Autoimmune thyroiditis

The autoimmune thyroid lesion was first described in 1912 by a Japanese doctor and scientist Hashimoto Hakaru . ^[1] Subsequently, the disease was named after the scientist - Hashimoto thyroiditis.

Autoimmune thyroiditis occurs in 3-4% of the world 's population ^[2] . The frequency of clinically expressed forms of the disease is 1% ^[3] .

The number of women with autoimmune thyroiditis exceeds the number of men by 4-8 times ^{[4] [5] [6]} . Most often, the disease is diagnosed in women over 60 years of age - the frequency in the population is 6-11% ^[7] .

The prevalence of the disease in children is 0.1-1.2%. ^[2]

The disease develops against the background of a genetically determined defect in the immune response, leading to T-lymphocytic aggression against thyroid cells of their own, ending in their destruction. Histologically, lymphocytic and plasmacytic infiltration, oncocytic transformation of thyrocytes (the formation of Gürtle-Ashkenazi cells), and destruction of follicles are determined histologically. AIT tends to manifest itself in the form of family forms. In patients with an increased frequency, haplotypes HLA-DR3, DR5, B8 are detected. In 50% of cases, relatives of patients with AIT show circulating antibodies to the thyroid gland. In addition, there is a combination of AIT in the same patient or within the same family with other autoimmune diseases - pernicious anemia, autoimmune primary hypocorticism, chronic autoimmune hepatitis, type 1 diabetes mellitus, vitiligo, rheumatoid arthritis, etc.

The basis of the pathogenesis of this condition is the development of autoantibodies by the immune system, which are directed by forgiving the cells of the thyroid parenchyma. Acting on thyrocytes, antibodies cause a destructive transformation in thyroid cells. The result is a decrease in thyroid function and a decrease in the production of thyroid hormones, which leads to an increase in the formation of thyroid stimulating hormone (TSH) and the development of hypothyroidism. Against the background of AIT, the development of temporary hyperthyroidism (thyrotoxicosis) is also possible - an increase in the production of thyroid hormones. Factors that can provoke AIT can be: pregnancy; childbirth; environmental degradation; deficiency or excess of iodine; radioactive pollution, etc.

Levanenko A.A. Autoimmune thyroiditis and the female reproductive system // Young Scientist. - 2018. - No. 13. - S. 77-78. - URL https://moluch.ru/archive/199/48980/ (accessed date: 08/13/2019).

It is confirmed by data on frequent cases of the occurrence of the disease in close relatives ^[8] . Patients with autoimmune thyroiditis often suffer from other autoimmune diseases of somatic and endocrine genesis: diffuse toxic goiter , myasthenia gravis , infiltrative (autoimmune) ophthalmopathy , Sjogren's syndrome , alopecia , vitiligo , collagen -lymphocytic lymphomas .

The occurrence of the disease can be preceded by any impact that leads to a violation of the integrity of the structure of the thyroid gland and the penetration of thyroid antigens into the bloodstream (various infectious diseases , inflammatory processes, less often a thyroid injury or surgery on the thyroid gland . Factors that can trigger autoimmune thyroiditis can also be: deterioration environmental conditions; deficiency or excess of iodine ; radioactive contamination and so on) ^[9] .

It was found that in regions with a high deficiency of selenium in soils, the incidence of autoimmune thyroiditis is significantly higher ^[10] .

Antibodies to the thyroid gland are found in the blood of most patients with autoimmune thyroiditis ^{[ specify ]} - proteins involved in the development of this disease ^[11] . This is due to a decrease in the activity of glutathione peroxidase in thyroid cells.

Clinical manifestations

In the euthyroid phase and the phase of subclinical hypothyroidism are absent. In some relatively rare cases, an increase in the volume of the thyroid gland (goiter), which quite rarely reaches significant degrees, comes to the fore in the euthyroid phase. With the development of hypothyroidism in the patient, the corresponding symptoms begin to increase.

Several forms of autoimmune thyroiditis are distinguished:

• Hypertrophic variant (Hashimoto's thyroiditis). The thyroid gland is diffusely dense, its function is not impaired or moderately impaired - hypothyroidism or thyrotoxicosis. ^[12] .
• Atrophic form of autoimmune thyroiditis. The thyroid gland at the time of examination is reduced, hypothyroidism is noted.
• Postpartum thyroiditis occurs in approximately 5-6% of women.

Conducted from ^[9] :

• subacute thyroiditis ;
• nodular goiter ;
• thyroid cancer ;
• other chronic thyroiditis .

No specific therapy for autoimmune thyroiditis has been developed.

Thyroid Treatment

In the presence of hypothyroidism, thyroid hormone preparations are prescribed ( thyroxine , triiodothyronine , thyroidin, L-thyroxine). The daily dose of thyroxine in adults is 1.4-1.7 μg per 1 kg of body weight (about 100-175 μg per person per day), and in children up to 4 μg per 1 kg of body weight. In some cases, in particular, with the atrophic form of autoimmune thyroiditis, an increased dose of thyroxine can be prescribed - 200-225 mcg / day. The appointment of thyroid drugs, especially in the elderly, should be started with small doses (25 mcg), increasing every 25-3 weeks by 25 mcg, controlling the clinical symptoms and serum TSH levels. Given the chronic nature of the disease, treatment with thyroid drugs is carried out for a long time. Serum TSH levels should be monitored no more than 1.5–2 months later. after starting treatment.

Glucocorticoid Treatment

Glucocorticoid drugs, as a rule, are prescribed only with a combination of autoimmune thyroiditis with subacute thyroiditis . Typically, prednisone is used in a daily dose of 40 mg, followed by a decrease.

Surgical Treatment

Surgical treatment is indicated only for rapidly growing goiter , compression of the trachea or vessels of the neck due to an enlarged thyroid gland , as well as suspected cancer in the presence of nodes.

The use of selenium preparations

In modern clinical practice, hypothyroidism is not an indication for the use of dietary supplements with selenium ^[13] .

Recommended as adjunctive therapy ^{[by whom? ]} taking selenium preparations. It was found that taking selenium preparations for 3 months leads to a significant decrease in the levels of autoantibodies to thyroid peroxidase and to improve the well-being of patients. ^[14] .

• Thyroid hormones
• Hypothyroidism
• Thyroid Peroxidase Antibodies
• Chronic thyroiditis
• Hashimoto Encephalopathy