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Autoimmune tireoidit

Autoimmune tireoidit (AIT) - the chronic inflammation of tissue of thyroid gland having autoimmune genesis and connected with damage and destruction of follicles and follicular cells of gland. In typical cases autoimmune tireoidit has an asymptomatic current, only occasionally being followed by increase in a thyroid gland. Diagnostics of an autoimmune tireoidit is carried out taking into account results of clinical analyses, ultrasonography of a thyroid gland, data of a histologic research of the material received as a result of a tonkoigolny biopsy. Treatment of an autoimmune tireoidit is performed by endocrinologists. It consists in correction of gormonoprodushchiruyushchy function of a thyroid gland and suppression of autoimmune processes.

Autoimmune tireoidit

Autoimmune tireoidit (AIT) - the chronic inflammation of tissue of thyroid gland having autoimmune genesis and connected with damage and destruction of follicles and follicular cells of gland. Autoimmune tireoidit makes 20-30% of number of all diseases of a thyroid gland. Occurs among women of AIT by 15 – 20 times more often than among men that is connected with violation of X - chromosomes and with influence on lymphoid system of estrogen. Age of patients with an autoimmune tireoidit usually from 40 to 50 years though recently the disease occurs at young people and children.

Classification of autoimmune tireoidit

Autoimmune tireoidit includes group of the diseases having one nature.

1. Chronic autoimmune tireoidit (limfomatozny, lymphocytic tireoidit, . - Hashimoto's craw) develops as a result of the progressing infiltration of T-lymphocytes in a parenchyma of gland, increase in quantity of antibodies to cages and leads to gradual destruction of a thyroid gland. As a result of violation of structure and function of a thyroid gland development of primary gipoterioz (decrease in level of hormones of a thyroid gland) is possible. Chronic AIT has the genetic nature, can be shown in the form of family forms, be combined with other autoimmune violations.

2. Postnatal tireoidit meets most often and it is most studied. As its reason serves excess reactivation of immune system of an organism after its natural oppression during pregnancy. At the available predisposition it can lead to development of a destructive autoimmune tireoidit.

3. Bezboleva tireoidit is an analog postnatal, but its emergence is not connected with pregnancy, its reasons are unknown.

4. Tsitokin-indutsirovanny tireoidit can arise during treatment by medicines of interferon of patients with hepatitis C and diseases of blood.

Such options of an autoimmune tireoidit as postnatal, bezbolevy and – induced, are similar staging of the processes happening in a thyroid gland. At the initial stage the destructive thyrotoxicosis, in the subsequent passing into the tranzitorny gipoterioz which in most cases is coming to an end with restoration of functions of a thyroid gland develops.

At all autoimmune tireoidit it is possible to allocate the following phases:

  • Eutireoidny phase of a disease (without dysfunction of a thyroid gland). Can proceed within several years, decades or all life.
  • Subclinical phase. In case of progressing of a disease, mass aggression of T-lymphocytes leads to destruction of cells of a thyroid gland and decrease in amount of tireoidny hormones. Due to increase in production of tireotropny hormone (TTG) which it is superfluous stimulates a thyroid gland, the organism manages to keep normal development of T4.
  • Tireotoksichesky phase. As a result of increase of aggression of T-lymphocytes and damage of cells of a thyroid gland there is a release in blood of the available tireoidny hormones and development of a thyrotoxicosis. Besides, to the blood course gets the destroyed parts of internal structures of follicular cages which provoke further development of antibodies to cells of a thyroid gland. When at further destruction of a thyroid gland, the number of gormonoprodutsiruyushchy cages falls below critical level, the content in T4 blood sharply decreases, there comes the phase of an obvious gipoterioz.
  • Gipotireoidny phase. About a year then usually there is a restoration of function of a thyroid gland proceeds. Sometimes the hypothyroidism remains resistant.

Autoimmune tireoidit can have monophase character (to have only tireotoksichesky, or only a gipotireoidny phase).

