Diffuse toxic goiter in children

Diffuse toxic goiter (synonyms: Graves' disease) is an organ-specific autoimmune disease in which thyroid-stimulating antibodies are produced.

ICD-10 code

E05.0 Thyrotoxicosis with diffuse goiter.

Causes of diffuse toxic goiter

Thyroid stimulating antibodies bind to TSH receptors on thyroid cells, and the process, normally triggered by TSH, is activated, a synthesis of thyroid hormones. The autonomous activity of the thyroid gland, which does not lend itself to central regulation, begins.

The disease is considered genetically determined. It is known that the development of thyroid-stimulating antibodies is due to the antigen-specific cell suppression defect. The provoking factor to the formation of thyroid-stimulating immunoglobulins can be an infectious disease or stress. In this case, most patients have a long-acting stimulant of the thyroid gland.

[1]

The pathogenesis of diffuse toxic goiter

Excess thyroid hormones lead to dissociation of respiration and phosphorylation in the cell, increased heat production, the rate of utilization of glucose. Gluconeogenesis and lipolysis are activated. Catabolic processes intensify, dystrophy of the myocardium, liver, and muscle tissue develop. The relative insufficiency of glucocorticoids, sex hormones is developing.

There are three stages in the development of the disease.

• I. Preclinical stage. The body accumulates antibodies, there are no clinical symptoms.
• II. Euthyroid stage. Progressively increasing hyperplasia of the thyroid gland, thyroid hormones in the blood do not exceed normal values.
• III. Hyperthyroid stage is accompanied by morphological lymphocytic infiltration of the thyroid gland, immunological reactions, cytolysis. There are clinical symptoms.

Symptoms of diffuse toxic goiter

There are three groups of symptoms:

• local symptoms - goiter;
• symptoms associated with hyperproduction of thyroid hormones;
• Symptoms due to concomitant autoimmune diseases. The thyroid gland is significantly enlarged, as a rule, the increase is noticeable upon examination. At a palpation the dense consistence is defined, above a gland vascular murmurs are listened.

Symptoms caused by thyrotoxicosis increase gradually over several months. The child becomes whiny, emotionally unstable, irritable, the dream is disturbed. On examination, the smooth velvety skin attracts attention, pigmentation occurs, especially in the eyelid region. Sweating is increased, muscle weakness is often noted. Appetite is increased, but the child is progressively losing weight. There are tremor of fingers, increased motor activity. Characteristic tachycardia at rest and increased pulsatile arthritic pressure. Mark a frequent stool, sometimes reveal hepatomegaly. Girls have amenorrhea.

Sympaticotonia provokes the appearance of eye symptoms: Gref's symptom is the exposure of the sclera site over the iris, while looking down, the Moebius symptom is the weakness of the convergence of the eyeballs, von Stellwagk's symptom is a rare flashing, the Dalrymple symptom is the widely open eye cracks,

Thyrotoxicosis, depending on the severity of tachycardia, is divided into three degrees:

• I degree - heart rate is increased by no more than 20%;
• II degree - heart rate is increased by no more than 50%;
• III degree - heart rate is increased by more than 50%.

Associated thyrotoxicosis autoimmune diseases include endocrine ophthalmopathy, pretybial myxedema, diabetes mellitus, juvenile polyarthritis. Endocrine ophthalmopathy is most often observed with diffuse toxic goiter. It is caused by the formation of antibodies to the membrane of the oculomotor muscles and their lymphocytic infiltration, which extends to the retrobulbar fiber. This causes edema, hyperpigmentation of the eyelids, exophthalmos.

Complications of diffuse toxic goiter

In the absence of treatment, the patient may develop a thyrotoxic crisis. In this case, the temperature rises, there is motor anxiety or apathy, vomiting, signs of acute heart failure, coma.

[2]

Diagnosis of diffuse toxic goiter

Diagnosis is based on clinical data and the determination of the thyroid hormone content in the blood. The following changes are noted:

• T ₃ and T ₄, in the serum are increased, and TSH is lowered - in 70% of patients;
• T ₃ increased, T ₄ normal, TSH decreased - in 30% of patients;
• antibodies to TSH receptors in blood serum;
• the content of cholesterol and beta-lipoproteins in blood serum is reduced;
• relative lymphocytosis in a clinical blood test;
• increased the content of ionized calcium in the blood serum;
• ECG - tachycardia, an increase in the voltage of the teeth.

[3], [4]

Differential diagnosis

Differential diagnosis should be carried out with vegetative-vascular dystonia, in which tachycardia and emotional arousal are not permanent.

Hyperthyroidism can also develop with other thyroid diseases. These include - acute purulent and subacute thyroiditis, autoimmune thyroiditis, functionally active nodes of the thyroid gland.

[5], [6]

Treatment of diffuse toxic goiter

The goal of the treatment is to eliminate the manifestations of hyprethyroidism and normalize the levels of thyroid hormones. Apply medication and surgical methods of treatment. Initial therapy is based on the use of drugs that have a thyreostatic effect. Thiamazole is prescribed for 1.5-2.5 years. The starting dose of thiamazole is 0.5-0.7 mg / kg per day, depending on the severity of thyrotoxicosis in three doses. Every 10-14 days the dose is reduced to maintenance. The maintenance dose is 50% of the initial dose. In the majority of patients, inhibition of thyroxine secretion by thiamazole leads to hypothyroidism and an increase in blood levels of TSH. In this regard, after 6-8 weeks from the start of treatment, thyroid administration is desirable to be combined with the appointment of levothyroxine sodium to maintain euthyroidism and to prevent the gastrointestinal effect of TSH.

With thyroid intolerance, inefficiency of conservative treatment, in the presence of nodes in the thyroid gland, subtotal strumectomy is indicated.

Prognosis for diffuse toxic goiter

After drug treatment lasting more than 1.5 years, remission occurs in 50% of patients. In half of patients with remission, thyrotoxicosis recurs. Evidence of achieving remission is the disappearance of thyroid-stimulating autoantibodies in the blood. Individual prognosis in patients with diffuse toxic goiter depends on the severity of autoimmune thyroid disease and does not depend on the antithyroid agent used. Combined treatment with thiamazole and levothyroxine for a long time and continued therapy with levothyroxine after thionamide discontinuation reduces the likelihood of relapse of thyrotoxicosis.