Is diffuse nodular nontoxic goiter dangerous or not? Suppressive therapy with L-thyroxine. Indications for surgical removal of goiter

Non-toxic diffuse goiter 1st degree and other degrees implies a condition in which the size of the thyroid gland increases, but its function does not change. Most often, this type of disorder is found in young people, as well as in women during puberty, during pregnancy and lactation, and during menopause. An increase in the size of the gland can occur evenly or with the formation of nodes, but the level of hormones always remains normal.

In this article we will talk about the causes of non-toxic goiter, and also consider its types and the symptoms that accompany them.

Forms of non-toxic goiter and its causes

Not toxic goiter accompanied by an increase in the size of the gland, while maintaining its function.

Nontoxic goiter can be:

diffuse;
single-node;
multi-node;
colloidal.

The reason most often is Not sufficient quantity iodine in the body (see). Iodine deficiency occurs due to a small amount of iodine in consumed food and water, as well as when its content in environment. Previous irradiation of the head and neck and exposure to excess amounts of goitrogenic substances are also considered factors influencing the development of the disease.

Various inflammatory, infectious and neoplastic processes are not the main cause of the development of non-toxic goiter, but can be predisposing factors, just like frequent stressful situations, complicated heredity and regular hypothermia.

Clinical manifestations of various forms of non-toxic goiter

Due to iodine deficiency in the thyroid tissues, a decrease in the concentration of iodinated lipids occurs, the normal content of which inhibits the activity of locally located growth factors. When the content of iodinated lipids is insufficient, thyrocytes divide and the number of thyroid cells increases, which causes hyperplasia.

Various forms of nontoxic goiter have characteristics and the symptoms we will look at:

Non-toxic diffuse goiter– the disease manifests itself gradually, with a feeling of discomfort in the throat, later soreness appears, and may occur painful sensations, as the thyroid gland grows, problems arise when swallowing food and water. Due to pressure on blood vessels And vocal cords there is a feeling of pulsation in the neck, the voice changes timbre and becomes more hoarse. If the size of the goiter reaches an impressive size, attacks of suffocation may occur (see), shortness of breath appears, and tongue mobility is impaired.
Non-toxic colloid goiter– occurs when colloid accumulates in the follicles. The follicle is functional unit thyroid gland, shaped like a sac no larger than 1 mm in size. Inside it consists of cells - thyrocytes, and outside - from blood vessels and nerve endings. A colloid is a substance that has a jelly-like consistency and contains iodine and amino acids. The occurrence of a goiter occurs if the process of outflow of colloid from the follicles is disrupted.

Nontoxic cellular goiter or colloid goiter is found when an enlarged thyroid gland causes discomfort. There is a feeling of squeezing in the neck, difficulty swallowing, and a soreness or lump in the throat. The disease is often accompanied by headaches and dizziness, as the enlarged gland puts pressure on the nerves and blood vessels.

Diffuse euthyroid goiter

Version: MedElement Disease Directory

Non-toxic diffuse goiter (E04.0)

Endocrinology

general information

Short description

Diffuse euthyroid goiter- general diffuse enlargement of the thyroid gland (TG) without disruption of its function. The most common cause is iodine deficiency.
The formation of endemic goiter is a compensatory reaction aimed at maintaining a constant concentration of thyroid hormones in conditions of iodine deficiency.
Clinical symptoms may be absent, manifested by a cosmetic defect in the neck ("thick" neck) or compression syndrome of the trachea and esophagus, which directly depends on the degree of enlargement of the thyroid gland.

Classification

A diffuse increase in the volume of the thyroid gland with preserved function is observed both in endemic goiter (found in iodine-deficient regions) and in sporadic goiter (not associated with a lack of iodine in the environment, but caused by congenital or acquired defects in the biosynthesis of thyroid hormones).

