Symptoms of autoimmune chronic 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.

Comparing the classification of thyroiditis by R. Volpe and the given classification of Hashimoto's thyroiditis, it can be concluded that the atrophic form of the latter is one of the causes of idiopathic myxedema. The atrophic asymptomatic variant of thyroiditis identified by R. Volpe, which, according to his data, was diagnosed on the basis of a puncture, is obviously the initial form of idiopathic myxedema without pronounced clinical symptoms of hypothyroidism.

The isolation of adolescent lymphocytic thyroiditis from the general group is due to the peculiarities of the disease course. The most common age of the onset of gland enlargement is 11-13 years without signs of hypothyroidism. The gland is moderately enlarged, painless, with a smooth surface and clear boundaries. ATA and AMA are either not detected or are determined in very low titers. The size of the gland quickly normalizes under the influence of thyroid hormones. Discontinuation of the drug after 8-12 months sometimes does not result in persistent hypothyroidism.

Postpartum thyroiditis develops in the postpartum period in women who have not previously noted thyroid disorders. It is usually enlarged to grade II-III, painless, signs of hypothyroidism are moderate: weakness, fatigue, chilliness, tendency to constipation. The administration of thyroid hormones leads to normalization of the condition. The combination of pregnancy and autoimmune diseases of the thyroid gland is one of the pressing problems. McGregor's data indicate that during pregnancy, the maternal immune response is suppressed, the number of T-suppressors increases and the number of T-helpers decreases. TSH-blocking antibodies from the mother can pass through the placenta to the fetus and cause neonatal hypothyroidism. The author notes that spontaneous recovery of the newborn occurs when maternal antibodies disappear from the child's blood, i.e. after 1.5-2 months. Thus, the presence of chronic autoimmune thyroiditis in the mother is not an absolute contraindication to pregnancy, and its presence does not aggravate autoimmune disorders in the mother's body. However, it is necessary to remember that normal fetal development requires good compensation of hypothyroidism in the mother. Sufficient clinical experience is needed to manage such pregnant women, since during pregnancy, the determination of T4 and T3 in the mother's blood serum using conventional kits may give incorrect results.

Endocrine ophthalmopathy occurs in autoimmune thyroiditis much less frequently than in diffuse toxic goiter. It is milder, and spontaneous long-term remissions are more common.

Thus, the outcome of autoimmune thyroiditis is the development of hypothyroidism with all the characteristic clinical symptoms. However, at the onset of the disease, a clinical picture of thyrotoxicosis may be observed. The duration of the hyperthyroid phase usually does not exceed several months, which can serve as one of the differential diagnostic signs: long-term thyrotoxicosis is observed in diffuse or mixed toxic goiter.

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