What you would like to know about Graves' disease - diffuse toxic goiter. Do not take medications occasionally

Graves' disease (Bazedow's disease, diffuse toxic goiter)- a systemic autoimmune disease that develops as a result of the production of antibodies to the thyroid hormone receptor, clinically manifested by damage to the thyroid gland with the development of thyrotoxicosis syndrome in combination with extrathyroid pathology: endocrine ophthalmopathy, pretibial myxedema, acropathy. The disease was first described in 1825 by Caleb Parry, in 1835 by Robert Graves, and in 1840 by Karl von Basedow.

Etiology

Diffuse toxic goiter is a multifactorial disease in which genetic features immune response are realized against the background of the action of factors environment. Along with ethnically associated genetic predisposition (carriage of haplotypes HLA-B8, -DR3 and -DQA1*0501 in Europeans), in the pathogenesis of diffuse toxic goiter some importance is attached to psychosocial advanced factors. Emotional stress and exogenous factors, such as smoking, can contribute to the implementation of a genetic predisposition to diffuse toxic goiter. Smoking increases the risk of developing diffuse toxic goiter by 1.9 times. Diffuse toxic goiter in some cases is combined with other autoimmune diseases endocrine diseases(diabetes mellitus type 1, primary hypocortisolism).

As a result of impaired immunological tolerance, autoreactive lymphocytes (CD4+ and CD8+ T lymphocytes, B lymphocytes) with the participation of adhesion molecules (ICAM-1, ICAM-2, E-selectin, VCAM-1, LFA-1, LFA-3, CD44 ) infiltrate the parenchyma of the thyroid gland, where they recognize a number of antigens that are presented by dendritic cells, macrophages and B lymphocytes. Subsequently, cytokines and signaling molecules initiate antigen-specific stimulation of B lymphocytes, resulting in the production of specific immunoglobulins against various components of thyrocytes. In the pathogenesis of diffuse toxic goiter, the main importance is given to the formation stimulating antibodies to TSH receptor (AT-rTSH).

Unlike other autoimmune diseases, diffuse toxic goiter does not cause destruction, but stimulation of the target organ. In this case, autoantibodies are produced to a fragment of the TSH receptor, which is located on the membrane of thyrocytes. As a result of interaction with the antibody, this receptor becomes active, triggering a post-receptor cascade of thyroid hormone synthesis (thyrotoxicosis) and, in addition, stimulating hypertrophy of thyrocytes (enlargement of the thyroid gland). For reasons that are not entirely clear, T-lymphocytes sensitized to thyroid antigens infiltrate and cause immune inflammation in a number of other structures, such as retrobulbar tissue (endocrine ophthalmopathy), tissue of the anterior surface of the leg (pretibial myxedema).

Pathogenesis

Clinically, the most significant syndrome that develops with diffuse toxic goiter due to hyperstimulation of the thyroid gland by antibodies to the TSH receptor is thyrotoxicosis. The pathogenesis of changes in organs and systems that develop during thyrotoxicosis is a significant increase in the level of basal metabolism, which over time leads to dystrophic changes. The structures most sensitive to thyrotoxicosis, in which the density of receptors for thyroid hormones is highest, are the cardiovascular (especially the atrial myocardium) and nervous systems.

Epidemiology

In regions with normal iodine intake, diffuse toxic goiter is the most frequent illness V nosological structure thyrotoxicosis syndrome (if you do not take into account diseases that occur with transient thyrotoxicosis, such as postpartum thyroiditis, etc.). Women get sick 8-10 times more often, in most cases between 30 and 50 years. The incidence of diffuse toxic goiter is the same among representatives of the European and Asian races, but lower among the Negroid race. The disease is quite rare in children and the elderly.

Clinical manifestations

Diffuse toxic goiter, in most cases, is characterized by a relatively short history: the first symptoms usually appear 4-6 months before visiting a doctor and making a diagnosis. As a rule, the key complaints relate to changes on the part of cardiovascular system, the so-called catabolic syndrome and endocrine ophthalmopathy.

The main symptom from cardiovascular system is tachycardia and quite pronounced sensations of heartbeat. Patients may feel palpitations not only in chest, but also the head, arms, stomach. Heart rate at rest with sinus tachycardia caused by thyrotoxicosis can reach 120-130 beats per minute.

With long-term thyrotoxicosis, especially in elderly patients, severe dystrophic changes in the myocardium, a frequent manifestation of which is supraventricular rhythm disturbances, namely atrial fibrillation (atrial fibrillation). This complication of thyrotoxicosis rarely develops in patients under 50 years of age. Further progression of myocardial dystrophy leads to the development of changes in the ventricular myocardium and congestive heart failure.

Typically expressed catabolic syndrome, manifested by progressive weight loss (sometimes by 10-15 kg or more, especially in persons with initial excess weight) against the background of increasing weakness and increased appetite. The skin of patients is hot, sometimes there is severe hyperhidrosis. A feeling of heat is typical; patients do not freeze at a sufficiently low temperature in the room. Some patients (especially the elderly) may experience evening low-grade fever.

Changes from nervous system are characterized by mental lability: episodes of aggressiveness, agitation, chaotic unproductive activity are replaced by tearfulness, asthenia (irritable weakness). Many patients are not critical of their condition and try to maintain active image life against the backdrop of a rather difficult somatic condition. Long-term thyrotoxicosis is accompanied by persistent changes in the patient’s psyche and personality. A frequent but nonspecific symptom of thyrotoxicosis is fine tremor: slight trembling fingers of outstretched arms is detected in most patients. In severe thyretoxicosis, tremors can be detected throughout the body and even make it difficult for the patient to speak.

