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Key Clinical Updates in Hyperthyroidism (Thyrotoxicosis)
The medication digoxin is a second-line agent for ventricular rate control in thyrotoxicosis-induced atrial fibrillation. It is reduced as hyperthyroidism is corrected. Serum digoxin levels should be kept below 1.2 ng/mL, since higher levels are associated with increased mortality.
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ESSENTIALS OF DIAGNOSIS
Sweating, weight loss or gain, anxiety, palpitations, loose stools, heat intolerance, menstrual irregularity.
Tachycardia; warm, moist skin; stare; tremor.
Graves disease: most common cause of hyperthyroidism; palpable goiter (sometimes with bruit) in most patients; ophthalmopathy also common.
Amiodarone: most common cause of thyrotoxic crisis (“thyroid storm”).
Suppressed TSH in primary hyperthyroidism; usually increased T4, FT4, T3, FT3.
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GENERAL CONSIDERATIONS
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The term “thyrotoxicosis” refers to the clinical manifestations associated with elevated serum levels of T4 or T3 that are excessive for the individual (hyperthyroidism).
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Graves disease is the most common cause of thyrotoxicosis. It is an autoimmune disorder, characterized by an increase in synthesis and release of thyroid hormones. Autoantibodies, known as thyroid-stimulating immunoglobulins (TSI) or thyrotropin receptor antibodies (TRAb), bind to the TSH receptors in the thyroid cell membranes and stimulate the gland to overproduce thyroid hormones. The presence of these antibodies distinguishes Graves disease from autoimmune chronic lymphocytic (Hashimoto) thyroiditis. Both conditions usually have present serum antithyroid antibodies (TPO Ab or Tg Ab or both).
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Graves disease is more common in women than in men (8:1). Its usual onset is between the ages of 20 and 40 years. It may be accompanied by infiltrative ophthalmopathy (Graves exophthalmos) and, less commonly, by infiltrative dermopathy (pretibial myxedema eFigure 28–5). The thymus gland is typically enlarged and serum ANA levels are usually elevated. Many patients with Graves disease have a family history of either Graves disease or Hashimoto autoimmune thyroiditis. Histocompatibility studies have shown an association with group HLA-B8 and HLA-DR3.
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Viral infections, including infections with SARS-CoV-2, have been reported to precipitate Graves disease. Vaccinations against SARS-CoV-2 also have triggered de novo Graves disease as well as relapses 4–30 days after infection or vaccination.
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Patients with Graves disease have an increased risk of other systemic autoimmune disorders, including Sjögren syndrome, celiac disease, pernicious anemia, Addison disease, alopecia areata, vitiligo, type 1 diabetes mellitus, hypoparathyroidism, myasthenia gravis, and cardiomyopathy.
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B. Toxic Multinodular Goiter and Thyroid Nodules
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Autonomous hyperfunctioning thyroid nodules that produce hyperthyroidism are known as toxic multinodular goiter (Plummer disease). They are more prevalent among older adults and in iodine-deficient regions. A single hyperfunctioning nodule can also produce hyperthyroidism. Activating TSH receptor mutations are responsible for some toxic nodules. Toxic multinodular goiter and Graves disease may sometimes ...