Hyperthyroidism (Nursing)

Learning Outcome

  1. List the causes of hyperthyroidism
  2. Describe the clinical features of hyperthyroidism
  3. Summarize the treatment of hyperthyroidism
  4. Recall the nurse care plans for hyperthyroidism


The thyroid gland is a bilobed structure located in the anterior aspect of the trachea between the cricoid cartilage and the suprasternal notch. Each lobe of the thyroid connects via a thyroid isthmus. It is supplied via the superior thyroid artery, which stems from the external carotid artery, and the inferior thyroid artery, a branch of the thyrocervical trunk.

Histologically, the thyroid gland is surrounded by a thin, connective tissue covering that penetrates the gland and divides the thyroid gland into compartments. The thyroid gland is composed of spherical, polarized follicular cells that surround a gel-like thyroglobulin-rich colloid. Thyroglobulin is the organic precursor for thyroid hormones and requires iodide to form thyroid hormone. Dietary iodine is transported into thyroid follicular cells via the sodium-iodide symporter after conversion to iodide via the thyroid peroxidase enzyme. The process of iodide becoming incorporated into monoiodotyrosine (MIT) or diiodotyrosine (DIT) molecules is referred to as organification, and the process is relatively self-regulated. Low dietary iodide facilitated upregulation of the sodium-iodide symporter, while high dietary iodide temporarily inhibits the organification process, a phenomenon known as the Wolff-Chaikoff effect.[1] Iodide incorporation into the thyroid hormone precursors, MIT and DIT, is due to the peroxidase enzyme. The organic coupling of one molecule of MIT with one molecule of DIT leads to triiodothyronine (T3) production, while the coupling of 2 DIT molecules leads to thyroxine (T4).

The thyroid gland secretes thyroxine (T4) in response to thyroid-stimulating hormone (TSH) originating from the anterior pituitary gland. The secreted T4 is converted to more potent triiodothyronine (T3) via deiodinase enzymes. Most of the conversion of T4 to T3 occurs outside the thyroid, although the thyroid gland possesses the intrinsic ability for T3 production.

From a physiologic perspective, the hypothalamus releases thyrotropin-releasing hormone (TRH) in response to low circulating thyroid stimulating hormone (TSH), T3, or T4. TRH promotes anterior pituitary secretion of thyroid-stimulating hormone (TSH), which, in turn, promotes T4 secretion from the thyroid gland. T4 and T3 exert negative feedback control on both the hypothalamus and the anterior pituitary.

The term "hyperthyroidism" defines a syndrome associated with excess thyroid hormone production. It is a common misconception that the terms thyrotoxicosis and hyperthyroidism are synonyms of one another. The term "thyrotoxicosis" refers to a state of excess thyroid hormone exposure to tissues. Although hyperthyroidism can lead to thyrotoxicosis and can be used interchangeably, it is important to note the difference between them.

Nursing Diagnosis

  • Fatigue
  • Tremor
  • Sweating
  • Hyperactive
  • Anxious
  • Palpitations
  • Heat intolerance
  • Nervous
  • Diarrhea


In the United States and most western countries, Graves disease is the most common cause of hyperthyroidism. As Graves disease is autoimmune in etiology, this form of hyperthyroidism tends to manifest itself in younger populations. In the older demographic, toxic multinodular goiter is the most common cause of hyperthyroidism.

Although Graves disease and toxic multinodular goiter are the more common causes of hyperthyroidism, other causes of hyperthyroidism include iodine-induced hyperthyroidism (Jod-Basedow phenomenon), thyroid adenomas, de Quervain thyroiditis (subacute thyroiditis), postpartum thyroiditis, and factitious thyroiditis (thyrotoxicosis factitia).

Factitious thyroiditis is hyperthyroidism associated with inappropriate or excessive use of pharmaceutical thyroid hormone. Due to a well-received side effect of weight loss, thyroxine has the potential for abuse, and any history of a hyperthyroid patient should include a medication list and an assessment of possible misuse (whether intentional or unintentional).

Other sources of hyperthyroidism include ectopic foci of thyroxine-secreting tissue. The more prevalent (although rare) form of this etiology is struma ovarii, consisting of ectopic and functional thyroid tissue (often compromising greater than 50% of total mass) in the ovary.

Amiodarone or other iodine-containing medications can induce iodine-associated hyperthyroidism or thyrotoxicosis. This iodine-induced hyperthyroidism is called the Jod-Basedow phenomenon (Jod is the German word for iodine).[2]

Risk Factors

The prevalence of hyperthyroidism is different according to the ethnic group, while in Europe, the frequency is affected by dietary intake of Iodine, and some cases are due to autoimmune disease. Subclinical hyperthyroidism occurs more in women older than 65 than in men, while overt hyperthyroidism rates are 0.4 per 1000 women and 0.1 per 1000 men and vary with age. 

Any analysis of the global epidemiology of hyperthyroidism will delineate along the lines of iodine-sufficient regions and iodine-deficient regions.[3] While iodine excess can lead to hyperthyroidism, iodine deficiency can lead to both hypothyroidism and hyperthyroidism.

Graves disease is typically seen in younger patients and is the most common cause of hyperthyroidism in that demographic. Toxic multifocal goiter is typically seen in older individuals and is the most common cause of hyperthyroidism in this respective demographic. Both Graves disease and toxic multifocal goiter have a female predilection and are typically seen in patients with pertinent family and personal medical histories.

The 1977 Whickham Survey was an evaluation of the spectrum of thyroid disorders in County Durham in northeastern England. Although the demographics of the Whickham Survey consisted of primary inhabitants of a community in northeast England (and hence, poor extrapolation potential), the survey did show interesting results of hyperthyroidism. The Whickham Survey demonstrated a prevalence of hyperthyroidism in women, approximately ten times more than that of men (2.7% versus 0.23%).[4]


Hyperthyroidism may manifest as weight loss despite an increased appetite, palpitation, nervousness, tremors, dyspnea, fatigability, diarrhea or increased GI motility, muscle weakness, heat intolerance, and diaphoresis. The signs and symptoms of thyroid hormone exposure to peripheral tissues reflect a hypermetabolic state. A patient with hyperthyroidism classically presents with signs and symptoms that reflect this state of increased metabolic activity. Common symptoms that a patient may report include unintentional weight loss despite unchanged oral intake, palpitations, diarrhea or increased frequency of bowel movements, heat intolerance, diaphoresis, and/or menstrual irregularities.

