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Graves Disease: Hyperthyroidism, Overview, Causes and Symptoms

Graves Disease – Hyperthyroidism:

Graves Disease is an autoimmune disease characterized by hyperthyroidism due to circulating autoantibodies. It is also the leading cause of hyperthyroidism, a condition in which the thyroid gland produces excessive hormones. It affects up to 2% of the female population, sometimes appears after childbirth, and occurs seven to eight times more often in women than in men. Once the disorder has been correctly diagnosed, it is quite easy to treat. In some cases, Graves’ disease goes into remission or disappears completely after several months or years. Left untreated, however, it can lead to serious complications and even death.

Pathophysiology:

Graves’ disease is an autoimmune disorder, in which the body produces antibodies to the receptor for thyroid-stimulating hormone (TSH). (Antibodies to thyroglobulin and to the thyroid hormones T3 and T4 may also be produced.)

These antibodies cause hyperthyroidism because they bind to the TSH receptor and chronically stimulate it. The TSH receptor is expressed on the follicular cells of the thyroid gland (the cells that produce thyroid hormone), and the result of chronic stimulation is an abnormally high production of T3 and T4. This, in turn, causes the clinical symptoms of hyperthyroidism, and the enlargement of the thyroid gland visible as goiter.

The infiltrative exophthalmos frequently encountered has been explained by postulating that the thyroid gland and the extraocular muscles share a common antigen which is recognized by the antibodies. Antibodies binding to the extraocular muscles would cause swelling behind the eyeball.

The “orange peel” skin has been explained by the infiltration of antibodies under the skin, causing an inflammatory reaction and subsequent fibrous plaques.

The three types of autoantibodies to the TSH receptor currently recognized are:

  1. Thyroid stimulating immunoglobulins (TSI): these antibodies (mainly IgG) act as long-acting thyroid stimulants, activating the cells in a longer and slower way than TSH, leading to an elevated production of thyroid hormone.
  2. Thyroid growth immunoglobulins (TGI): these antibodies bind directly to the TSH receptor and have been implicated in the growth of thyroid follicles.
  3. Thyrotrophin binding-inhibiting immunoglobulins (TBII): these antibodies inhibit the normal union of TSH with its receptor. Some will actually act as if TSH itself is binding to its receptor, thus inducing thyroid function. Other types may not stimulate the thyroid gland, but will prevent TSI and TSH from binding to and stimulating the receptor.

Another effect of hyperthyroidism is bone loss from osteoporosis, caused by an increased excretion of calcium and phosphorus in the urine and stool. The effects can be minimized if the hyperthyroidism is treated early. Thyrotoxicosis can also augment calcium levels in the blood by as much as 25%. This can cause stomach upset, excessive urination, and impaired kidney function.

 

Signs and Symptoms:

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Differential Diagnosis:

 

Diagnosis:

Laboratory studies:
Imagine Studies:
Histologic Findings:

 

Treatment:

 

Graves Ophthalmopathy:
Graves’ orbitopathy is an autoimmune disease of the retroocular tissues occurring in patients with Graves’ disease. Although it has often been referred to as Graves’ ophthalmopathy, or simply thyroid eye disease (TED), it is primarily a disease of the orbit and is better termed Graves’ orbitopathy.

 

Sources: [1][2][3][4]

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