Thyrotoxicosis is characterized by muscle weakness and a decrease in muscle volume, especially the proximal muscles of the arms and legs. Sometimes quite pronounced myopathy develops. Very rare complication is thyrotoxic hypokalemic periodic paralysis, which manifests itself periodically sudden attacks muscle weakness. Laboratory tests reveal hypokalemia and increased CPK levels. It is more common among representatives of the Asian race.

Intensification of bone resorption leads to the development osteopenia syndrome, and thyrotoxicosis itself is considered one of the most important factors risk of osteoporosis. Frequent complaints patients are hair loss, brittle nails.

Changes from gastrointestinal tract develop quite rarely. Elderly patients may have diarrhea in some cases. With long-term severe thyrotoxicosis, dystrophic changes in the liver (thyrotoxic hepatosis) can develop.

Menstrual irregularities are quite rare. Unlike hypothyroidism, moderate thyrotoxicosis may not be accompanied by a decrease in fertility and does not exclude the possibility of pregnancy. Antibodies to the TSH receptor penetrate the placenta, and therefore in children born (1%) to women with diffuse toxic goiter (sometimes years after radical treatment), transient neonatal thyrotoxicosis may develop. In men, thyrotoxicosis is often accompanied by erectile dysfunction.

In severe thyrotoxicosis, a number of patients exhibit symptoms of thyroidogenic (relative) adrenal insufficiency, which must be differentiated from the true one. Hyperpigmentation of the skin and exposed parts of the body is added to the symptoms already listed. (Jellinek's sign), arterial hypotension.

In most cases, diffuse toxic goiter occurs enlargement of the thyroid gland, which, as a rule, is diffuse in nature. Often the gland is significantly enlarged. In some cases, you can listen above the thyroid gland systolic murmur. However, goiter is not an obligate symptom of diffuse toxic goiter, since it is absent in at least 25-30% of patients.

Of key importance in the diagnosis of diffuse toxic goiter are changes in the eyes, which are a kind of “calling card” of diffuse toxic goiter, i.e. their detection in a patient with thyrotoxicosis almost unambiguously indicates diffuse toxic goiter, and not another disease. Very often, due to the presence of severe ophthalmopathy in combination with symptoms of thyrotoxicosis, the diagnosis of diffuse toxic goiter is obvious already upon examination of the patient.

Another rare (less than 1% of cases) disease associated with diffuse toxic goiter is pretibial myxedema. The skin of the anterior surface of the leg becomes swollen, thickened, purple-red in color (“orange peel”), often accompanied by erythema and itching.

The clinical picture of thyrotoxicosis may vary from classic version. So, if young people Diffuse toxic goiter is characterized by a detailed clinical picture; in elderly patients, its course is often oligo- or even monosymptomatic (heart rhythm disturbance, low-grade fever). In the “apathetic” version of the course of diffuse toxic goiter, which occurs in elderly patients, clinical manifestations include loss of appetite, depression, physical inactivity.

A very rare complication of diffuse toxic goiter is a thyrotoxic crisis, the pathogenesis of which is not entirely clear, since a crisis can develop without an extreme increase in the level of thyroid hormones in the blood. The cause of thyrotoxic crisis may be acute acute goiter accompanying diffuse toxic goiter. infectious diseases, performing surgery or therapy with radioactive iodine against the background of severe thyrotoxicosis, canceling thyreostatic therapy, administering an iodine-containing contrast drug to the patient.

Clinical manifestations of a thyrotoxic crisis include a sharp worsening of the symptoms of thyrotoxicosis, hyperthermia, confusion, nausea, vomiting, and sometimes diarrhea. Registered sinus tachycardia over 120 beats/min. It is often noted atrial fibrillation, high pulse pressure followed by severe hypotension. IN clinical picture heart failure may predominate, respiratory distress syndrome. Manifestations of relative adrenal insufficiency are often expressed in the form of skin hyperpigmentation. Skin may be icteric due to the development of toxic hepatosis. Laboratory tests may reveal leukocytosis (even in the absence of concomitant infection), moderate hypercalcemia, increased levels alkaline phosphatase. Mortality during thyrotoxic crisis reaches 30-50%.

Diagnostics

TO diagnostic criteria Diffuse toxic goiter includes:

Laboratory confirmed thyrotoxicosis (decrease in TSH, increase in T4 and/or T3).

Endocrine ophthalmopathy (60-80% of cases).

Diffuse increase in the volume of the thyroid gland (60-70%).

Diffuse enhancement of 99m Tc uptake according to thyroid scintigraphy.

Increased level of antibodies to the TSH receptor.

At the first stage of diagnosing diffuse toxic goiter, it is necessary to confirm that the patient has clinical symptoms(tachycardia, weight loss, tremor) is caused by thyrotoxicosis syndrome. For this purpose, a hormonal study is carried out, which reveals a decrease or even complete suppression TSH level and increased levels of T4 and/or T3. Further diagnosis is aimed at differentiating diffuse toxic goiter from other diseases occurring with thyrotoxicosis. In the presence of clinically significant endocrine ophthalmopathy, the diagnosis of diffuse toxic goiter is almost obvious. In some cases, in the absence of obvious endocrine ophthalmopathy, it makes sense to actively search for it using instrumental methods(Ultrasound and MRI of the orbits).