Etiology and pathogenesis

Etiology
The most common cause of an enlarged thyroid gland (goiter) is iodine deficiency.
Goiter detected in conditions of iodine deficiency is designated by the term endemic, and in regions with normal iodine consumption - sporadic.
Quite rarely, endemic goiter is associated not with iodine deficiency, but with the action of other goitrogenic factors (flavonoids, thiocyanates).
The etiology of sporadic goiter has been little studied and, apparently, is heterogeneous. In some cases, it is associated with congenital defects of enzyme systems involved in the synthesis of thyroid hormones.

Pathogenesis
The pathogenesis of iodine deficiency goiter has been most studied. The formation of endemic goiter is a compensatory reaction aimed at maintaining a constant concentration of thyroid hormones in the body under conditions of iodine deficiency. An increase in the proliferative activity of thyrocytes is promoted by TSH, as well as local growth factors (IGF-1, epidermal growth factor, fibroblast growth factor, transforming growth factor ß). Powerful inhibitors of the production of local growth factors are iodinated lipids (iodolactones).

Epidemiology

Diffuse euthyroid goiter develops more often in individuals young up to 20 years - in 50% of cases, in another 20% of cases - up to 30 years
It occurs 2-3 times more often in women than in men.
As a rule, euthyroid goiter occurs during periods increased need in iodine - sexual development, pregnancy and lactation.

Risk factors and groups

Main risk group development of iodine deficiency diseases:
- children under 3 years of age;
- pregnant women;
- breastfeeding;

A group at particular risk for the formation of the most threatening consequences of iodine deficiency in medical and social terms:
- girls during puberty;
- women of childbearing (fertile) age;
- pregnant and lactating women;
- children and teenagers.

Clinical picture

Symptoms, course

The clinical picture of diffuse euthyroid goiter depends on the degree of enlargement of the thyroid gland, since its function remains normal.
The mere fact of a slight enlargement of the thyroid gland with its normal function practically does not affect the work of other organs and systems.
In the vast majority of cases, in conditions of mild and moderate iodine deficiency, a slight enlargement of the thyroid gland is detected only with a targeted examination.
In conditions of severe iodine deficiency, goiter can reach gigantic sizes. It is also possible to experience compression syndrome of nearby organs (esophagus, trachea), which is manifested by difficulty swallowing and breathing, and discomfort in the neck.

Diagnostics

Anamnesis. When collecting anamnesis, it is necessary to take into account the region of residence, the number of pregnancies, and smoking. As a rule, diffuse euthyroid goiter is asymptomatic; with a significant increase in the size of the thyroid gland (TG), it can manifest itself as compression of the trachea and esophagus.

Physical examination. Palpation of the thyroid gland is the main method for assessing the structure of the thyroid gland and should be performed in all patients. If, based on the results of palpation, a conclusion is made about an increase in the size of the thyroid gland or the presence of nodular formations, the patient is indicated for further ultrasound of the thyroid gland.

Ultrasound thyroid gland
The study allows us to characterize the size, shape and volume of the thyroid gland, the presence of nodes in it, its topographic-anatomical relationship with other organs of the neck, echogenicity and echostructure.
Using ultrasound, palpation examination data is clarified and the degree of thyroid enlargement is determined. The volume of each share is calculated using the formula:

V = V left beat + V right beat
V shares = (a+b+c) x 0.479

The normal thyroid volume for European residents is up to 18 ml for women, and up to 25 ml for men. The lower limit of normal thyroid volume has not been established.
In a child, the volume of the thyroid gland depends on the degree of physical development, therefore, before the study, the child’s height and weight are measured and the body surface area is calculated using a special scale or formula. In children, the volume of the thyroid gland is compared with standard indicators(depending on age or body surface area) obtained in regions without iodine deficiency.

Thyroid scintigraphy carried out to diagnose substernal goiter.

X-ray examination chest with barium contrast of the esophagus is recommended in the presence of goiter large sizes accompanied by symptoms of compression of the trachea and esophagus.

