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HASHIMOTO DISEASE (H. Haslii-moto, Japanese surgeon and pathologist, 1881 — 1934; synonym: an autoimmune thyroiditis, an autoallergichesky thyroiditis, a lymphocytic thyroiditis, a lymphomatous craw, a Hashimoto's disease, a chronic not purulent thyroiditis, a chronic nonspecific thyroiditis, a limfoadenoidny thyroiditis) — the autoimmune disease of a thyroid gland leading, as a rule, to disturbance of its function.

The disease is described in 1912 by Hashimoto. Develops at women at the age of 40 — 50 years more often, but quite often meets at children's and youthful age.

Etiology and pathogeny. X. is an autoimmune disease (see Autoallergichesky diseases). The autoimmune nature of a disease is confirmed by existence in blood serum of sick antibodies to thyreoglobulin, microsomal and to other antigens of a thyroid gland (see), existence of autoantibodies to a thyroid gland at relatives of patients, increase in the sizes of a thymus (see), existence of a hypergammaglobulinemia (see Immunoglobulin), presence of immunoglobulins at tissue of a thyroid gland, limfokletochny and plazmotsitarno-cellular infiltration of a thyroid gland of patients of X., combination of X. with other autoimmune diseases (a pseudorheumatism, pernicious anemia, an addisonovy disease, etc.), and also a possibility of creation of pilot models of X. by immunization of animals thyreoglobulin of own thyroid gland. In a pathogeny of X. much in common with a diffusion toxic craw (see the Craw diffusion toxic). Both diseases are connected with existence of specific defect immunol. protection of an organism, to-ry the thymus gland of dependent lymphocytes — T lymphocytes is characterized by emergence of self-reactive «forbidden» clones (see. Immunocompetent cells). The system of suppressors existing in a healthy organism suppresses activity of T lymphocytes and prevents their interaction with complementary antigens of a thyroid gland. At X. as a result of defect of this system (possibly, genetic) it is broken immunol. tolerance (see Tolerantnost immunological.), and «forbidden» clones of T lymphocytes interact with complementary antigens of cells of a thyroid gland, causing thereby a local cell-mediated immune response. At the same time T lymphocytes interact with V-lymphocytes with the subsequent transformation of the last in plasmocytes (see), to-rye form polyclonal autoantibodies (see) to a thyroid gland. The last render destructive action on cells of follicles of a thyroid gland. In blood serum of patients of X. constantly autoantibodies to a tireoglobtslin (see), to components of a colloid of a thyroid gland, microsomes of ferruterous cells, thyroxine are found (see) and to triiodothyronine (see), to receptors of thyritropic hormone of a hypophysis on membranes of thyrocytes, demonstrating that in a pathogeny of X. matters not only cell-mediated, but also humoral immunity.


Provocative moment in development of X. any damage causing disturbance of integrity of a thyroid gland and intake of thyreoglobulin in blood (operation, use of radioisotopes, an inflammation, inadequate treatment can serve as thyreostatic drugs or drugs of iodine, at a local or sporadic craw, injuries). A certain value have insufficient receipt in an organism of iodine (see), and also genetic predisposition to disturbances immunol. tolerances what overseeing by enzygotic twins and relatives of patients of X testifies to., existence of associations between some antigens of histocompatability (see Immunity transplant, t. 20, additional materials) and development of a disease.

Progressing of autoimmune process leads to the expressed destructive changes in a thyroid gland and development of a hypothyroidism (see). Development of a hypothyroidism at X. it is connected: with disturbance of biosynthesis of hormones of a thyroid gland as a result of lymphocytic infiltration, destruction of thyroid fabric and the subsequent atrophy of body; with presence of immunoglobulins. blocking linkng of thyritropic hormone with receptors; with blocking by the iodine which is released from the destroyed thyroid fabric, biol. effect of thyritropic hormone; with inhibition the somatostatin synthesized by parakrinovy cells of a thyroid gland, education and release of triiodothyronine and tetraiodine-tironina.

Development of a hyperthyroidism (see the Thyrotoxicosis) at X. it is caused by synthesis of the antibodies stimulating proliferation and hyperfunction a shooting gallery e about c of 11 t about in (t and p e about and d with t and m at l and r at yu shch and x

antibodies) that pulls together pathogenetic H.b. with a diffusion toxic craw. The hyperthyroidism arising at the beginning of a disease is connected with destruction of follicles of a thyroid gland and an exit of large amounts of thyroxine and triiodothyronine in blood.