Ultrasound for diffuse toxic goiter usually reveals diffuse increase thyroid gland and hypoechogenicity, characteristic of all its autoimmune diseases. Determining the volume of the thyroid gland is, in addition, necessary for choosing a treatment method, since the prognosis of conservative thyreostatic therapy for goiter large size bad enough. Thyroid scintigraphy is not necessary in typical cases (thyrotoxicosis, endocrine ophthalmopathy, diffuse goiter, young age of the patient). In less obvious situations, this method makes it possible to differentiate diffuse toxic goiter from diseases occurring with destructive thyrotoxicosis (postpartum, subacute thyroiditis etc.) or from the functional autonomy of the thyroid gland (multi-nodular toxic goiter with “hot” nodes).

In diffuse toxic goiter, at least 70-80% of patients have circulating antibodies to thyroid peroxidase (AT-TPO) and thyroglobulin (AT-TG), however, they are nonspecific for this disease and occur in any other autoimmune pathology thyroid gland ( autoimmune thyroiditis, postpartum thyroiditis). In some cases, an increase in the level of AT-TPO can be regarded as indirect diagnostic sign diffuse toxic goiter, when we're talking about about her differential diagnosis from non-autoimmune diseases occurring with thyrotoxicosis (functional autonomy of the thyroid gland). A fairly specific test for the diagnosis and differential diagnosis of diffuse toxic goiter is to determine the level antibodies to TSH receptor which in this disease are given the main pathogenetic significance. However, it should be taken into account that in some cases these antibodies are not detected in patients with obvious diffuse toxic goiter, which is due to the imperfection of relatively recently developed test systems.

Treatment

There are three methods of treating diffuse toxic goiter (conservative treatment with thyreostatic drugs, surgical treatment and therapy 131 I), while none of them is etiotropic. IN different countries The proportion of use of these treatment methods traditionally differs. Thus, in European countries, the most accepted method of treatment is conservative therapy thyreostatics, in the United States the vast majority of patients receive 131 I therapy.

Conservative therapy carried out using thiourea preparations, which include thiamazole(mercazolyl, tyrosol, methizol) and propylthiouracil(PTU, propitsil). The mechanism of action of both drugs is that they actively accumulate in the thyroid gland and block the synthesis of thyroid hormones due to inhibition of thyroid peroxidase, which adds iodine to tyrosine residues in thyroglobulin.

Purpose surgical treatment, as well as therapy 131 I is the removal of almost the entire thyroid gland, on the one hand, ensuring the development of postoperative hypothyroidism (which is quite easily compensated), and on the other, eliminating any possibility of relapse of thyrotoxicosis.

In most countries of the world, the majority of patients with diffuse toxic goiter, as well as with other forms of toxic goiter, receive radioactive 131 I therapy as the main method of radical treatment. This is due to the fact that the method is effective, non-invasive, relatively inexpensive, and devoid of those complications which can develop during thyroid surgery. The only contraindications to treatment with 131 I are pregnancy and breast-feeding. IN significant quantities 131 I accumulates only in the thyroid gland; after entering it, it begins to disintegrate with the release of beta particles, which have a path length of about 1-1.5 mm, which ensures local radiation destruction of thyrocytes. A significant advantage is that 131 I treatment can be carried out without preliminary preparation thyreostatics. For diffuse toxic goiter, when the goal of treatment is destruction of the thyroid gland, therapeutic activity taking into account the volume of the thyroid gland, the maximum uptake and half-life of 131 I from the thyroid gland is calculated based on the estimated absorbed dose of 200-300 Gray. With an empirical approach, a patient without preliminary dosimetric studies is prescribed about 10 mCi for a small goiter, and 15-30 mCi for a larger goiter. Hypothyroidism usually develops within 4-6 months after administration of 131 I.

Peculiarity treatment of diffuse toxic goiter during pregnancy is that a thyreostatic agent (preference is given to PTU, which penetrates the placenta worse) is prescribed in a minimal amount required dose(only according to the “block” scheme), which is necessary to maintain the level of free T4 at upper limit norm or slightly above it. Usually, as the duration of pregnancy increases, the need for thyreostatic drugs decreases and most women after 25-30 weeks do not take the drug at all. However, most of them develop a relapse of the disease after childbirth (usually 3-6 months).

Treatment thyrotoxic crisis involves intensive activities with appointment large doses thyreostatics. Preference is given Vocational school at a dose of 200-300 mg every 6 hours, if not possible self-administration by the patient - through a nasogastric tube. In addition, beta-blockers are prescribed (propranolol: 160-480 mg per day per os or intravenously at a rate of 2-5 m g/hour), glucocorticoids (hydrocortisone: 50-100 mg every 4 hours or prednisolone (60 mg/day), detoxification therapy ( saline solution, 10% glucose solution) under hemodynamic control. Effective method The treatment for thyrotoxic crisis is plasmapheresis.

Forecast

In the absence of treatment, it is unfavorable and is determined by the gradual development of atrial fibrillation, heart failure, and exhaustion (marantic thyrotoxicosis). In the case of normalization of thyroid function, the prognosis of thyrotoxic cardiomyopathy is favorable - in most patients, cardiomegaly regresses and is restored sinus rhythm. The probability of relapse of thyrotoxicosis after a 12-18-month course of thyreostatic therapy is 70-75% of patients.

