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Autoimmune Chronic Thyroiditis - Information Overview
Last reviewed: 05.07.2025

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In recent years, there has been an increase in the incidence of the disease, which is obviously associated with increased stimulation of the immune system by newly created artificial antigens, with which the human body had no contact during the process of photogenesis.
Autoimmune thyroid disease (4 cases) was first described by Hashimoto in 1912, the disease was called Hashimoto's thyroiditis. For a long time, this term was identical to the term chronic autoimmune or lymphocytic thyroiditis. However, clinical observations have shown that the latter can occur in various forms, accompanied by symptoms of hypo- and hyperthyroidism, enlargement or atrophy of the gland, which made it appropriate to distinguish several forms of autoimmune thyroiditis. A number of classifications of autoimmune thyroid diseases have been proposed. The most successful, in our opinion, is the classification proposed by R. Volpe in 1984:
- Graves' disease (Basedow's disease, autoimmune thyrotoxicosis);
- Chronic autoimmune thyroiditis:
- Hashimoto's thyroiditis;
- lymphocytic thyroiditis in children and adolescents;
- postpartum thyroiditis;
- idiopathic myxedema;
- chronic fibrous variant;
- atrophic asymptomatic form.
All forms of chronic thyroiditis meet the requirements of E. Witebsky (1956) for autoimmune diseases: the presence of antigens and antibodies, an experimental model of the disease on animals, the possibility of transferring the disease with the help of antigens, antibodies and immunocompetent cells from sick animals to healthy ones.
Causes of autoimmune thyroiditis
The study of the HLA system showed that Hashimoto's thyroiditis is associated with the DR5, DR3, B8 loci. The hereditary genesis of the disease (thyroiditis) Hashimoto is confirmed by data on frequent cases of the disease among close relatives. Genetically determined defect of immunocompetent cells leads to a breakdown of natural tolerance and infiltration of the thyroid gland by macrophages, lymphocytes, plasma cells. Data on subpopulations of peripheral blood lymphocytes in patients with autoimmune diseases of the thyroid gland are contradictory. However, most authors adhere to the point of view of the primary qualitative antigen-dependent defect of T-suppressors. But some researchers do not confirm this hypothesis and suggest that the immediate cause of the disease is an excess of iodine and other drugs, which are assigned the role of a resolving factor in the breakdown of natural tolerance. It has been proven that the production of antibodies occurs in the thyroid gland, is carried out by derivatives of beta cells, is a T-dependent process.
Causes and pathogenesis of autoimmune chronic thyroiditis
Symptoms of autoimmune thyroiditis
Hashimoto's thyroiditis most often occurs at the age of 30-40 years, and less often in men than in women (1:4-1:6, respectively). The disease may have individual characteristics.
Hashimoto's thyroiditis develops gradually. At first, there are no signs of dysfunction, since the destructive changes mentioned above are compensated by the work of the intact areas of the gland. As the process progresses, destructive changes can affect the functional state of the gland: provoke the development of the first phase of hyperthyroidism due to the entry of a large amount of previously synthesized hormone into the blood or symptoms of increasing hypothyroidism.
Classical antithyroid antibodies are detected in 80-90% of cases of autoimmune thyroiditis and, as a rule, in very high titers. The frequency of detection of antimicrosomal antibodies is higher than in diffuse toxic goiter. It is not possible to correlate the titer of antithyroid antibodies with the severity of clinical symptoms. The presence of antibodies to thyroxine and triiodothyronine is a rare finding, so it is difficult to judge their role in the clinical picture of hypothyroidism.
Diagnosis of autoimmune thyroiditis
Until recently, detection of antibodies to thyroglobulin (or microsomal antigen), especially at high titers, served as a diagnostic criterion for autoimmune thyroiditis. It has now been established that similar changes are observed in diffuse toxic goiter and some forms of cancer. Therefore, these studies help to conduct a differential diagnosis with extrathyroidal disorders and play an auxiliary, rather than absolute, role. A thyroid function test with 131 1 usually gives reduced absorption and accumulation figures. However, there may be variants with normal or even increased accumulation (due to an increase in the mass of the gland) against the background of clinical symptoms of hypothyroidism.
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Treatment of autoimmune thyroiditis
Treatment of autoimmune thyroiditis should begin with the administration of thyroid hormones. Increasing the concentration of thyroxine and triiodothyronine in the blood inhibits the synthesis and release of thyroid-stimulating hormone, thereby stopping further growth of the goiter. Since iodine can play a provoking role in the pathogenesis of autoimmune thyroiditis, it is necessary to prefer dosage forms with a minimum iodine content. These include thyroxine, triiodothyronine, combinations of these two drugs - thyrotom and thyrotom forte, Novotirol.
Thyreocomb, containing 150 mcg of iodine per tablet, is preferable for the treatment of hypothyroidism in endemic goiter, as it replenishes the iodine deficiency and stimulates the work of the gland itself. Despite the fact that sensitivity to thyroid hormones is strictly individual, people over 60 years of age should not be prescribed a dose of thyroxine over 50 mcg, and triiodothyronine intake should begin with 1-2 mcg, increasing the dose under ECG control.
Prognosis for autoimmune thyroiditis
The prognosis with early diagnosis and active treatment is favorable. Data on the frequency of goiter malignancy in chronic thyroiditis are contradictory. However, their reliability is higher (10-15%) than in euthyroid nodular goiters. Most often, chronic thyroiditis is combined with adenocarcinomas and lymphosarcomas.
The ability to work of patients with autoimmune thyroiditis depends on the success of hypothyroidism compensation. Patients should be constantly monitored by a dispensary.