Thyroiditis de Kervena, treatment
In malignant tumors of the thyroid gland in 2/3 of cases, infiltration with lymphocytes is detected. In 50% of patients, antibodies to thyroid tissue antigens are detected, mostly in very low titers, approximately in 10% of cases it corresponds to that in patients with thyroiditis Hashimoto, therefore, differential diagnosis is not always possible. It should be borne in mind that with thyroiditis Hashimoto may develop adenocarcinoma and lymphosarcoma( in 5% of cases).In such situations it is necessary to use all diagnostic methods, including puncture biopsy.
The pathogenesis of autoimmune thyroiditis has not yet been fully explored. Results of immunological methods in vitro indicate that autoantibodies( especially to the microsomal antigen) have pathogenetic significance. Until now, it has not been possible to reproduce the experimental model of thyroiditis by administering animal serum to a human containing specific antibodies. Of course, this can be explained by the species specificity of the antigens. The idea of the pathogenetic significance of antibodies confirms the immediate cytotoxic effect, the reaction of immune complexes, and AZKTS.Immunomorphological studies show the deposition of immune complexes along the basal membrane of the follicles, as well as in different parts of the thyroid tissue, which leads to fibrosis and proliferation of connective tissue cells.
To date, it has not been possible to obtain convincing evidence of transplacental transfer of factors that cause thyroiditis. With the help of sensitive methods, circulating immune complexes were detected in 25% of cases, and in single cases - morphological changes corresponding to the picture of nephritis caused by immune complexes.
The expressed lymphocytic infiltration testifies to participation of reactions of cellular immunity. The effect of antibodies largely depends on them( modulation from cytotoxicity to the activity of blocking antibodies).The frequency and simultaneous detection of serum autoantibodies to different thyroid tissue antigens, a combination with other autoimmune disorders, the existence of family forms of the disease, including identical twins, all suggest that a certain role is played by genetic factors.
The trigger mechanisms have not yet been precisely established. Most researchers among the most crucial influences call a viral infection, as well as a link with other infections. In the latter case, we are talking about forms of infectious thyroiditis complicated by immunological disorders.
The fact that focal thyroiditis and autoantibodies to thyroid tissue antigens often appear in elderly people with obvious defects in the immune system, suggests a variety of factors contributing to the development of thyroiditis, but not all patients experience pronounced immune disorders. In this connection, attention is drawn to the fact described by different scientific groups: DR-expression on the thyrocytes as a result of a viral infection accompanied by interferon production. According to Bottazzo et al., Through this expression normal membrane structures are modified and should lead to the appearance of autoantigens and the creation of a Circulus vitiosus situation. Such DR-expression should be considered yet as a normal process in the course of inflammation, lymphocytic infiltration and cell activation, and irreversible. Decisive in the maintenance of Circulus vitiosus, in all probability, is still an unknown factor.
The usual leaching and release of thyroglobulin into the circulation leads only to temporary antibody formation, for example, in patients with subacute thyroiditis of de Kerven, and also after a course of treatment with radioactive iodine and surgical intervention. The importance of genetic factors is indicated by the detection of antibodies to thyroid tissue antigens from relatives. The most commonly identified HLA-DR5.
Combination with other autoimmune diseases. Quite often a combination of Hashimoto's thyroiditis with other autoimmune disorders, for example, with collagen diseases, Addison's disease, Myasthenia gravis, chronic hepatitis and pernicious anemia. In 5-20% of patients, ANF sera are detected, and sometimes other types of autoantibodies. The Wasserman reaction in these cases can be false positive.
Treatment of .Relatively reliable substitution therapy, therefore, immunosuppressants should be prescribed according to strict indications( strengthening autoaggression mechanisms).
As a symptomatic treatment to reduce the functional activity of the thyroid gland, thyroxine is prescribed.
It is suggested that direct exposure to immune mechanisms is possible by translating the antigen into a tolerogenic form( hapten blockade).In some cases, this can reduce the activity of the autoimmune process.
Very often after a clinical recovery for a long time in the serum of the patient, antibodies to thyroid tissue antigens are detected. Along with the main treatment, you can prescribe corticosteroids, starting with 50 mg of prednisolone per day. When determining the initial dose of the drug, it is necessary to take into account the overall clinical picture of the disease. Corticoids are prescribed for several weeks. Due to the existing danger of development of hypothyroidism, clear indications for surgical intervention and treatment with radioactive iodine should be determined.