Autoimmune thyroiditis (AIT) is a chronic inflammation of thyroid tissue that has an autoimmune genesis and is associated with damage and destruction of follicles and follicular cells of the gland. In typical cases, autoimmune thyroiditis has an asymptomatic course, only occasionally accompanied by an increase in the thyroid gland. Diagnosis of autoimmune thyroiditis is carried out taking into account the results of clinical tests, ultrasound of the thyroid gland, data from histological examination of the material obtained as a result of fine needle biopsy. Treatment of autoimmune thyroiditis is carried out by endocrinologists. It consists in correcting the hormone-producing function of the thyroid gland and suppressing autoimmune processes.
ICD 10
E06.3 Autoimmune thyroiditis
Meaning
Autoimmune thyroiditis accounts for 20-30% of all thyroid diseases. Among women, AIT occurs 15-20 times more often than among men, which is associated with a violation of the X chromosome and with the effect of estrogens on the lymphoid system. The age of patients with autoimmune thyroiditis is usually from 40 to 50 years, although recently the disease has been found in young people and children.
Causes
Even with a hereditary predisposition, additional adverse provoking factors are necessary for the development of autoimmune thyroiditis:
- past acute respiratory viral diseases;
- foci of chronic infection (on the palatine tonsils, in the sinuses of the nose, carious teeth);
- ecology, excess of iodine, chlorine and fluorine compounds in the environment, food and water (affects the activity of lymphocytes);
- prolonged uncontrolled use of medications (iodine-containing drugs, hormonal agents);
- radiation exposure, long exposure to the sun;
- traumatic situations (illness or death of loved ones, loss of work, resentment and disappointment).
Classification
Autoimmune thyroiditis includes a group of diseases that have the same nature.
- Chronic autoimmune thyroiditis (lymphomatous, lymphocytic thyroiditis, obsolete.- Hashimoto’s goiter) develops as a result of progressive infiltration of T-lymphocytes into the parenchyma of the gland, an increase in the number of antibodies to cells and leads to gradual destruction of the thyroid gland. As a result of a violation of the structure and function of the thyroid gland, the development of primary hypothyroidism (a decrease in the level of thyroid hormones) is possible. Chronic AIT has a genetic nature, can manifest itself in the form of family forms, combined with other autoimmune disorders.
- Postpartum thyroiditis occurs most often and is the most studied. Its cause is excessive reactivation of the body’s immune system after its natural suppression during pregnancy. With an existing predisposition, this can lead to the development of destructive autoimmune thyroiditis.
- Pain-free thyroiditis is an analogue of postpartum, but its occurrence is not associated with pregnancy, its causes are unknown.
- Cytokine-induced thyroiditis may occur during treatment with interferon drugs in patients with hepatitis C and blood diseases.
Such variants of autoimmune thyroiditis as postpartum, pain-free and cytokine-induced are similar in the phase of the processes occurring in the thyroid gland. At the initial stage, destructive thyrotoxicosis develops, subsequently turning into transient hypothyroidism, in most cases ending with the restoration of thyroid functions.
- The following phases can be distinguished in all autoimmune thyroiditis:
- The euthyroid phase of the disease (without thyroid dysfunction). It can last for several years, decades, or a lifetime.
- Subclinical phase. In case of disease progression, mass aggression of T–lymphocytes leads to the destruction of thyroid cells and a decrease in the amount of thyroid hormones. By increasing the production of thyroid-stimulating hormone (TSH), which excessively stimulates the thyroid gland, the body manages to maintain normal production of T4.
- Thyrotoxic phase. As a result of the increase in aggression of T-lymphocytes and damage to thyroid cells, the release of existing thyroid hormones into the blood and the development of thyrotoxicosis occurs. In addition, destroyed parts of the internal structures of follicular cells enter the bloodstream, which provoke further production of antibodies to thyroid cells. When, with further destruction of the thyroid gland, the number of hormone-producing cells falls below the critical level, the T4 content in the blood decreases sharply, a phase of obvious hypothyroidism occurs.
- Hypothyroid phase. It lasts about a year, after which the thyroid gland is usually restored. Sometimes hypothyroidism remains persistent.
Autoimmune thyroiditis can be monophasic in nature (have only a thyrotoxic, or only a hypothyroid phase).
According to clinical manifestations and changes in the size of the thyroid gland , autoimmune thyroiditis is divided into forms:
- Latent (there are only immunological signs, there are no clinical symptoms). The gland is of normal size or slightly enlarged (1-2 degrees), without seals, the functions of the gland are not impaired, sometimes moderate symptoms of thyrotoxicosis or hypothyroidism may be observed.
- Hypertrophic (accompanied by an increase in the size of the thyroid gland (goiter), frequent moderate manifestations of hypothyroidism or thyrotoxicosis). There may be a uniform enlargement of the thyroid gland throughout the volume (diffuse form), or there may be the formation of nodes (nodular form), sometimes a combination of diffuse and nodular forms. Hypertrophic form of autoimmune thyroiditis may be accompanied by thyrotoxicosis in the initial stage of the disease, but usually the function of the thyroid gland is preserved or reduced. As the autoimmune process in the thyroid tissue progresses, the condition worsens, the function of the thyroid gland decreases, and hypothyroidism develops.
- Atrophic (the size of the thyroid gland is normal or reduced, according to clinical symptoms – hypothyroidism). It is more often observed in the elderly, and in young people – in the case of exposure to radiation. The most severe form of autoimmune thyroiditis, due to the massive destruction of thyrocytes – the function of the thyroid gland is sharply reduced.