Fig. of Mikropreparata of a thyroid gland is normal («) and at Hashimoto's disease:

and — follicles of a thyroid gland are filled with a colloid (1) and covered by an epithelium (2); — follicles of a thyroid gland are sharply reduced in sizes, contain a pale colloid (i), in a stroma diffusion infiltration lymphoid and plasmocytes (2) \coloring hematoxylin-eosine is observed; x 7 0.

Pathological anatomy. Allocate hypertrophic and atrophic forms of a disease. At a hypertrophic form X. the thyroid gland is increased in sizes already at early stages of a disease. As a rule, both shares increase, it is rare only a pyramidal share. Gland dense, a surface its hilly, on a section the lobular structure is expressed, has white marble, light pink color is more rare. In some cases in a thyroid gland there are nodes. At microscopic examination find the expressed lymphoid infiltration with formation of lymphoid follicles and considerable impurity of plasmocytes, destruction of thyroid follicles, disappearance of a colloid, presence at a cavity of thyroid follicles of large multinucleate cells, transformation of a follicular epithelium in large multinucleate cells with oksifilno the painted protoplasm — Gyurtle's cells — Askanazi; in places — a hyperplasia of thyrocytes. In intersticial fabric along with lymphoid infiltration of an otmech to Utah I the phenomena of a sclerosis (fig.) expressed in different degree. At gistokhy. a research in thyrocytes find reduction of activity of peroxidase (see) and acid phosphatase (see), up to their total disappearance. At electronic microscopic examination cystous expansion of elements en to a plasmatic reticulum is noted (see).

Growth of the fibrous fabric replacing thyroid, besides, is characteristic of an atrophic form.

Clinical picture. The disease usually develops gradually within several years though also more bystry course of a disease is possible. The preclinical (latent) stage is characterized by immune shifts and morfol. disturbances — increase in an antiserum capacity to thyroid antigens and immunoglobulins of blood, development lympho-plazmotsitarnoy infiltrations of a thyroid gland. Function of a thyroid gland in this stage is not broken. Further the wedge, manifestations depend on a form of a disease (hypertrophic or atrophic) and a functional condition of a thyroid gland.

The atrophic form meets more often at elderly people and is, as a rule, shown by slackness, weakness, drowsiness, decrease in working capacity, a hearing impairment, a xeroderma, puffiness of the person, change of a timbre and hoarseness of a voice, bradikardny and other signs of a hypothyroidism (see).

At a hypertrophic form one of the most precursory and characteristic symptoms of a disease is the enlargement of the thyroid gland. Patients complain also of feeling of pressure, sometimes pains in a neck, the osiplost of a voice caused by a prelum of branches of a recurrent guttural nerve the increased thyroid gland or with hypostasis of a mucous membrane of a throat. The thyroid gland is increased, dense, with a pulled surface, mobile, painless is more often. Regional limf, nodes are not increased. Depending on a functional condition of a thyroid gland at a hypertrophic form X. allocate hyper thyroid, hypo-thyroid and euthyroid forms. Often - it is phases of the same process. Hyper thyroid form X. (hashitoksikoz) it is shown by a thyrotoxicosis of easy, is more rare moderately severe (an indisposition, perspiration, temperature increase, weight loss, heartbeat and other symptoms of a thyrotoxicosis). Further the thyrotoxicosis is replaced by a hypothyroidism, however displays of a thyrotoxicosis can periodically repeat throughout all disease. The Gipotireo-idny form is characterized by signs of a hypothyroidism. At an eutireo-idiy form the dense thyroid gland for many years can be the only sign of X. Sometimes euthyroid form X. it is combined with the phenomena of the endocrine ophthalmopathy which is shown an exophthalmos (see) and an ophthalmoplegia (see).

Allocate X. at children and young men. The disease is characterized less expressed, than at adults, its functions, lower caption or lack of antiti-reoidny antibodies are an enlargement of the thyroid gland without disturbance.

Current of X. slow, progressing from the outcome in a hypothyroidism.

