Graves' disease symptoms. What you would like to know about Graves' disease - diffuse toxic goiter

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 familial predisposition to Graves' disease. Important role genetic factors play a role in the pathogenesis of the disease.

Hyperthyroidism occurs as a result of 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 an increase in thyroid gland.

The reasons for the formation of autoantibodies to thyroid-stimulating hormone receptors are unknown, but it is assumed that infectious and environmental factors, as well as stress-induced immunosuppression, underlie this mechanism. The causes of Graves' disease manifestations in the skin and eyes are also unknown. Perhaps these manifestations are the result of a cross-reaction of thyroid-stimulating immunoglobulins with thyroid-stimulating hormone receptors on fibroblasts in the orbit and in the dermis. This interaction triggers the production of numerous cytokines and the synthesis of glycosaminoglycans by fibroblasts. Changes associated with the accumulation of glycosaminoglycans and tissues are clinically manifested by skin changes and ophthalmopathy.

Symptoms of Graves' Disease

Graves' disease often presents for the first time in various common symptoms and signs of thyrotoxicosis. Hypertension, heart failure and exacerbation may be detected, especially in elderly patients with accompanying illnesses of cardio-vascular 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
• Elevated systolic pressure
• Fine silky hair
• Fine tremor of hands and tongue
• Hyperkinesia
• hyperreflexia
• Onycholysis
• Weakness skeletal muscle upper shoulder girdle
• Wide palpebral fissure, lag upper eyelid from the iris of fixing the gaze on an object slowly moved down
• Tachycardia
• Warm moist smooth skin

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

Patients with Graves' disease may have eye socket changes (orbitopathy), including exophthalmos and proptosis. These changes can lead to complications ranging from mild hyperemia (with chemosis, conjunctivitis, and periorbital swelling) to corneal ulceration, neuritis ophthalmic 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 region in the form of raised, thickened hyperpigmented areas (" Orange peel"). Such lesions may be accompanied by itching and dense swelling.

Diagnosis of Graves' disease

Laboratory and instrumental research

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

Differential Diagnosis

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

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 that secretes thyroid-stimulating hormone, as well as conditions associated with trophoblastic stimulation of the thyroid gland ( hydatidiform mole and choriocarcinoma). Palpation of a single nodular mass may indicate a toxic adenoma, while multiple nodular masses suggest the presence of a multinodular goiter. Sensitive to palpation thyroid in patients who have undergone viral disease, suggests subacute thyroiditis. The absence of a palpable 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 the radiopharmaceutical during radioisotope scanning. Conversely, thyroiditis caused by excessive release of thyroid hormone depots is characterized by low rates 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. Sometimes thionamides are used as first-line drugs to induce remission. In other cases, they are used for short-term therapy to manage the symptoms of the disease before being treated with radioactive iodine preparations or before surgery.

Conservative treatment

Therapy with thionamides

Propylthiouracil (PTU), methimazole, and β-adrenergic antagonists (β-blockers) are effective in the treatment of Graves' disease. b-Adrenergic blockers are used as adjuvants because they reduce many of the clinical manifestations of excessive sympathetic stimulation—tremor, palpitations, and anxiety.

In general, with the susceptibility of the patient, thionamides can very effectively stop hyperthyroidism.

In groups of children, adolescents and patients with small goiters and mild hyperthyroidism, spontaneous recovery is most characteristic when treated with thionamide drugs alone. It is noted that with longer treatment with thionamide drugs, prolonged 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 is the preferred treatment of choice by many for the treatment of elderly 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 the 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 preparations are prescribed, which reduces the level of thyroid hormones. After taking thionamide preparations, 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 year of follow-up of patients after radioisotope therapy, it was found that permanent hypothyroidism is detected in at least 50% of patients receiving high-dose therapy, while the results of a 25-year follow-up show that permanent 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 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 amount of glandular tissue left is determined based on the volume of the enlarged gland.

Indications for Graves' disease

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

Preoperative preparation

Preparation of a patient with thyrotoxicosis for planned surgical treatment begins with the appointment 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 the operation, potassium iodide is administered 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 for 5 days with betamethasone (0.5 mg every 6 hours), iopanoic Θ acid (500 mg every 6 hours), and propranolol (40 mg every 8 hours) before surgery. It has been proven that this dosing regimen allows safe and effective prevention of postoperative thyroid storm.

