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Hypothyroidism: Mimicker of Common Complaints Matthew C Emerg Med Clin N Am 23 (2005) 649–667 Hypothyroidism: Mimicker of Common Complaints Matthew C. Tews, DOa, Sid M. Shah, MD, FACEPb,*, Ved V. Gossain, MD, FACP, FACEPc aCollege of Osteopathic Medicine, Emergency Medicine Residency Program, Michigan State University–Lansing, P.O. Box 30480, Lansing, MI 48909, USA bMichigan State University, Attending Physician Emergency Medicine, Ingham Regional Medical, Center 401 W. Greenlawn Avenue, Lansing, MI 48910, USA cDivision of Endocrinology, Department of Medicine, Michigan State University, Lansing, MI 48909, USA Patients with hypothyroidism may present with vague symptoms such as fatigue, arthralgias, myalgias, muscle cramps, headaches, and ‘‘not feeling well.’’ These are also among the more common complaints encountered by the emergency physicians. The disease spectrum of hypothyroidism ranges from an asymptomatic, subclinical condition to the rare, life-threatening myxedema coma, and thus can be a challenging diagnosis to make. A progressive and chronic disease, hypothyroidism results from diminished thyroid hormone production. It slows metabolic functions in every organ system in the body. Commonly, clinical presentation of hypothyroidism can be confused with effects of aging in the elderly, musculoskeletal or a psychiatric illness such as depression in the younger patients. Spontaneously occurring hypothyroidism is relatively common, with prevalence between 1% to 2%, and is 10 times more common in women than in men [1]. The probability of developing spontaneous hypothyroidism increases with age, with women having a mean age at diagnosis of around 60 years [2]. A recent survey showed that 9.5% out of nearly 26,000 visitors to a statewide health fair in Colorado had elevated circulating thyroid stimulating hormone (TSH) levels, indicating underlying hypothyroidism [3]. One large study performed in England found the prevalence of hypothyroidism to be around 18/1000 women and less than 1/1000 men in the general population studied [4]. The study also revealed a higher * Corresponding author. E-mail address: [email protected] (S.M. Shah). 0733-8627/05/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.emc.2005.03.013 emed.theclinics.com 650 TEWS et al prevalence of subclinical hypothyroidism, defined as an asymptomatic elevation of TSH, found in roughly 8% of women and 3% of men. In a 20-year follow-up to this original study, the authors found the mean incidence from all causes of hypothyroidism to be 4.1/1000 of women and 0.6/1000 of men in survivors [5]. Thyroid disorders pose a particular challenge to emergency physicians because a significant number of patients with thyroid dysfunction are unaware of their condition. A well-known endocrinologist estimates that almost half the people with thyroid dysfunction are not properly diagnosed [6]. Because of this, the American Thyroid Association has recommended measuring serum TSH concentrations in adults starting at age 35 and continuing every 5 years, or more often in those at risk for thyroid dysfunction [7]. Pathophysiology The production and release of thyroid hormone is the result of a delicate balance of the hypothalamic–pituitary–thyroid axis, which is controlled by a negative feedback loop involving circulating free thyroxine (T4) and triiodothyronine (T3), and TSH release from the thyroid gland. This delicate balance can be altered by causes such as the destruction or removal of the thyroid gland, alterations in the synthesis, release, and conversion of thyroid hormone (secondary to disease or medications), and diseases of the pituitary gland. The substrate for the synthesis of thyroid hormones is the circulating iodides. The thyroid gland is able to ‘‘trap’’ iodide from the blood stream by an energy requiring mechanism. The trapped iodide is oxidized by the enzyme Peroxidase. The next step in the synthesis of triiodothyronine (T3) and tetraiodothyronine (T4) is iodination of tyrosine to monoiodotyrosine (MIT) and diiodotyrosine (DIT). Coupling of two DIT molecules results in the formation of T4. Some T3 is also formed within the thyroid gland by condensation of one molecule of MIT and DIT. The formed T4 and T3 are stored in the thyroid gland in combination with thyroglobulin. Release of T4 and T3 then occurs by proteolysis and is regulated by TSH. After its release from the thyroid gland, T4 is bound almost exclusively to proteins in the blood including thyroid-binding globulin (TBG), trans- thyretin (prealbumin), and albumin for transportation to target tissues [8]. Over 99% of T4 is bound to these proteins, leaving !1% free in circulation. It is this small amount of free hormone that is responsible for the negative feedback inhibition on the anterior pituitary and hypothalamus