The sensitive equilibrium of the thyroid hormone loop can be disturbed due to the presence of different autoantibodies. Autoimmune thyroid diseases are characterised by antibodies against thyroid microsomes, whose main target antigen is thyroperoxidase (TPO), and antibodies against thyroglobulin (TG) or the receptor of thyrotropin (also known as thyroid stimulating hormone (TSH). The most frequent autoimmune thyroid diseases are Hashimoto’s autoimmune thyroiditis (AIT) and immunohyperthyroidism, also known as Graves’ disease. While AIT can manifest as a thyroid overfunction (hyperthyroidism) or underfunction (hypothyroidism), Graves’ disease is always associated with hyperthyroidism.
Hashimoto’s thyroiditis leads to autoimmune-mediated lymphocytic infiltration and consequently to a destruction of the thyroid tissue, in the long term often resulting in reduced thyroid hormone production.
A special form of autoimmune thyroiditis is post-partum thyroiditis, a temporary hypothyroid functional disorder of the thyroid accompanied by high titers of anti-TPO antibodies. The disease affects around 5 to 9% of women after giving birth, and the risk is especially high in diabetes mellitus patients.
The permanent stimulation of TSH receptors by binding of autoantibodies is one of the most relevant factors for the pathogenesis of Graves’ disease. The permanent binding activates signal cascades leading to an increased uptake of iodine by the thyroid. As a consequence, the thyroid hormones triiodothyronine (T3) and thyroxine (T4) are produced and secreted in larger quantities.