Autoimmune Chronic Thyroiditis: A Review of Information
Last reviewed: 23.04.2024
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In recent years, there has been an increase in the incidence, which is obviously associated with increased stimulation of the immune system with newly created artificial antigens, which the human body did not have contact with during photogenesis.
The first autoimmune thyroid lesion (4 cases) was 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 different versions, accompanied by symptoms of hypo- and hyperthyroidism, an increase or atrophy of the gland, which made it expedient to isolate several forms of autoimmune thyroiditis. A number of classifications of autoimmune diseases of the thyroid gland was proposed. The most successful is the classification proposed by R. Volpe in 1984:
- Graves' disease (Graves disease, autoimmune thyrotoxicosis);
- Chronic autoimmune thyroiditis:
- Hashimoto's thyroiditis;
- lymphocyte thyroiditis of children and adolescents;
- postpartum thyroiditis;
- idiopathic myxedema;
- chronic fibrous variant;
- atrophic asymptomatic form.
All forms of chronic thyroiditis correspond to the requirements of E. Witebsky (1956) for autoimmune diseases: the presence of antigens and antibodies, the experimental model of the disease in animals, the possibility of disease transfer by means of antigens, antibodies and immunocompetent cells from healthy animals.
Causes of autoimmune thyroiditis
A study of the HLA system showed that Hashimoto's thyroiditis is associated with loci DR5, DR3, B8. Hereditary genesis of the disease (thyroiditis) of Hashimoto is confirmed by data on frequent cases of the disease among close relatives. Genetically caused defect of immunocompetent cells leads to a breakdown of natural tolerance and infiltration of the thyroid gland by macrophages, lymphocytes, and plasma cells. Data on subpopulations of peripheral blood lymphocytes in patients with autoimmune thyroid diseases 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 that play the role of a resolving factor in a breakdown of natural tolerance. It is proved that the production of antibodies occurs in the thyroid gland, is carried out by the derivatives of beta-cells, is a T-dependent process.
Causes and pathogenesis of autoimmune chronic thyroiditis
Symptoms of autoimmune thyroiditis
Thyroiditis Hashimoto often begin to ache at the age of 30-40 years, and less often than men (1: 4-1: 6, respectively). The disease can have individual characteristics.
Thyroiditis Hashimoto develops gradually. Initially, there are no signs of a disruption of the function, since those destructive changes, mentioned above, are compensated by the work of undamaged sections of the gland. As the process increases, destructive changes can affect the functional state of the gland: to provoke the development of the first phase of hyperthyroidism due to the receipt of a large amount of previously synthesized hormone in the blood or symptoms of increasing hypothyroidism.
Classical antithyroid antibodies are determined in autoimmune thyroiditis in 80-90% of cases and, as a rule, in very high titres. In this case, the frequency of detection of antimycrosomal antibodies is higher than in diffuse toxic goiter. A correlation between the titer of antithyroid antibodies and the severity of clinical symptoms is not possible. 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, the detection of antibodies to thyroglobulin (or microsomal antigen), especially with a large titer, served as a diagnostic criterion for autoimmune thyroiditis. It is now established that similar changes are observed in diffuse toxic goiter and some forms of cancer. Therefore, these studies help to make a differential diagnosis with vnnetireoidnymi violations and play the role of auxiliary, rather than absolute. Examination of the thyroid function with 131 1 usually gives a reduced number of absorption and accumulation. However, there may be variants with normal or even increased accumulation (due to an increase in the gland mass) against the background of clinical symptoms of hypothyroidism.
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Treatment of autoimmune thyroiditis
Treatment of autoimmune thyroiditis should begin with the appointment of thyroid hormones. An increase in the concentration of thyroxin and triiodothyronine in the blood inhibits the synthesis and release of the thyroid-stimulating hormone, thereby stopping further growth of the goiter. Since iodine can play a provocative role in the pathogenesis of autoimmune thyroiditis, it is preferable to prefer dosage forms with a minimum iodine content. These include thyroxine, triiodothyronine, a combination of these two drugs - thyrotoxic and thyrotope forte, novotyrol.
Thyreocomb, containing 150 mcg of iodine in a tablet, is preferred for the treatment of hypothyroidism in endemic goiter, as it compensates for the deficiency of iodine and stimulates the proper functioning of the gland. Despite the fact that sensitivity to thyroid hormones is strictly individual, individuals over 60 years should not be prescribed a dose of thyroxin over 50 mcg, and triiodothyronine should be started with 1-2 mcg, increasing the dose under ECG monitoring.
Prognosis for autoimmune thyroiditis
The prognosis for 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 with euthyroid nodular goiter. Most often, chronic thyroiditis combines adenocarcinomas and lymphosarcomas.
The ability to work for patients with autoimmune thyroiditis depends on success in compensating for hypothyroidism. Patients should always be on dispensary records.