controlling the release of TSH. Even small changes in free hormone levels are reflected in exaggerated changes in TSH secretion; making serum TSH a sensitive marker of thyroid function [9]. Although most of the thyroid hormone released from the thyroid gland is in the form of T4, only about 20% of T3 is released from thyroid, while the other 80% of T3 is formed by deiodination of T4 in peripheral tissues such HYPOTHYROIDISM: MIMICKER OF COMMON COMPLAINTS 651 as the pituitary, liver, kidneys, and hypothalamus [9]. It is T3, however, that has greater biologic activity than T4 at the cellular level. Etiology Hypothyroidism is broadly classified either as primary or central hypothyroidism. Ninety-nine percent of cases are primary hypothyroidism, typically resulting from destruction of the gland from either iatrogenic or autoimmune causes [10]. Depending on the cause, patients with hypothy- roidism can present with or without a goiter. Central hypothyroidism is divided into pituitary (secondary) or hypothalamic (tertiary) causes, depending on the underlying etiology. Central causes of hypothyroidism make up a very small percentage of hypothyroid cases, with prevalence in the general population of about 0.005% [2]. Congenital hypothyroidism has a prevalence of about 1 in 4000 newborns worldwide. Eighty-five percent of cases of congenital hypothyroidism are due to thyroid dysgenesis, and the remainder are due to central causes [11]. Table 1 lists the causes of hypothyroidism, and the most common causes are discussed here. Causes of primary hypothyroidism The most common form of hypothyroidism worldwide is iodine deficiency typically associated with endemic goiter [12]. In iodine-replete Table 1 Causes of hypothyroidism Primary hypothyroidism Chronic autoimmune thyroiditis Reversible autoimmune thyroiditis (silent and postpartum) Radioiodine ablation Surgery Irradiation Infiltrative and infectious diseases Congenital thyroid dysgenesis Iodine excess or deficiency Drugs Central hypothyroidism Tumors Trauma Vascular Infectious Infiltrative Congenital Drugs Data from Wiersinga WM. Hypothyroidism and myxedema coma. In: DeGroot LJ, Jameson JL, editors. Endocrinology. 4th edition, volume 2. Philadelphia: W.B. Saunders Company; 2001. p. 1493. 652 TEWS et al regions, such as the United States, chronic autoimmune disease involving the thyroid gland forms the majority of cases of hypothyroidism. Autoimmune thyroiditis Hashimoto’s thyroiditis is the most common form of thyroiditis, making this the number one cause of primary hypothyroidism in the developed countries with adequate iodine intake. Hashimoto’s thyroiditis is charac- terized by chronic lymphocytic infiltration and destruction of the thyroid gland over time. It is associated with the presence of antithyroid antibodies. Antithyroid peroxidase (TPO) antibodies are present in more than 90% of cases of chronic autoimmune thyroiditis [13,14]. Hashimoto’s thyroiditis is also associated with other autoimmune diseases, and specific association with certain histocompatibility antigens (HLA DR3 and HLA DR5) has also been described [14]. Postpartum thyroiditis is a variant of autoimmune thyroiditis with an incidence of 6.0% to 8.8% in the postpartum period. It typically presents as transient hyperthyroidism, usually between 6 weeks to 6 months postpartum [15]. This period is typically followed by a ‘‘hypothyroid phase,’’ which resolves spontaneously in the majority of the cases approximately 1 year postpartum. However, permanent hypothyroidism can develop in up to 23%. It may recur in subsequent pregnancies. Subacute thyroiditis, thought to be due to an autoimmune viral infection, results in an enlarged, painful, and tender thyroid gland. Patients initially present with hyperthyroidism due to release of preformed hormone, after which there is a brief period of hypothyroidism. The patient typically recovers in a few weeks; although recurrences may occur [16]. Iatrogenic causes Iatrogenic causes of hypothyroidism are common. Surgical procedures, such as total thyroidectomy, may quickly result in hypothyroidism within 1 month after surgery, while hypothyroidism after subtotal resection for Grave’s disease may take up to 10 years to develop [2]. The use of radioiodine (I131) as destructive treatment for thyrotoxicosis frequently causes hypothyroidism. Radioiodine therapy and surgery have an incidence of overt hypothyroidism that is greatest within the first year after treatment [12]. Medications Often overlooked in the emergency department (ED), medications are a well-known cause of hypothyroidism. Those with underlying autoimmune thyroiditis are more sensitive to the effect of commonly prescribed medications such as lithium, amiodarone, and cytokine therapy [9] Table 2 lists the effects of some medications
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