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What is Grave's Disease (GD)? Who gets GD? GD in Chilhood/Pregnancy Symptoms Laboratory Tests Treatment Options Alternative Med Radioiodine Ablation Autoimmune Thyroid Disease Graves' Ophthalmopathy aka Thyroid Eye Disease Subclinical Hyperthyroidism Subclinical Hypothyroidism Hashitoxicosis Goiter Lymphoma Other Autoimmune Diseases Environmental Causes Nutrient Deficiencies Provocative Links Favorite Links My Graves Disease Book My Articles on Suite 101 Sign My Guest Book View My Guest Book Contact Me About Me  |
There are many GD variants or subtypes, and each individual case of GD is unique. Graves' disease is caused by stimulating TSH receptor antibodies, which are also known as thyroid stimulating immunoglobulins or TSI. These antibodies activate receptors on the surface of thyroid cells, ordering thyroid cells to produce more thyroid hormone. Like a key opening a lock, these antibodies cause a sustained increase in thyroid hormone levels. Graves' disease primarily targets women between the ages of 30-50. However, it also affects men, and it can affect individuals of any age. GD can also affect muscle, causing muscle weakness, and it can affect heart muscle. See "thyroid storm" on the symptoms page. Graves Disease 1, med student text Patients with pretibial myxedema (PTM) may rarely develop a soft tissue disorder known as acropachy that primarily affects the fingers and toes. GD patients may also exhibit symptoms of clubbing which is different than acropachy. See symptoms page to learn more about the skin disorders associated with GD. What are thyroid cysts? As mentioned, the stimulating thyrotropin (or TSH) receptor antibodies seen in Graves' disease are also called thyroid stimulating immunoglobulins (TSI). These antibodies are directly responsible for the hyperthyroidism of Graves' disease. Acting in place of TSH, they direct the thyroid gland to keep producing and secreting excess thyroid hormone. See Page describing Thyroid Laboratory Tests. TSI activate the TSH receptor on thyroid cells, mimicking the action of TSH, a hormone released by the pituitary gland. Normally, TSH stimulates the thyroid gland to produce and release thyroid hormone. Bypassing all normal regulatory controls, TSI cause the thyroid gland to release excess thyroid hormone, causing hyperthyroidism. TSI also stimulate orbital cells, causing Graves' ophthalmopathy and they stimulate dermal cells, causing pretibial myxedema. TSH is a pituitary hormone which regulates thyroid hormone levels in the blood. The concentration of TSH present in the blood is generally a good indicator of thyroid status, and levels of TSH are often used to diagnose thyroid disorders. When thyroid hormone levels in the blood are low, the hypothalamus orders the pituitary to secrete more TSH and TSH levels are high. When thyroid hormone levels are elevated, the hypothalamus halts TSH release. Thus, in hyperthyroidism, levels of TSH are low, frequently lower than the detection level (usually <0.01 IU/L). Thyroid hormones include thyroxine (T4)and triiodothyronine (T3). Normally, the thyroid primarily produces T4 along with a small amount of T3. T3, which is 10 times more active than T4, is mainly produced in the body by conversion (or losing one iodine molecule) from T4. Thyroid hormone is 65% iodine. T4 has 4 iodine atoms, whereas T3 has 3 iodine atoms. However, in GD the thyroid gland produces more T3 relative to T4 than usual. This results in a condition known as T3 toxicosis. Despite it's ominous sound, T3 toxicosis is a good indicator of a favorable response to ant-thyroid drug therapy.  This site is for educational purposes only and is not intented as a substitute for medical treatment. This is a private site. Visitor information is not shared with any other groups or organizations.Copyright 2004, Elaine Moore. |