Hyperthyroidism can result from genetic and immunologic factors. In Graves’ disease, thyroid–stimulating antibodies bind to and then stimulate the TSH receptors of the thyroid gland. The trigger for this autoimmune disease is unclear. Increased incidence in monozygotic twins suggests an inherited factor, probably a polygenic inheritance pattern. Graves’ disease occasionally coexists with abnormal iodine metabolism and other endocrine abnormalities, such as diabetes mellitus, thyroiditis, and hyperparathyroidism. It’s also associated with production of autoantibodies
(long–acting thyroid stimulator [LATS], LATS–protector, and human thyroid adenylate cyclase stimulators), possibly caused by a defect in suppressor–T–lymphocyte function that allows the formation of these autoantibodies.

In a patient with latent hyperthyroidism, excessive intake of iodine and, possibly, stress can induce clinical hyperthyroidism. Also, in a patient with inadequately treated hyperthyroidism, stressful conditions (such as surgery, infection, toxemia of pregnancy, and diabetic ketoacidosis) can precipitate thyrotoxic crisis.

Because thyroid hormones have widespread effects on almost all body tissues, the complications of hypersecretion may be far–reaching and varied. Cardiovascular complications are most common in elderly patients and include arrhythmias, especially atrial fibrillation; cardiac insufficiency;
cardiac decompensation; and resistance to the usual therapeutic dose of cardiac glycosides. Additional complications include muscle weakness and atrophy; paralysis; osteoporosis; vitiligo and skin hyperpigmentation; corneal ulcers; myasthenia gravis; impaired fertility; decreased libido; and gynecomastia.