Physical examination of the thyroid may or may not reveal an enlarged thyroid (goiter). The thyroid may be diffusely enlarged, or one or more nodules may be palpated. The thyroid may be painless to palpation or extremely tender to even light palpation.[5]


Thyroid-stimulating hormone (TSH) is the initial diagnostic test of choice and is considered the best screening test for assessing the pathology of the thyroid and for the monitoring of thyroid replacement therapy. Due to the negative feedback that T3 and T4 exert on the pituitary gland, elevated T3 and/or elevated T4 will cause decreased TSH production from the anterior pituitary gland. Abnormal TSH is often followed up with a measurement of free T4 and/or free T3.[6] Concerns for an autoimmune process such as Graves disease will warrant further evaluation by assessing serum levels of TSH-receptor antibodies.[7]

TSH levels in the context of acute illness should be interpreted with more discretion as TSH levels are considerably more susceptible to the effects of illness.

Hyperthyroidism is a common etiology for atrial fibrillation; thus, further workup with an ECG may be warranted, especially in a patient complaining of palpitations. Obtaining troponin levels is not routine unless the clinical presentation warrants further cardiac ischemic workup, such as active chest pain.

Radiological diagnostics such as chest x-rays serve little diagnostic utility in managing hyperthyroidism. Diagnostics such as ultrasound are not useful in diagnosing hyperthyroidism, but the ultrasound findings of nodules could potentially determine an etiology.

Since a majority of cases of hyperthyroidism are due to Graves disease or toxic multinodular goiter, confirmation of the diagnosis can be made based on history, clinical findings, and palpating of the thyroid. In cases of diffuse goiter or no thyroid enlargement, a 24-hour radioactive iodine uptake (RAIU) is needed to distinguish between Graves disease and other hyperthyroidism etiologies. Radioactive iodine uptake is the percentage of iodine-131 retained by the thyroid after 24 hours. For the typical western diet, the normal range of RAIU is typically 10% to 30%.

Graves disease, toxic multinodular goiter, and thyroid adenoma are etiologies of hyperthyroidism with increased RAIU, reflecting an increased synthesis of thyroid hormone. Subacute thyroiditis, painless thyroiditis, iodine-induced hyperthyroidism, and factitious hyperthyroidism have decreased RAIU. Thyroiditis represents a disruption of the thyroid follicles with the subsequent release of thyroid hormone. Since there is no increased thyroid hormone synthesis, RAIU will be low in thyroiditis.[8]

If RAIU is not available or is contraindicated, then measurement of thyroid receptor antibodies can be used as an alternative test for diagnosis of Graves disease.[9]

A radioisotope thyroid scan is a diagnostic tool that utilizes technetium-99m pertechnetate as a radioactive tracer. The technetium-99m pertechnetate is taken up by the thyroid gland by the sodium-iodide symporter. The scan itself assesses the functional activity of thyroid nodules, classifying them as either "cold" (hypofunctioning), "warm" (isofunctioning), or "hot" (hyperfunctioning). "Cold" nodules raise concern for potential malignancy due to ineffective uptake of iodide and synthesis of thyroid hormone typically seen in thyroid carcinomas.

Medical Management

Treatment of hyperthyroidism depends on the underlying etiology and can be divided into two categories: symptomatic therapy and definitive therapy. The symptoms of hyperthyroidism, such as palpitations, anxiety, and tremor, can be controlled with a beta-adrenergic antagonist such as atenolol. Calcium channel blockers, such as verapamil, can be used as second-line therapy for patients who are beta-blocker intolerant or have contraindications to beta-blocker therapy.[10]

Transient forms of hyperthyroidism, such as subacute thyroiditis or postpartum thyroiditis, should be managed with symptomatic therapy alone, as hyperthyroidism in these clinical situations tends to be self-limiting.

Three definitive treatments of hyperthyroidism predispose the patient to potential long-term hypothyroidism: radioactive iodine therapy (RAI), thionamide therapy, and subtotal thyroidectomy. Clinical assessment and monitoring of free T4 are imperative for patients who undergo any of these treatments. TSH-monitoring status after definitive therapy is of poor utility since TSH remains suppressed until the patient becomes euthyroid. Thus, TSH monitoring for thyroid status is not recommended immediately following definitive therapy.

The choice of which definitive treatment modality depends on the etiology. Due to its high efficacy, RAI therapy is considered the treatment of choice in almost all patients with Graves disease. Despite the relative safety and high efficacy, RAI is contraindicated in patients who are pregnant or patients who are breastfeeding.

In RAI therapy, radioactive iodine-131 is administered with subsequent destruction of thyroid tissue. A single dose is sufficient to control hyperthyroidism in a significant portion of patients, and the effects on other parts of the human body are essentially negligible due to the high thyroid uptake of the radioactive iodine-131. In a female patient of reproductive potential, it is highly recommended to obtain a beta-hCG to rule out pregnancy prior to initiation of RAI therapy. Patients on a thionamide (methimazole or propylthiouracil) should be instructed to discontinue this therapy approximately one week before RAI therapy since thionamide administration can interfere with the therapeutic benefit of RAI therapy. Several months are typically needed status post-RAI therapy to achieve euthyroid status. Typically, patients are evaluated in 4 to 6-week intervals with increased time intervals for stable, plasma-free T4 levels. Failure to achieve euthyroidism after RAI therapy may indicate the need for either repeat RAI therapy (for symptomatic hyperthyroidism) or the initiation of thyroxine therapy (for hypothyroidism).

RAI therapy involves the release of stored thyroid hormone, leading to transient hyperthyroidism. This is generally well tolerated, although this transient hyperthyroidism is of concern in patients with significant cardiac disease. For patients with cardiac disease, pretreatment with a thionamide to deplete the stored hormone is recommended to avoid the potential exacerbation of cardiac disease.

Thionamide therapy is used as a definitive treatment for hyperthyroidism inpatient unwilling to undergo RAI therapy or have contraindications to RAI therapy, for example, allergy or pregnancy. Methimazole and propylthiouracil both inhibit thyroid hormone synthesis by thyroid peroxidase. Thyroid peroxidase is the enzyme responsible for converting dietary iodine into iodide. Propylthiouracil (PTU) also lowers peripheral tissue exposure to active thyroid hormone by blocking the extrathyroidal conversion of T4 to T3. Thionamide therapy has no permanent effect on thyroid function, and remission of hyperthyroidism is common in patients who discontinue thionamide therapy.

Establishing a euthyroid status typically requires several months after initiation of thionamide therapy. Although methimazole and PTU are equally effective, methimazole is preferred due to a relatively better safety profile. An exception to this recommendation is in pregnant patients, in which PTU is preferred. Methimazole is associated with an increased risk of congenital defects; thus, PTU is preferred in managing gestational hyperthyroidism.

Side effects of thionamide therapy include agranulocytosis, hepatitis, vasculitis, and drug-induced lupus. Although these are rare side effects, patients should be warned about the potential for these side effects. Patients should also be advised to discontinue the thionamide immediately and notify their physician if symptoms suggestive of agranulocytosis occur (fever, chills, rapidly progressive infection, sore throat, among others). Routine monitoring of leukocyte counts is not recommended when starting a patient on a thionamide due to the rapid onset of agranulocytosis. A baseline comprehensive metabolic panel (CMP) to assess hepatic status would not be unreasonable due to the potential for hepatitis.

