Graves’ disease (ChGB) is an autoimmune disease. The body’s immune system secretes antibodies to the TSH receptor (so-called TRAb or anti-TSHR), which results in increased thyroid gland activity and overproduction of thyroid hormones – triiodothyronine (T3), thyroxine (T4) and calcitonin. This disease mainly affects women who are sick up to ten times more often than men, which prompts some specialists to make the thesis that female hormones may have the disease. The disease proceeds with periods of spontaneous exacerbation and resolution of hyperthyroidism.
Graves’ disease – causes
As a result of disorders of the immune control mechanism, anti-TSH receptor (anti-TSHR) autoantibodies appear that stimulate follicular cell function, leading to hyperthyroidism. Anti-TSHR, by attaching to the TSH receptor present on the cell membrane of thyocytes, provokes their excessive activation, leading to increased secretion of hormones. An important role in the development of Graves-Basedov disease (ChGB) is the presentation of thyroid antigens to T lymphocytes, which in turn activate B lymphocytes that transform into plasmocytes and produce anti-TSHR. Activation of cellular response mechanisms against TSH receptors present in orbital fibroblasts leads to thyroid orbitopathy. It involves activated TH1-type lymphocytes that secrete cytokines that increase fibroblast proliferation. Activation of Th 2 lymphocytes causes steatosis and fibrosis within the orbit, which leads to impaired ocular function and fixation of exophthalmos.
Graves’ disease – symptoms
Symptoms of Graves’ disease are the same as those seen with hyperthyroidism. Their severity provides information on the stage of the disease. Overproduction of thyroid hormones leads to hypermetabolism, which adversely affects the work of the nervous and cardiovascular systems.
People suffering from ChGB struggle with excessive sweating and constant heat, as well as trembling hands and weakening of muscular strength. They are nervous and irritable, they have serious problems with concentration, as well as trouble filling. The consequence of accelerated metabolism is weight loss, even despite increased appetite. In addition, there are:
- feeling palpitations and increased heart rate
- recurrent diarrhea
- menstrual cycle disorders
- deterioration of the skin, hair and nails,
- libido disorders.
With ChGB, 8 out of 10 patients develop a thyroid gland and goiter, which increases neck circumference but does not cause a feeling of pressure. The goiter is soft, enlarged evenly and without palpable nodules. The patient may complain of hoarseness or shortness of breath.
A characteristic symptom of hyperthyroidism in Graves’ disease is thyroid orbitopathy. As a result of accelerating the metabolism, orbital tissues increase their volume, thereby pressing on the eyeball. This moves under the influence of pressure, which results in staring eyes. There may also be pre-shaved edema as well as thyroid acropathy, i.e. thickening of the fingers, although these are very rare symptoms.