Operation technique

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

Most prefer to divide the infrahyoid muscle vertically in the midline and separate it from the thyroid capsule using a blunt technique and lateral traction. After the detection of the upper pole of the thyroid gland, with care - so as not to damage the external branch of the laryngeal nerve - the superior thyroid artery and vein are ligated throughout. The release of the upper pole allows you to mobilize the lateral and posterior surfaces of the thyroid lobe and identify the inferior thyroid artery to the side of the gland.

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

From this moment of the operation, it is safe to treat the lower and posterior venous branches of the thyroid gland. The isthmus of the gland is crossed between the clamps and the lobe of the thyroid gland 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 relapse of hyperthyroidism.

Patients with Graves' disease most often undergo bilateral subtotal resection of the thyroid gland. Such an operation requires repeating the steps described above on the opposite side. An alternative variant of the operation is a lobectomy on one side and a subtotal resection on the opposite side (Dunhill operation), in which a slightly larger piece of tissue remains, but it is much easier to carry out subsequent treatment.

Operation complications

Due to slight swelling due to tracheal intubation, signs of nerve damage may not be noticed immediately after extubation, but this is suggested by the 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 with a special stimulator and palpate the contraction of the muscles of the larynx. If the patient develops 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 talking and a slight change in voice, especially at high notes. Such damage can be critical for singers and public speakers. Therefore, every effort must be made during surgery to clearly identify and preserve the nerves, since the location of the nerves near the vascular thyroid pedicle contributes to such injuries. Transient nerve paresis occurs in 3-5% of patients. Restoration of nerve function in this case 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 the operation, it is necessary to isolate these glands and make every effort to preserve their blood supply, which in 30% of patients is carried out directly from the capsule of the thyroid gland. In case of violation of the blood supply to the parathyroid glands or when they are removed along with the thyroid gland, it is important to perform their autotransplantation. Transient hypoparathyroidism after thyroidectomy occurs in 3-5% of patients. Such a condition in the immediate postoperative period requires the appointment of vitamin D3 preparations and maintenance therapy with calcium preparations. Permanent hypoparathyroidism occurs in less than 1% of patients.

In the postoperative period, the patient needs close observation for early detection of bleeding or airway obstruction. In patients with progressive hematomas, increasing pain sometimes leads to hoarseness and the 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 administration of corticosteroids.

The article was prepared and edited by: surgeon

Graves' disease(diffuse toxic goiter, Graves' disease) is considered to be a life-threatening disease of the thyroid gland. The defeat of almost all organs and systems makes Graves' disease very dangerous. Patients sometimes have different attitudes towards their disease, ranging from anxious-manic self-limitation in everything to complete disregard and refusal to recognize their illness.

Naturally, such extremes in behavior cannot go unnoticed. For some, this can result in severe depression, for others, severe complications or, even worse, early death. Hello, my name is Dilyara Lebedeva. I am an endocrinologist, and you can find out more about me on the About the Author page.

A person with Graves' disease is a person with a "big" heart. And the point is not that such qualities as kindness, cordiality, understanding or sympathy appear in him. Such people have a big heart in the most direct, anatomical sense of the word.

An excess of thyroid hormones made him so. Because it is so big and ... weak. Yes, an increase in volume in this case does not mean an increase in strength, rather, on the contrary. Unfortunately, this is not the only weakness in patients with Graves' disease. You can read more about this disease in the article

Forced Restrictions in Graves' Disease

This article is written for patients who want to take control (under reasonable control) of their disease. I will try to describe as clearly as possible what you can’t do with Graves’ disease, and not succumb to near-medical delirium and prejudices that can be imposed on you by people “out of touch” (as they say now).

So, here are the “don’ts” that will improve the quality of your life.

Do not take drugs on a case-by-case basis

Since it so happened that your doctor has decided to treat you with antithyroid drugs, then the key to the success of treatment is the regular intake of drugs. The constant fluctuation of the level of hormones (sometimes higher, sometimes lower) in case of irregular intake of them negatively affects the organs, and, possibly, the sensitivity to the drug in the future.

However, you have the right to demand that the doctor revise the tactics of treatment if taking pills is a burden for you. Moreover, the success of this method of treatment is only 30%, in other cases relapse occurs.

