Autoimmune thyroid disorders develop in people with certain predisposing genes when they're exposed to specific environmental triggers. This article describes these triggers.
Most thyroid diseases, whether they cause hypothyroidism, hyperthyroidism or thyroid eye disease (TED), are autoimmune disorders. Here, a defect in the immune system's response leads to diminished or excessive thyroid function or characteristic eye changes. The specific disorder that someone develops depends on the particular thyroid antibodies produced during this faulty immune response. The particular disorder can change over time and it can also improve, stabilize, or resolve when the immune system heals.
Most people with Graves' disease, which is autoimmune hyperthyroidism, are initially hypothyroid before hyperthyroidism develops although the hypothyroidism is usually mild and not diagnosed. Many people with autoimmune hypothyroidism, either Hashimoto's thyroiditis or atrophic thyroiditis, later develop Graves' disease. Autoimmune thyroid disorders occur in people with specific immune system and thyroid regulatory genes that predispose them to developing thyroid disease in the presence of certain environmental triggers. Many people have these predisposing genes but only a fraction of them develop autoimmune thyroid diseases. Certain environmental triggers are known to trigger or induce thyroid disease in these people.
This article describes the known and suspected triggers of autoimmune thyroid disease. Known triggers include cigarette smoke, stress, low selenium levels, seasonal and food allergies, sex steroids particularly estrogens, excess dietary iodine, and trauma. Thyroid cells may also be injured by oxidative stress related to the immune system's response to low antioxidant levels. Suspected environmental triggers include retroviruses, Yersinia and other enteric bacteria, and aspartame in artificial sweeteners. The immune mechanisms that contribute to disease from environmental agents include: increased cell destruction or apoptosis, thyroid autoantibody production, inflammation as white blood cells invade thyroid tissue, and the production of cytotoxic (destructive to cells) immune system chemicals known as cytokines.
Thyroid antibodies are seen in all forms of autoimmune thyroid disease. Thyroglobulin and thyroid peroxidase (TPO) antibodies, which are associated with thyroid cell inflammation, are seen in Hashimoto's thyroiditis, autoimmune atrophic thyroiditis, Hashitoxicosis, Graves' disease, and in lower levels in patients with silent or postpartum thyroiditis.
Stimulating TSH receptor antibodies (thyroid stimulating immunoglobulins or TSI) are seen in Graves' disease, Hashitoxicosis and in patients with thyroid eye disease. Blocking TSH receptor antibodies (thyrotropin blocking antibodies or TBA) prevent TSH from reacting with thyroid cells, which, in turn, reduces thyroid hormone production. TBA are seen in autoimmune atrophic thyroiditis, at lower levels than TSI in patients with Graves' disease, in higher levels than TSI in patients with Hashitoxicosis, in patients with thyroid eye disease.
In euthyroid Graves' disease, a condition of normal thyroid function and thyroid eye disease, levels of stimulating and blocking antibodies are both elevated to the same degree.
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