, is the most common disease of the thyroid gland, which occurs with the development of thyrotoxicosis. Graves' disease is often diagnosed in women between the ages of 30 and 50. With such a pathology in in rare cases faced by persons in old age or childhood.

Diffuse goiter is an autoimmune disease. This pathology is hereditary. Therefore, the risk of developing the disease in children whose parents suffered from goiter is quite high. In this case, patients synthesize antibodies, which, in turn, affect the cells of the thyroid gland. As a result, cells produce large number hormones.

The causes of goiter are associated with the following ailments:

traumatic brain injury;
stress;
nasopharyngeal disease;
infectious disease.

The causative factor in the development of Graves' disease may be a lack of iodine in the body through food or water. Those at risk are those who take medicines based on iodine without doctor's recommendations. According to data medical statistics, persons who work in areas where iodine is extracted are at twice the risk of illness.

Doctors also call diffuse toxic goiter Bazedow's disease. Since this pathology is autoimmune in nature, it is more often diagnosed in people suffering from diabetes mellitus, rheumatoid arthritis or scleroderma.

In some cases, prolonged experiences, stress, severe physical labor, bad habits or hypothermia.

Classification by degree

According to classification World Organization Graves' disease has 3 stages of development.

On initial stage development of pathology clinical symptoms may not appear. Palpation does not detect any changes.
On next stage Graves' disease does not manifest itself visually, but when palpating the thyroid gland, its enlargement is observed.
On last stage changes become noticeable not only upon palpation, but also visually.

To determine the stage of Graves' enlargement, in some cases another classification is used. On initial stage the disease is asymptomatic. The first clinical symptoms appear in the second stage, when thyroid gland becomes noticeable when swallowing. At the next stage, the thyroid gland noticeably enlarges. The patient's neck contour changes. If treatment is not started in a timely manner, Graves' disease becomes the most severe degree. In this case, the thyroid gland becomes huge. It begins to compress neighboring organs.

Based on severity, Bazedow's disease is classified into mild, moderate and severe. Mild form The pathology is characterized by nervous excitability and weight loss. The patient's heart rate increases to 80-100 beats per minute. General condition gradually getting worse. The patient loses his ability to work. Treatment at this stage is more effective.

At average shape severity, the patient exhibits excitability and nervousness. The number of beats per minute is 100-120. Weight loss reaches 15-20% of total mass bodies.

The most difficult is last stage diffuse toxic goiter. The patient's condition sharply worsens, and serious problems with heart and liver. Nervous excitability leads to complete loss of performance. Patients lose about half of their total body weight.

Symptoms of the disease

With Basedow's disease, patients experience sleep problems, rapid heartbeat, nervousness, agitation and irritability. Persons suffering from toxic goiter do not tolerate high temperature environment. In some cases, patients have complaints about stabbing pain in the chest area. Despite weight loss, appetite remains the same. Diarrhea may also be added to the symptoms.

Basedow's disease manifests itself in disruption of the heart. Diffuse goiter is characterized by an increase in systolic and a decrease in diastolic heart pressure. The blood vessels dilate, causing the skin to become moist and warm. In some cases, patients may experience hives, darkening of skin folds, and itching. Hair loss may occur in 5-10% of patients.

Symptoms diffuse goiter appear as trembling fingers. Sometimes, due to strong trembling of the hands, it is difficult for the patient to perform usual actions. As the pathology progresses, patients are unable to dress, eat, comb their hair, and take care of themselves due to finger trembling.

With diffuse goiter, disturbances in the functioning of the central nervous system are observed. Patients complain of feeling constant worry and irritability. The characteristic symptom is frequent changes mood and sleep disorders. In this regard, depression appears.

When Basedow's disease manifests itself ophthalmological symptoms. The patient develops pain in the eyes and constant lacrimation. The eyes widen, the eyeball bulges, and an impression of surprise or fear is created on the face. The upper eyelid rises and the eyelids do not close completely. Without treatment, the disease progresses and leads to severe eye pain and complete blindness.

An enlarged thyroid gland can cause difficulty breathing, choking and coughing, dizziness and difficulty swallowing. In persons suffering from diffuse goiter, the voice changes and hoarseness appears.

If Bazedow's disease is suspected, doctors carry out ultrasound examination, palpation of the thyroid gland and blood is taken for further examination of the level of pancreatic hormones.

Treatment of Graves' disease

Goiter treatment is carried out based on the diagnostic results and the severity of symptoms. At the initial stage of development of the pathology, treatment is carried out by medication. The main goal of therapy is to regulate the production of thyroid hormone.

The patient is prescribed thyreostatic drugs, which short period over time can reduce the productivity of the thyroid gland.

These drugs include Mercazolil, Carbimazole and Propylthiouracil. Treatment is carried out under the strict supervision of a doctor, because the drugs cause side effects. Self-medication can lead to the complete disappearance of all types of leukocytes in the blood.

In addition, doctors prescribe beta blockers, for example, Anaprilin or Obzidan. These drugs reduce heart rate, improve myocardial nutrition and normalize blood pressure.

In case of severe diffuse goiter, the patient is prescribed glucocorticosteroids.

An overactive thyroid gland is treated with hormone replacement therapy, which uses tyrosine analogues. This treatment is carried out until the end of life.

In combination with basic treatment, doctors prescribe medications that effectively combat existing symptoms. For nervous system disorders, doctors prescribe sedatives, for example Seduxen or Relanium. They have a hypnotic, anticonvulsant and muscle relaxant effect.

