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Hyperthyroidism: Diagnosis and Treatment IGOR KRAVETS, MD, Stony Brook University School of Medicine, Stony Brook, New York

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Hyperthyroidism: Diagnosis and Treatment IGOR KRAVETS, MD, Stony Brook University School of Medicine, Stony Brook, New York Hyperthyroidism: Diagnosis and Treatment IGOR KRAVETS, MD, Stony Brook University School of Medicine, Stony Brook, New York Hyperthyroidism is an excessive concentration of thyroid hormones in tissues caused by increased synthesis of thyroid hormones, exces- sive release of preformed thyroid hormones, or an endogenous or exogenous extrathyroidal source. The most common causes of an excessive production of thyroid hormones are Graves disease, toxic multinodular goiter, and toxic adenoma. The most common cause of an excessive passive release of thyroid hormones is painless (silent) thyroiditis, although its clinical presentation is the same as with other causes. Hyperthyroidism caused by overproduction of thyroid hor- mones can be treated with antithyroid medications (methimazole and propylthiouracil), radioactive iodine ablation of the thyroid gland, or surgical thyroidectomy. Radioactive iodine ablation is the most widely used treatment in the United States. The choice of treatment depends on the underlying diagnosis, the presence of contraindications to a particular treatment modality, the severity of hyperthyroidism, and the patient’s preference. (Am Fam Physician. 2016;93(5):363-370. Copyright © 2016 American Academy of Family Physicians.) ILLUSTRATION TODD BY BUCK More online yperthyroidism is an excessive cells that leads to a somatic activating muta- at http://www. concentration of thyroid hor- tion of TSH receptors.4 A single nodule is aafp.org/afp. mones in tissues causing a char- called a toxic adenoma (Plummer disease). CME This clinical content acteristic clinical state. In the In contrast with these three disorders, conforms to AAFP criteria HUnited States, the overall prevalence of hyper- painless or transient (silent) thyroiditis for continuing medical education (CME). See thyroidism is 1.2%, and the prevalences of causes a destruction of thyroid follicles via CME Quiz Questions on overt hyperthyroidism and subclinical hyper- an autoimmune mechanism and a release of page 351. thyroidism are 0.5% and 0.7%, respectively.1 preformed thyroid hormones into the circu- Author disclosure: No rel- lation.5 Its clinical presentation is the same evant financial affiliations. Etiology and Pathogenesis as with other causes. In a Danish study, its ▲ Patient information: The common endogenous causes of hyper- prevalence among patients with thyrotoxi- A handout on this topic, thyroidism are Graves disease, toxic multi- cosis was 0.5%, as evaluated by scintigra- written by the author of nodular goiter, toxic adenoma, and painless phy.6 Painless thyroiditis can be triggered this article, is available 1-9 at http://www.aafp.org/ thyroiditis (Table 1). Graves disease, the by childbirth (postpartum thyroiditis) or afp/2016/0301/p363-s1. most common cause of hyperthyroidism in by use of medications such as lithium, inter- html. the United States,2 is an autoimmune disor- feron alfa, interleukin-2, and amiodarone.7 der in which thyroid-stimulating antibodies Gestational hyperthyroidism develops in activate thyroid-stimulating hormone (TSH) the first trimester of pregnancy as a result receptors, triggering thyroid hormone syn- of the stimulatory action of placental beta thesis. Risk factors for Graves disease include human chorionic gonadotropin (β-hCG), female sex and personal or family history of which shares structural features with TSH, an autoimmune disorder.2,3 on the thyroid gland.8 β-hCG-mediated Toxic multinodular goiter is the second hyperthyroidism can occasionally be caused most common cause of hyperthyroidism by hyperemesis gravidarum and, rarely, by a in the United States and the most common gestational trophoblastic tumor.8 cause in older persons living in iodine- Other rare causes of hyperthyroidism are deficient areas.2 Over time, nodules arise TSH-secreting pituitary adenoma, metastatic from the frequent replication of clonogenic follicular thyroid cancer, and struma ovarii.9 MarchDownloaded 1, 2016 from ◆ theVolume American 93, FamilyNumber Physician 5 website at www.aafp.org/afp.www.aafp.org/afp Copyright © 2016 American Academy of FamilyAmerican Physicians. Family For the Physician private, noncom 363- mercial use of one individual user of the website. All other rights reserved. Contact [email protected] for copyright questions and/or permission requests. Hyperthyroidism SORT: KEY RECOMMENDATIONS FOR PRACTICE Evidence Clinical recommendation rating References The choice of treatment modality for hyperthyroidism caused by overproduction of thyroid