On clinical manifestations and change of the sizes of a thyroid gland autoimmune tireoidita subdivide into forms:

  • Latent (there are only immunological signs, clinical symptoms are absent). Gland of the usual size or is a little increased (1-2 degrees), without consolidations, functions of gland are not broken, moderate symptoms of a thyrotoxicosis or a hypothyroidism can sometimes be observed.
  • Hypertrophic (is followed by increase in the sizes of a thyroid gland (craw), frequent moderate manifestations of a hypothyroidism or a thyrotoxicosis). There can be a uniform increase in a thyroid gland on all volume (a diffusion form), or to be observed formation of knots (a nodal form), sometimes a combination of diffusion and nodal forms. The hypertrophic form of an autoimmune tireoidit can be followed by a thyrotoxicosis in an initial stage of a disease, but usually function of a thyroid gland is kept or reduced. As autoimmune process in tissue of a thyroid gland progresses, there is a deterioration in a state, function of a thyroid gland decreases, and the hypothyroidism develops.
  • Atrophic (the size of a thyroid gland is normal or is reduced, on clinical symptoms – ). It is more often observed at advanced age, and at young people – in case of impact of radiation exposure. The most severe form of an autoimmune tireoidit, in connection with mass destruction of tirotsit – function of a thyroid gland is sharply lowered.

Reasons of autoimmune tireoidit

Even at hereditary predisposition, additional adverse provocative factors are necessary for development of an autoimmune tireoidit:

  • the postponed sharp respiratory viral diseases;
  • the centers of a chronic infection (on palatal almonds, in nose bosoms, carious teeth);
  • ecology, surplus of compounds of iodine, chlorine and fluorine in the environment, food and water (influences activity of lymphocytes);
  • prolonged uncontrolled use of drugs (iodinated medicines, hormonal means);
  • radiation, long stay in the sun;
  • the psychoinjuring situations (disease or the death of close people, loss of work, offense and disappointment).

Symptoms of autoimmune tireoidit

The majority of cases of a chronic autoimmune tireoidit (in an eutireoidny phase and a phase of a subclinical gipoterioz) a long time proceeds asymptomatically. The thyroid gland is not increased in a size, at a palpation is painless, function of gland is normal. Very seldom increase in the size of a thyroid gland can be defined (craw), the patient complains of unpleasant feelings in a thyroid gland (pressure sense, a coma in a throat), easy fatigue, weakness, joint pains.

The clinical picture of a thyrotoxicosis at an autoimmune tireoidit is usually observed in the first years of development of a disease, has passing character and in process of an atrophy of the functioning tissue of a thyroid gland passes to some time into an eutireoidny phase, and then into a hypothyroidism.

Postnatal tireoidit, is usually shown by a slight thyrotoxicosis on the 14th week after the delivery. Fatigue, by the general weakness, weight reduction is in most cases observed. Sometimes the thyrotoxicosis is considerably expressed (tachycardia, feeling of heat, excess perspiration, a tremor of extremities, emotional lability, an insomniya). The Gipotireoidny phase of an autoimmune tireoidit is shown on the 19th week after the delivery. In certain cases it is combined with a postnatal depression.

Bezboleva tireoidit (silent) it is expressed by slight, often subclinical thyrotoxicosis. Tsitokin-indutsirovanny tireoidit also usually is not followed by a heavy thyrotoxicosis or a hypothyroidism.

Diagnostics of an autoimmune tireoidit

Before manifestation of a hypothyroidism it is rather difficult to diagnose AIT. Endocrinologists establish the diagnosis of an autoimmune tireoidit on a clinical picture, these laboratory researches. Presence at other members of the family of autoimmune violations confirms probability of an autoimmune tireoidit.

