Simple nontoxic goiter (euthyroid goiter)

A simple nontoxic goiter, which can be diffuse or nodular, is a non-tumor hypertrophy of the thyroid without an evolving state of hyperthyroidism, hypothyroidism, or inflammation. The cause is usually unknown, but it is believed that this can be the result of prolonged hyperstimulation by thyroid stimulating hormone, most often in response to iodine deficiency (endemic colloid goiter) or by taking various food components or drugs that inhibit the synthesis of thyroid hormones. Except for cases of expressed iodine deficiency, thyroid function is normal and patients are asymptomatic, a markedly enlarged, dense thyroid gland is defined. The diagnosis is established based on clinical examination and laboratory confirmation of normal thyroid function. Therapeutic measures are aimed at eliminating the leading cause of the disease, in the case of developing too large goiter, surgical treatment (partial thyroidectomy) is preferable.

[1], [2], [3], [4], [5]

Causes of the simple nontoxic goiter (euthyroid goiter)

Simple non-toxic goiter - the most common and typical cause of enlargement of the thyroid gland, most often detected in the pubertal period, the period of pregnancy and in menopause. The reason to this point in most cases is not clear. The known causes are the established defects in the production of thyroid hormones in the body and the iodine deficiency in certain countries, as well as the consumption of food containing components that suppress the synthesis of thyroid hormones (so-called zobogenic nutritional components, for example, cabbage, broccoli, cauliflower, cassava). Other known causes are caused by the use of drugs that reduce the synthesis of thyroid hormones (eg, amiodarone or other iodine-containing drugs, lithium).

Iodine deficiency is rare in North America, but remains the main cause of the goiter epidemic all over the world (called endemic goiter). There are compensatory low elevations of TSH that prevent the development of hypothyroidism, but the TTG stimulation itself speaks in favor of nontoxic nodular goiter. Nevertheless, the true etiology of most non-toxic goiter occurring in regions where iodine is sufficient is unknown.

[6], [7]

Symptoms of the simple nontoxic goiter (euthyroid goiter)

Patients may have an anamnesis of low intake of iodine in the body with food or a high content of food in the diet of zobogenic components, but this phenomenon is rare in North America. In the early stages, the enlarged thyroid gland is usually soft and smooth, both segments are symmetrical. Later, multiple nodes and cysts can develop.

The accumulation of radioactive iodine by the thyroid gland is determined, scanning and determination of laboratory parameters of thyroid function (T3, T4, TTG) are carried out. In the early stages, the accumulation of radioactive iodine by the thyroid gland can be normal or high with a normal scintigraphic pattern. Laboratory indicators are usually normal. Antibodies to thyroid tissue are determined to identify differences with Hashimoto's thyroiditis.

With endemic goiter, serum TSH can be slightly elevated, and serum T3 - at the lower limit of the norm or slightly reduced, but serum T3 is usually normal or slightly elevated.

Treatment of the simple nontoxic goiter (euthyroid goiter)

Iodized salt is used in regions with iodine deficiency; oral or intramuscular administration of iodine oil solutions annually; iodization of water, cereals or the use of animal feed (fodder) reduce the incidence of iodine deficiency goiter. It is necessary to exclude the ingestion of zobilogenic components.

In other regions, the hypothalamic-hypophyseal zone is suppressed by thyroid hormones blocking the THH production (hence the stimulation of the thyroid gland). TTG-suppressive doses of L-thyroxine, necessary for its complete suppression (100-150 mcg / day orally, depends on the level of serum TSH), are especially effective in young patients. The appointment of L-thyroxine is contraindicated in elderly and senile patients, with non-toxic nodular goiter, since these species of goiter rarely decrease in size and may contain areas with autonomous (non-TTG-dependent) function, in which case taking L-thyroxin can lead to development of the hyperthyroid state. Patients with large goiter often require surgery or radioiodine therapy (131-I) to reduce the size of the gland sufficient to prevent the development of difficulty breathing or swallowing or problems associated with cosmetic correction.