Laboratory diagnostics

The main hormonal markers for diagnosing thyroid diseases are TSH and free thyroxine(T 4).
With euthyroidism TSH level and free T4 are within normal limits.

Differential diagnosis

Diffuse euthyroid goiter is differentiated from chronic autoimmune thyroiditis Autoimmune thyroiditis is a chronic inflammatory disease of the thyroid gland (TG) of autoimmune origin, in which, as a result of chronically progressive lymphoid infiltration gradual destruction of thyroid tissue occurs, most often leading to the development of primary hypothyroidism
and sporadic goiter Sporadic goiter is a disease characterized by the appearance of a goiter, usually without pronounced dysfunction of the gland, developing in people living outside goiter-endemic areas
.

Complications

The main complication of diffuse non-toxic goiter may be compression of surrounding organs due to the large size of the goiter; in such cases, it is indicated surgery.

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Treatment

The purpose of treatment is a decrease in the size of the thyroid gland (TG).

Today there are three options conservative therapy diffuse euthyroid goiter:
1. Monotherapy with iodine preparations.
2. Suppressive therapy with levothyroxine sodium (L-thyroxine).
3. Combination therapy with iodine and L-thyroxine.

1. Monotherapy with iodine preparations
At the first stage of treatment, the vast majority of children, adolescents and people under 45-50 years of age are prescribed iodine at a dose of 100-200 mcg/day, which leads to a fairly rapid suppression of the hypertrophic component of the goiter (an increase in the size of thyrocytes).

Advantages of iodine therapy: etiotropic nature, safety, no need for dose selection and frequent hormonal studies. Duration of treatment is 1.5-2 years.
Efficacy is assessed 6 months after the start of treatment. If a tendency towards a decrease in the size of the thyroid gland is detected, therapy is continued for 1.5-2 years. After discontinuation of potassium iodide, it is recommended to use table salt, seafood.

2. Suppressive therapy with L-thyroxine

If there is no effect from monotherapy with iodine preparations after 6 months, L-thyroxine therapy is carried out in doses that allow maintaining the TSH level at the lower limit of normal.
The goal of L-thyroxine therapy for diffuse euthyroid goiter is to maintain TSH in the range of 0.1-0.4 mIU/l, which in adults requires the administration of at least 100-150 mcg of L-thyroxine.
The effectiveness of treatment is assessed after 6 months. When normal thyroid volume is achieved, L-thyroxine is discontinued and iodine preparations are prescribed, against which the thyroid volume is monitored.

Disadvantages of suppressive therapy with levothyroxine sodium: high probability of goiter relapse after discontinuation of the drug, risk of complications of drug-induced thyrotoxicosis, need to adjust the dose, which requires frequent hormonal studies.
Suppressive therapy with levothyroxine sodium is not considered the treatment of choice for diffuse euthyroid goiter.

3. Combination therapy with iodine and L-thyroxine

Has proven itself well in clinical studies combination therapy iodine preparations and L-thyroxine (200 mcg of iodine and 100-150 mcg of L-thyroxine).
The main advantage of combination therapy is the rapid achievement of a reduction in thyroid volume due to iodine, which prevents the decrease in intrathyroidal iodine content that occurs during monotherapy with L-thyroxine.
It is also possible to sequentially prescribe L-thyroxine first, and then add iodine. In case of normalization of thyroid volume, iodine intake in a physiological dose is prescribed for life.

Features of monitoring elderly patients
In people over 60 years of age, goiter does not big size with or without nodal changes, active surveillance is most justified, involving ultrasound and TSH determination at intervals of 1-2 years.

Treatment during pregnancy
For all pregnant women living in an iodine-deficient region, it is advisable to prescribe 250 mcg of iodine along with iodized salt. During pregnancy, the treatment of choice is iodine monotherapy, less often - combination therapy with iodine and L-thyroxine. In both cases, monitoring of thyroid function is necessary, since during a short period of pregnancy there is no significant decrease in the volume of the thyroid gland, and with sufficient iodine consumption, the volume of the thyroid gland naturally increases slightly.