Subtotal thyroidectomy is utilized for long-term control of hyperthyroidism. Preparation of the patient for a subtotal thyroidectomy includes pretreatment with methimazole to achieve a nearly euthyroid status. Supersaturated potassium iodide is then added daily approximately two weeks before surgery and discontinued postoperatively. Alternatively, atenolol can be started 1 to 2 weeks before surgery to reduce resting heart rate. Supersaturated potassium iodide is also dosed and discontinued postoperatively. The rationale behind these management plans is to reduce complications associated with perioperative exacerbation of hyperthyroidism.

Complications of subtotal thyroidectomy include hypothyroidism due to the decreased secretory potential of T4. Hypothyroidism remains the most common complication associated with subtotal thyroidectomy. The proximity of the parathyroid glands to the thyroid gland can result in the removal of parathyroid glands along with thyroid tissue, resulting in hypoparathyroidism. Due to the risk of iatrogenic injury to the recurrent laryngeal nerve, vocal cord paralysis is also a complication of subtotal thyroidectomy. All of these complications should be discussed with the patient, and the discussion should be documented.

Nursing Management

  • Monitor vital signs, especially heart rate and blood pressure (both increase in hyperthyroidism)
  • Ask if the patient has chest pain (Due to increased heart work)
  • Listen to the heart for murmurs
  • Obtain ECG (atrial arrhythmias may occur in hyperthyroidism)
  • Teach the patient to relax
  • Administer medications as prescribed (beta-blockers)
  • Check intake and output (diarrhea is a common feature in hyperthyroidism)
  • Weigh patient daily
  • Administer antithyroid medications as prescribed
  • Educate the patient about thyroid surgery
  • Educate the patient on radioactive iodine and how it can destroy the thyroid gland
  • Provide oxygen if the saturation is less than 94%
  • If the patient has a fever, provide a cooling blanket
  • Check thyroid function labs

When To Seek Help

  • Loss of consciousness
  • Altered mental status
  • Chest pain and dyspnea
  • High blood pressure
  • Abnormal heart rate
  • Fever

Outcome Identification

  • Normal thyroid function
  • No symptoms

Coordination of Care

Except for thyroid storm, hyperthyroidism in itself is rarely life-threatening but can pose a significant burden on a patient’s day-to-day routine. Inpatient management of a patient with hyperthyroidism does not always necessarily require consultation with an endocrinologist, but the presence of thyroid storm may warrant consultation with an endocrinologist and possible admission to the intensive care unit due to potentially life-threatening complications such as tachycardia and hypertensive crisis. Nurses involved with patient care should be vigilant about the signs and symptoms of thyroid storm.

As mentioned previously, any consideration of RAI therapy in a female of reproductive potential should follow a negative beta-hCG, as pregnancy is an absolute contraindication to RAI therapy. Incorporating a mandatory pregnancy test as part of an overall care plan would help avoid potentially damaging radiation exposure.

Health Teaching and Health Promotion

Patient education regarding hyperthyroidism is similar to other diseases. Patients should be educated on the importance of compliance with therapy and educated on the signs and symptoms of extreme hyperthyroidism (thyroid storm).

Discharge Planning

Except for thyroid storm, hyperthyroidism in itself is rarely life-threatening but can pose a significant burden on a patient’s day-to-day routine. Hyperthyroidism can present with many symptoms and, if not managed, can lead to poor quality of life. Because there are many causes of hyperthyroidism, the condition is best managed by an interprofessional team.

The primary care providers, including the nurse practitioner, should educate patients on the importance of medication compliance. In addition, the patient should be informed by the pharmacist that certain products like contrast dyes, expectorants, food supplements, and seaweed tablets may contain high levels of iodine and interfere with therapy.

Inpatient management of a patient with hyperthyroidism does not always necessarily require consultation with an endocrinologist, but the presence of a thyroid storm may warrant consultation with an endocrinologist and possible admission to the intensive care unit due to potentially life-threatening complications such as tachycardia and hypertensive crisis. Nurses involved with patient care should be vigilant about the signs and symptoms of thyroid storm.

As mentioned previously, any consideration of RAI therapy in a female of reproductive potential should follow a negative beta-hCG, as pregnancy is an absolute contraindication to RAI therapy. Incorporating a mandatory pregnancy test as part of an overall care plan would help avoid potentially damaging radiation exposure.

Patients with graves disease will need an ophthalmology consult. For those who undergo thyroidectomy, lifelong treatment with levothyroxine is required.

The interprofessional team must communicate with other members to ensure that the patient is receiving the current standard of care treatment.

Pearls and Other issues

Acute coronary syndrome (ACS) may be complicated by thyroid dysfunction. A recent study has shown that thyroid dysfunction is seen in up to 23.3% of patients with coronary artery disease and both overt and subclinical hyperthyroidism in 2.5%.[11]

Pregnancy and concurrent thyroid pathology can pose medical management challenges. PTU is recommended in pregnant women presenting with hyperthyroidism due to methimazole’s association with congenital defects. Close monitoring is recommended with PTU administration, as overcorrection can potentially cause fetal hypothyroidism. Thyroid hormone is essential due to its role in fetal neurodevelopment. Recent literature indicates that previously recommended TSH cutoffs in pregnant women lead to overcorrection of thyroid disease in pregnant patients.[12] As fetal exposure to thyroid hormone plays a significant role, careful monitoring and close supervision are warranted.

Neonatal thyrotoxicosis results from fetal tissue exposure to excessive thyroid hormone. There are typically two variants of neonatal thyrotoxicosis: autoimmune-mediated and non-autoimmune-mediated. Autoimmune fetal hyperthyroidism involves the transplacental passage of TSH receptor-stimulating antibodies. Hyperthyroidism is generally transient as symptoms cease 5 to 6 months after birth following clearance of maternal antibodies. Non-autoimmune fetal hyperthyroidism is associated with an activating mutation of either the TSH receptor or the GNAS gene (leading to McCune-Albright syndrome). Unlike the autoimmune etiology, the non-autoimmune variant is permanent, long persisting after birth.[13]

(Click Image to Enlarge)
Algorithm for evaluation of patients presenting with hyperthyroidism
Algorithm for evaluation of patients presenting with hyperthyroidism
Contributed by Jasleen Kaur, MD. Created using BioRender.