hormones depends C 25, 26 on the patient’s age, symptoms, comorbidities, and preference. The diagnostic workup for hyperthyroidism includes measuring thyroid-stimulating hormone, free thyroxine C 20, 21 (T4), and total triiodothyronine (T3) levels to determine the presence and severity of the condition, as well as radioactive iodine uptake and scan of the thyroid gland to determine the cause. Methimazole (Tapazole) is the preferred antithyroid medication except in the first trimester of pregnancy and B 26 in patients with an adverse reaction to the medication. A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to http://www.aafp.org/afpsort. Clinical Manifestations Table 1. Etiology and Pathogenesis of Hyperthyroidism The clinical presentation of hyperthyroid- ism ranges from asymptomatic to thyroid Etiology Mechanism storm (Table 2).10-18 Elevated thyroid hor- Most common causes mone levels amplify catecholamine signaling Graves disease Autoimmune process in which antibodies through increased numbers of cell surface stimulate the TSH receptor leading to beta-adrenergic receptors. The resulting overproduction of thyroid hormones adrenergic symptoms (e.g., palpitations, heat Painless or transient Autoimmune destruction of thyroid tissue leading (silent) thyroiditis to a release of preformed thyroid hormones intolerance, diaphoresis, tremor, stare [an Toxic adenoma (Plummer Somatic mutation in TSH receptor or Gs alpha appearance of a fixed look due to retraction disease) gene in a thyroid nodule of eyelids], lid lag, hyperdefecation) are the Toxic multinodular goiter Expansion of clonogenic cells with an activating most common manifestations of hyperthy- TSH receptor mutation roidism.10 Hypermetabolism induces weight Less common causes loss despite an increased appetite. Neu- Drug-induced thyroiditis Overproduction of thyroid hormones (amiodarone-induced thyrotoxicosis type 1) romuscular symptoms include weakness or release of preformed thyroid hormones of proximal muscles.11 Psychiatric symp- (amiodarone-induced thyrotoxicosis type 2, toms range from anxiety to frank psycho- interferon alfa, interleukin-2, or lithium) sis.12 Patients with long-standing untreated Hyperemesis gravidarum High level of β-hCG stimulates TSH receptors hyperthyroidism may develop atrial fibril- Postpartum thyroiditis Variant of painless thyroiditis with the same 13,14 mechanism, occurring after delivery lation (10% to 15% of patients ) or heart 15 Subacute granulomatous Painful inflammation of the thyroid gland caused failure (5.8% of patients ). (de Quervain) thyroiditis by viral infection, often with fever, triggering a Signs that are pathognomonic for Graves release of preformed thyroid hormones disease include orbitopathy, pretibial myx- Rare causes edema (thyroid dermopathy), and thyroid Factitious thyrotoxicosis Surreptitious ingestion of thyroid hormones acropachy, which occur in 25%, 1.5%, and Metastatic follicular Metastasis of functional follicular thyroid cancer 16 thyroid cancer 0.3% of patients, respectively. Goiters that Struma ovarii Ectopic thyroid tissue in ovarian dermoid tumor develop in Graves disease are usually smooth produces thyroid hormones and may have a thrill on palpation or a bruit Trophoblastic tumor or Tumor produces β-hCG, which stimulates thyroid on auscultation. Single or multiple nod- a germ cell tumor TSH receptors ules on palpation raise suspicion for a toxic TSH-secreting pituitary Tumor secreting large quantities of TSH, and not adenoma or a toxic multinodular goiter, adenoma responding to thyroxine and triiodothyronine feedback although nonfunctioning thyroid nodules may coexist with a goiter in Graves disease.16 β-hCG = beta human chorionic gonadotropin; TSH = thyroid-stimulating hormone. Graves orbitopathy manifests as exoph- Information from references 1 through 9. thalmos or periorbital edema, and it can trigger photophobia, excessive lacrimation, 364 American Family Physician www.aafp.org/afp Volume 93, Number 5 ◆ March 1, 2016 Hyperthyroidism 1 increased eye sensitivity to wind or smoke, or a sen- (T3) levels (free T3 assays are poorly validated ) if the sation of a foreign body in the eyes. In severe cases, TSH level is low. Others prefer to order all three tests blurred vision, diplopia, or reduced color perception if hyperthyroidism is suspected to make the diagnosis 16 may develop. Smoking increases the risk of developing more efficiently. Many laboratories perform reflex free4 T Graves orbitopathy (odds ratio = 3.7).17 testing if TSH is suppressed. Table 3 lists patterns of thy- Pretibial myxedema, a less common finding, develops roid function tests in hyperthyroidism.20,21 The serum from fibroblast activation and manifests as swelling over level of thyroid-stimulating immunoglobulins or TSH- the tibiae with the skin assuming
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