Laboratory researches at an autoimmune tireoidit include:

  • the general blood test - is defined increase in quantity of lymphocytes
  • to immunogramm – existence of antibodies to a tireoglobulin, a tireoperoksidaza, the second colloidal anti-gene, antibodies to tireoidny hormones of a thyroid gland is characteristic
  • determination of T3 and T4 (the general and free), the TTG level in blood serum. Increase in the TTG level at the maintenance of T4 normal testifies to a subclinical gipotiroz, the increased TTG level at the reduced concentration of T4 – to a clinical hypothyroidism
  • Ultrasonography of a thyroid gland - shows increase or reduction of the sizes of gland, change of structure. Results of this research serve as addition to a clinical picture and other results of laboratory researches
  • the tonkoigolny biopsy of a thyroid gland - allows to reveal the large number of lymphocytes and other cages characteristic of an autoimmune tireoidit. It is applied in the presence of data on possible malignant regeneration of nodal formation of a thyroid gland.

Serve as criteria of diagnostics of an autoimmune tireoidit:

  • increase in level of the circulating antibodies to a thyroid gland (AT-TPO);
  • detection at ultrasonography of a gipoekhogennost of a thyroid gland;
  • signs of primary hypothyroidism.

In the absence of at least one of these criteria the diagnosis of an autoimmune tireoidit has only probabilistic character. As increase in the AT-TPO level, or a gipoekhogennost of a thyroid gland in itself do not prove autoimmune yet tireoidit, it does not allow to establish the exact diagnosis. Treatment is shown to the patient only in a gipotireoidny phase therefore there is no urgent need in diagnosis in an eutireoidny phase, as a rule.

Treatment of an autoimmune tireoidit

Specific therapy of an autoimmune tireoidit is not developed. Despite modern achievements of medicine, the endocrinology has yet no effective and safe methods of correction of autoimmune pathology of a thyroid gland at which process would not progress to a gipoterioz.

In case of a tireotoksichesky phase of an autoimmune tireoidit purpose of the medicines suppressing function of a thyroid gland - tirostatik (, , propiltiouratsit) are not recommended as at this process there is no hyperfunction of a thyroid gland. At the expressed symptoms of cardiovascular violations apply beta .

At manifestations of a hypothyroidism individually appoint replacement therapy tiroidny medicines of hormones of a thyroid gland - levotiroksiny (L-tiroksinom). It is carried out under control of a clinical picture and the maintenance of TTG in blood serum.

Glucocorticoids (Prednisolonum) are shown only at a simultaneous current of an autoimmune tireoidit with a subsharp tireoidit that is quite often observed during the autumn and winter period. For decrease in a caption autoantitet nonsteroid resolvents are applied: indometacin, diclofenac. Use also medicines for immunity correction, vitamins, adaptogens. At a hypertrophy of a thyroid gland and the expressed squeezing of bodies of a sredosteniye carry out by it expeditious treatment.

The forecast at an autoimmune tireoidit

Forecast of development of an autoimmune tireoidit satisfactory. At in due time begun treatment process of destruction and decrease in function of a thyroid gland it is possible to slow down and reach long remission of a disease considerably. The satisfactory health and normal efficiency of patients in certain cases remain more than 15 years, despite the arising short-term aggravations of AIT.

Autoimmune tireoidit and the raised caption of antibodies to a tireoperoksidaza (AT-TPO) needs to be considered as risk factors of emergence in the future of a hypothyroidism. In case of a postnatal tireoidit the probability of its recurrence after the following pregnancy at women makes 70%. About 25-30% of women with a postnatal tireoidit have further chronic autoimmune tireoidit with transition to a resistant hypothyroidism.

Prevention of an autoimmune tireoidit

At the revealed autoimmune tireoidit without dysfunction of a thyroid gland observation of the patient is necessary as soon as possible to find and in due time to compensate manifestations of a hypothyroidism.

Women are bearers of AT-TPO without change of function of a thyroid gland, are in risk group of development of a gipoterioz in case of pregnancy approach. Therefore it is necessary to control a state and function of a thyroid gland as on early terms of pregnancy, and after the delivery.

Autoimmune tireoidit - treatment

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