Surgery with diffuse euthyroid goiter, it can be indicated only if it is gigantic in size and/or if there are signs of compression of surrounding organs.

Forecast

The prognosis for diffuse euthyroid goiter is favorable. Normalization of the volume of the thyroid gland occurs after 1.5-2 years of treatment. To avoid relapse of the disease, constant consumption of iodized salt is recommended.

Hospitalization

Hospitalization is not indicated.

Prevention

The goal of prevention is to normalize iodine consumption by the population. The iodine requirement is:
- 90 mcg per day - at the age of 0-59 months;
- 120 mcg per day - at the age of 6-12 years;
- 150 mcg/day - for adolescents and adults;
- 250 mcg/day - for pregnant and lactating women.

Ensuring normal iodine consumption in regions of iodine deficiency is possible through the introduction of mass, group and individual prevention methods.

Mass prevention
Universal salt iodization is recommended by WHO, the Ministry of Health of the Republic of Kazakhstan and the Russian Federation as a universal and highly effective method of mass iodine prophylaxis.
Universal salt iodization means that virtually all salt for human consumption (i.e., sold in stores and used in Food Industry) must be iodized. To achieve optimal iodine intake (150 mcg/day), WHO and the International Council for the Control of Iodine Deficiency Diseases recommend adding an average of 20-40 mg of iodine per 1 kg of salt. It is recommended to use potassium iodide as an iodized supplement.
Subsequently, mass iodine prophylaxis leads to a significant reduction in the prevalence of all forms of goiter.

Group and individual iodine prophylaxis carried out during certain periods of life (pregnancy, lactation, childhood and adolescence), when physiological need in iodine increases, and consists of taking pharmacological agents containing a physiological dose of potassium iodide.
In groups increased risk it is permissible to use only pharmacological agents, containing a precisely standardized dose of iodine. In these population groups, the prevalence of endemic goiter is especially high, and, therefore, taking drugs with precise dosage has not only preventive, but also therapeutic value.
Recommended doses of potassium iodide for prophylaxis in high-risk groups:

Potassium iodide long-term orally 50-100 mcg/day. - children under 12 years old;
- 100-200 mcg/day. - teenagers and adults;
- 200 mcg/day. - pregnant and lactating women.

Information

Sources and literature

Braverman L. Diseases of the thyroid. - Humana Press, 2003
Valdina E.A. Thyroid diseases. Guide, St. Petersburg: Peter, 2006
Dedov I.I., Melnichenko G.A. Endocrinology. National leadership, 2012.
Dedov I.I., Melnichenko G.A., Andreeva V.N. Rational pharmacotherapy of diseases endocrine system and metabolic disorders. Guide for practicing doctors, M., 2006
Kubarko A.I., S.Yamashita Thyroid gland. Functional aspects, Minsk-Nagasaki, 1997
Cattail W.M., Arki R.A. Pathophysiology of the endocrine system / trans. from English edited by Smirnova N.A., M.: Binom publisher, St.-Pb.: Nevsky dialect, 2001 (with completed justification form) coming until March 29, 2019:[email protected] , [email protected] , [email protected]
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Nontoxic goiter is an enlargement of the thyroid gland that is not accompanied by hormonal disorders. Another name for the disease is simple goiter. The main reasons for its development are considered to be heredity, medications and unfavorable living conditions. However, women get sick 10 times more often than men, which suggests the role of estrogen in the development of this pathology.
The main symptom that patients complain about is a visual enlargement of the front of the neck. Patients may also be bothered by a sore throat, cough, difficulty swallowing, etc. To make an accurate diagnosis, it will be necessary to undergo an ultrasound and other tests.