Nurse Editor

Kristina Fortes


Philip Mathew


Jasleen Kaur


Prashanth Rawla


3/19/2023 4:04:19 PM



Ross DS, Burch HB, Cooper DS, Greenlee MC, Laurberg P, Maia AL, Rivkees SA, Samuels M, Sosa JA, Stan MN, Walter MA. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid : official journal of the American Thyroid Association. 2016 Oct:26(10):1343-1421     [PubMed PMID: 27521067]


Biondi B, Cooper DS. Subclinical Hyperthyroidism. The New England journal of medicine. 2018 Jun 21:378(25):2411-2419. doi: 10.1056/NEJMcp1709318. Epub     [PubMed PMID: 29924956]


Biondi B, Palmieri EA, Fazio S, Cosco C, Nocera M, Saccà L, Filetti S, Lombardi G, Perticone F. Endogenous subclinical hyperthyroidism affects quality of life and cardiac morphology and function in young and middle-aged patients. The Journal of clinical endocrinology and metabolism. 2000 Dec:85(12):4701-5     [PubMed PMID: 11134131]


Vadiveloo T, Donnan PT, Cochrane L, Leese GP. The Thyroid Epidemiology, Audit, and Research Study (TEARS): morbidity in patients with endogenous subclinical hyperthyroidism. The Journal of clinical endocrinology and metabolism. 2011 May:96(5):1344-51. doi: 10.1210/jc.2010-2693. Epub 2011 Feb 23     [PubMed PMID: 21346066]


Selmer C, Olesen JB, Hansen ML, Lindhardsen J, Olsen AM, Madsen JC, Faber J, Hansen PR, Pedersen OD, Torp-Pedersen C, Gislason GH. The spectrum of thyroid disease and risk of new onset atrial fibrillation: a large population cohort study. BMJ (Clinical research ed.). 2012 Nov 27:345():e7895. doi: 10.1136/bmj.e7895. Epub 2012 Nov 27     [PubMed PMID: 23186910]


Cappola AR, Fried LP, Arnold AM, Danese MD, Kuller LH, Burke GL, Tracy RP, Ladenson PW. Thyroid status, cardiovascular risk, and mortality in older adults. JAMA. 2006 Mar 1:295(9):1033-41     [PubMed PMID: 16507804]


Selmer C, Olesen JB, Hansen ML, von Kappelgaard LM, Madsen JC, Hansen PR, Pedersen OD, Faber J, Torp-Pedersen C, Gislason GH. Subclinical and overt thyroid dysfunction and risk of all-cause mortality and cardiovascular events: a large population study. The Journal of clinical endocrinology and metabolism. 2014 Jul:99(7):2372-82. doi: 10.1210/jc.2013-4184. Epub 2014 Mar 21     [PubMed PMID: 24654753]


Roti E, Uberti ED. Iodine excess and hyperthyroidism. Thyroid : official journal of the American Thyroid Association. 2001 May:11(5):493-500     [PubMed PMID: 11396708]


Brucker-Davis F, Oldfield EH, Skarulis MC, Doppman JL, Weintraub BD. Thyrotropin-secreting pituitary tumors: diagnostic criteria, thyroid hormone sensitivity, and treatment outcome in 25 patients followed at the National Institutes of Health. The Journal of clinical endocrinology and metabolism. 1999 Feb:84(2):476-86     [PubMed PMID: 10022404]


Mittra ES, Niederkohr RD, Rodriguez C, El-Maghraby T, McDougall IR. Uncommon causes of thyrotoxicosis. Journal of nuclear medicine : official publication, Society of Nuclear Medicine. 2008 Feb:49(2):265-78. doi: 10.2967/jnumed.107.041202. Epub 2008 Jan 16     [PubMed PMID: 18199610]


Dunzendorfer T, deLas Morenas A, Kalir T, Levin RM. Struma ovarii and hyperthyroidism. Thyroid : official journal of the American Thyroid Association. 1999 May:9(5):499-502     [PubMed PMID: 10365682]


Taylor PN, Albrecht D, Scholz A, Gutierrez-Buey G, Lazarus JH, Dayan CM, Okosieme OE. Global epidemiology of hyperthyroidism and hypothyroidism. Nature reviews. Endocrinology. 2018 May:14(5):301-316. doi: 10.1038/nrendo.2018.18. Epub 2018 Mar 23     [PubMed PMID: 29569622]


Tsang W, Houlden RL. Amiodarone-induced thyrotoxicosis: a review. The Canadian journal of cardiology. 2009 Jul:25(7):421-4     [PubMed PMID: 19584973]


Lazarus JH. Lithium and thyroid. Best practice & research. Clinical endocrinology & metabolism. 2009 Dec:23(6):723-33. doi: 10.1016/j.beem.2009.06.002. Epub     [PubMed PMID: 19942149]


Illouz F, Braun D, Briet C, Schweizer U, Rodien P. Endocrine side-effects of anti-cancer drugs: thyroid effects of tyrosine kinase inhibitors. European journal of endocrinology. 2014 Sep:171(3):R91-9. doi: 10.1530/EJE-14-0198. Epub 2014 May 15     [PubMed PMID: 24833135]


Tomer Y, Blackard JT, Akeno N. Interferon alpha treatment and thyroid dysfunction. Endocrinology and metabolism clinics of North America. 2007 Dec:36(4):1051-66; x-xi     [PubMed PMID: 17983936]


Guaraldi F, La Selva R, Samà MT, D'Angelo V, Gori D, Fava P, Fierro MT, Savoia P, Arvat E. Characterization and implications of thyroid dysfunction induced by immune checkpoint inhibitors in real-life clinical practice: a long-term prospective study from a referral institution. Journal of endocrinological investigation. 2018 May:41(5):549-556. doi: 10.1007/s40618-017-0772-1. Epub 2017 Oct 17     [PubMed PMID: 29043574]


Iddah MA, Macharia BN. Autoimmune thyroid disorders. ISRN endocrinology. 2013:2013():509764. doi: 10.1155/2013/509764. Epub 2013 Jun 26     [PubMed PMID: 23878745]


Pearce EN, Farwell AP, Braverman LE. Thyroiditis. The New England journal of medicine. 2003 Jun 26:348(26):2646-55     [PubMed PMID: 12826640]


Smith TJ, Hegedüs L. Graves' Disease. The New England journal of medicine. 2016 Oct 20:375(16):1552-1565     [PubMed PMID: 27797318]


Vitti P, Rago T, Tonacchera M, Pinchera A. Toxic multinodular goiter in the elderly. Journal of endocrinological investigation. 2002:25(10 Suppl):16-8     [PubMed PMID: 12508907]


Laurberg P, Pedersen KM, Vestergaard H, Sigurdsson G. High incidence of multinodular toxic goitre in the elderly population in a low iodine intake area vs. high incidence of Graves' disease in the young in a high iodine intake area: comparative surveys of thyrotoxicosis epidemiology in East-Jutland Denmark and Iceland. Journal of internal medicine. 1991 May:229(5):415-20     [PubMed PMID: 2040867]


Abraham-Nordling M, Byström K, Törring O, Lantz M, Berg G, Calissendorff J, Nyström HF, Jansson S, Jörneskog G, Karlsson FA, Nyström E, Ohrling H, Orn T, Hallengren B, Wallin G. Incidence of hyperthyroidism in Sweden. European journal of endocrinology. 2011 Dec:165(6):899-905. doi: 10.1530/EJE-11-0548. Epub 2011 Sep 9     [PubMed PMID: 21908653]