What other methods are used in the treatment of Graves' disease, read the article

Don't let your hormones go unchecked

The second "can't" follows directly from the first. In the treatment of Graves' disease with thyreostatics, monthly monitoring of the level of hormones TSH, free T4 and T3 is necessary.

In response, the pituitary gland begins to produce more TSH, and the hormone, in turn, causes an increase in the thyroid gland.

That is why, sometimes, against the background of treatment with thyreostatics, iron can increase. In this case, a certain dose of L-thyroxine is prescribed. This treatment regimen is called “block and replace.”

You can't get pregnant

I don't mean when Graves' disease occurs against the background of an existing pregnancy. There will be a tactic here. We are also interested in women who are just planning a pregnancy. When there is Graves' disease, pregnancy is contraindicated, because very toxic drugs are used in the treatment of this disease, and the disease itself carries a number of complications for both the mother and the fetus.

Reliable methods of contraception must be used. Pregnancy can be planned only after a complete cure of the disease, against the background of persistent euthyroidism. When remission of the disease is achieved after long-term therapy with thyreostatics, there is no 100% guarantee that a relapse will not begin during pregnancy. Such a guarantee, or close to it, can only be given by surgical and radiation treatment of Graves' disease.

Pregnancy planning after surgery can be immediately after recovery, and after radiation treatment, pregnancy can be planned after 1 year. This is very convenient, especially in cases where a woman is already at the age when delay can deprive her of the chance to have a child.

Do not use iodine-containing drugs and products

The thyroid gland in Graves' disease is very active in taking iodine from the products entering the body. And iodine, as you know, is a substrate for thyroid hormones. Therefore, a reasonable restriction in the consumption of iodine-containing products, as well as the use of ordinary (non-iodized) salt, takes place.

You can find out which foods contain a large amount of iodine from the tables in. You should also pay attention to the drugs you take, because some of them may contain iodine.

Can't self-medicate

Graves' disease- This is a life-threatening disease, and there is no place for amateur performances. When this diagnosis is established, immediate treatment is required.

Some patients are not ready or willing to take synthetic drugs. A long and painful search for alternative treatments begins. All this is a waste of precious time and health in the search for the perfect cure.

I declare with all responsibility that there are no effective alternative treatments for Graves' disease. Yes, in the days of our great-grandfathers and great-great-grandfathers, they were treated with various herbs or something else. But at the same time, no one says what was the mortality rate for this disease and what is the percentage of cure for Graves' disease.

We use all the benefits of civilization: electricity, TV, telephone, Internet, cars, planes. So why do we reject advanced technologies and developments in both the pharmaceutical industry and traditional medicine? Is our body really simpler than the latest iPad model?

The conclusion is this: look for a doctor who keeps up with modern medicine.

You can’t deprive yourself of sleep and expose yourself to pointless stress

This rule is not only for patients suffering from Graves' disease, but for people in general. But for my patients, this rule is also relevant because they have a very active sympathetic autonomic nervous system, i.e. such people are sympathetic.

And stress and lack of sleep cause even more activity of the sympathetic nervous system, increasing the already existing anxiety, fussiness and irritability. The conclusion is simple, as in one cartoon about imp No. 13 - "love yourself, spit on everyone and success awaits you in life."

You can not stay in the active sun for a long time

And this rule can be recommended to all inhabitants of the planet. Staying in the summer under the sun at the peak of its activity (from 11 am to 4 pm) is dangerous for any person. And for a patient with Graves' disease, it is also important that thyrotoxicosis be well compensated, i.e., the level of free T4 should be within the normal range.

If the patient also has eye symptoms, then wearing sunglasses is a must in hot climates, plus the use of special moisturizing eye drops.

Don't Skip Calcium-Rich Foods

Therefore, in order to preserve your bones as much as possible, you need to give preference to foods that contain a large amount of calcium. Remember that a person should receive at least 1 g of calcium per day. In some cases, it is possible to prescribe calcium and vitamin D tablets in tablets, but this appointment is made only on the recommendation of your doctor.

If you have not been prescribed calcium supplements, then ask your doctor about the appropriateness of such an appointment.

Can't lie on the couch

The benefits of physical activity cannot be overestimated. But in everything you need to know the measure. If earlier, before your illness, you regularly visited the gym, then classes can be continued provided that thyrotoxicosis is well compensated. Classes at first should not be intense, the pace of training should increase gradually.