Features of the treatment of non-toxic goiter are that it is very important not to harm the patient and not disrupt hormonal background. Therefore, it is not advisable to prescribe hormonal drugs or surgery. A wait-and-see approach is used. To prevent further development illness, we recommend using folk remedies, which return the thyroid gland to normal size.

Causes of non-toxic goiter and risk factors

Previously, the most common cause of nontoxic goiter was iodine deficiency. However, this problem has now been overcome in almost all regions of our country (produced iodized salt, prevention is carried out). Therefore, other reasons come to the fore:

hereditary predisposition;
autoimmune disorders;
Hashimoto's thyroiditis;
mild disturbances in the production of thyroid hormones (in this case, the hormonal balance is not disturbed, but the thyroid gland turns on the compensatory mechanism and begins to increase in size);
congenital defects of certain enzymes;
long-term use some pharmacological drugs;
constant contact with chemicals having a goitrogenic effect.

Risk factors include bad habits (especially smoking), frequent stress, untreated infectious and inflammatory diseases, deficiency of microelements (except iodine; selenium, calcium and magnesium are important for the health of the thyroid gland) and age over 40 years.

Pathogenesis

The development of the disease occurs against the background of impaired biosynthesis TSH hormones and iodine metabolism in the blood. The level of hormones increases slightly (but is within normal limits), which stimulates the thyroid gland to turn on the compensatory mechanism and increase in size. In this case, the function of the organ is not impaired.

As a result of enlargement (hyperplasia), the thyroid tissue suffers. Hemorrhages and necrosis appear in them. The number of pathological foci is increasing. If a disorder is observed in one of the cell clones, then hyperplasia will be nodular in nature. In this case, the nodes can accumulate iodine (so-called hot nodes), not accumulate iodine (cold nodes), or consist of colloidal liquid (colloid node). Over time, if the disease is not treated, the thyroid gland will not be able to perform its role normally, and a non-toxic goiter will turn into a toxic (hormone-dependent) one.

Signs

Usually the thyroid gland slowly increases in size and does not hurt when palpated. Pain is only possible if there is hemorrhage into the parenchymal tissue. One of the main signs of the disease is a visual enlargement of the neck in front. If the goiter greatly increases in size, it can compress the trachea, recurrent laryngeal nerve and other neighboring organs, which will lead to coughing, change in voice timbre, flushing of the face, dizziness, etc. Other possible symptoms:

characteristic wheezing or whistling when breathing (especially when lying down);
increased fatigue;
sleep problems;
night sweats;
sensation of a foreign body in the neck;
difficulty swallowing;
intolerance to cold and heat;
increased irritability;
constipation.

Not all of these symptoms will necessarily be observed in the patient. It all depends on the size of the goiter and its type.

Classification of non-toxic goiter

There are several types of non-toxic goiter, depending on the nature of tissue damage.

Diffuse non-toxic (sporadic) goiter of the thyroid gland. A type of ND in which the thyroid gland is uniformly enlarged; no nodes, cysts, hemorrhages, necrosis or other changes were detected in the parenchymal tissue. This is the most common and harmless form of the disease.
. One of the cells of the thyroid gland develops pathological process, it divides, turning into a knot. Over time, the size of the node increases more and more, disfiguring the neck.
Multinodular goiter. As the name implies, this is a disease in which several nodes grow in the thyroid tissue at once.
Diffuse nodular goiter. Here two processes are combined at once: the thyroid gland increases in size, and one or more nodes grow in its tissues.
Colloid nodular goiter. It develops as a result of excessive accumulation of colloid (a viscous protein substance) in the follicles.
Simple non-toxic goiter. It is divided into diffuse and spherical shape. Such a goiter does not pose a health risk and often disappears on its own. It is the simple non-toxic variety that is most often found during pregnancy or during puberty.

There are also 3 stages of goiter, depending on its size (zero, first and second). Zero stage is not visible or palpable, the disease can be detected accidentally during ultrasound or other instrumental studies. The first stage is palpable, but almost invisible visually. The second stage spoils the shape of the neck and is noticeable to others.