Garmendia Madariaga A, Santos Palacios S, Guillén-Grima F, Galofré JC. The incidence and prevalence of thyroid dysfunction in Europe: a meta-analysis. The Journal of clinical endocrinology and metabolism. 2014 Mar:99(3):923-31. doi: 10.1210/jc.2013-2409. Epub 2014 Jan 1     [PubMed PMID: 24423323]


Franklyn JA. The management of hyperthyroidism. The New England journal of medicine. 1994 Jun 16:330(24):1731-8     [PubMed PMID: 7910662]


Hegedüs L, Bonnema SJ, Bennedbaek FN. Management of simple nodular goiter: current status and future perspectives. Endocrine reviews. 2003 Feb:24(1):102-32     [PubMed PMID: 12588812]


Tunbridge WM, Evered DC, Hall R, Appleton D, Brewis M, Clark F, Evans JG, Young E, Bird T, Smith PA. The spectrum of thyroid disease in a community: the Whickham survey. Clinical endocrinology. 1977 Dec:7(6):481-93     [PubMed PMID: 598014]


Vanderpump MP, Tunbridge WM, French JM, Appleton D, Bates D, Clark F, Grimley Evans J, Hasan DM, Rodgers H, Tunbridge F. The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickham Survey. Clinical endocrinology. 1995 Jul:43(1):55-68     [PubMed PMID: 7641412]


Hollowell JG, Staehling NW, Flanders WD, Hannon WH, Gunter EW, Spencer CA, Braverman LE. Serum TSH, T(4), and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III). The Journal of clinical endocrinology and metabolism. 2002 Feb:87(2):489-99     [PubMed PMID: 11836274]


Wang C, Li Y, Teng D, Shi X, Ba J, Chen B, Du J, He L, Lai X, Li Y, Chi H, Liao E, Liu C, Liu L, Qin G, Qin Y, Quan H, Shi B, Sun H, Tang X, Tong N, Wang G, Zhang JA, Wang Y, Xue Y, Yan L, Yang J, Yang L, Yao Y, Ye Z, Zhang Q, Zhang L, Zhu J, Zhu M, Shan Z, Teng W. Hyperthyroidism Prevalence in China After Universal Salt Iodization. Frontiers in endocrinology. 2021:12():651534. doi: 10.3389/fendo.2021.651534. Epub 2021 May 28     [PubMed PMID: 34122333]


Bogazzi F, Tomisti L, Bartalena L, Aghini-Lombardi F, Martino E. Amiodarone and the thyroid: a 2012 update. Journal of endocrinological investigation. 2012 Mar:35(3):340-8. doi: 10.3275/8298. Epub 2012 Mar 19     [PubMed PMID: 22433945]


Martino E, Safran M, Aghini-Lombardi F, Rajatanavin R, Lenziardi M, Fay M, Pacchiarotti A, Aronin N, Macchia E, Haffajee C. Environmental iodine intake and thyroid dysfunction during chronic amiodarone therapy. Annals of internal medicine. 1984 Jul:101(1):28-34     [PubMed PMID: 6428291]


Krohn K, Führer D, Bayer Y, Eszlinger M, Brauer V, Neumann S, Paschke R. Molecular pathogenesis of euthyroid and toxic multinodular goiter. Endocrine reviews. 2005 Jun:26(4):504-24     [PubMed PMID: 15615818]


Hamburger JI. Evolution of toxicity in solitary nontoxic autonomously functioning thyroid nodules. The Journal of clinical endocrinology and metabolism. 1980 Jun:50(6):1089-93     [PubMed PMID: 7372787]


Stanbury JB, Ermans AE, Bourdoux P, Todd C, Oken E, Tonglet R, Vidor G, Braverman LE, Medeiros-Neto G. Iodine-induced hyperthyroidism: occurrence and epidemiology. Thyroid : official journal of the American Thyroid Association. 1998 Jan:8(1):83-100     [PubMed PMID: 9492158]


Bervini S, Trelle S, Kopp P, Stettler C, Trepp R. Prevalence of Iodine-Induced Hyperthyroidism After Administration of Iodinated Contrast During Radiographic Procedures: A Systematic Review and Meta-Analysis of the Literature. Thyroid : official journal of the American Thyroid Association. 2021 Jul:31(7):1020-1029. doi: 10.1089/thy.2020.0459. Epub 2021 Mar 15     [PubMed PMID: 33327840]


Dunne P, Kaimal N, MacDonald J, Syed AA. Iodinated contrast-induced thyrotoxicosis. CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne. 2013 Feb 5:185(2):144-7. doi: 10.1503/cmaj.120734. Epub 2012 Nov 12     [PubMed PMID: 23148056]


Fradkin JE, Wolff J. Iodide-induced thyrotoxicosis. Medicine. 1983 Jan:62(1):1-20     [PubMed PMID: 6218369]


Bogazzi F, Bartalena L, Martino E. Approach to the patient with amiodarone-induced thyrotoxicosis. The Journal of clinical endocrinology and metabolism. 2010 Jun:95(6):2529-35. doi: 10.1210/jc.2010-0180. Epub     [PubMed PMID: 20525904]


Bahn Chair RS, Burch HB, Cooper DS, Garber JR, Greenlee MC, Klein I, Laurberg P, McDougall IR, Montori VM, Rivkees SA, Ross DS, Sosa JA, Stan MN, American Thyroid Association, American Association of Clinical Endocrinologists. Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. Thyroid : official journal of the American Thyroid Association. 2011 Jun:21(6):593-646. doi: 10.1089/thy.2010.0417. Epub 2011 Apr 21     [PubMed PMID: 21510801]


Şahlı E, Gündüz K. Thyroid-associated Ophthalmopathy. Turkish journal of ophthalmology. 2017 Apr:47(2):94-105. doi: 10.4274/tjo.80688. Epub 2017 Apr 1     [PubMed PMID: 28405484]


Bartalena L, Kahaly GJ, Baldeschi L, Dayan CM, Eckstein A, Marcocci C, Marinò M, Vaidya B, Wiersinga WM, EUGOGO †. The 2021 European Group on Graves' orbitopathy (EUGOGO) clinical practice guidelines for the medical management of Graves' orbitopathy. European journal of endocrinology. 2021 Aug 27:185(4):G43-G67. doi: 10.1530/EJE-21-0479. Epub 2021 Aug 27     [PubMed PMID: 34297684]


Bahn RS. Graves' ophthalmopathy. The New England journal of medicine. 2010 Feb 25:362(8):726-38. doi: 10.1056/NEJMra0905750. Epub     [PubMed PMID: 20181974]


Fatourechi V. Pretibial myxedema: pathophysiology and treatment options. American journal of clinical dermatology. 2005:6(5):295-309     [PubMed PMID: 16252929]


