Pathogenic autoantibodies to the TSHR disturb normal hypothalamus-pituitary-thyroid regulation of thyroid function [8-10] (Fig. 14.1). GD is characterized by hyperthyroidism, which often leads to tachycardia, anxiety, excessive sweating, and acute weight loss. On the other hand, autoimmune PM is characterized by hypothyroidism that can lead to physical and mental lethargy, bradycardia, and weight gain. Pathogenic antibodies (TSAbs) from patients with GD bind to TSHR and stimulate thyroid, but in PM, pathogenic antibodies (TSBAbs) block either the binding of TSH or TSH-mediated activation of thyroid cells. Unlike in HT, the primary cause of thyroid dysfunction in GD and PM is not due to glandular destruction but rather to physiological perturbation of thyroid function mediated by anti-TSHR antibodies. The important question is how one develops pathogenic antibodies against the thyroid. Since self-tolerance prevents development of autoimmune responses, breakdown in self-tolerance must precede the generation of autoantibodies.
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