Laboratory data and diagnostics

For diagnosis, the doctor will interview the patient, collect anamnesis, perform palpation and send for an ultrasound. If cancer is suspected, a biopsy is done. Scintiography, CT and MRI will be useful - they will provide more knowledge about the nature of the lesion.

Laboratory findings include a blood test for thyroid hormones. They should be normal.

Does non-toxic mean not dangerous?

A goiter is dangerous if it reaches a large size and puts pressure on the respiratory organs or blood vessels. There is also a risk that the nodular form will develop into cancer. So patients must do everything to cure this disease.

How to prevent the disease from occurring?

Healthy image life - best prevention. You must ensure that your body gets enough iodine. Also very important:

treat all infections and inflammations in a timely manner;
check with an endocrinologist once a year;
if possible, avoid contact with hazardous chemicals;
go to the sea once a year;
avoid depression and stress.

It has been established that tobacco smoke negatively affects the functioning of the thyroid gland, so try to say goodbye to this bad habit.

Treatment with traditional methods

Observational tactics are usually used. The patient must adjust his diet and remove risk factors. Once every six months he undergoes examination by an endocrinologist. The doctor makes sure that the goiter does not increase and does not stop in malignancy.

If the goiter has reached a large size, the patient is prescribed surgery complete removal thyroid glands But this is an extreme measure, since in order for the body to function without the thyroid gland, the patient will have to take hormonal medications all his life. This is fraught side effects and a significant deterioration in health.

Treatment of nodular non-toxic goiter with folk remedies

Treatment with folk remedies helps patients avoid surgery, eliminate unpleasant symptoms, gradually return the thyroid gland to normal sizes. We will offer the most effective recipes.

Cherry twig tea

Prepare young cherry branches (dry them and chop them into pieces no larger than 0.5 cm). Every day, brew tea from cherry twigs in the proportion of 1 tablespoon of raw material to 2 glasses of water. Boil the mixture for half an hour over low heat. Drink half a glass three times a day. Treatment must be long-term in order to fully restore thyroid function.

Laminaria slates

To compensate for iodine deficiency and relieve constipation associated with non-toxic goiter, you need to take dry kelp shale daily. They are sold at pharmacies or traditional healers. It is best to eat them at night, a tablespoon at a time, with plenty of water. For children, the dosage is reduced. You can take kelp for as long as you like, it is not addictive and does not harm the body.

Juice treatment

Treatment with juices helps with any form of non-toxic goiter. The juice from raw potatoes– take half a glass once a day on an empty stomach. You can also make mixtures of carrot, celery, beet, and spinach juices. It is useful to add a tablespoon of dandelion grass juice, nettle leaves, and chokeberry fruits to the drink.

Silver cinquefoil

Tea made from dry silverweed herb helps patients well. To prepare it, boil water, pour 2 pinches of chopped herbs into a mug and pour boiling water over it. After 10 minutes of infusion, the tea will be ready. Drink 2-3 servings per day. Treatment must be long-term in order to completely restore the thyroid gland.

Compresses for large goiter

Sometimes a non-toxic goiter grows to large sizes and produces large nodules. Then funds are needed not only for internal, but also for external use. We give several recipes for compresses.

Grind raw onion in a blender and mix with the same amount of honey. Add a couple of drops of iodine. Place the resulting pulp on gauze and apply to the sore spot. Keep the compress for about two hours. Repeat the procedure every 2 days.
Oak bark helps a lot. You should boil it in a small amount of water, and then apply the softened bark to your neck and wrap it with oilcloth (keep for at least an hour). Such compresses can be done every day until the thyroid gland begins to shrink.
For nodular non-toxic goiter, make an ointment from hop cones. To do this, grind the plant, mix with lard and simmer for 1 hour over low heat. 10 minutes before the end of cooking, add lanolin (10 g of lanolin is enough for 500 ml of mixture). Strain, cool, place in a glass jar. Apply oil to your goiter in the evening and apply oilcloth on top.
Juniper berry ointment has helped many patients. To prepare it, mix 1 part chopped fruit with 3 parts butter, boil for 20 minutes, strain. Apply on your neck in the evening and place a diaper on top.