Jadidi J, Sigari M, Efendizade A, Grigorian A, Lehto SA, Kolla S. Thyroid acropachy: A rare skeletal manifestation of autoimmune thyroid disease. Radiology case reports. 2019 Aug:14(8):917-919. doi: 10.1016/j.radcr.2019.04.021. Epub 2019 May 23     [PubMed PMID: 31193617]


Fatourechi V, Ahmed DD, Schwartz KM. Thyroid acropachy: report of 40 patients treated at a single institution in a 26-year period. The Journal of clinical endocrinology and metabolism. 2002 Dec:87(12):5435-41     [PubMed PMID: 12466333]


De Leo S, Lee SY, Braverman LE. Hyperthyroidism. Lancet (London, England). 2016 Aug 27:388(10047):906-918. doi: 10.1016/S0140-6736(16)00278-6. Epub 2016 Mar 30     [PubMed PMID: 27038492]


Favresse J, Burlacu MC, Maiter D, Gruson D. Interferences With Thyroid Function Immunoassays: Clinical Implications and Detection Algorithm. Endocrine reviews. 2018 Oct 1:39(5):830-850. doi: 10.1210/er.2018-00119. Epub     [PubMed PMID: 29982406]


Li D, Radulescu A, Shrestha RT, Root M, Karger AB, Killeen AA, Hodges JS, Fan SL, Ferguson A, Garg U, Sokoll LJ, Burmeister LA. Association of Biotin Ingestion With Performance of Hormone and Nonhormone Assays in Healthy Adults. JAMA. 2017 Sep 26:318(12):1150-1160. doi: 10.1001/jama.2017.13705. Epub     [PubMed PMID: 28973622]


McKee A, Peyerl F. TSI assay utilization: impact on costs of Graves' hyperthyroidism diagnosis. The American journal of managed care. 2012 Jan 1:18(1):e1-14     [PubMed PMID: 22435785]


Autilio C, Morelli R, Locantore P, Pontecorvi A, Zuppi C, Carrozza C. Stimulating TSH receptor autoantibodies immunoassay: analytical evaluation and clinical performance in Graves' disease. Annals of clinical biochemistry. 2018 Jan:55(1):172-177. doi: 10.1177/0004563217700655. Epub 2017 Oct 9     [PubMed PMID: 28388869]


Kahaly GJ. Bioassays for TSH Receptor Antibodies: Quo Vadis? European thyroid journal. 2015 Mar:4(1):3-5. doi: 10.1159/000375445. Epub     [PubMed PMID: 25960955]


Chung J, Lee YJ, Choi YJ, Ha EJ, Suh CH, Choi M, Baek JH, Na DG, Korean Society of Thyroid Radiology (KSThR), Korean Society of Radiology. Clinical applications of Doppler ultrasonography for thyroid disease: consensus statement by the Korean Society of Thyroid Radiology. Ultrasonography (Seoul, Korea). 2020 Oct:39(4):315-330. doi: 10.14366/usg.20072. Epub 2020 Aug 25     [PubMed PMID: 32892523]


Daniels GH. Amiodarone-induced thyrotoxicosis. The Journal of clinical endocrinology and metabolism. 2001 Jan:86(1):3-8     [PubMed PMID: 11231968]


Burch HB, Burman KD, Cooper DS. A 2011 survey of clinical practice patterns in the management of Graves' disease. The Journal of clinical endocrinology and metabolism. 2012 Dec:97(12):4549-58. doi: 10.1210/jc.2012-2802. Epub 2012 Oct 5     [PubMed PMID: 23043191]


Balazs C, Kiss E, Leövey A, Farid NR. The immunosuppressive effect of methimazole on cell-mediated immunity is mediated by its capacity to inhibit peroxidase and to scavenge free oxygen radicals. Clinical endocrinology. 1986 Jul:25(1):7-16     [PubMed PMID: 3024872]


Lechpammer M, Lukac J, Lechpammer S, Kusić Z. Antithyroid drug-induced immunomodulation in Graves' disease patients. Acta medica Croatica : casopis Hravatske akademije medicinskih znanosti. 2002:56(1):21-6     [PubMed PMID: 12455450]


Laurberg P, Andersen SL. Therapy of endocrine disease: antithyroid drug use in early pregnancy and birth defects: time windows of relative safety and high risk? European journal of endocrinology. 2014 Jul:171(1):R13-20. doi: 10.1530/EJE-14-0135. Epub 2014 Mar 24     [PubMed PMID: 24662319]


Hackmon R, Blichowski M, Koren G. The safety of methimazole and propylthiouracil in pregnancy: a systematic review. Journal of obstetrics and gynaecology Canada : JOGC = Journal d'obstetrique et gynecologie du Canada : JOGC. 2012 Nov:34(11):1077-1086. doi: 10.1016/S1701-2163(16)35438-X. Epub     [PubMed PMID: 23231846]


Burch HB, Cooper DS. ANNIVERSARY REVIEW: Antithyroid drug therapy: 70 years later. European journal of endocrinology. 2018 Oct 12:179(5):R261-R274. doi: 10.1530/EJE-18-0678. Epub 2018 Oct 12     [PubMed PMID: 30320502]


Klein I, Becker DV, Levey GS. Treatment of hyperthyroid disease. Annals of internal medicine. 1994 Aug 15:121(4):281-8     [PubMed PMID: 7518659]


Mohlin E, Filipsson Nyström H, Eliasson M. Long-term prognosis after medical treatment of Graves' disease in a northern Swedish population 2000-2010. European journal of endocrinology. 2014 Mar:170(3):419-27. doi: 10.1530/EJE-13-0811. Epub 2014 Feb 4     [PubMed PMID: 24366943]


Komiya I, Yamada T, Sato A, Kouki T, Nishimori T, Takasu N. Remission and recurrence of hyperthyroid Graves' disease during and after methimazole treatment when assessed by IgE and interleukin 13. The Journal of clinical endocrinology and metabolism. 2001 Aug:86(8):3540-4     [PubMed PMID: 11502776]


Suzuki N, Noh JY, Yoshimura R, Mikura K, Kinoshita A, Suzuki A, Mitsumatsu T, Hoshiyama A, Fukushita M, Matsumoto M, Yoshihara A, Watanabe N, Sugino K, Ito K. Does Age or Sex Relate to Severity or Treatment Prognosis in Graves' Disease? Thyroid : official journal of the American Thyroid Association. 2021 Sep:31(9):1409-1415. doi: 10.1089/thy.2020.0881. Epub 2021 May 26     [PubMed PMID: 33882721]


Allahabadia A, Daykin J, Sheppard MC, Gough SC, Franklyn JA. Radioiodine treatment of hyperthyroidism-prognostic factors for outcome. The Journal of clinical endocrinology and metabolism. 2001 Aug:86(8):3611-7     [PubMed PMID: 11502786]