The diagnosis is made on the basis of the anamnesis, survey (the increased dense, mobile thyroid gland), by a wedge, pictures and data a lab., immunol., tsitol. and other methods of a research.

At patients of X. frequent increase in a caption of anti-thyroid antibodies (to thyreoglobulin, microsomes of ferruterous cells, to I and

II components of a colloid), increase in level of thyritropic hormone in blood (sometimes even against the background of an euthyroid state), decrease in maintenance of at-, a2-is noted and it r-globuli-is new, increase in contents at-glo-bulinov (first of all IgM and IgG) in blood, a lymphocytosis, a monocytopenia, sometimes acceleration of ROE, at later stages — hypochromia anemia.

At a radio isotope research absorption 131J a thyroid gland in most cases normal, especially at early stages of a course of a disease. At nek-ry patients decrease in absorption 131J in 24 hours after administration of drug is noted. In cases of a hashitoksikoz absorption 131J can be normal or slightly raised. After administration of thyritropic hormone (see) absorption of a radioiodine does not increase as it is observed normal. On a skanogramma (see Scanning) the illegibility of contours of a thyroid gland, mosaicity of accumulation of a radioiodine is defined.

At rentgenol. a research narrowing and (or) shift of a trachea and gullet because of a prelum is in some cases observed by their increased dense thyroid gland.

In some cases diagnosis is helped by performing trial treatment by Prednisolonum (on 15 — 20 mg a day within 7 — 10 days). In the presence of X. the craw can decrease in sizes, to become less dense.

For diagnosis, especially at children, the aspiration biopsy has great value (see); at the same time it is necessary to define the place of a puncture correctly. At microscopic examination of the received material about N and r and in and yut about l sh about e quantity of lymphoid elements, among to-rykh cells of the light centers of lymphoid follicles, plasmocytes, and also macrophages and multinuclear histiocytes meet. On this background rare accumulations of follicular cells and (or) Gyurtle's cells — Askanazi meet. Usually there is a correlation between data tsitol. researches and the raised caption of anti-thyroid antibodies (is more often than microsomal).

For identification of X. at early stages it is necessary to consider persons with risk factors. The people who had a diffusion toxic craw, underwent a thyroid gland operation, patients with various forms of a craw (see), relatives of patients of X treat them. and a diffusion toxic craw, and also the persons having other autoimmune diseases, especially a myasthenia (see), vitiligo (cm), acanthosis nigricans (see), etc.

Differential diagnosis is carried out with a sporadic craw (see the Craw sporadic), is more often conglomerate, cancer of thyroid gland (see. A thyroid gland, tumors), a diffusion toxic craw (see the Craw diffusion toxic), Ridel's thyroiditis and specific thyroidites (see Tireoi-dipg).

At an euthyroid form of a sporadic craw the thyroid gland is usually elastic and does not reach density observed at patients of X., the antiserum capacity to thyreoglobulin and microsomal elements of a thyroid gland low or is not defined. At an aspiration biopsy of a thyroid gland do not reveal specific to X. changes.

Cancer of a thyroid gland is characterized by the stony density of gland, its small mobility, increase regional limf, nodes. On a skanogramma blurring and irregularity of contours of a thyroid gland, sites with lack of absorption of radioisotope are noted. Caption of autoantibodies low. During the performing trial treatment by Prednisolonum at patients with cancer of a thyroid gland of effect it is not observed.

At differentiation of X. with a diffusion toxic craw consider anamnestic data (the long absence of dysfunction of a thyroid gland or decrease it, and also tendency of displays of a thyrotoxicosis to spontaneous regressing is not characteristic of a diffusion toxic craw), the accruing weight loss, the expressed changes of a cardiovascular and nervous system, lack of a high antiserum capacity (especially microsomal), data tsitol. researches, indicators radioisotope of whom of a research.

At a fibrous thyroiditis of Ridel a thyroid gland of stony density, a caption of autoantibodies it is a little raised, but is much lower, than at X.

At differential diagnosis of X. with specific thyroidites (tubercular, with ifit and-tichesky) consider the anamnesis and results of serological and specific tests, and also data tsitol. researches of the material taken at a puncture.

