Páginas: 28 (6812 palabras) Publicado: 24 de octubre de 2010
Emerg Med Clin N Am 23 (2005) 669–685

Nathanael J. McKeown, DOa, Matthew C. Tews, DOa, Ved V. Gossain, MD, FACP, FACEPb, Sid M. Shah, MD, FACEPc,*
College of Osteopathic Medicine, Emergency Medicine Residency Program, Michigan State University, PO Box 30480, Lansing, MI 48909, USA b Division of Endocrinology, Department of Medicine, B234 Clinical Center, 138 Service Road,Michigan State University, Lansing, MI 48824, USA c Michigan State University, Emergency Medicine, Ingham Regional Medical Center, 401 West Greenlawn, Lansing, MI 48910, USA

Hyperthyroidism is a hypermetabolic state that results from excess synthesis and release of thyroid hormone from the thyroid gland. Thyrotoxicosis is a general term referring to all causes of excess thyroid hormone in thebody, including exogenous intake of thyroid hormone preparations. Although the terms hyperthyroidism and thyrotoxicosis are by definition not the same, they often are used interchangeably [1]. The clinical spectrum of hyperthyroidism varies from asymptomatic, subclinical hyperthyroidism to the life-threatening thyroid storm. Subclinical hyperthyroidism is diagnosed in asymptomatic patients on thebasis of abnormal laboratory tests (low thyrotropin [TSH] but normal free T4 and free T3), and is probably more common than generally believed. Overt clinical hyperthyroidism presents with typical signs and symptoms. Thyroid storm is the severe life-threatening form of hyperthyroidism. It usually is brought about by a precipitating event in patients with undiagnosed or undertreated hyperthyroidism.Epidemiology and pathophysiology The overall incidence of subclinical and overt hyperthyroidism has been estimated to be 0.05 to 0.1% in the general population [2]. It occurs at all ages, but it is more common in women than in men. In a recent US study

* Corresponding author. E-mail address: sidshah@comcast.net (S.M. Shah). 0733-8627/05/$ - see front matter Ó 2005 Elsevier Inc. All rightsreserved. doi:10.1016/j.emc.2005.03.002 emed.theclinics.com



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(National Health and Nutrition Examination Survey III), the prevalence of hyperthyroidism was found to be 1.2% (0.5% clinical and 0.7% subclinical) in a sample of randomly selected people [3]. Of those who have hyperthyroidism, only 1% to 2% will progress to thyroid storm [4]. Overall, Graves’ disease is themost common cause of spontaneously occurring thyrotoxicosis, except in the elderly, where toxic nodular goiter is more common than Graves’ disease [5]. Thyroid function is controlled by a negative feedback loop that is regulated by circulating TSH and thyroid hormones (T4 and T3). Thyroid gland mainly produces T4 and a smaller amount of T3. Most T3 (80%) is formed in the periphery by conversion ofT4 to T3 [6]. T3 is approximately three to four times more biologically active compared with T4. Excess T3 triggers a sequence of molecular events that cause the tissue responses seen in hyperthyroidism such as excessive energy and heat production and deleterious effects on the central nervous system and cardiac function. Etiologies The most common cause of hyperthyroidism in the developedcountries, Graves’ disease is an autoimmune disease in which antibodies against TSH receptors develop. The result is unopposed stimulation of the thyroid gland causing increased synthesis and release of thyroid hormone and enlargement of the thyroid gland. Laboratory abnormalities include high serum thyroid hormone levels and a high radioiodine uptake by the thyroid gland. Graves’ disease is more commonin areas of high iodine intake, such as the United States, and generally presents between 30 to 40 years of age [6,7]. There is also a genetic component leading to an increased risk of developing the disease in those with a family history of hyperthyroidism or in those with an autoimmune disease such as type 1 diabetes mellitus [6]. Other triggers include stressful events, sex steroids, smoking,...
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