Autoimmune thyroiditis: how to recognize and how to treat?

Among the diseases of the endocrine system, chronic inflammation of the thyroid gland - autoimmune thyroiditis - occupies a special place, since it is a consequence of the body's immune reactions against its own cells and tissues. In the IV class of diseases, this pathology (other names - autoimmune chronic thyroiditis, Hashimoto's disease or thyroiditis, lymphocytic or lymphomatous thyroiditis).

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Pathogenesis of autoimmune thyroiditis

The causes of the organ-specific autoimmune process in this pathology are the perception by the body's immune system of thyroid 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 the parenchyma of the thyroid gland and accumulate there, forming lymphocytic (lymphoplasmocytic) infiltrates. Against this background, the gland tissue undergoes destructive changes: the integrity of the follicle membranes and the walls of thyrocytes (follicular cells that produce hormones) is disrupted, part of the glandular tissue can be replaced by fibrous tissue. Follicular cells, naturally, are destroyed, their number decreases, and as a result, the thyroid gland functions are disrupted. This leads to hypothyroidism – low levels 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 thyroid hormone levels in the blood are within normal limits. Then the disease begins to progress, causing a hormone deficiency. The pituitary gland, which controls the thyroid gland, reacts to this and, by increasing the synthesis of thyroid-stimulating hormone (TSH), stimulates the productionof thyroxine for some time. Therefore, months and even years may pass before the pathology becomes apparent.

Predisposition to autoimmune diseases is determined by an inherited dominant genetic trait. Studies have shown that half of the closest relatives of patients with autoimmune thyroiditis also have antibodies to thyroid tissue in their blood serum. Today, 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, or rather, those combined with it:

• diabetes type 1,
• gluten enteropathy (celiac disease),
• pernicious anemia,
• rheumatoid arthritis,
• systemic lupus erythematosus,
• Addison's disease,
• Werlhof's disease,
• biliary cirrhosis of the liver (primary),
• as well as Down, Shereshevsky-Turner and Klinefelter syndromes.

In women, autoimmune thyroiditis occurs 10 times more often than in men, and usually manifests itself after 40 years (according to The European Society of Endocrinology, the typical age of 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 old, but already in adolescents it accounts for 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 in the body, the functioning of the cardiovascular system, gastrointestinal tract and central nervous system, the symptoms of autoimmune thyroiditis can vary.

Some people experience no signs of illness, while others experience various combinations of symptoms.

Hypothyroidism in autoimmune thyroiditis is characterized by the following symptoms:

• fatigue, lethargy and drowsiness;
• difficulty breathing;
• hypersensitivity to cold;
• pale dry skin;
• hair thinning and loss;
• brittle nails;
• puffiness of the face;
• hoarseness;
• constipation;
• unexplained weight gain;
• muscle pain and joint stiffness;
• menorrhagia (in women);
• depressive state.

A goiter, a swelling in the thyroid gland area at the front of the neck, may also develop.

Hashimoto's disease can have complications:

• a large goiter makes it difficult to swallow or breathe;
• the level of low-density lipoprotein (LDL) cholesterol in the blood increases;
• Long-term depression sets in, cognitive abilities and libido decline.

The most serious consequences of autoimmune thyroiditis, caused by a critical deficiency of thyroid hormones, are myxedema, that is, mucinous edema, and its result in the form of hypothyroid coma.

Diagnosis of autoimmune thyroiditis

Endocrinologists diagnose autoimmune thyroiditis (Hashimoto's disease) based on the patient's complaints, existing symptoms and blood test results.

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

Antibodies are also necessarily determined in autoimmune thyroiditis:

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

To visualize pathological changes in the structure of the thyroid gland and its tissues under the influence of antibodies, instrumental diagnostics are carried out - ultrasound or computer. Ultrasound allows you to detect and assess the level of these changes: damaged tissues with lymphocytic infiltration will give the so-called diffuse hypoechogenicity.

Aspiration puncture biopsy of the thyroid gland and cytological examination of the biopsy are 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 identify lymphoid elements in its tissues.

Since in most cases of thyroid pathologies, differential diagnostics are required to distinguish autoimmune thyroiditis from follicular or diffuse endemic goiter, toxic adenoma and several dozen other thyroid pathologies. In addition, hypothyroidism can be a symptom of other diseases, in particular, those associated with dysfunction of the pituitary gland.

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Treatment of autoimmune thyroiditis

Doctors do not hide the fact that the treatment of autoimmune thyroiditis is one of the current (and still unresolved) problems of endocrinology.

Since there is no specific treatment for this pathology, the simplest and most effective method is hormone replacement therapy, which is widely used today, with drugs containing synthetic analogues of thyroxine (L-Thyroxine, Levothyroxine, Euthyrox). Such drugs are taken daily and for life - with regular testing of the level of thyroid-stimulating hormone in the blood.

They cannot cure autoimmune thyroiditis, but by increasing the level of thyroxine, they alleviate the symptoms caused by its deficiency.

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

There have been no cases of spontaneous regression of autoimmune thyroiditis, although the size of the goiter may decrease significantly over time. Removal of the thyroid gland is performed only in the case of its hyperplasia, which interferes with normal breathing, compression of the larynx, and also when malignant neoplasms are detected.

Lymphocytic thyroiditis is an autoimmune condition and cannot be prevented, so prevention of this pathology is impossible.

The prognosis for those who treat their health correctly, are under the supervision of an experienced endocrinologist and follow his recommendations is positive. Both the disease itself and its treatment methods still raise many questions, and even the most highly qualified doctor cannot answer the question of how long people live with autoimmune thyroiditis.