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Auto-Antibodies in Graves and Hashimotos Jim Lowrance

Major Thyroid Disease Causing Antibodies

Thyroid autoimmunity is the most common cause of thyroid disease in industrialized countries, causing overactive and under-active hormone disorders.

Thyroid antibodies attack key proteins in the thyroid gland and in some cases, stimulate production of excessive amounts of hormone. These killer cells that are manufactured by the immune system become confused for reasons yet to be fully understood by medical science and they begin to identify thyroid cells as threats in the body. As they attack these cells, the thyroid gland becomes damaged, resulting in inflammation, enlargement of the gland and thyroid hormone imbalances.

Protein-Enzyme Cell Destroying Antibodies

The antibodies, also called auto-antibodies, that enter into thyroid protein-enzymes, causing destruction of them, are called the Anti-thyroidperoxidase and the Anti-thyroglobulin. Abbreviations commonly used for these on medical blood lab documents are TPO ABs” and TG ABs or Anti-TPO and Anti-TG.

Once these proteins called thyroidperoxidase and thyroglobulin are destroyed by these antibodies, they are rendered incapable of aiding in the process of converting iodine absorbed by the thyroid gland, into thyroid hormones that regulate the metabolism of all other cells in the body. This is the rate at which the body burns fuels that enter the body, converting them into energy.

As less hormone becomes available the metabolism can be slowed down (hypothyroidism). These proteins are also part of what keeps thyroid tissue healthy and so as the level of them begins to diminish, thyroid tissue will also begin to die within the gland. As this process occurs, the thyroid gland can become inflamed (thyroiditis) and/or enlarged (goiter).

Thyroid Stimulating Antibodies

These antibodies are also called Thyroid Stimulating Immunoglobulins (abbreviated TSI). These type auto-antibodies stimulate excessive release of T3-triiodothyronine and T4-thyroxine from the thyroid gland. They do this by binding to receptors in the blood that normally attach to the Thyroid Stimulating Hormone (TSH) which is another hormone that comes from the pituitary brain-gland that regulates hormone release from the thyroid gland.

TSH in-essence is a messenger hormone, telling the thyroid gland how much hormone is needed in the body and keeps the levels in-balance for proper metabolism via ongoing communication. Once the TSI antibodies attach to TSH-receptors, the message from them to the thyroid gland mimics the communication of TSH which stimulates an increase in thyroid hormone levels. They are in-essence tricking the thyroid gland into producing more thyroid hormone when it is not needed, causing a sped up metabolism in the body (hyperthyroidism).

Graves Disease and Hashimotos Thyroiditis

All three types of antibodies described in the previous subheadings can be present in both Graves disease and Hashimotos thyroiditis. Graves, results in eventual hyperthyroidism in most cases and Hashimotos results in hypothyroidism. The diseases are differentiated and diagnosed by the balance of auto-antibodies found, by levels of thyroid hormones in the body (imbalances) and by the symptom manifestations caused by the combination of these two factors.

The TPO and TG antibodies are typically found in higher titers (lab measurements) in Hashimotos patients than in Graves patients, so both diseases cause thyroid gland destruction but at a much slower rate with Graves disease. The TSI antibodies that stimulate excessive hormone release from the thyroid gland are found to be high-positive in the vast majority of Graves patients but are not found to be positive in all Hashimotos patients and when they are, it is usually in low titers. If a Hashimotos patient does have significant levels of TSI, it can cause, intermittent phases of hyperthyroidism, called Hashitoxicosis which is most often a temporary condition.

These facts about antibodies point to how closely related Graves and Hashimotos are and may also explain as to why patients with one disease may transition over to the other in rare cases when a significant change in the balance of auto-antibodies and thyroid hormone levels takes place.

Thyroid antibodies attack key proteins in the thyroid gland and in some cases, stimulate production of excessive amounts of hormone.

These killer cells that are manufactured by the immune system become confused for reasons yet to be fully understood by medical science and they begin to identify thyroid cells as threats in the body.

As they attack these cells, the thyroid gland becomes damaged, resulting in inflammation, enlargement of the gland and thyroid hormone imbalances.

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