If drug therapy turned out to be ineffective, then doctors perform a subtotal resection of the thyroid gland. During the operation, the gland is partially removed and a small area is left glandular tissue. During the recovery period after surgery, doctors prescribe replacement therapy which allows you to avoid hormonal disorder in the body.

Surgeries do not worsen autoimmune diseases, but on the contrary, allow the patient to return to everyday life after long period recovery.

Radical methods of treatment also include iodine therapy. The principle of the procedure is to remove thyroid tissue from further development hypothyroidism.

During the rehabilitation period, doctors recommend performing therapeutic exercises and hardening procedures. For preventive purposes, a diet is prescribed that includes a high content of plant and animal proteins. Tinctures and decoctions based on medicinal herbs which have a sedative effect.

Graves' disease is the most common thyroid disease. In medical sources you can find other names: diffuse toxic goiter, Graves' disease, Flayani's disease.

Graves' disease most often affects residents of regions where the soil and water are characterized by a deficiency of the element iodine. Mostly women are affected. However, even in relatively iodine-rich areas it is diagnosed large percentage violations. Scientists indicate several reasons for the prevalence of Graves' disease:

genetic factor;
poor nutrition;
harmful working conditions;
radiation;
stress.

What is the basis of the disease

As mentioned above, Graves' disease is associated with the accumulation of genetic mutations under the influence of consanguineous marriages, infections various kinds, radiation and stress conditions.

Under the influence of immune aggression, abnormal stimulation of thyroid cells and tissue proliferation occurs. , which has negative impact As a result of this abnormal symbiosis, the synthesis of triiodothyronine and thyroxine increases on the hypothalamus and pituitary gland, which leads to a condition called thyrotoxicosis.

Clinical picture of the disorder

Most often, patients complain of heart problems, which is expressed in the development of shortness of breath, arrhythmia, and hypertension. Patients with Graves' disease symptoms such as chest pain, swelling, poor appetite, insomnia.

Other symptoms of the disorder:

sudden weight loss;
trembling of legs and arms;
damp skin;
sweating;
heartburn;
diarrhea;
pain in the intestines.

In women, Graves' disease can cause infertility, amenorrhea and decreased libido.

Violation calcium metabolism leads to tooth loss and frequent fractures bones.

Ophthalmopathy as one of the main signs of the disease

With Graves' disease, a symptom develops such as ophthalmopathy associated with damage to the fiber of the eyes. Endocrine ophthalmopathy is characterized by bulging eyes and impaired eyelid closure.

During examination, the endocrinologist pays attention to the following characteristic symptoms:

unclosed palpebral fissure;
no blinking;
when looking down, the upper eyelid lingers;
the gaze cannot fixate a close object.

If Graves' disease is left untreated, blindness develops due to destruction of the optic nerve. The disorder is treatable with corticosteroids, and patients are offered plastic surgery to eliminate a cosmetic defect.

Diagnostic measures

To diagnose Graves' disease, patients undergo the following procedures:

Primary visual inspection and palpation.
Blood tests, including hormone tests.
Radioisotope scanning.
Computed tomography.
Cytology of gland tissue.
X-ray.

The main symptoms that distinguish Graves' disease are thyrotoxicosis and overgrown gland tissue.

A blood test confirms the disease if thyrotropin levels are low and T3 and T4 are high.

An autoimmune disease is confirmed by tests for antibodies to TSH, an increased titer of antibodies indicates inflammatory process in iron.

Ultrasound is necessary to determine the volume of the gland, structure and quality of blood supply.

Therapy for Graves' disease

Treatment for Graves' disease is with thyreostatics, which block the production of hormones. The duration of treatment with thyreostatics is at least one year. Its effectiveness is approximately 35%. In some cases, reducing the dose provokes the return of symptoms of thyrotoxicosis. The problem of progressive thyrotoxicosis is solved surgically.

Graves' disease is also amenable to radioisotope treatment, which requires preliminary preparation. On preparatory stage carried out full examination, identifying the causes of the disease, normalization hormonal levels, treatment of major diseases.

Radical treatment can lead to the appearance of symptoms of hypothyroidism, requiring additional intake of synthetic thyroxine.

The set of measures that eliminate the symptoms of Graves' disease includes special diet, the purpose of which is to replenish glycogens, restoring the functionality of the liver and heart muscles.

The energy value of the diet should be increased, since patients lose weight and become weaker, the cause of weight loss is accelerated exchange substances. The protein norm must be increased by thirty percent. The patient should eat at least one hundred grams of protein per day, half the norm for protein of animal origin. Carbohydrates must be included in the diet.

Graves' disease in children

Congenital toxic goiter is rare in children.

Reasons congenital disease Graves in children:

Lack of nutrients in the diet of the mother carrying the child.
Infectious diseases during pregnancy.
The effect of aggressive toxic substances on the fetus.
Developmental abnormalities of the hypothalamus or pituitary gland.
Injury to the thyroid gland of the expectant mother.

Graves' disease can manifest itself during the hormonal maturation of a child, when the content of hormones in the blood increases significantly.

The driving force of the process is:

autoimmune processes;
increased production of thyrotropin;
disturbances in the sympathoadrenal system.

Increased synthesis of hormones leads to acceleration metabolic processes, the child sharply loses weight, in addition to this, other symptoms appear:

dwarfism;
physical underdevelopment;
increased body temperature;
nervous excitability;
exophthalmos;
disruption of the heart.

