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Autoimmune Thyroid Diseases

© Elaine Moore

Autoimmune diseases (AITDs) refer to a number of different disorders in which the immune system either targets or attacks the cells of the thyroid gland, causing symptoms of thyroid disease. AITDs include both disorders of hypothyroidism, or reduced thyroid hormone production and hyperthyroidism, disorders caused by excess thyroid hormone production.

The most common AITDs are: 1) Hashimoto's thyroiditis (HT) a disorder of hypothyroidism, which is also called autoimmune thyroiditis, lymphocytic thyroiditis or lymphadenitis; 2) Graves' disease (GD) a disorder of hyperthyroidism, which is also known as Basedow's disease and diffuse toxic goiter; 3) Primary myxedema or autoimmune thyroid failure, a hypothyroid disorder marked by thyroid cell destruction. Primary myxedema eventually progresses to thyroid failure; 4) Hashitoxicosis, a condition characterized by symptoms of hyperthyroidism in patients with HT.

Rarely, autoimmune thyroid disorders may also progress to another condition known as thyroid lymphoma. Thyroid lymphoma results from ongoing immune system changes, including chronic autoantibody production.

Symptoms in AITD are primarily caused by thyroid autoantibodies and lymphocytic infiltration (clusters of lymphocytes aggregating in tissue, causing inflammation and cell destruction). Thyroid autoantibodies exert their effects on either thyroid cells or the TSH cell receptor where they may block or stimulate thyroid hormone production. Symptoms are also caused by an infiltration of specialized white blood cells, primarily lymphocytes and macrophage. Chemicals known as cytokines that are released by T lymphocytes during the autoimmune process also contribute to symptoms.

Although AITDs are basically caused by a hyperactive or hypervigilant immune system (due to changes in B lymphocytes), at the same time the immune system is suppressed. A defect in or diminished amount of the T suppressor (CD8) lymphocyte cells which normally stop the immune system cells from producing autoantibodies is also responsible for AITD. This T cell defect is thought to result from a reduced number of suppressor cells or from immune system changes such as anergy or apoptosis which alter these cells.

Other suppressor cells known as natural killer (NK) cells are also reduced in quantity in Graves disease, and this also contributes to the production of thyroid autoantibodies. Like suppressor T lymphocytes, NK cells normally destroy autoreactive (reacting against slef-tissue) cells.

The various autoimmune thyroid disorders may occur in the same patient at different times during their lifetime. It's not uncommon for patients with HT to later develop GD, and most patients with GD exhibit symptoms of hypothyroidism before their diagnosis. What symptoms predominate is a direct effect of the predominant type of predominant autoantibody in one's blood. Many of the immune system changes and symptoms of AITD also tend to overlap.