Symptoms
Most cases of chronic autoimmune thyroiditis (in the euthyroid phase and the phase of subclinical hypothyroidism) are asymptomatic for a long time. The thyroid gland is not enlarged in size, it is painless on palpation, the function of the gland is normal. Very rarely, an increase in the size of the thyroid gland (goiter) can be determined, the patient complains of unpleasant sensations in the thyroid gland (a feeling of pressure, a coma in the throat), mild fatigue, weakness, joint pain.
The clinical picture of thyrotoxicosis in autoimmune thyroiditis is usually observed in the first years of the development of the disease, has a transient character and as the atrophy of the functioning thyroid tissue passes for a while into the euthyroid phase, and then into hypothyroidism.
Postpartum thyroiditis, usually manifested by mild thyrotoxicosis at 14 weeks after delivery. In most cases, fatigue, general weakness, weight loss are observed. Sometimes thyrotoxicosis is significantly pronounced (tachycardia, feeling of heat, excessive sweating, tremor of the extremities, emotional lability, insomnia). The hypothyroid phase of autoimmune thyroiditis manifests itself at the 19th week after delivery. In some cases, it is combined with postpartum depression.
Pain-free (silent) thyroiditis is expressed by mild, often subclinical thyrotoxicosis. Cytokine-induced thyroiditis is also usually not accompanied by severe thyrotoxicosis or hypothyroidism.
Diagnostics
Before the manifestation of hypothyroidism, it is quite difficult to diagnose AIT. The diagnosis of autoimmune thyroiditis is determined by endocrinologists according to the clinical picture, laboratory data. The presence of autoimmune disorders in other family members confirms the likelihood of autoimmune thyroiditis.
Laboratory tests for autoimmune thyroiditis include:
- blood test – an increase in the number of lymphocytes is determined
- immunogram – the presence of antibodies to thyroglobulin, thyroperoxidase, the second colloidal antigen, antibodies to thyroid hormones of the thyroid gland is characteristic
- determination of T3 and T4 (total and free), TSH levels in blood serum. An increase in TSH levels with a normal T4 content indicates subclinical hypothyroidism, an increased TSH level with a reduced T4 concentration indicates clinical hypothyroidism
- ultrasound of the thyroid gland – shows an increase or decrease in the size of the gland, a change in structure. The results of this study complement the clinical picture and other laboratory results
- fine needle biopsy of the thyroid gland – it allows you to identify a large number of lymphocytes and other cells characteristic of autoimmune thyroiditis. It is used if there is evidence of a possible malignant degeneration of the nodular formation of the thyroid gland.
The criteria for the diagnosis of autoimmune thyroiditis are:
- increasing the level of circulating antibodies to the thyroid gland (AT-TPO);
- detection of thyroid hypo-echogenicity by ultrasound;
- signs of primary hypothyroidism.
In the absence of at least one of these criteria, the diagnosis of autoimmune thyroiditis is only probabilistic. Since an increase in the level of AT-TPO, or hypo-echogenicity of the thyroid gland by itself does not yet prove autoimmune thyroiditis, this does not allow an accurate diagnosis. Treatment is indicated to the patient only in the hypothyroid phase, so there is usually no urgent need for a diagnosis in the euthyroid phase.
Treatment
Specific therapy for autoimmune thyroiditis has not been developed. Despite the modern achievements of medicine, endocrinology does not yet have effective and safe methods of correction of autoimmune pathology of the thyroid gland, in which the process would not progress to hypothyroidism.
In the case of the thyrotoxic phase of autoimmune thyroiditis, the appointment of drugs that suppress the function of the thyroid gland – thyrostatics (thiamazole, carbimazole, propylthiouracil) is not recommended, since there is no hyperfunction of the thyroid gland in this process. With pronounced symptoms of cardiovascular disorders, beta-blockers are used.
In cases of hypothyroidism, replacement therapy with thyroid hormone preparations – levothyroxine (L-thyroxine) is prescribed individually. It is carried out under the control of the clinical picture and the content of TSH in the blood serum.
Glucocorticoids (prednisolone) are indicated only in the simultaneous course of autoimmune thyroiditis with subacute thyroiditis, which is often observed in the autumn-winter period. Nonsteroidal anti-inflammatory drugs are used to reduce the titer of autoantibodies: indomethacin, diclofenac. They also use drugs to correct immunity, vitamins, adaptogens. With hypertrophy of the thyroid gland and pronounced compression of the mediastinal organs by it, surgical treatment is carried out.
Forecast
The prognosis for the development of autoimmune thyroiditis is satisfactory. With timely treatment, the process of destruction and reduction of thyroid function can be significantly slowed down and achieve long-term remission of the disease. Satisfactory well-being and normal working capacity of patients in some cases persist for more than 15 years, despite the emerging short-term exacerbations of AIT.
Autoimmune thyroiditis and an increased titer of antibodies to thyroperoxidase (AT-TPO) should be considered as risk factors for hypothyroidism in the future. In the case of postpartum thyroiditis, the probability of its recurrence after the next pregnancy in women is 70%. About 25-30% of women with postpartum thyroiditis later have chronic autoimmune thyroiditis with the transition to persistent hypothyroidism.
Prevention
If autoimmune thyroiditis is detected without thyroid dysfunction, it is necessary to monitor the patient in order to detect and compensate for the manifestations of hypothyroidism as early as possible.
Women who carry AT-TPO without changing the function of the thyroid gland are at risk of developing hypothyroidism in case of pregnancy. Therefore, it is necessary to monitor the condition and function of the thyroid gland both in the early stages of pregnancy and after childbirth.