If you didn’t go to the gym before and didn’t go nearby, and now after an illness you decided to go in for sports, then you shouldn’t rush right off the bat and prepare for the Olympic Games.

It is enough to start with daily walks along the street, gradually increasing the speed and distance. The main thing is the regularity of training. Naturally, this should be done only after stable compensation of thyrotoxicosis.

You can not lose heart and give up

This is perhaps the most important rule of all. Only in this way will you have an incentive to live, and it is not easy to live, but to live well. And remember the words from the famous song: "Everything will pass, both sadness and joy."

With warmth and care, endocrinologist Dilyara Lebedeva

Description:

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

Symptoms:

You may have hyperthyroidism if you:

      *Experiencing weakness, exhaustion, or irritability.
      *Notice tremors in the hands, an 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.
      *Lose weight with your usual diet.

In addition, some women experience irregular periods or no periods at all, and some men may experience breast enlargement. Symptoms of hyperthyroidism depend on the individual characteristics of the body, age and the amount of thyroid hormone.

Specific symptoms of Graves' disease

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

      * Enlargement of the thyroid gland.
      * Thickening of nails.
      *Mixedema - rough, reddish, thick skin on the front of the legs.
      *Thickening of the terminal phalanges of the fingers.
      *Protrusion and redness of the eyes.

Complications

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

If hyperthyroidism is not treated, the patient begins:

      *Lose weight.
      *Experiencing heart problems: , atrial fibrillation and .
      *Notice the difficulty in the absorption of calcium and other beneficial minerals.

Rarely, hyperthyroidism can cause a life-threatening condition called thyroid storm. usually occurs due to a serious infection or severe stress.

Causes of occurrence:

Other common reasons include:

      *Thyroid nodules. 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. Initially, thyroiditis may cause an increase in thyroid hormone levels, later this level may decrease (hypothyroidism) until the gland recovers.

Rare causes of hyperthyroidism include eating foods or medicines 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 goiter and severe 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, focusing on the signs of elimination of thyrotoxicosis: pulse stabilization (70-80 beats per minute), weight gain, disappearance and sweating, normalization of pulse pressure. It is necessary to conduct a clinical blood test every 10-14 days (with maintenance therapy with Mercazolil - 1 time per month). In addition to antithyroid drugs, b-blockers, glucocorticoids, sedatives, and potassium preparations are used.

Radioiodine therapy.

Radioiodine therapy (RIT) is one of the modern methods of treating diffuse toxic goiter and other thyroid diseases. During treatment, radioactive iodine (isotope I-131) is administered into the body in the form of gelatin capsules orally (in rare cases, a liquid solution of I-131 is used). Radioactive iodine, which accumulates in the cells of the thyroid gland, exposes the entire gland to beta and gamma radiation. In this case, the cells of the gland and tumor cells that have spread beyond its limits are destroyed. Conducting radioiodine therapy implies mandatory hospitalization in a specialized department.

Surgery.

Absolute indications for surgical treatment are allergic reactions or a persistent decrease in leukocytes observed during conservative treatment, large goiter (enlargement of the thyroid gland above grade III), heart rhythm disturbances by type

Graves' disease (Graves' disease, hyperthyroidism or diffuse toxic goiter) is an autoimmune disease in which there is an increased production of thyroid hormones (triiodothyronine and thyroxine) by the tissues of the thyroid gland. An excess of these substances in the blood serum leads to thyrotoxicosis - poisoning of the body by thyroids.

Diffuse toxic goiter occurs most often in women aged 30-50 years. Men get sick much less often. According to the average statistics of the Ministry of Health (Ministry of Health), out of 8 sick people, only one is male. What this is connected with is still unknown.

The content of the article:
1. Etiology of the disease

Etiology of the disease

Graves' disease is most common among residents of regions where the soil and water contain little or no iodine. However, despite this, iodine deficiency is not the main factor provoking the development of pathology. Scientists believe that the causes of the disease are genetic in nature.

