Autoimmune thyroiditis symptoms
Autoimmune thyroiditis is one of the most common thyroid diseases. Among the population of different countries, autoimmune thyroiditis occurs in 0.1-1.2%( in children) - 6-11%( in women over 60 years) cases. At the same time, antibodies to the thyroid gland circulating in the blood can be detected in 10-15% of practically healthy individuals. The ratio of the number of sick men and women is 1: 4- 1: 10. Autoimmune thyroiditis is one of the most typical autoimmune diseases. This disease was first described by Hashimoto in 1912. There are two main forms of autoimmune thyroiditis : hypertrophic( Hashimoto's goiter) and atrophic( primary myxedema).
The disease develops against a background of a genetically determined defect in the immune system. As a result of this defect in the blood, antibodies are formed to the cells of the thyroid gland, under the influence of which the cells are destroyed.
Autoimmune thyroiditis has the property of manifesting itself in the form of family forms. Observation of idolized twins indicates the simultaneous occurrence of a given disease in them in 3-9% of cases, and in identical twins - in 30-60% of cases. The latter fact speaks in favor of the presence of a genetic defect leading to the development of autoimmune thyroiditis. In addition, within the same family, there is a combination of this disease with other autoimmune diseases, such as pernicious anemia, autoimmune primary hypocorticism, chronic autoimmune hepatitis, insulin-dependent diabetes mellitus, allergic alveolitis, vitiligo, alimentary baldness, Sjogren's syndrome, rheumatoid arthritis and many others. There are cases when one of the twins suffered from diffuse toxic goiter and the other with Hashimoto's thyroiditis. In families of people suffering from diffuse toxic goiter, there are a large number of relatives with Hashimoto's thyroiditis. In 50% of cases, relatives of people with autoimmune thyroiditis have antibodies to the thyroid gland cells circulating in the blood.
In the course of the development of the autoimmune process in thyroid autoimmune thyroid function undergoes numerous changes with a practically obligatory outcome in hypothyroidism, i.e., a condition developing with prolonged persistent deficiency of thyroid hormones. Among people with autoimmune thyroiditis, the majority are those who have the disease in mild form or even without any characteristic signs of hypothyroidism. At some part of persons with autoimmune thyroiditis at the beginning of the disease, the presence of thyrotoxicosis( state in excess of the thyroid hormones in the body) is possible. The development of this condition is associated with the process of decay of thyroid tissue due to the effect of antibodies on it and the intake of a large number of previously synthesized hormones into the blood. Another possible cause of temporary thyrotoxicosis( hashitoxicosis) may be the presence of antibodies that stimulate the formation of thyroid hormones. Hypothyroidism due to autoimmune thyroiditis is usually seen as an irreversible condition, but there are isolated reports that even with prolonged hypothyroidism, thyroid function can spontaneously normalize. In some cases, even the state of increased production of thyroid hormones is developing. Autoimmune thyroiditis is a benign disease of the thyroid gland. Transformation of it into a malignant pathology is unlikely, except for very rare thyroid lymphoma. Moreover, with autoimmune thyroiditis, the area of the thyroid gland malignant tumor is surrounded by blood cells, which have a protective effect, reducing the frequency of tumor metastasis formation.
In most cases, autoimmune thyroiditis first appears between 30 and 60 years. The course of the disease is long and at the very beginning - asymptomatic. Hashitoksikoz( thyrotoxicosis in autoimmune thyroiditis) can be difficult to distinguish from diffuse toxic goiter, since in both cases, an increase in the thyroid gland can be determined, and ultrasound reveals similar changes. In this case, the study of certain antibodies can help. In addition, a long, more than half a year, course of thyrotoxicosis testifies to the diffuse toxic goiter. At a hypertrophic form of illness in the field of a neck the struma is defined. In the case of formation in the thick of the gland of the nodes, it becomes necessary to exclude their malignant degeneration, which can occur with autoimmune thyroiditis. In some cases with autoimmune thyroiditis, the organ of vision may be affected.
Autoimmune thyroiditis is a disease that is recognized only when there are characteristic manifestations and results of laboratory and instrumental research methods. None of the methods, even the most informative, in itself makes it possible to diagnose autoimmune thyroiditis. In general, the more there are the characteristic manifestations and laboratory-instrumental signs of the disease, the more likely the presence of autoimmune thyroiditis.
People with autoimmune thyroiditis usually have an elevated level of antibodies to thyroid hormones. The presence of a large number of antibodies in the blood is a serious sign of either having, or a high risk of developing an autoimmune thyroid disease. It should be noted that a moderate increase in the level of antibodies to the thymus glands occurs in about 20% of healthy people and does not have a definite value. Thus, the diagnosis of autoimmune thyroiditis only on the basis of the detection of a small increase in the level of antibodies is an error.
Puncture biopsy can also be used to identify autoimmune thyroiditis, as well as diseases with similar manifestations. The most typical indication for this type of study is the combination of autoimmune thyroiditis with nodular formation in the thyroid gland to exclude oncological pathology. At the same time, when identifying typical data of laboratory and instrumental studies that clearly indicate the presence of autoimmune thyroiditis, there is no need for a needle biopsy of the thyroid gland.
Even if hypothyroidism with autoimmune thyroiditis occurs without severe symptoms, this in any case leads to activation of the adrenal glands. At the same time from time to time, their hormones are released into the blood, which is accompanied by the appearance of periodic heart attacks, sweating, trembling of hands, a sense of fear. The combination of such manifestations in this disease is often referred to as "panic attacks".Often the mention of such manifestations makes doctors seek such a disease as thyrotoxicosis. With hypothyroidism, there is a moderate decrease in prolactin( female sex hormone), which often leads to the formation of polycystic ovaries.
Treatment. In the vast majority of cases with autoimmune thyroiditis, conservative treatment is performed. In the thyrotoxic phase of autoimmune thyroiditis, one should theoretically confine oneself only to the use of funds that promote the disappearance of all manifestations of the disease( symptomatic agents).In the future, it is necessary to include thyroid hormone preparations( substitution therapy) in the treatment. In practice, the thyrotoxic phase of autoimmune thyroiditis is usually regarded as a manifestation of a diffuse toxic goiter, in connection with which another treatment is prescribed.
In most cases, the treatment of autoimmune thyroiditis is conservative, but there are situations when it is necessary to carry out the operation. Indications for surgical treatment of patients with hypertrophic form of autoimmune thyroiditis are: a combination of autoimmune thyroiditis with oncological processes in the thyroid gland, as well as large goiter with signs of compression of a number of located organs.
In the pathogenesis of most diseases of the thyroid gland( diffuse toxic goiter, toxic nodular goiter, primary hypothyroidism, etc.), autoimmune processes play a decisive role, so their diagnosis requires the definition of antithyroid antibodies. Currently, the diagnosis uses the definition:
- of thyroid auto-antibodies;
- AT to thyroglobulin;
- autoantibodies to thyroid peroxidase.