Treatment is directed to elimination of a lack of own hormones of a thyroid gland and decrease of the activity of autoimmune processes in a thyroid gland. Appoint drugs of thyroid hormones (Thyreoidinum, triiodothyronine) in combination with glucocorticoid hormones. Reception of thyroid hormones is begun with small doses (Thyreoidinum — on 25 — 100 mg, triiodothyronine — on 10 — 25 mkg a day), gradually raising doses respectively to 200 — 300 mg and 50 — 100 mkg a day. Treatment by drugs of thyroid hormones is carried out under, control of pulse, the ABP and an ECG. At treatment by Thyreoidinum the effect is noted usually when the dose reaches 100 — 200 mg a day, at treatment by triiodothyronine — 25 — 50 mkg a day. Further appoint maintenance doses: Thyreoidinum of 50 — 100 mg a day, triiodothyronine of 10 — 25 mkg a day. Patients shall receive maintenance doses of thyroid hormones constantly. Corticosteroids (Prednisolonum) appoint on 20 — 30 mg a day with a gradual dose decline during 11/2 — 2 months. Apply also elektrofonoforez with a hydrocortisone on area of a thyroid gland. Sometimes for the purpose of increase in activity of T-suppressors appoint immunostimulators — Leva Mi of the evils

, etc.

Criteria of efficiency of treatment are reduction of the sizes of a craw up to a normal amount of a thyroid gland, decrease in an antiserum capacity to thyreoglobulin and microsomal elements of a thyroid gland, good health of the patient.

Operational treatment of X. carry out at a prelum by the increased thyroid gland of bodies of a neck, a craw of the big sizes and suspicion on its malignancy. The issue of the volume of an operative measure is resolved individually taking into account the sizes of a craw and data tsitol. researches (express biopsy). Make a subtotal resection of a thyroid gland more often (see Shchitovid-paya of iron, operation), is more rare — its extirpation (I eat. Thyroidectomy). In the postoperative period drugs of thyroid hormones are appointed.

Patients of X. shall be on dispensary observation at the endocrinologist.

The forecast for life favorable. Working capacity depends on degree of a hypothyroidism. At timely begun treatment in some cases perhaps absolute recovery.

Prevention consists in timely and effective treatment acute inf. diseases, sanitation hron. the centers of an infection, especially at persons with risk factors on X.

Bibliography: Yefimov A. S., Baud

of plank beds P. N. and Zelinsky B. A. Endokrinologiya, Kiev, 1983; 3 e f and -

G. S., Shepetkov L. V. and Ibragimov V. G. rova. Autoimmune thyroiditis, Kazansk. medicalballot boxes., t. 60, No. 4, page 26, 1979; Levitte I. D. Use the expert pi a ratsionny puncture of a thyroid gland and definition of the thyroid autoantibodies circulating in blood for diagnosis of an autoimmune tireo-kdit, Owls. medical, No. 1, page 82, 1982; R the expert to and A. M N. Autoimmune processes in pathology of a thyroid gland, L., 1973; With p e with and in c e in and V. G. Autoimmune thyroiditis (clinic, diagnosis, treatment), Owls. medical, No. 12, page 59, 1983;

De Groot L. J. a. Stanbu-r at J. Century of The thyroid and its diseases, N. Y., 1975; Doniach D.

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D o-niach D., Bottazzo G. F. a. Russell R. C. Goitrous autoimmune thyroiditis (Hashimoto’s disease), Clin. Endocr. Metabol., v. 8, p. 63, 1979; H a-shimoto H.< Zur Kenntnis des lympho-matosen Veranderung der Schilddriise Struma lymphomatosa), Arch. klin. Chir., Bd 97, S. 219, 1912; H j o r t T., L a u-ridsen U. B. a. Persson I. Thyroid antibodies and thyroglobulin-like products in serum during antithyroid therapy, Acta med. scand., v. 188, p. 431, 1970; Knecht H., Saremalsani P. Hedinger C. Immunohistological findings in Hashimoto's thyroiditis, focal limphocytic thyroiditis and thyroiditis de Quervain, Virchows Arch. path. Anat., Bd 393, S. 215, 1981; Roitt I. M.

a. o. Auto-antibodies in Hashimoto’s disease (lymphadenoid goiter), Lancet, v. 271, p. 820, 1956; V about 1 p e R. Auto-immunity in the endocrine system, V. a. o., 1981.

V. V. Talantov, I. D. Levitte.