Factors leading to the development of thyrotoxicosis:

• genetic predisposition;
• acute lack of iodine in the body;
• severe stress;
• chronic diseases of the nasopharynx;
• head injuries (concussion, traumatic brain injury);
• severe infectious diseases;
• brain encephalitis;
• type 1 diabetes mellitus (characterized by a deficiency of insulin and an excess of glucose in the blood);
• disturbances in the work of the organs of the endocrine system, in particular, the sex glands and the pituitary gland;
• chronic insufficiency of the adrenal cortex.

All these factors together can be an impetus for the production of antibodies by the human immune system that provokes an overactive thyroid gland. It happens in the following way:

1. Antibodies secreted by the immune system block the body's sensitivity to TSH (thyroid-stimulating hormone secreted by the pituitary gland).
2. A serious hormonal imbalance begins in the body, which leads to a sharp increase in the activity of the thyroid gland and, as a result, an increased synthesis of thyroxine and triiodtropine.
3. An excess of thyroid hormones in the blood causes thyrotoxicosis, which entails negative changes not only in the patient's well-being, but also in his appearance.
4. Thyroid tissues begin to grow, diffuse toxic goiter develops.

All organs of the body suffer from Basedow's disease, in women in half of the cases there are problems with conception. Symptoms of the disease are not always pronounced, especially if diffuse goiter is only at the first stage of development. However, the further the disease progresses, the more noticeable its symptoms become.

Diffuse toxic goiter has 3 pronounced symptoms, which directly indicate that the disease not only has a place to be, but is at least at 2-3 stages of development. This:

• hyperthyroidism (increased levels of thyroid hormones in the blood);
• enlargement of the thyroid gland in size;
• exophthalmos (pathological protrusion of the eyeballs, popularly called "bulging eyes").

These symptoms are the most pronounced and, with a complex manifestation, indicate problems with the thyroid gland. However, due to the fact that Graves' disease directly affects the hormonal background, its clinical signs can be much wider.

From the side of the cardiovascular system, the symptoms are as follows:

• arrhythmia, including extrasystole (untimely depolarization and contraction of the heart or its individual chambers);
• tachycardia (rapid heartbeat);
• arterial hypertension (in other words, hypertension, characterized by high blood pressure from 140/90 mm Hg and above);
• stagnation of blood in the heart cavities;
• chronic heart failure, accompanied by edema of the extremities.

Symptoms from the hormonal system:

• metabolic failure, sudden weight loss even with good appetite;
• women may develop oligomenorrhea (menstruation occurs less frequently than once every 40 days), or complete amenorrhea (menstruation stops completely);
• increased sweating;
• headaches, constant fatigue, decreased mental and physical activity.

Failures are observed in the work of the nervous system. A person becomes restless, nervous, when stretching his arms in front of him, he has a strong tremor of the fingers, insomnia appears.

It is also worth paying attention to the nails and the condition of the fingers. With Graves' disease, onycholysis (destruction of the nail plate) or thyroid acropachy (thickening and swelling of the soft tissues of the fingers) is possible. The latter symptom is quite rare and occurs only in 1-2% of patients.

On the part of the gastrointestinal tract, there is a constant intestinal disorder (diarrhea) and dysbacteriosis.

Separately, it is necessary to highlight the symptoms associated with eye health. Graves' disease is characterized by the symptoms of Graefe (when looking down, the upper eyelid lags behind the iris), Dalrymple (hypertonicity of the muscles of the upper eyelid, which leads to expansion of the palpebral fissure), Stelvag (retraction of the upper eyelid and rare blinking), Krause (strong eye shine). Also, in 80% of cases in the later stages of the disease, exophthalmos (protruding eye syndrome) and eyelid tremor are observed.

All these symptoms appear due to the growth of periorbital tissues. The overgrown areas begin to crowd the eyeballs, thereby increasing intraocular pressure and leading to the above ophthalmological problems. Patients often complain of a decrease in visual acuity, a feeling of sand and dryness in the eyes. Due to hypertonicity of the muscles, the eyelids often cannot close completely, which leads to the development of chronic conjunctivitis.

