotoxicosis is being carried out, 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
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
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 (DTG) - Graves-Basedow's disease
- thyrotoxic adenoma
- multinodular toxic goiter
- iodine-induced thyrotoxicosis- (iodine-Basedow)
- well-differentiated thyroid cancer
- 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 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 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;
- heart rhythm disturbances: 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 of thyrotoxicosis associated with a violation of the autonomic innervation of the 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).
To assess the size of the thyroid gland, the WHO classification of 1994 is recommended. This international classification is simplified, accessible 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 thumb of the subject.
Grade 2 - goiter is palpable and visible to the eye.
- damage to other organs of internal secretion:
- development of thyroid adrenal insufficiency;
- ovarian dysfunction with menstrual dysfunction up to amenorrhea, miscarriage;
- fibrocystic mastopathy in women, gynecomastia in men;
- 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 :
|
Outcomes of conservative thyrostatic therapy with thiamazole ( n=80) |
Thyroid functions |
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 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, surgical treatment is recommended. 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 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 fever, sore throat, and 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 "ideal" and etiotropic treatment, standard recommendations for monitoring, continuity of inpatient and outpatient treatment, and minimally effective maintenance doses remain unresolved.
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 when euthyroidism is achieved 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 direction in the treatment is the use of octreotide, human immunoglobulin, treatment regimens for which 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 damage to the cardiovascular system and myopathy is noted, 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 a 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 oncological 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 has not yet been a consensus on this issue, and there is no experience in using the drug in our country.
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 of hypothyroidism are not very specific, so the initial stages of the disease are usually not recognized and patients are unsuccessfully treated by various specialists.
Patients complain of a feeling of chilliness, an unmotivated increase in body weight against the 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; due to 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 analysis of blood - determination of the level of TSH. 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 of primary hypothyroidism, characteristic markers can be determined:
- "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 of the 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 the lesion and the cause that caused the hypothyroidism syndrome, replacement therapy with levothyroxine is prescribed (recently, combined drugs T3 and T4 are used much less frequently).
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 concomitant pathology, 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. It is possible to transfer thyroid-stimulating antibodies (TSH Ab) from mother to fetus, 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 a malignant process in the thyroid gland, or the need to use large 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 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, a decrease in the level of TSH in combination with an increase in free T4 in early pregnancy will indicate; 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 maternal hypertension, fetal malformations, premature birth, and 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 advised 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.
