Definition of the Disease

Thyroid Factor

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Hyperthyroidism and thyrotoxicosis are synonymous terms. Excess thyroid hormone elevates the basal metabolic rate (e.g., causing weight loss) and causes the classic findings exhibited in this patient involving the nervous system (e.g., personality changes, tremor, hyperreflexia), cardiovascular system (tachycardia with a hyperdynamic heart, bounding pulses and wide pulse pressure), and gastrointestinal tract (e.g., loose stools or diarrhea). In extreme cases, high output heart failure can result. Many other systems can be affected such as the tissues of the retroorbital space, the skin, the hair, and the reproductive system. The patient's oligomenorrhea is likely a consequence of her disordered metabolism, the stress of illness and weight loss.

Goiter with hyperthyroidism, exophthalmos, and pretibial myxedema are the pathognomonic triad of Graves disease. Graves disease is a classic organ-specific autoimmune disease where there is a humoral autoimmune response to the TSH receptor. In Graves disease goiter [i.e., hyperplasia of the thyroid with palpable (and often visible) gland enlargement] and hyperthyroidism (i.e., hyperfunction of the thyroid) result from IgG autoantibodies that bind to and stimulate the TSH receptor. Such agonist autoantibodies [i.e., thyroid-stimulating immunoglobulins (TSIs)] can be identified in 80-100% of subjects with Graves disease. In contrast, TSIs are detected in 0-10% of control populations and up to 20% of subjects with Hashimoto thyroiditis.

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