Degrees of the disease

There are three types of Graves' disease in terms of severity:

1. Easy degree. It is characterized by a loss of no more than 10% of the total body weight, the pulse in a calm state rises to 100 beats per minute. Working capacity decreases, concentration of attention decreases, a person quickly gets tired. The thyroid gland is slightly enlarged and palpable only on close examination.
2. Average degree. The patient loses about 20% of body weight, the pulse is even more rapid - from 100 to 120 beats per minute, tachycardia is pronounced. The person becomes nervous and irritable. The thyroid gland becomes visually noticeable when swallowing, easily palpable on palpation.
3. Severe degree. Weight is reduced by more than 20%, in women, amenorrhea is possible, working capacity drops completely, and abnormalities in the liver appear. The patient has mental problems. The heart rate is high - more than 120 heart beats per minute. The thyroid gland is greatly enlarged, a noticeable goiter appears.

Severe disease usually requires surgery. If untreated, the goiter begins to squeeze the throat.

Diagnosis of Graves' disease

To diagnose toxic goiter, you need to contact an immunologist, since the disease belongs to the category of autoimmune. In addition to the immunologist, you should also visit an endocrinologist.

Diagnosis of Graves' Disease is carried out in stages and includes the following procedures and studies:

• Primary history taking, visual examination and palpation of the anterior part of the neck.
• Blood test for hormones. It allows you to accurately determine whether the patient suffers from Graves' disease, or the reasons for his poor health lie in another disease. If the concentration of thyroid hormones is within the normal range, then the thyroid gland works correctly and there can be no talk of diffuse goiter. With an overestimated level of hormones, further examination is prescribed.
• Ultrasound examination of the thyroid gland. Allows you to determine the exact size of the body.
• Scintigraphy. The patient is given an injection of a radiopharmaceutical that accumulates in the tissues of the thyroid gland. Its distribution is recorded by the detectors of the gamma camera and transmitted to a computer. From the resulting image, the radiologist can determine which tissues of the organ are healthy and which are not.

An accurate diagnosis can only be made after a complete examination. When a disease is detected, the doctor prescribes the appropriate treatment.

Treatment of diffuse goiter

Treatment options for the disease:

1. Medical therapy. The main drugs for the treatment of goiter are mercasolil and propylthiouracil. The daily dosage of the first is 30-40 mg, but with large goiters, it can be increased to 60 mg. After successful treatment, additional therapy is carried out for another 1-2 years, in which the daily dose of Mercazolil is reduced to 10 mg. Also, in addition to the main treatment, the patient is prescribed potassium preparations, b-blockers, sedatives and glucocorticoids. Once a month, a laboratory blood test is done to monitor the progress of treatment.
2. Radioiodine therapy. Treatment is with radioactive iodine preparations. The isotope is administered orally into the body, after which it accumulates in the tissues of the thyroid gland and begins to release gamma and beta radiation. Tumor cells of the gland die, the organ returns to normal size and restores its functions. This method of treatment implies mandatory hospitalization of the patient.
3. Operational intervention. It is carried out in exceptional cases, when the size of the goiter is too large, heart rhythm failures are observed, and the level of leukocytes in the blood is reduced to a critical state.

Graves' disease is a serious pathology that requires timely treatment. With successful therapy, the patient quickly returns to his usual way of life, but in the future, constant monitoring of the health of the thyroid gland is necessary.

Graves' disease (Basedow'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 Carl von Basedow.

Etiology

Diffuse toxic goiter is a multifactorial disease in which the genetic features of the immune response are realized against the background of environmental factors. Along with ethnically associated genetic predisposition (carriage of haplotypes HLA-B8, -DR3 and -DQA1 * 0501 in Europeans), psychosocial advanced factors are of particular importance in the pathogenesis of diffuse toxic goiter. Emotional stressors and environmental factors, such as smoking, may contribute to the realization 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 endocrine diseases (type 1 diabetes mellitus, primary hypocorticism).

As a result of impaired immunological tolerance, autoreactive lymphocytes (CD4+ and CD8+ T-lymphocytes, B-lymphocytes) with the participation of adhesive molecules (ICAM-1, ICAM-2, E-selectin, VCAM-1, LFA-1, LFA-3, CD44 ) infiltrate the thyroid parenchyma, 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 attached to the formation stimulatory antibodies to TSH receptor (AT-rTTH).

