Symptoms of autoimmune chronic 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. At first, 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.

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

Isolation from the general group of lymphocytic thyroiditis of adolescents is due to the peculiarities of the course of the disease. The most frequent age of onset of enlargement of the gland is 11-13 years without signs of hypothyroidism. The gland is moderately enlarged, painless, with an even surface and clear boundaries. ATA and AMA are either not detected, or are determined in very low titres. Dimensions of the gland quickly normalize under the influence of thyroid hormones. Abolition of the drug after 8-12 months sometimes does not give stable hypothyroidism.

Postpartum thyroiditis develops in the postpartum period in women who have not previously noticed a violation of the thyroid gland. It is usually increased to grade II-III, painless, signs of hypothyroidism are moderately expressed: weakness, fatigue, chilliness, propensity to constipation. The appointment of thyroid hormones leads to the normalization of the condition. The combination of pregnancy and autoimmune thyroid diseases is one of the topical problems. Data from McGregor indicate that during pregnancy, the maternal immune response is suppressed, the number of T suppressors increases and the number of T-helpers decreases. TTG-blocking antibodies of the mother can pass through the placenta to the fetus and cause neonatal hypothyroidism. The author notes that spontaneous recovery of a newborn occurs when maternal antibodies disappear from the blood of the child, 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 exacerbate autoimmune disorders in the maternal organism. However, it must be remembered that the normal development of the fetus requires a good compensation of hypothyroidism in the mother. To conduct such pregnant patients need sufficient clinical experience, because on the background of pregnancy, the determination of T4 and T3 in the mother's blood serum using conventional sets can give incorrect results.

Endocrine ophthalmopathy occurs with autoimmune thyroiditis much less often than with diffuse toxic goiter. It proceeds milder, spontaneous long-term remissions are more frequent.

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.

[1], [2], [3], [4], [5], [6]