Treatment of Graves' disease in children

Treatment of the disease in children includes the following:

medication therapy;

Description:

Graves' disease (diffuse toxic goiter) is the most common cause. Graves' disease causes increased production of thyroid hormones. Most often, it is transmitted genetically.

Symptoms:

You may have hyperthyroidism if you:

      *Experience weakness, exhaustion or irritability.
      *Notice trembling in hands, accelerated irregular heart rate or difficulty breathing at rest.
      *You sweat a lot and notice itching or redness of the skin.
      *Have frequent bowel movements or diarrhea.
      *Notice excessive hair loss.
      *You lose weight with your usual diet.

In addition, some women experience irregular menstrual cycle or a complete cessation of menstruation, and in some men, breast enlargement may occur. Symptoms of hyperthyroidism depend on individual characteristics body, age and amount of thyroid hormone.

Certain symptoms of Graves' disease

People with Graves' disease often have additional symptoms, including:

      *Enlarged thyroid gland.
      *Thickening of nails.
      *Myxedema is rough, reddish, thick skin on the front side of the legs.
      *Thickening of the terminal phalanges of the fingers.
      *Bulging and redness of the eyes.

Complications

The most common complication of the disease is ophthalmopathy, which can develop before, after, or simultaneously with other symptoms of hyperthyroidism. Patients with ophthalmopathy develop vision problems, bulging and red eyes, sensitivity to light, blurred vision, etc. Smokers are more susceptible to ophthalmopathy.

If hyperthyroidism is not treated, the patient begins to:

      *Lose weight.
      *Facing cardiac problems: , atrial fibrillation and.
      *Notice difficult absorption of calcium and other useful minerals.

In rare cases, hyperthyroidism can cause a life-threatening condition called thyrotoxic crisis. usually occurs due to a serious infection or severe stress.

Causes:

Other common reasons include:

*Nodules of the thyroid gland. Thyroid nodules are pathological formations that provoke excessive production of thyroid hormones.
*Thyroiditis occurs when the body produces antibodies that damage the thyroid gland. Thyroiditis can also develop due to a viral or bacterial infection. At first, thyroiditis may cause an increase in thyroid hormone levels, but later these levels may decrease (hypothyroidism) until the thyroid gland recovers.

Rare causes of hyperthyroidism include consuming foods or medications that contain large amounts of iodine.

Treatment:

Conservative pharmacological treatment.
The main means of conservative treatment are the drugs Mercazolil and methylthiouracil (or propylthiouracil). The daily dose of Mercazolil is 30-40 mg, sometimes with very large goiters and severe course thyrotoxicosis it can reach 60-80 mg. The maintenance daily dose of Mercazolil is usually 10-15 mg. The drug is taken continuously for 1/2-2 years. Reducing the dose of Mercazolil is strictly individual, it is carried out based on the signs of elimination of thyrotoxicosis: stabilization of the pulse (70-80 beats per minute), increase in body weight, disappearance of sweating, normalization pulse pressure. It is necessary to conduct a clinical blood test every 10-14 days (with maintenance therapy with Mercazolil - once a month). In addition to antithyroid drugs, b-blockers, glucocorticoids, sedatives, potassium supplements.

Radioiodine therapy.

Radioiodine therapy (RIT) is one of the modern methods of treating diffuse toxic goiter and other diseases of the thyroid gland. During treatment, radioactive iodine (isotope I-131) is introduced into the body in the form gelatin capsules orally (in rare cases used liquid solution I-131). Radioactive iodine, which accumulates in the cells of the thyroid gland, exposes the entire gland to beta and gamma radiation. This destroys the gland cells and tumor cells, spreading beyond its borders. Radioiodine therapy requires mandatory hospitalization in a specialized department.

Surgical treatment.

The absolute indications for surgical treatment are allergic reactions or persistent decrease in white blood cells, noted with conservative treatment, large sizes goiter (enlargement of the thyroid gland above III degree), heart rhythm disturbances by type

Graves' disease is a type of hyperthyroidism that occurs mainly in women (7 times more often than in men) and most often manifests itself during the 3rd-4th decade of life. The disease is characterized by goiter, eye and skin lesions, but all three manifestations do not always occur together.

Causes of Graves' disease

There is a known family predisposition to Graves' disease. Important role Genetic factors play a role in the pathogenesis of the disease.

Hyperthyroidism occurs due to stimulation of thyroid-stimulating hormone receptors by autoantibodies to these receptors - the so-called thyroid-stimulating immunoglobulins. Excessive stimulation leads to an increase in the synthesis and secretion of thyroid hormones, as well as growth of the thyroid gland.

The reasons for the formation of autoantibodies to thyroid-stimulating hormone receptors are unknown, but the mechanism is believed to be infectious and environmental factors, as well as stress-related immunosuppression. The causes of the skin and eye manifestations of Graves' disease are also unknown. Perhaps these manifestations are a consequence of the cross-reaction of thyroid-stimulating immunoglobulins with thyroid-stimulating hormone receptors on fibroblasts in the orbit and dermis. This interaction triggers the production of numerous cytokines and the synthesis of glycosaminoglycans by fibroblasts. Changes associated with glycosaminoglycan and tissue accumulation are clinically manifested by skin changes and ophthalmopathy.

Symptoms of Graves' disease

Graves' disease often first manifests in a variety of ways. general symptoms and signs of thyrotoxicosis. Hypertension, heart failure and exacerbation may be detected, especially in elderly patients with concomitant diseases cardiovascular system.

