Simple non-toxic goiter (euthyroid goiter)

Simple nontoxic goiter, which may be diffuse or nodular, is a nonneoplastic hypertrophy of the thyroid gland without underlying hyperthyroidism, hypothyroidism, or inflammation. The cause is usually unknown, but is thought to result from prolonged hyperstimulation of thyroid-stimulating hormone, most commonly in response to iodine deficiency (endemic colloid goiter) or to various foods or drugs that inhibit thyroid hormone synthesis. Except in cases of severe iodine deficiency, thyroid function is normal and patients are asymptomatic, with a markedly enlarged, firm thyroid gland. Diagnosis is based on clinical examination and laboratory confirmation of normal thyroid function. Treatment is directed at the underlying cause, with surgical treatment (partial thyroidectomy) being preferred if the goiter is too large.

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Causes simple nontoxic goiter (euthyroid goiter)

Simple nontoxic goiter is the most common and typical cause of thyroid enlargement, most often detected during puberty, pregnancy and menopause. The cause is still unclear in most cases. Known causes are established defects in the production of thyroid hormones in the body and iodine deficiency in certain countries, as well as the use of food containing components that suppress the synthesis of thyroid hormones (the so-called goitrogenic food components, such as cabbage, broccoli, cauliflower, cassava). Other known causes are due to the use of drugs that reduce the synthesis of thyroid hormones (for example, amiodarone or other iodine-containing drugs, lithium).

Iodine deficiency is rare in North America but remains a major cause of the goiter epidemic worldwide (called endemic goiter). Compensatory low TSH elevations are seen to prevent hypothyroidism, but TSH stimulation itself favors nontoxic nodular goiter. However, the true etiology of most nontoxic goiters occurring in iodine-rich areas is unknown.

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Symptoms simple nontoxic goiter (euthyroid goiter)

Patients may have a history of low dietary iodine intake or high dietary goitrogenic components, but this phenomenon is rare in North America. In the early stages, the enlarged thyroid gland is usually soft and smooth, with both lobes symmetrical. Later, multiple nodules and cysts may develop.

The thyroid gland is assessed for radioactive iodine accumulation, thyroid scanning, and thyroid function laboratory parameters (T3, T4, TSH). In the early stages, thyroid gland radioactive iodine accumulation may be normal or high with a normal scintigraphic picture. Laboratory parameters are usually normal. Thyroid antibodies are measured to differentiate from Hashimoto's thyroiditis.

In endemic goiter, serum TSH may be slightly elevated and serum T3 may be at the lower limit of normal or slightly decreased, but serum T3 levels are usually normal or slightly elevated.

Treatment simple nontoxic goiter (euthyroid goiter)

In regions with iodine deficiency, salt iodization is used; oral or intramuscular administration of oil solutions of iodine annually; iodization of water, cereals or the use of animal feed (forage) reduces the incidence of iodine-deficiency goiter. It is necessary to exclude the intake of goitrogenic components in food.

In other regions, hypothalamic-pituitary suppression with thyroid hormones that block TSH production (hence the stimulation of the thyroid gland) is used. TSH-suppressive doses of L-thyroxine, necessary for its complete suppression (100-150 mcg/day orally, depending on the serum TSH level), are especially effective in young patients. L-thyroxine is contraindicated in elderly and senile patients with nontoxic nodular goiters, since these types of goiter rarely decrease in size and may contain areas with autonomous (non-TSH-dependent) function, in which case L-thyroxine intake may lead to the development of a hyperthyroid state. Patients with large goiters often require surgery or radioiodine (131-I) therapy to reduce the size of the gland enough to prevent breathing or swallowing difficulties or cosmetic problems.