Apply ointment compresses until the goiter begins to shrink.

Diffuse nontoxic goiter

When the thyroid gland is enlarged in degrees I-III, potassium iodide is indicated (100-200 mcg of iodine per day). Surgical treatment subtotal resection of the thyroid gland is necessary only for large goiters.

Diffuse toxic goiter

Diffuse toxic goiter (Graves-Parry-Bazedow disease) - genetically determined autoimmune disease. It is manifested by persistent excessive production of thyroid hormones by a diffusely enlarged thyroid gland under the influence of specific thyroid-stimulating autoantibodies with impaired functional state various organs and systems, primarily the cardiovascular and central nervous system. The disease most often manifests itself between the ages of 16 and 40 years, mainly in females.

Etiology and pathogenesis

The main role in the development of the disease is given to hereditary predisposition. 15% of patients with diffuse toxic goiter have relatives with the same disease; in approximately half of the relatives, circulating thyroid autoantibodies are detected in the blood. Provoking factors - mental trauma, infectious diseases, pregnancy, intake large doses iodine, massive insolation, etc.

According to modern ideas In this disease, TSH receptors of thyrocytes serve as primary autoantigens. Congenital deficiency of T-suppressors promotes the survival and proliferation of “forbidden” clones of T-lymphocytes that interact with self-antigens. As a result, in immune reaction B lymphocytes are involved, responsible for the formation of autoantibodies. With the participation of T-helper cells, B-lymocytes and plasma cells secrete thyroid-stimulating autoantibodies (autoantibodies to the TSH receptor). They bind to the TSH receptors of thyrocytes and have a stimulating effect on the thyroid gland, similar to the action of TSH: they activate adenylate cyclase and stimulate the formation of cAMP.

As a result, the mass and vascularization of the thyroid gland increase, and the formation of thyroid hormones increases. Excessive synthesis of thyroid hormones activates catabolic processes, oxidative phosphorylation changes, which leads to disruption of energy accumulation in cells. As a result of these processes, it develops muscle weakness, low-grade body temperature appears, patients progressively lose weight.

Clinical picture

Clinical symptoms are caused by the influence of excess thyroid hormones on various organs and systems of the body. The complexity and multiplicity of factors involved in pathogenesis determine the diversity clinical manifestations diseases. When analyzing complaints and results objective examination identify symptoms that can be combined into certain syndromes.

The thyroid gland, as a rule, is enlarged due to both lobes and the isthmus, palpable elastic consistency, painless, displaced when swallowing.

Defeat syndrome of cardio-vascular system manifested by tachycardia, atrial fibrillation, development of dishormonal myocardial dystrophy (“thyrotoxic heart”), high pulse pressure. Cardiac disorders are associated both with the direct toxic effect of hormones on the myocardium and with hard work heart due to the increased needs of peripheral tissues for oxygen under conditions of excessively intense metabolism. As a result of the increase in shock and minute volumes heart and acceleration of blood flow, systolic blood pressure increases, at the apex of the heart and above carotid arteries listen to systolic murmur. The mechanism for reducing diastolic blood pressure is associated with the development of adrenal insufficiency and insufficient synthesis of glucocorticoids, the main regulators of vascular wall tone.

Hypocortisolism syndrome, in addition to decreased blood pressure, is also characterized by hyperpigmentation skin. Pigmentation often appears around the eyes - Jellinek's sign.

