Thyroiditis is based on thyroid inflammation. The following thyroiditis are distinguished: Hashimoto, subacute granulomatous, subacute lymphocytic, Riedel fibrous, purulent.
Hashimoto’s thyroiditis (autoimmune, lymphomatous struma, lymphadenoid goiter) occurs in most cases in older women with a genetic predisposition due to certain histocompatibility antigens (HLA DR5, DR3). The leading role in the genesis of the disease is played by autoimmune damage to the organ parenchyma by thyroid-specific T cells. Diffuse lymphoplasmacytic gland infiltration develops with the formation of lymphoid follicles with germinal centers. The organ is enlarged, sometimes unevenly in both lobes (a variant of Hashimoto’s thyroiditis with goiter).
Subacute Graiulomatous thyroiditis de Curven
Subacute giulomatous thyroiditis de Kerven (giant cell) is associated with the HLA B35 haplotype and usually develops in women aged 25–45 years. The painful gland is asymmetrically enlarged due to the defeat of individual sites, less often – of the entire organ. White-yellow foci of dense consistency bulging above the cut surface are found. Focal infiltrate, consisting of polymorphonuclear leukocytes that form microabscesses that melt the gland tissue, is characteristic.
Subacute lymphocytic thyroiditis
Subacute lymphocytic thyroiditis (painless, silent) is asymptomatic and is detected by chance during a morphological study of surgical or autopsy material. In the iron, lymphoplasmacytic small focal infiltrates are found, located mainly subcapsularly. Riedel’s fibrous thyroiditis (struma) (stone goiter) is characterized by hypothyroidism, which develops due to severe follicular atrophy due to the expanding fibrous stroma, which gives the gland a higher density.
Purulent (infectious) thyroiditis
Purulent (infectious) thyroiditis rarely occurs, as a rule, secondarily with hematogenous introduction of infection (streptococci, staphylococci, salmonella, enterobacteria, tuberculosis mycobacteria, fungi). There is a painful increase in the organ due to its purulent inflammation, accompanied by a slight decrease in thyroid function.
Goiter (struma) is called an enlargement of the thyroid gland, which is based on its hyperplasia. Diffuse toxic goiter (Graves’ disease, Bazedov’s disease) takes 2nd place in frequency of development (after diabetes mellitus) among endocrine diseases, is observed in most cases in women aged 20-40 years and manifests itself as severe hyperthyroidism. A genetic predisposition to the disease is associated with HLA B8 and DR3 haplotypes. The disease is due to the appearance for unknown reasons of thyroid-stimulating antibodies related to IgG, enhancing the production of hormones in the gland and causing the proliferation of follicular cells. The organ is diffusely enlarged, with a uniform soft consistency. Microscopic examination noted the transformation of the cylindrical follicular epithelium into prismatic, proliferation of the epithelium with the formation of pseudo-papillae, the presence of liquid vacuolated colloid in irregular stellate follicles, lymphoid cell (CD4 and CD8) gland stroma infiltrate.
Diffuse non-toxic goiter
Diffuse non-toxic (simple) goiter is characterized by a uniform increase in the entire thyroid gland due to the accumulation of a colloid in the follicles (colloid goiter). Distinguish between endemic and sporadic variants of the disease.
Endemic goiter is found in special geographical areas, most often in mountainous areas, characterized by a lack of iodine in water and food. Iodine deficiency (especially with an excess of calcium salts) causes a decrease in the synthesis of thyroid hormones. In response, there is a compensatory increase in the formation of thyroid stimulating hormone of the pituitary gland, leading to an increase in the thyroid gland due to hyperplasia and hypertrophy of follicular cells. Initially, an euthyroid state is formed, replaced by hypothyroidism over time. In this case, myxedema develops in adults, and in young children there is a lag in mental and physical development, called endemic cretinism.
Sporadic goiter is a relatively rare disease that is ubiquitous; manifested by an euthyroid state, rarely hypothyroidism. With any variant of the course of diffuse non-toxic goiter, a hyperplastic stage is initially noted, manifested by a moderate increase in the gland (up to 100-150 g). Microscopic examination reveals small follicles lined with prismatic epithelium and containing a small amount of colloid. After reaching the euthyroid state, the proliferation of follicular cells ceases and the stage of colloid involution begins. In this case, the follicles increase significantly due to the accumulation of colloidal eosinophilic and SIC-positive contents. The follicular epithelium flattenes, atrophies. The mass of the gland can reach 500 g or more, the organ becomes dense, gelatinous in the section (colloid goiter).