Thyroiditis

Subacute thyroiditis of de Kerven, or granulomatous thyroiditis, is one of the most common forms of the disease. Etiological factors of thyroiditis of de Kerven include measles virus, infectious mumps, adenovirus infection, influenza. Thyroiditis develops in 3-6 weeks after the transferred viral infections.

During subacute thyroiditis, 4 stages are isolated.

■ Stage I - thyrotoxic: inflammatory destruction of follicular cells of the thyroid leads to the release of excess amounts of T4 and T3 into the blood, which can cause thyrotoxicosis.

■ Stage II - an interim period( 1-2 weeks) of euthyroidism occurs after the removal of excess T4 from the body.

■ Stage III - hypothyroid, develops in severe cases of the disease.

■ Stage IV - restorative( euthyroid status).

With subacute thyroid concentration in blood TTG is normal or decreased, T4 and T3 - high or above normal, then they are normalized. The change in the level of thyroid hormones in the blood with thyroiditis depends on the stage of the disease. Thus, in the first stage( duration 1-1.5 months) there is an increase in the concentration of cT4( T4 and T3) in the blood and normal

or a decreased level of TSH.Clinically observed symptoms of thyrotoxicosis. These changes are due to the excessive intake of previously synthesized hormones and thyroglobulin into the blood, due to increased vascular permeability against inflammation. After 4-5 weeks, a violation of the synthesis of hormones in the inflamed thyroid leads to a normalization of their content in the blood, and then to a decrease( 3-4 months of the disease).Reducing the formation of T4 and T3 activates the release of TSH by the pituitary gland, its concentration in the blood increases and can be increased 4-6 months. Approximately to the end of the 10th month from the moment of the disease, the concentrations of TSH, T4 and T3 in the blood are normalized. The content of thyroglobulin in the blood is increased for a long time. The disease is prone to relapse, which requires long-term monitoring of thyroid function. With the development of relapse the concentration of thyroglobulin in the blood increases again.

Chronic lymphocytic thyroiditis( Hashimoto's thyroiditis) is a disease caused by the genetic defect of immunocompetent cells( T-suppressors), leading to infiltration of the thyroid gland by macrophages, lymphocytes, and plasma cells. As a result of these processes in the thyroid gland, there is formation of AT to thyreoglobulin, thyroid peroxidase, TSH receptors. The interaction of AT with Ar leads to the appearance of immune complexes, the release of biologically active substances, which ultimately causes destructive changes in thyreocytes and leads to a decrease in thyroid function.

In the development of chronic autoimmune thyroiditis, the thyroid gland function undergoes stage changes with a virtually mandatory outcome in hypothyroidism. As the gland failure progresses, the blood concentrations of T4 and then T3 decrease, and the TSH content gradually increases. In the future, hypothyroidism develops with characteristic laboratory manifestations. In some patients with autoimmune thyroiditis, signs of hyperthyroidism( decrease in TSH concentration and an increase in CT4) are possible in the onset of the disease, which is caused by destruction of the thyroid tissue.