Other gland syndrome internal secretion. In addition to the adrenal glands, damage to the pancreas often occurs with the development of thyroiditis. diabetes mellitus. Increased breakdown of glycogen with the entry of large amounts of glucose into the blood forces the pancreas to work at maximum voltage, which ultimately leads to exhaustion compensatory mechanisms and the development of insulin deficiency. The course of existing diabetes mellitus in patients with diffuse toxic goiter significantly worsens. To correct hyperglycemia before surgery, such patients often have to be switched from oral hypoglycemic drugs to fractional administration of insulin.

From others endocrine disorders that can develop in patients with diffuse toxic goiter, ovarian dysfunction with impaired menstrual cycle, fibrocystic mastopathy(thyrotoxic mastopathy, Velyaminov’s disease), men may develop gynecomastia.

Syndrome of central and peripheral lesions nervous system. Increased excitability, psycho-emotional lability, decreased concentration, tearfulness, fatigue, sleep disturbance, tremor of the fingers (Marie's symptom) and the whole body (telegraph pole syndrome) are noted. increased sweating, persistent red dermographism, increased tendon reflexes.

Catabolic disorder syndrome is manifested by weight loss with increased appetite, low-grade fever body and muscle weakness.

Organ damage syndrome digestive system manifests itself unstable stool with a tendency to diarrhea, attacks of abdominal pain, and sometimes jaundice associated with impaired liver function.

Eye syndrome is manifested by the following symptoms.

Dalrymple's sign (thyroid exophthalmos) is a widening of the palpebral fissure with the appearance of a white strip of sclera between the iris and the upper eyelid.
Graefe's symptom - lag upper eyelid from the iris when fixing the gaze on an object slowly moving downward, while a white strip of sclera remains between the upper eyelid and the iris.
Kocher's sign - when you fix your gaze on an object slowly moving upward, a white strip of sclera remains between the lower eyelid and the iris.
Stellwag's sign is a rare blinking of the eyelids.
Möbius sign - loss of the ability to fix the gaze at close range due to weakness of the adductors eye muscles the eyeballs fixed on a nearby object diverge and take their original position.
The Repnev-Melekhov symptom is an “angry look.”

Their development is based on hypertonicity of the muscles of the eyeball and upper eyelid due to disruption of autonomic innervation under the influence of excess thyroid hormones in the blood.

Thyroid exophthalmos in diffuse toxic goiter should be distinguished from endocrine ophthalmopathy- an autoimmune disease, which is not a manifestation of diffuse toxic goiter, but is often (40-50% of cases) combined with it. With endocrine ophthalmopathy, an autoimmune process affects the periorbital tissues. Due to the infiltration of orbital tissues by lymphocytes, the deposition of acidic glycosaminoglycans secreted by fibroblasts, edema and an increase in the volume of retrobulbar tissue, myositis and proliferation develop connective tissue in the extraocular muscles. Gradually, infiltration and edema turn into fibrosis, changes in the eye muscles become irreversible.

Endocrine ophthalmopathy is clinically manifested by impaired functioning oculomotor muscles, trophic disorders and exophthalmos. Patients complain of pain, double vision and a feeling of “sand” in the eyes, lacrimation. Sometimes the disease takes a malignant course, asymmetry of the apples develops up to the complete loss of one of them. According to domestic classification, there are three stages of endocrine ophthalmopathy:

I - swelling of the eyelids, feeling of “sand” in the eyes, lacrimation;
II - diplopia, abduction limitation eyeballs, gaze paresis;
III - incomplete closure of the palpebral fissure, corneal ulceration, persistent diplopia, optic nerve atrophy.

Another autoimmune disease that accompanies diffuse toxic goiter is pretibial myxedema (1-4%). In this case, the skin of the anterior surface of the leg is damaged, it becomes swollen and thickened. The condition is often accompanied by itching and erythema.

Savelyev V.S.

Surgical diseases

Colloidal in varying degrees proliferating nodular goiter, nodular colloid proliferating goiter, colloid nodular goiter, solitary nodule, simple sporadic goiter, simple non-toxic goiter

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Non-toxic uninodular goiter (E04.1)

Endocrinology