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Hashimoto thyroiditis — also known as Hashimoto’s disease or chronic lymphocytic thyroiditis — is an autoimmune condition, meaning antibodies from a person’s own immune system attack a part of the body. In the case of Hashimoto’s, the target of the antibodies is the thyroid gland .
The thyroid is a butterfly-shaped gland in the neck that controls metabolism. Unlike in Graves disease, in which antibodies stimulate the thyroid to overproduce thyroid hormones (a condition known as hyperthyroidism), Hashimoto’s disease starts with a short period of hyperthyroidism and ends with low thyroid function. This is known as hypothyroidism , or an underactive thyroid.
The number of people who have Hashimoto’s disease in the United States is unknown, according to the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), but it is the most common cause of hypothyroidism which affects about 5 in 100 Americans. However, while Hashimoto’s disease is the most common cause of hypothyroidism, a person can be hypothyroid without a Hashimoto’s etiology.
What causes Hashimoto’s disease?
The nature of the immune attack on the thyroid explains why Hashimoto’s can begin with hyperthyroidism and end with hypothyroidism. Thyroid cells contain the hormones triiodothyronine (T3) and thyroxine (T4), which are waiting to be released into the blood as needed. When Hashimoto antibodies — such as thyroid peroxidase (TPO), thyroglobulin (TG), and thyroid-stimulating immunoglobulin (TSI) — strike the thyroid, however, a couple of things happen. If TSI is among the antibodies striking the thyroid, thyroid cells are stimulated to release their hormones. Whether or not TSI is among the antibodies striking the thyroid, other antibodies, such as TPO damage thyroid tissue, causing the hormones (T3 and T4) to leak into the blood fairly rapidly. The damage is generally permanent, so, ultimately, the thyroid cells will not be able to produce more hormones.
Meanwhile, high levels of thyroid hormones have been released, so, over a period of several days, levels of T3 and T4 in the blood rise. This causes hyperthyroidism (high concentrations of thyroid hormones) that typically lasts up to two weeks.
However, because the gland is damaged, it cannot produce more hormones. After this brief spike, the amounts of T3 and T4 in the blood begin dropping. The person goes through a period of having normal levels of thyroid hormones in the blood (this is called being euthyroid).
Because the hyperthyroid period is so brief and because the person then goes through a euthyroid state on the way to becoming hypothyroid, temporary hyperthyroid symptoms are not always noticed. The thyroid hormone levels then keep dropping, so the person becomes increasingly hypothyroid and remains that way.
It isn’t clear what causes the immune system to attack thyroid cells, according to the Mayo Clinic . Genetic factors, environmental triggers (such as an infection or stress) or a combination of the two may play a role.
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