Autoimmune thyroiditis: how to recognize and how to treat?

, medical expert
Last reviewed: 29.06.2022

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Among diseases of the endocrine system, chronic inflammation of the thyroid gland - autoimmune thyroiditis - takes a special place, because it is a consequence of immune reactions of the body against its own cells and tissues. In the fourth class of diseases, this pathology (other names - autoimmune chronic thyroiditis, Hashimoto's disease or thyroiditis, lymphocytic or lymphomatous thyroiditis) has a code for ICD 10 - E06.3.

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Pathogenesis of autoimmune thyroiditis

The causes of the organ-specific autoimmune process in this pathology consist in the perception by the immune system of the body of the thyroid gland cells as foreign antigens and the production of antibodies against them. Antibodies begin to "work", and T-lymphocytes (which must recognize and destroy foreign cells) rush into the gland tissue, triggering inflammation - thyroiditis. In this case effector T-lymphocytes penetrate into the thyroid parenchyma and accumulate there, forming lymphocytic (lymphoplasmocytic) infiltrates. Against this background, the gland tissue undergoes destructive changes: integrity of membranes of follicles and walls of thyrocytes (follicular cells that produce hormones) is violated, part of the glandular tissue can be replaced by fibrous tissue. Follicular cells, naturally, are destroyed, their number is reduced, and as a result, there is a violation of the thyroid gland. This leads to hypothyroidism - a lower level of thyroid hormones.

But this does not happen immediately, the pathogenesis of autoimmune thyroiditis is characterized by a long asymptomatic period (euthyroid phase), when the blood levels of the thyroid hormones are within normal limits. Then the disease begins to progress, causing a deficiency of hormones. This reacts to the control of the thyroid gland pituitary gland and, by increasing the synthesis of thyroid-stimulating hormone (TSH), stimulates the production of thyroxin for a time. Therefore, it can take months and even years until the pathology becomes obvious.

Predisposition to autoimmune diseases is determined by an inherited dominant genetic trait. Studies have shown that half of the immediate relatives of patients with autoimmune thyroiditis also have antibodies to the thyroid gland in serum. To date, scientists associate the development of autoimmune thyroiditis with mutations in two genes - 8q23-q24 on chromosome 8 and 2q33 on chromosome 2.

As endocrinologists note, there are immune diseases that cause autoimmune thyroiditis, more precisely, combined with it: type I diabetes, gluten enteropathy (celiac disease), pernicious anemia, rheumatoid arthritis, systemic lupus erythematosus, Addison's disease, Verlhof disease, biliary cirrhosis (primary) , as well as syndromes of Down, Shereshevsky-Turner and Klinefelter.

In women, autoimmune thyroiditis occurs 10 times more frequently than in men, and usually occurs after 40 years (according to The European Society of Endocrinology, the typical age of the manifestation of the disease is 35-55 years). Despite the hereditary nature of the disease, autoimmune thyroiditis is almost never diagnosed in children under 5 years, but already in adolescents it is up to 40% of all thyroid pathologies.

Symptoms of autoimmune thyroiditis

Depending on the level of deficiency of thyroid hormones, which regulate protein, lipid and carbohydrate metabolism, cardiovascular system, gastrointestinal tract and central nervous system functioning in the body, the symptoms of autoimmune thyroiditis can vary.

However, some people do not feel any signs of the disease, while others have different combinations of symptoms.

For hypothyroidism, autoimmune thyroiditis is characterized by such signs as: fatigue, lethargy and drowsiness; difficulty breathing; hypersensitivity to cold; pale dry skin; thinning and hair loss; brittle nails; puffiness of the face; hoarseness; constipation; causeless weight gain; pain in the muscles and stiffness of the joints; menorrhagia (in women), a depressive state. Also, goitre - swelling in the thyroid gland on the front of the neck can form.

In Hashimoto's disease, there may be complications: a large goiter makes swallowing or breathing difficult; the blood level of low-density cholesterol (LDL); there is a long depression, cognitive abilities and libido decrease. The most serious consequences of autoimmune thyroiditis, caused by a critical shortage of thyroid hormones - myxedema, that is, mucinous edema, and its result in the form of a hypothyroid coma.

Where does it hurt?

Diagnosis of autoimmune thyroiditis

Endocrinology specialists diagnose autoimmune thyroiditis (Hashimoto's disease) on the basis of patient complaints, existing symptoms and blood test results.

First of all, blood tests are necessary - to the level of thyroid hormones: triiodothyronine (T3) and thyroxine (T4), as well as pituitary thyroid-stimulating hormone (TSH).

It is also necessary to determine antibodies for autoimmune thyroiditis:

  • antibodies to thyroglobulin (TGAb) - AT-TG,
  • antibodies to thyroid peroxidase (TPOAb) - AT-TPO,
  • antibodies to the thyroid-stimulating hormone receptor (TRAb) - AT-rTTG.

To visualize the pathological changes in the structure of the thyroid gland and its tissues under the influence of antibodies, instrumental diagnostics, such as ultrasound or computer, is performed. Ultrasound can detect and assess the level of these changes: damaged tissue with lymphocytic infiltration will give the so-called diffuse gipoehogenicity.

Aspiration puncture biopsy of the thyroid gland and cytological examination of the biopsy specimen is performed in the presence of nodes in the gland - to determine oncological pathologies. In addition, the cytogram of autoimmune thyroiditis helps to determine the composition of the gland cells and to reveal lymphoid elements in its tissues.

Since most thyroid pathologies require differential diagnosis to distinguish autoimmune thyroiditis from follicular or diffuse endemic goiter, toxic adenoma and several dozen other pathologies of the thyroid gland. In addition, hypothyroidism can be a symptom of other diseases, in particular, associated with impaired functions of the pituitary gland.

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Treatment of autoimmune thyroiditis

Doctors do not hide that the treatment of autoimmune thyroiditis is one of the actual (and not yet solved) problems of endocrinology.

Since there is no specific treatment for this pathology, the most simple and effective method is the hormone replacement therapy widely used today with preparations containing synthetic analogs of thyroxine (L-thyroxine, Levothyroxine, Eutirox). Such drugs are taken daily and for life - with a regular check of the level of thyroid-stimulating hormone in the blood.

Cure autoimmune thyroiditis, they can not, but, increasing the level of thyroxine, alleviate the symptoms caused by its insufficiency.

In principle, this problem is all autoimmune diseases of man. And drugs for immune correction, given the genetic nature of the disease, are also powerless.

The cases of spontaneous regression of autoimmune thyroiditis were not fixed, although the size of goiter could decrease significantly over time. The thyroid gland is removed only with its hyperplasia, which prevents normal breathing, compression of the larynx, and also when malignant neoplasms are detected.

Lymphocytic thyroiditis is an autoimmune condition and can not be prevented, therefore, prevention of this pathology is impossible.

The prognosis for those who correctly treat their health is on the dispensary account of an experienced endocrinologist and carries out his recommendations, positive. And the disease itself, and the methods of its treatment still cause a lot of questions, and even a doctor of the highest qualification can not answer the question of how many live with autoimmune thyroiditis.

More information of the treatment

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