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Why is my TSI level 241 but my FT3 and FT4 and TSH in normal range?
What causes this, and should I be worried my doctor may have overlooked something. She says my Graves disease is in "remission".
What causes this, and should I be worried my doctor may have overlooked something. She says my Graves disease is in "remission".
Excerpt from Elaine Moore's article Graves’ Disease Revisited...
"Graves’ disease is considered an antibody-mediated autoimmune disorder. Here, stimulating TSH receptor antibodies (also known as thyroid stimulating immunoglobulins or TSI) react with the TSH receptor protein on thyroid cells, ordering these cells to produce excess thyroid hormone.
While the immediate goals in treating Graves’ disease are to reduce thyroid hormone levels and lessen the effects of hyperthyroidism, the long-term goals are to heal the immune system and reduce the production of TSI.
There is some variation in TSI. This explains why Graves’ patients with very high TSI levels can have mild symptoms and Graves’ patients with moderate TSI levels can have severe symptoms. It’s suspected that there are several subtypes of TSI. Presumably, these subtypes determine the type of epitopes or binding sites on the TSH receptor that TSI can bind to. TSI may bind to epitopes that result in stimulation of thyroid cells or they may bind to epitopes that are less potent.
Many patients with Graves’ disease also have blocking TSH receptor antibodies. These antibodies block both TSH and TSI from reacting with the TSH receptor, thereby preventing thyroid cells from producing excess thyroid hormone."
"Graves’ disease is considered an antibody-mediated autoimmune disorder. Here, stimulating TSH receptor antibodies (also known as thyroid stimulating immunoglobulins or TSI) react with the TSH receptor protein on thyroid cells, ordering these cells to produce excess thyroid hormone.
While the immediate goals in treating Graves’ disease are to reduce thyroid hormone levels and lessen the effects of hyperthyroidism, the long-term goals are to heal the immune system and reduce the production of TSI.
There is some variation in TSI. This explains why Graves’ patients with very high TSI levels can have mild symptoms and Graves’ patients with moderate TSI levels can have severe symptoms. It’s suspected that there are several subtypes of TSI. Presumably, these subtypes determine the type of epitopes or binding sites on the TSH receptor that TSI can bind to. TSI may bind to epitopes that result in stimulation of thyroid cells or they may bind to epitopes that are less potent.
Many patients with Graves’ disease also have blocking TSH receptor antibodies. These antibodies block both TSH and TSI from reacting with the TSH receptor, thereby preventing thyroid cells from producing excess thyroid hormone."
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