Manifestations of Graves' disease

Anxiety
Excessive sweating
Fatigue
Feeling hot ( poor tolerance heat)
Frequent defecation
Irritability
Menstrual irregularities
Heartbeat
Shortness of breath or feeling short of breath
Weight loss
Energetic and strong pulse
Increased systolic pressure
Fine silky hair
Minor tremor of hands and tongue
Hyperkinesia
Hyperreflexia
Onycholysis
Weakness skeletal muscles upper shoulder girdle
Wide palpebral fissure, lag upper eyelid from the iris fixation of gaze on an object slowly moving downwards
Tachycardia
Warm moist smooth skin

The thyroid gland in Graves' disease is usually diffusely enlarged, and its consistency can vary from soft to dense. Noise or vibration may be felt over the gland, indicating increased vascularity. Often, palpation reveals an enlarged pyramidal lobe.

Patients with Graves' disease may have changes in the eye sockets (orbitopathy), including proptosis and proptosis. These changes can lead to complications - from mild hyperemia (with chemosis, conjunctivitis and swelling of the periorbital region) to corneal ulceration, neuritis optic nerve, atrophy optic nerve, exophthalmic ophthalmoplegia. Rapidly progressive exophthalmos is called malignant exophthalmos. Graves' disease also affects the extraocular muscles, leading to inflammation, muscle enlargement and subsequent fibrosis, dysfunction, and sometimes diplopia.

Skin lesions associated with Graves' disease usually appear on back side feet or in the pretibial area as raised, thickened, hyperpigmented areas (“orange peel”). Such lesions may be accompanied by itching and dense swelling.

Diagnosis of Graves' disease

Laboratory and instrumental studies

In Graves' disease and other forms of thyrotoxicosis, elevated levels freely circulating T4 and T3, with undetectable concentrations of thyroid-stimulating hormone. Sometimes, only an increase in T3 concentration is detected. This condition is called T3 thyrotoxicosis. At radioisotope research Graves' disease is characterized by diffusely increased uptake of a radioisotope by the thyroid gland.

Differential diagnosis

The presence of thyrotoxicosis, goiter and ophthalmopathy is considered an actual sign of Graves' disease. If a patient has a combination of such symptoms, radioisotope scanning is indicated only in rare cases.

A symmetrical goiter, especially in the presence of noise above it, is most characteristic of Graves' disease, although occasionally the causes of such manifestations can be an adenoma secreting thyroid-stimulating hormone, as well as conditions associated with trophoblastic stimulation of the thyroid gland ( hydatidiform mole and choriocarcinoma). Palpation of a single nodular formation may indicate a toxic adenoma, while multiple nodular formations suggest the presence of a multinodular goiter. The thyroid gland is sensitive to palpation in patients who have undergone viral disease, suggests subacute thyroiditis. The absence of a palpably detectable thyroid gland indicates an exogenous supply of thyroid hormones (artificial thyrotoxicosis) or, much less frequently, an ectopic source of thyroid hormone production (ovarian goiter).

Hyperthyroidism, with the exception of iodine-induced hyperthyroidism, is characterized by increased accumulation of radiopharmaceuticals during radioisotope scanning. Conversely, thyroiditis caused by excessive release of thyroid hormone depots is characterized by: low performance radiopharmaceutical accumulation (usually<1%). У пациентов с эктопической тиреоидной тканью, как при яичниковом зобе, отмечается повышенное накопление радиофармпрепарата в области яичников.

Treatment of Graves' disease

All patients with Graves' disease require treatment with antithyroid drugs. Thionamides are sometimes used as first-line drugs to induce remission. In other cases, they are used for short-term therapy to manage symptoms of the disease before treatment with radioactive iodine drugs or before surgery.

Conservative treatment

Thionamide therapy

Propylthiouracil (PTU), methimazole, and beta-adrenergic receptor antagonists (beta-blockers) are effective in treating Graves' disease. β-Blockers are used as adjuvant drugs because they reduce many of the clinical manifestations of excessive sympathetic stimulation - tremor, palpitations and anxiety.

In general, if the patient is receptive, thionamides can very effectively stop hyperthyroidism.

In groups of children, adolescents and patients with small goiters and mild hyperthyroidism, spontaneous recovery is most common when treated with thionamide drugs alone. It has been noted that with longer treatment with thionamide drugs, long-term remissions are more common. Therefore, most experts recommend taking thionamide drugs for at least 1 year.

Radioisotope therapy

Radioisotope therapy has been used to treat hyperthyroidism since the 1940s, and many specialists prefer this treatment for older patients with Graves' disease. The method is also used for the treatment of toxic multinodular goiter and single (solitary) toxic adenomas, as well as for ablation of residual thyroid tissue or malignant cells after subtotal thyroidectomy. Radioisotope therapy is absolutely contraindicated during pregnancy, as it can lead to fetal hypothyroidism.

When preparing patients for radioiodine therapy, thionamide drugs are prescribed, which reduces the level of thyroid hormones. After taking thionamide drugs, radioisotope therapy is carried out for 4-5 days, prescribing sodium iodide (131I) orally.

Although the goal of radioiodine therapy is to achieve a euthyroid state, hypothyroidism often develops as a result of treatment depending on the dose. Based on the results of a one-year observation of patients after radioisotope therapy, it was found that persistent hypothyroidism is detected in at least 50% of patients receiving high-dose therapy, while the results of a 25-year observation show that persistent hypothyroidism after low-dose therapy is observed in at least 25% of patients . Therefore, all patients treated with 131I require long-term follow-up. There is currently no evidence to suggest that radioiodine therapy increases the risk of developing thyroid cancer.