Santos RB, Romaldini JH, Ward LS. A randomized controlled trial to evaluate the effectiveness of 2 regimens of fixed iodine (¹³¹I) doses for Graves disease treatment. Clinical nuclear medicine. 2012 Mar:37(3):241-4. doi: 10.1097/RLU.0b013e31823ea6e0. Epub     [PubMed PMID: 22310249]


Roque C, Santos FS, Pilli T, Dalmazio G, Castagna MG, Pacini F. Long-term Effects of Radioiodine in Toxic Multinodular Goiter: Thyroid Volume, Function, and Autoimmunity. The Journal of clinical endocrinology and metabolism. 2020 Jul 1:105(7):. pii: dgaa214. doi: 10.1210/clinem/dgaa214. Epub     [PubMed PMID: 32320467]


Kang AS, Grant CS, Thompson GB, van Heerden JA. Current treatment of nodular goiter with hyperthyroidism (Plummer's disease): surgery versus radioiodine. Surgery. 2002 Dec:132(6):916-23; discussion 923     [PubMed PMID: 12490836]


Holm LE, Lundell G, Israelsson A, Dahlqvist I. Incidence of hypothyroidism occurring long after iodine-131 therapy for hyperthyroidism. Journal of nuclear medicine : official publication, Society of Nuclear Medicine. 1982 Feb:23(2):103-7     [PubMed PMID: 7057248]


Yano Y, Sugino K, Akaishi J, Uruno T, Okuwa K, Shibuya H, Kitagawa W, Nagahama M, Ito K, Ito K. Treatment of autonomously functioning thyroid nodules at a single institution: radioiodine therapy, surgery, and ethanol injection therapy. Annals of nuclear medicine. 2011 Dec:25(10):749-54. doi: 10.1007/s12149-011-0526-7. Epub 2011 Oct 5     [PubMed PMID: 21971604]


Nygaard B, Hegedüs L, Ulriksen P, Nielsen KG, Hansen JM. Radioiodine therapy for multinodular toxic goiter. Archives of internal medicine. 1999 Jun 28:159(12):1364-8     [PubMed PMID: 10386513]


Ferrari C, Reschini E, Paracchi A. Treatment of the autonomous thyroid nodule: a review. European journal of endocrinology. 1996 Oct:135(4):383-90     [PubMed PMID: 8921817]


Ceccarelli C, Bencivelli W, Vitti P, Grasso L, Pinchera A. Outcome of radioiodine-131 therapy in hyperfunctioning thyroid nodules: a 20 years' retrospective study. Clinical endocrinology. 2005 Mar:62(3):331-5     [PubMed PMID: 15730415]


Erbil Y, Ozluk Y, Giriş M, Salmaslioglu A, Issever H, Barbaros U, Kapran Y, Ozarmağan S, Tezelman S. Effect of lugol solution on thyroid gland blood flow and microvessel density in the patients with Graves' disease. The Journal of clinical endocrinology and metabolism. 2007 Jun:92(6):2182-9     [PubMed PMID: 17389702]


Ansaldo GL, Pretolesi F, Varaldo E, Meola C, Minuto M, Borgonovo G, Derchi LE, Torre GC. Doppler evaluation of intrathyroid arterial resistances during preoperative treatment with Lugol's iodide solution in patients with diffuse toxic goiter. Journal of the American College of Surgeons. 2000 Dec:191(6):607-12     [PubMed PMID: 11129808]


Guo Z, Yu P, Liu Z, Si Y, Jin M. Total thyroidectomy vs bilateral subtotal thyroidectomy in patients with Graves' diseases: a meta-analysis of randomized clinical trials. Clinical endocrinology. 2013 Nov:79(5):739-46. doi: 10.1111/cen.12209. Epub 2013 Apr 19     [PubMed PMID: 23521078]


Limonard EJ, Bisschop PH, Fliers E, Nieveen van Dijkum EJ. Thyroid function after subtotal thyroidectomy in patients with Graves' hyperthyroidism. TheScientificWorldJournal. 2012:2012():548796. doi: 10.1100/2012/548796. Epub 2012 Feb 1     [PubMed PMID: 22448136]


Al-Adhami A, Snaith AC, Craig WL, Krukowski ZH. Changing trends in surgery for Graves' disease: a cohort comparison of those having surgery intended to preserve thyroid function with those having ablative surgery. Journal of otolaryngology - head & neck surgery = Le Journal d'oto-rhino-laryngologie et de chirurgie cervico-faciale. 2013 May 29:42(1):37. doi: 10.1186/1916-0216-42-37. Epub 2013 May 29     [PubMed PMID: 23718902]


Dogan L, Karaman N, Yilmaz KB, Ozaslan C, Atalay C. Total thyroidectomy for the surgical treatment of multinodular goiter. Surgery today. 2011 Mar:41(3):323-7. doi: 10.1007/s00595-009-4272-6. Epub 2011 Feb 23     [PubMed PMID: 21365410]


Hussain M, Hisham AN. Total thyroidectomy: the procedure of choice for toxic goitre. Asian journal of surgery. 2008 Apr:31(2):59-62. doi: 10.1016/S1015-9584(08)60059-7. Epub     [PubMed PMID: 18490216]


Vidal-Trecan GM, Stahl JE, Eckman MH. Radioiodine or surgery for toxic thyroid adenoma: dissecting an important decision. A cost-effectiveness analysis. Thyroid : official journal of the American Thyroid Association. 2004 Nov:14(11):933-45     [PubMed PMID: 15671772]


Otsuka F, Noh JY, Chino T, Shimizu T, Mukasa K, Ito K, Ito K, Taniyama M. Hepatotoxicity and cutaneous reactions after antithyroid drug administration. Clinical endocrinology. 2012 Aug:77(2):310-5. doi: 10.1111/j.1365-2265.2012.04365.x. Epub     [PubMed PMID: 22332800]


Wang MT, Lee WJ, Huang TY, Chu CL, Hsieh CH. Antithyroid drug-related hepatotoxicity in hyperthyroidism patients: a population-based cohort study. British journal of clinical pharmacology. 2014 Sep:78(3):619-29     [PubMed PMID: 25279406]


Nakamura H, Miyauchi A, Miyawaki N, Imagawa J. Analysis of 754 cases of antithyroid drug-induced agranulocytosis over 30 years in Japan. The Journal of clinical endocrinology and metabolism. 2013 Dec:98(12):4776-83. doi: 10.1210/jc.2013-2569. Epub 2013 Sep 20     [PubMed PMID: 24057289]


Noh JY, Yasuda S, Sato S, Matsumoto M, Kunii Y, Noguchi Y, Mukasa K, Ito K, Ito K, Sugiyama O, Kobayashi H, Nihojima S, Okazaki M, Yokoyama S. Clinical characteristics of myeloperoxidase antineutrophil cytoplasmic antibody-associated vasculitis caused by antithyroid drugs. The Journal of clinical endocrinology and metabolism. 2009 Aug:94(8):2806-11. doi: 10.1210/jc.2008-2700. Epub 2009 Jun 2     [PubMed PMID: 19491223]


