Riedel’s thyroiditis

Riedel’s goiter is a chronic fibrotic process in the thyroid gland. Fibrous thyroiditis can be combined with retroperitoneal and mediastinal fibrosis, primary sclerosing cholangitis, retrobulbar fibrosis, which suggests a common origin. A morphological study reveals proliferation of connective tissue in the thyroid gland, atrophy of its parenchyma. The disease progresses slowly. The thyroid gland is enlarged and compacted. Sometimes it compresses the larynx, esophagus, blood vessels and nerves of the neck. The skin with the gland is not welded. Riedel’s goiter has to be differentiated with a thyroid tumor, often diagnosis is possible only with histological examination. If there are signs of hypothyroidism, thyroid hormone replacement therapy is performed, in the case of compression of the surrounding organs, surgery. Subacute thyroiditis de Curven. The disease is 1-2% in the structure of all pathological processes in the thyroid gland. Often occurs after an acute respiratory infection, sometimes childbirth. In a morphological study, along with a destructive and dystrophic process in the follicles, inflammatory infiltration with the appearance of multinucleated cells and granulomas resembling tuberculous, but without caseous necrosis is noted.

In clinical terms, the disease proceeds with fever or subfebrile condition, asthenic syndrome, often pain caused by stretching of the thyroid capsule. Pain can occur in the neck, but often they begin in the ear, lower jaw, and only later do the discomfort in the thyroid gland appear. Sometimes only one lobe of the gland increases, in the area of ​​which the pain is localized. The disease can last for months, but more often its manifestations quickly decrease after 1-2 weeks. The disease lasts 8-12 weeks. In the acute period, symptoms of hyperthyroidism with an increase in T4 level, absorption of radioactive iodine may be observed. Symptoms of transient hypothyroidism later appear. ESR can be increased for a long time, the titer of antithyroid antibodies is usually normal, although it can be temporarily slightly increased. In the presence of local symptoms (pain, inflammation), acetylsalicylic acid is treated. With its ineffectiveness, prednisone is prescribed at 20-40 mg / day, followed by a gradual dose reduction. With small hyperthyroidism, propranolol is prescribed at 40-60 mg / day. Relapses are possible. Goiter Hashimoto. Autoimmune thyroiditis occurs mainly in middle-aged women.

The role of immune disorders in the development of the disease is indicated by: 1) the presence of massive lymphocytic and plasmacytic infiltration of thyroid tissue); 2) an increase in the content of immunoglobulins in the blood; 3) an increase in the titer of antibodies to various components of thyroid tissue, primarily thyroglobulin and microsomes, v 90% of patients; 4) a combination of thyroiditis with a number of diseases that are considered autoimmune (pernicious anemia, chronic active hepatitis, Sjogren’s syndrome, SLE, RA), all these diseases are quite common in the same families.

The disease develops gradually. The thyroid gland is enlarged, usually painless, of moderate density, sometimes with an uneven surface. Patients may complain of weakness. Compression manifestations are rare. After 3-4 months from the onset of the disease, symptoms of hypothyroidism sometimes appear, T4 and T3 levels in the blood decrease, and the content of thyroid-stimulating hormone increases. The diagnosis can be confirmed by thyroid biopsy. Detection of antibodies to thyroid components is of certain diagnostic value. Treatment is carried out with thyroid hormones, which not only have a substitution effect, but also affect the course of the autoimmune process. Sometimes glucocorticoids have to be used.

Symptom complex

hypothyroidism, the thyroid gland is not palpable. Hypothyroidism manifests itself early and goes away, in most cases, very hard, with extensive clinical manifestations. Ultrasound and X-ray scanning does not reveal thyroid tissue. Sometimes a small amount of ectopic thyroid tissue is found along the ductus thyreoglossus or in the area of ​​the root of the tongue. A hormonal examination reveals a sharp increase in TSH level and a significant decrease in T “T., as well as STB and BEY. Indication of
gland dysgenesis, rather than atyroidism, can be detected by detection of T3 with a low T4 in the blood. Iodine and thyroid function is sharply reduced. Disease occurs 4 times more often in females.
Type of inheritance . Most likely AR.

Medical and genetic counseling for hereditary forms of hypothyroidism proceeds from the established fact of AR type of inheritance for absolute about most syndromes. Genetic risk for siblings is high. The exception is cases of hypothyroidism with the formation of abnormal iodine proteins that are inherited by blood pressure, where the risk is high for the offspring of patients. Given the incomplete penetrance and variable expression of the pathological gene for this pathology, a directed examination of healthy individuals is possible carriers of the gene It must also be remembered that in some cases dysgenesis of the thyroid gland is not hereditarily determined. Thus, in sporadic cases, in the absence of blood viability between spouses, the risk for siblings is 5%. Identification of heterozygous carriers of the recessive gene for individual symptoms of the disease may be important for genetic counseling. In heterozygotes, an enlargement of the thyroid gland, hearing loss, subclinical signs of hypothyroidism are often detected. Currently, prenatal diagnosis of hypothyroidism is not performed. However, it is quite possible to detect a disease in a newborn with the help of hormonal examination in families with burdened heredity. Early treatment can help most patients. In addition, when consulting should take into account the mild clinical course of a number of syndromes. Thus, there is no reason to significantly limit childbearing in families with hereditarily determined forms of hypothyroidism.

local_offerevent_note April 30, 2020

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