Surgical treatment

The main goal of surgical treatment is to eliminate hyperthyroidism by reducing the volume of functioning thyroid tissue. The volume of glandular tissue left is determined based on the volume of the enlarged gland.

Indications for Graves' disease

Since radioisotope therapy cannot be performed during pregnancy, surgical treatment is indicated for all pregnant women with intolerance to thionamide drugs or if it is impossible to control hyperthyroidism with medication. Surgical treatment is also indicated for other patients with intolerance to thionamide drugs or radioiodine therapy, with large goiter causing compression of the airways or dysphagia, or when patients choose surgical treatment instead of conservative therapy.

Preoperative preparation

Preparing a patient with thyrotoxicosis for planned surgical treatment begins with the administration of thionamide drugs until a euthyroid state is achieved or, at least, until the symptoms of hyperthyroidism are controlled before surgery. β-blockers are used to reduce signs and symptoms associated with adrenergic stimulation. 7-10 days before surgery, potassium iodide is prescribed orally in the form of a saturated solution or Lugol's solution (contains 7 mg of iodine in one drop).

Patients requiring emergency thyroidectomy are treated with betamethasone (0.5 mg every 6 hours), iopanoic acid (500 mg every 6 hours), and propranolol (40 mg every 8 hours) before surgery for 5 days. It has been proven that this dosing regimen allows for the safe and effective prevention of postoperative thyrotoxic crisis.

Operation technique

In most cases, thyroidectomy can be performed through a low transverse cervical incision (Kocher approach). The skin, together with the subcutaneous muscle, is separated upward to the apex of the thyroid cartilage, downward to the sternoclavicular joints and laterally to the inner edge of the sternocleidomastoid muscles.

Most prefer to divide the infrahyoid muscle vertically along the midline and separate it from the thyroid capsule using blunt force and lateral traction. After identifying the upper pole of the thyroid gland, with caution - so as not to damage the external branch of the laryngeal nerve - the upper thyroid artery and vein are ligated along the length. Release of the upper pole allows you to mobilize the lateral and posterior surfaces of the thyroid lobe and identify the inferior thyroid artery lateral to the gland.

The recurrent laryngeal nerve is found medially near the capsule of the gland at the intersection with the inferior thyroid artery. From this point, the recurrent laryngeal nerve is carefully traced to pass through the cricothyroid membrane, where it is separated from the overlying thyroid gland. In the same area, the upper parathyroid glands can be detected. As a rule, they are formations with a diameter of up to 1 cm, located at the intersection of the inferior thyroid artery and the recurrent nerve. Every effort should be made to preserve the parathyroid glands.

From this point in the operation, the inferior and posterior venous branches of the thyroid gland can be safely treated. The isthmus of the gland is divided between the clamps and the thyroid lobe is directly separated from the underlying trachea. If there is a pyramidal lobe located anterior to the trachea and larynx, it should be removed, as it can cause a relapse of hyperthyroidism.

Patients with Graves' disease most often undergo bilateral subtotal thyroid resection. This operation requires repeating the steps described above on the opposite side. An alternative surgical option is lobectomy on one side and subtotal resection on the opposite side (Dunhill operation), which leaves a slightly larger fragment of tissue, but makes subsequent treatment much easier.

Complications of the operation

Due to the slight swelling associated with tracheal intubation, signs of nerve damage may not be noticed immediately after extubation, but this is suggested by deterioration of the patient's voice in the next 12-24 hours after surgery. Intraoperatively, to prevent such a complication, it is useful to stimulate the recurrent nerve using a special stimulator and palpate the contraction of the laryngeal muscles. If the patient experiences hoarseness after surgery, the surgeon must ensure that nerve conduction is not impaired. If the external branch of the laryngeal nerve is damaged, the patient may experience rapid fatigue when speaking and a slight change in voice, especially on high notes. Such damage can be critical for singers and public speakers. Therefore, during surgery, every effort must be made to clearly identify and preserve the nerves, since the location of the nerves close to the vascular pedicle of the thyroid gland contributes to such injuries. Transient nerve palsy occurs in 3-5% of patients. Restoration of nerve function requires from several days to 4 months. Complete nerve damage occurs in 1% of cases or less.

When the parathyroid glands are damaged or excised, hypoparathyroidism develops. During surgery, it is necessary to isolate these glands and make every effort to preserve their blood supply, which in 30% of patients comes directly from the thyroid capsule. If the blood supply to the parathyroid glands is disrupted or if they are removed along with the thyroid gland, it is important to perform their autotransplantation. Transient hypoparathyroidism after thyroidectomy is observed in 3-5% of patients. This condition in the immediate postoperative period requires the administration of vitamin D3 supplements and maintenance therapy with calcium supplements. Permanent hypoparathyroidism occurs in less than 1% of patients.

In the postoperative period, the patient needs close monitoring for early detection of bleeding or airway obstruction. In patients with growing hematomas, increasing pain sometimes leads to hoarseness and rapid development of symptoms of airway obstruction, stridor, and respiratory depression. If bleeding is suspected, it is necessary to remove the stitches, open the wound and immediately evacuate the hematoma (if necessary, right in the ward). Sometimes airway obstruction occurs as a result of subglottic or supraglottic edema. Treatment is conservative - inhalation of humidified oxygen and intravenous corticosteroids.

The article was prepared and edited by: surgeon