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 thyrocytes, activating the process normally triggered by TSH - the synthesis of thyroid hormones. Autonomous thyroid activity begins, which is not subject to central regulation.

The disease is considered genetically determined. It is known that the production of thyroid-stimulating antibodies is due to an antigen-specific defect in cellular suppression. An infectious disease or stress may be a provoking factor for the formation of thyroid-stimulating immunoglobulins. In most patients, a long-acting thyroid stimulator is detected.

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Pathogenesis of diffuse toxic goiter

Excess thyroid hormones lead to uncoupling of respiration and phosphorylation in the cell, heat production and the rate of glucose utilization increase, gluconeogenesis and lipolysis are activated. Catabolic processes intensify, myocardial, liver, and muscle tissue dystrophy develop. Relative deficiency of glucocorticoids and sex hormones develops.

There are three stages in the development of the disease.

• I. Preclinical stage. Antibodies accumulate in the body, clinical symptoms are absent.
• II. Euthyroid stage. Hyperplasia of the thyroid gland progressively increases, thyroid hormones in the blood do not exceed normal values.
• III. The hyperthyroid stage is accompanied by morphologically lymphocytic infiltration of the thyroid gland, immunological reactions, cytolysis. Clinical symptoms appear.

Symptoms of diffuse toxic goiter

There are three groups of symptoms:

• local symptoms - goiter;
• symptoms associated with hyperproduction of thyroid hormones;
• symptoms caused by concomitant autoimmune diseases. The thyroid gland is significantly enlarged, as a rule, the enlargement is noticeable upon examination. Palpation reveals a dense consistency, vascular noises are heard above the gland.

Symptoms caused by thyrotoxicosis gradually increase over several months. The child becomes whiny, emotionally unstable, irritable, and sleep is disturbed. On examination, smooth velvety skin attracts attention, there may be pigmentation, especially in the eyelid area. Sweating is increased, muscle weakness is often noted. Appetite is increased, but at the same time the child progressively loses weight. Finger tremors and increased motor activity appear. Tachycardia at rest and increased pulse arterial pressure are characteristic. Frequent stools are noted, and hepatomegaly is sometimes detected. Amenorrhea is observed in girls.

Sympathicotonia provokes the appearance of eye symptoms: Graefe's symptom - exposure of the sclera above the iris when looking down, Mobius's symptom - weakness of convergence of the eyeballs, von Stellwag's symptom - rare blinking, Dalrymple's symptom - wide-open eye slits, etc.

Depending on the severity of tachycardia, thyrotoxicosis is divided into three degrees:

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

Autoimmune diseases associated with thyrotoxicosis include endocrine ophthalmopathy, pretibial myxedema, diabetes mellitus, and juvenile polyarthritis. Endocrine ophthalmopathy is most often observed in diffuse toxic goiter. It is caused by the formation of antibodies to the membrane of the extraocular muscles and their lymphocytic infiltration, which also extends to the retrobulbar tissue. This causes edema, hyperpigmentation of the eyelids, and exophthalmos.

Complications of diffuse toxic goiter

If left untreated, the patient may develop a thyrotoxic crisis. This is accompanied by a rise in temperature, motor restlessness or apathy, vomiting, signs of acute heart failure, and coma.

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Diagnosis of diffuse toxic goiter

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

• T3 and T4 _in the blood serum are elevated, and TSH is reduced in 70% of patients _;
• T3 is elevated, T4 _isnormal, TSH is reduced - in 30% of patients;
• antibodies to TSH receptors in blood serum;
• the content of cholesterol and beta-lipoproteins in the blood serum is reduced;
• relative lymphocytosis in clinical blood analysis;
• increased levels of ionized calcium in the blood serum;
• ECG - tachycardia, increased voltage of the teeth.

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Differential diagnosis

Differential diagnosis should be carried out with vegetative-vascular dystonia, in which tachycardia and emotional arousal are intermittent.

Hyperthyroidism can also develop with other thyroid diseases. These include acute purulent and subacute thyroiditis, autoimmune thyroiditis, functionally active thyroid nodules.

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Treatment of diffuse toxic goiter

The goal of treatment is to eliminate the manifestations of hyperthyroidism and normalize the levels of thyroid hormones. Medication and surgical treatment are used. 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 the maintenance dose. The maintenance dose is 50% of the initial dose. In most patients, inhibition of thyroxine secretion by thiamazole leads to hypothyroidism and an increase in the level of TSH in the blood. In this regard, 6-8 weeks after the start of treatment, it is advisable to combine the use of thyreostatics with the prescription of sodium levothyroxine to maintain euthyroidism and prevent the goitrogenic effect of TSH.

In case of intolerance to antithyroid drugs, ineffectiveness of conservative treatment, and the presence of nodules 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 the patients with remission, thyrotoxicosis recurs. Evidence of remission is the disappearance of thyroid-stimulating autoantibodies in the blood. The individual prognosis in patients with diffuse toxic goiter depends on the severity of the autoimmune thyroid lesion and does not depend on the antithyroid drug used. Combined treatment with thiamazole and levothyroxine for a long time and continuation of levothyroxine therapy after discontinuation of thionamides reduces the likelihood of relapse of thyrotoxicosis.