Thyrotoxicosis is a clinical state of inappropriately high levels of circulating thyroid hormones (T3 and/or T4) in the body from any cause. It is often incorrectly used interchangeably with hyperthyroidism, which is a form of thyrotoxicosis caused by excessive endogenous thyroid hormone production.

The clinical presentation varies, ranging from asymptomatic or subclinical, to life-threatening thyroid storm. Typical symptoms are due to the hypermetabolic state induced by excess thyroid hormones and include weight loss, heat intolerance, and palpitations. The differential for thyrotoxicosis is broad and will need a combination of a thorough physical exam, laboratory studies, and imaging to determine the underlying etiology for appropriate treatment. If not adequately treated, thyrotoxicosis can lead to serious complications including delirium, altered mental status, osteoporosis, muscle weakness, atrial fibrillation, congestive heart failure (CHF), thromboembolic disease, cardiovascular collapse, and death.

Thyrotoxicosis results from thyroid hormone excess either from endogenous over-secretion of T3 and T4 or from exogenous ingestion of synthetic thyroid hormone. Thyroid hormone affects almost every tissue and organ system in the body by increasing basal metabolic rate and tissue thermogenesis by upregulating alpha-adrenergic receptors leading to an increase in sympathetic activity. Thyroid hormone causes increased expression of myocardial sarcoplasmic reticulum calcium-dependent ATP, increasing heart rate and myocardial contractility with the net effect of increased cardiac output. Decreased systemic vascular resistance (SVR) and decreased afterload results from arterial smooth muscle relaxation by metabolic end products, such as lactic acid, produced with increased consumption of oxygen. Decreased SVR leads to activation of the renin-angiotensin system, increasing reabsorption of sodium and expanding blood volume to increase preload. If left untreated, this may lead to left ventricular hypertrophy and congestive heart failure.

Graves’ disease is an autoimmune disease comprised of antibodies that stimulate TSH receptors to cause excess secretion of thyroid hormones via a type II hypersensitivity reaction. This results in hyperplasia of thyroid follicular cells causing a diffuse goiter. The cause of Graves’ disease is not known, but genetic and environmental factors, such as smoking, stress, and dietary iodine play a role. The thyroid-stimulating immunoglobulin (TSI) triggers the hyperthyroidism.

In toxic multinodular goiter and toxic adenoma, autonomously functioning nodules over-secrete thyroid hormone independently without stimulation from TSH. Rarely, these Nnontoxic adenomas or goiter can convert to toxic adenomas after exposure to iodinated contrast, such as from a cardiac catheterization or undergoing a CT study with contrast.

In thyroiditis, thyrotoxicosis is caused by the release of preformed thyroid hormone into the circulation as inflammation destroys thyroid follicles. This causes transient thyrotoxicosis that most often self-resolves. Inflammation can be precipitated by a variety of insults to the thyroid gland, including autoimmune, infectious, chemical, or mechanical insults.

Gestational hyperthyroidism generally occurs in the first trimester of pregnancy, due to increased stimulation of the thyroid gland by excess human chorionic gonadotropin (HCG), which is similar in structure to TSH and binds the TSH receptor.

Reference:
Blick C, Nguyen M, Jialal I. Thyrotoxicosis. [Updated 2020 Dec 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: [ Ссылка ]
Kopp P. Thyrotoxicosis of other Etiologies. [Updated 2010 Dec 1]. In: Feingold KR, Anawalt B, Boyce A, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: [ Ссылка ]
Doubleday AR, Sippel RS. Hyperthyroidism. Gland Surg. 2020;9(1):124-135. doi:10.21037/gs.2019.11.01
Pearce EN. Diagnosis and management of thyrotoxicosis. BMJ. 2006;332(7554):1369-1373. doi:10.1136/bmj.332.7554.1369

Image credit: Kjpargeter / Freepik @ [ Ссылка ]
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Iwen KA, Oelkrug R, Brabant G. Effects of thyroid hormones on thermogenesis and energy partitioning. J Mol Endocrinol. 2018 Apr;60(3):R157-R170. doi: 10.1530/JME-17-0319. Epub 2018 Feb 6. PMID: 29434028.


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