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Graves’ disease is an autoimmune disease of the thyroid gland that causes an overactive thyroid gland. Hereditary predisposition plays an important role in morbidity – the role of HLA-DR3 and the CTLA-4 gene has been demonstrated. The disease is 10 times more common in women than in men, and often manifests itself after childbirth.
Graves’ disease – causes
As a result of disorders of the immune system control mechanism, autoantibodies against the TSH receptor (anti-TSHR) appear, which stimulate the activity of follicular cells, leading to hyperthyroidism. By binding to the TSH receptor present on the plasma membrane of thyrocytes, anti-TSHR causes their excessive activation, leading to increased secretion of hormones. In the development of Graves and Basedov’s disease (ChGB), an important role is played by the presentation of thyroid antigens to T lymphocytes, which in turn activate B lymphocytes, which transform into plasmocytes and produce anti-TSHR. Activation of the cellular response mechanisms against TSH receptors present in orbital fibroblasts leads to thyroid orbitopathy. It involves activated TH1 lymphocytes, secreting cytokines that intensify the proliferation of fibroblasts. As a result of the activation of Th 2 lymphocytes, steatosis and fibrosis in the orbital area occur, which leads to impaired function of the eyeball and to the fixation of exophthalmos.
Graves’ disease – symptoms
A typical feature of Graves’ disease is its recurrent course with periods of exacerbation and remission. The thyroid gland becomes enlarged. The typical symptoms of an overactive thyroid gland predominate:
- nervousness,
- tiredness,
- increased sweating,
- heat intolerance,
- palpitations,
- weight loss,
- tachycardia,
- muscle tremors
- increased pulse tension.
They are accompanied by the symptoms of autoimmune inflammation of the soft tissues of the orbit (exophthalmos) or skin (myxedema) and thyroid acropathy (EMO syndrome) specific for ChGB. Sometimes other autoimmune diseases are also found, such as pernicious anemia, myasthenia gravis, rheumatoid arthritis, and autoimmune cirrhosis. The diagnosis of a vascular goiter facilitates the diagnosis of ChGB. Vitiligo and alopecia areata are common in the course of Graves’ disease.
Graves’ disease is diagnosed on the basis of the results of hormonal tests (decrease in TSH, increase in FT4, less often increase in FT3), imaging of the thyroid gland (USG, scintigraphy), fine-needle aspiration biopsy and after an ophthalmological examination.
Graves’ disease – treatment
The treatment of Graves’ disease is not causal. Hyperthyroidism is treated (thyrostatic drugs – thiamazole, iodine salt of L-T4 left-handed thyroxine) and thyroid orbitopathy (pulse therapy – iv methylprednisolone), radioiodine treatment, surgery.
In untreated hyperthyroidism in the course of diabetes mellitus, it may go into spontaneous remission, but before that, life-threatening complications (thyroid crisis, stroke, heart attack) may occur. Drug treatment speeds up remission, but does not prevent relapse, which occurs in 50% of cases.
Lit.: [1] Ludgate M., Baker G.: Inducing Graves’ ophthalmopathy. J Endocrinol Invest 2004, 27; 211-5. [2] Bartalena L., Tanda M.L., Piantanida E. i wsp.: Relationship between management of hyperthyroidism and course of the ophthalmopathy. J Endocrinol Invest 2004, 27; 288-94.
Source: A. Kaszuba, Z. Adamski: “Lexicon of dermatology”; XNUMXst edition, Czelej Publishing House