Gao Y, Zhao MH, Guo XH, Xin G, Gao Y, Wang HY. The prevalence and target antigens of antithyroid drugs induced antineutrophil cytoplasmic antibodies (ANCA) in Chinese patients with hyperthyroidism. Endocrine research. 2004 May:30(2):205-13     [PubMed PMID: 15473130]


Yazisiz V, Ongüt G, Terzioğlu E, Karayalçin U. Clinical importance of antineutrophil cytoplasmic antibody positivity during propylthiouracil treatment. International journal of clinical practice. 2010 Jan:64(1):19-24. doi: 10.1111/j.1742-1241.2007.01485.x. Epub 2008 Feb 14     [PubMed PMID: 18284438]


Aloush V, Litinsky I, Caspi D, Elkayam O. Propylthiouracil-induced autoimmune syndromes: two distinct clinical presentations with different course and management. Seminars in arthritis and rheumatism. 2006 Aug:36(1):4-9     [PubMed PMID: 16887463]


Hess E. Drug-related lupus. The New England journal of medicine. 1988 Jun 2:318(22):1460-2     [PubMed PMID: 3259288]


Gomez Cruz MJ, Jabbar M, Saini N, Eng D, Crawford B, Vazquez DM, Menon R, Chen M. Severe hypoglycemia secondary to methimazole-induced insulin autoimmune syndrome in a 16 year old African-American male. Pediatric diabetes. 2012 Dec:13(8):652-5. doi: 10.1111/j.1399-5448.2012.00884.x. Epub 2012 Jul 3     [PubMed PMID: 22759245]


Jain N, Savani M, Agarwal M, Kadaria D. Methimazole-induced insulin autoimmune syndrome. Therapeutic advances in endocrinology and metabolism. 2016 Aug:7(4):178-81. doi: 10.1177/2042018816658396. Epub 2016 Jul 19     [PubMed PMID: 27540463]


Rosato L, Avenia N, Bernante P, De Palma M, Gulino G, Nasi PG, Pelizzo MR, Pezzullo L. Complications of thyroid surgery: analysis of a multicentric study on 14,934 patients operated on in Italy over 5 years. World journal of surgery. 2004 Mar:28(3):271-6     [PubMed PMID: 14961204]


Bhattacharyya N, Fried MP. Assessment of the morbidity and complications of total thyroidectomy. Archives of otolaryngology--head & neck surgery. 2002 Apr:128(4):389-92     [PubMed PMID: 11926912]


Safioleas M, Stamatakos M, Rompoti N, Mouzopoulos G, Iannescu R, Salichou V, Skandalakis P. Complications of thyroid surgery. Chirurgia (Bucharest, Romania : 1990). 2006 Nov-Dec:101(6):571-81     [PubMed PMID: 17283832]


Thiyagarajan A, Platzbecker K, Ittermann T, Völzke H, Haug U. Estimating Incidence and Case Fatality of Thyroid Storm in Germany Between 2007 and 2017: A Claims Data Analysis. Thyroid : official journal of the American Thyroid Association. 2022 Nov:32(11):1307-1315. doi: 10.1089/thy.2022.0096. Epub 2022 Sep 28     [PubMed PMID: 36006371]


Dekkers OM, Horváth-Puhó E, Cannegieter SC, Vandenbroucke JP, Sørensen HT, Jørgensen JO. Acute cardiovascular events and all-cause mortality in patients with hyperthyroidism: a population-based cohort study. European journal of endocrinology. 2017 Jan:176(1):1-9     [PubMed PMID: 27697972]


Abrahamsen B, Jørgensen HL, Laulund AS, Nybo M, Bauer DC, Brix TH, Hegedüs L. The excess risk of major osteoporotic fractures in hypothyroidism is driven by cumulative hyperthyroid as opposed to hypothyroid time: an observational register-based time-resolved cohort analysis. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. 2015 May:30(5):898-905. doi: 10.1002/jbmr.2416. Epub     [PubMed PMID: 25431028]


Mintziori G, Kita M, Duntas L, Goulis DG. Consequences of hyperthyroidism in male and female fertility: pathophysiology and current management. Journal of endocrinological investigation. 2016 Aug:39(8):849-53. doi: 10.1007/s40618-016-0452-6. Epub 2016 Mar 8     [PubMed PMID: 26956000]


Siu CW, Pong V, Zhang X, Chan YH, Jim MH, Liu S, Yiu KH, Kung AW, Lau CP, Tse HF. Risk of ischemic stroke after new-onset atrial fibrillation in patients with hyperthyroidism. Heart rhythm. 2009 Feb:6(2):169-73. doi: 10.1016/j.hrthm.2008.10.023. Epub 2008 Nov 1     [PubMed PMID: 19187905]


Xu N, Wang Y, Xu Y, Li L, Chen J, Mai X, Xu J, Zhang Z, Yang R, Sun J, Chen H, Chen R. Effect of subclinical hyperthyroidism on osteoporosis: A meta-analysis of cohort studies. Endocrine. 2020 Jul:69(1):39-48. doi: 10.1007/s12020-020-02259-8. Epub 2020 Mar 23     [PubMed PMID: 32207036]


Collet TH, Gussekloo J, Bauer DC, den Elzen WP, Cappola AR, Balmer P, Iervasi G, Åsvold BO, Sgarbi JA, Völzke H, Gencer B, Maciel RM, Molinaro S, Bremner A, Luben RN, Maisonneuve P, Cornuz J, Newman AB, Khaw KT, Westendorp RG, Franklyn JA, Vittinghoff E, Walsh JP, Rodondi N, Thyroid Studies Collaboration. Subclinical hyperthyroidism and the risk of coronary heart disease and mortality. Archives of internal medicine. 2012 May 28:172(10):799-809. doi: 10.1001/archinternmed.2012.402. Epub     [PubMed PMID: 22529182]


Abdulaziz Qari F. Thyroid Hormone Profile in Patients With Acute Coronary Syndrome. Iranian Red Crescent medical journal. 2015 Jul:17(7):e26919. doi: 10.5812/ircmj.26919v2. Epub 2015 Jul 22     [PubMed PMID: 26421178]


Korevaar TIM, Medici M, Visser TJ, Peeters RP. Thyroid disease in pregnancy: new insights in diagnosis and clinical management. Nature reviews. Endocrinology. 2017 Oct:13(10):610-622. doi: 10.1038/nrendo.2017.93. Epub 2017 Aug 4     [PubMed PMID: 28776582]


Samuels SL, Namoc SM, Bauer AJ. Neonatal Thyrotoxicosis. Clinics in perinatology. 2018 Mar:45(1):31-40. doi: 10.1016/j.clp.2017.10.001. Epub 2017 Dec 16     [PubMed PMID: 29406005]