Unlike other autoimmune diseases, diffuse toxic goiter does not destroy, but stimulates the target organ. In this case, autoantibodies are produced to a fragment of the TSH receptor, which is located on the thyrocyte membrane. As a result of interaction with the antibody, this receptor becomes active, triggering the post-receptor cascade of thyroid hormone synthesis (thyrotoxicosis) and, in addition, stimulating thyrocyte hypertrophy (enlargement of the thyroid gland). For unknown reasons, 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 with antibodies to the TSH receptor is thyrotoxicosis. The pathogenesis of changes in organs and systems that develop with thyrotoxicosis consists in a significant increase in the level of basal metabolism, which eventually 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 common disease in the 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 rare in children and the elderly.

Clinical manifestations

For diffuse toxic goiter, in most cases, a relatively short history is characteristic: the first symptoms usually appear 4-6 months before going to the doctor and making a diagnosis. As a rule, key complaints are associated with changes in the cardiovascular system, the so-called catabolic syndrome and endocrine ophthalmopathy.

The main symptom from of cardio-vascular system is tachycardia and quite pronounced sensations of palpitations. Patients can feel heartbeats not only in the chest, but also in the head, arms, and abdomen. Heart rate at rest with sinus tachycardia due to thyrotoxicosis can reach 120-130 beats per minute.

With long-term thyrotoxicosis, especially in elderly patients, pronounced dystrophic changes in the myocardium develop, a frequent manifestation of which is supraventricular arrhythmias, namely atrial fibrillation (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.

Usually expressed catabolic syndrome, manifested by progressive weight loss (sometimes by 10-15 kg or more, especially in people with initial excess weight) against the background of increasing weakness and increased appetite. The skin of patients is hot, sometimes there is a pronounced hyperhidrosis. A feeling of heat is characteristic, patients do not freeze at a sufficiently low temperature in the room. In some patients (especially in the elderly) evening subfebrile condition may be detected.

Changes from nervous system characterized by mental lability: episodes of aggressiveness, excitement, chaotic unproductive activity are replaced by tearfulness, asthenia (irritable weakness). Many patients are not critical to their condition and try to maintain an active lifestyle against the background of a rather severe somatic condition. Long-term thyrotoxicosis is accompanied by persistent changes in the psyche and personality of the patient. A frequent but nonspecific symptom of thyrotoxicosis is a fine tremor: a fine tremor of the fingers of outstretched hands is detected in most patients. In severe thyrotoxicosis, tremor can be determined 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. A very rare complication is thyrotoxic hypokalemic periodic paralysis, which is manifested by intermittent sharp bouts of muscle weakness. In a laboratory study, hypokalemia and an increase in the level of CPK are detected. It is more common in representatives of the Asian race.

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

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

Menstrual irregularities are 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 cross the placenta, and therefore, children born (1%) to women with diffuse toxic goiter (sometimes years after radical treatment) may develop transient neonatal thyrotoxicosis. In men, thyrotoxicosis is often accompanied by erectile dysfunction.

In severe thyrotoxicosis, a number of patients have symptoms of thyroid (relative) adrenal insufficiency, which must be differentiated from the true. To the already listed symptoms are added hyperpigmentation of the skin, exposed parts of the body (symptom of Jellinek), arterial hypotension.

In most cases, diffuse toxic goiter occurs enlargement of the thyroid gland, which is usually diffuse. Often, the gland is enlarged significantly. In some cases, a systolic murmur can be heard over the thyroid gland. Nevertheless, 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 unequivocally 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 already obvious when examining the patient.

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

The clinical picture of thyrotoxicosis may have deviations from the classical variant. So, if the young diffuse toxic goiter is characterized by a detailed clinical picture; in elderly patients, its course is often oligo- or even monosymptomatic (cardiac arrhythmia, subfebrile condition). In the "apathetic" variant 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 a prohibitive increase in the level of thyroid hormones in the blood. The cause of a thyrotoxic crisis may be acute infectious diseases associated with diffuse toxic goiter, surgical intervention or radioactive iodine therapy against the background of severe thyrotoxicosis, cancellation of thyrostatic therapy, administration of a contrast iodine-containing drug to the patient.

Clinical manifestations of a thyrotoxic crisis include a sharp increase in the symptoms of thyrotoxicosis, hyperthermia, confusion, nausea, vomiting, and sometimes diarrhea. Sinus tachycardia over 120 beats / min is recorded. Often there is atrial fibrillation, high pulse pressure, followed by severe hypotension. The clinical picture may be dominated by heart failure, respiratory distress syndrome. Often expressed manifestations of relative adrenal insufficiency in the form of hyperpigmentation of the skin. The skin may be icteric due to the development of toxic hepatosis. In a laboratory study, leukocytosis (even in the absence of concomitant infection), moderate hypercalcemia, and an increase in the level of alkaline phosphatase can be detected. Mortality in thyrotoxic crisis reaches 30-50%.

Diagnostics

TO diagnostic criteria diffuse toxic goiter include:

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

Endocrine ophthalmopathy (60-80% of cases).

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

Diffuse enhancement of 99m Tc uptake by thyroid scintigraphy.

Elevated levels of antibodies to the TSH receptor.

At the first stage of diagnosis of diffuse toxic goiter, it is necessary to confirm that the patient's clinical symptoms (tachycardia, weight loss, tremor) are due to thyrotoxicosis syndrome. For this purpose, a hormonal study is carried out, which detects a decrease or even complete suppression of the level of TSH and an increase in the levels of T4 and / or TK. Further diagnostics is aimed at differentiating diffuse toxic goiter from other diseases that occur with thyrotoxicosis. In the presence of clinically pronounced 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 with diffuse toxic goiter, as a rule, detects a diffuse enlargement of the thyroid gland and hypoechogenicity characteristic of all its autoimmune diseases. Determining the volume of the thyroid gland, in addition to everything, is necessary for choosing a method of treatment, since the prognosis of conservative thyrostatic therapy for large goiters is rather poor. Thyroid scintigraphy in typical cases (thyrotoxicosis, endocrine ophthalmopathy, diffuse goiter, young age of the patient) is not necessary. In less obvious situations, this method allows you to differentiate diffuse toxic goiter from diseases that occur with destructive thyrotoxicosis (postpartum, subacute thyroiditis, etc.) or from functional autonomy of the thyroid gland (multinodular toxic goiter with "hot" nodes).

With diffuse toxic goiter, at least 70-80% of patients have circulating antibodies to thyroid peroxidase (Ab-TPO) and thyroglobulin (Ab-TG), however, they are nonspecific for this disease and occur in any other autoimmune pathology of the thyroid gland (autoimmune thyroiditis, postpartum thyroiditis). In some cases, an increase in the level of AT-TPO can be regarded as an indirect diagnostic sign of diffuse toxic goiter when it comes to its 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 the determination of the level antibodies to the TSH receptor which in this disease is given the main pathogenetic significance. Nevertheless, it should be taken into account that in some cases these antibodies are not detected in patients with obvious diffuse toxic goiter, which is associated with the imperfection of the relatively recent test systems.

Treatment

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

Conservative therapy carried out with the help of thiourea preparations, which include thiamazole(mercasolil, tyrosol, metizol) and propylthiouracil(vocational school, propycil). 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 the inhibition of thyroid peroxidase, which carries out the addition of iodine to tyrosine residues in thyroglobulin.

aim 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, excluding any possibility of recurrence 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. that can develop during thyroid surgery. The only contraindications to treatment with 131 I are pregnancy and breastfeeding. Significant amounts of 131 I accumulate only in the thyroid gland; after entering it, it begins to decompose 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 lies in the fact that treatment with 131 I can be carried out without prior preparation with thyreostatics. In diffuse toxic goiter, when the goal of treatment is destruction of the thyroid gland, the therapeutic activity, taking into account the volume of the thyroid gland, the maximum uptake and the half-life of 131 I from the thyroid gland, is calculated from an estimated absorbed dose of 200-300 Gy. With an empirical approach, a patient without preliminary dosimetric studies with a small goiter is assigned about 10 mCi, with a larger goiter - 15-30 mCi. Hypothyroidism usually develops within 4-6 months after administration of 131 I.

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

Treatment thyrotoxic crisis implies intensive measures with the appointment of large doses of thyreostatics. Preference is given vocational school at a dose of 200-300 mg every 6 hours, if self-administration by the patient is impossible - through a nasogastric tube. In addition, ß-blockers are prescribed (propranolol: 160-480 mg per day per os or IV at the rate of 2-5 mg/hour), glucocorticoids (hydrocortisone: 50-100 mg every 4 hours or prednisolone (60 mg/day), detoxification therapy ( saline, 10% glucose solution) under hemodynamic control. Plasmapheresis is an effective treatment for thyroid storm.

Forecast

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