Overview
Related Diseases & Conditions
Summary
Thyroid function tests (TFTs) are the most commonly used endocrine test. A serum thyroid-stimulating hormone (TSH) assay is the test of choice to screen for thyroid function disorders in the absence of hypothalamic or a pituitary pathology.[1] [2] [3] Suppressed or elevated TSH confirms presence of thyroid dysfunction but not its cause. Free secreting thyroxine (T4) assay is the test of choice to evaluate an abnormal TSH level.Summary
Graves disease is the most common form of hyperthyroidism in countries with sufficient iodine intake. Graves disease is caused by TSH receptor antibodies. Extrathyroidal manifestations can include orbitopathy, pretibial myxoedema (thyroid dermopathy), and acropachy, which do not occur with other causes of hyperthyroidism. Diagnosis is mostly clinical. The main goal of treatment is to normalize thyroid function parameters.Summary
A toxic multinodular goiter (MNG; also known as Plummer disease) contains multiple autonomously functioning nodules, resulting in hyperthyroidism. Nodules function independently of TSH and are almost always benign. However, nonfunctioning thyroid nodules in the same goiter may be malignant.[4] Key risk factors include iodine deficiency, age >40 years, and head and neck irradiation. Diagnosis is made by assessing signs and symptoms, biochemical evidence of hyperthyroidism, and radioisotope scan with typical uptake and appearance. Spontaneous remission is rare.Summary
Summary
Painless lymphocytic thyroiditis, also known as painless thyroiditis or silent thyroiditis, is characterized by autoimmune-mediated inflammation of the thyroid gland with release of thyroid hormone, resulting in transient hyperthyroidism. This is frequently followed by a hypothyroid phase before recovery of normal thyroid function.[7] [8] Thyroiditis may occur sporadically, postpartum, during drug treatment or radiation therapy, or as the result of bacterial or viral infection. The diagnosis of painless thyroiditis can be established based on history, clinical features, TFTs, and radioiodine uptake. Some patients progress to permanent hypothyroidism.Summary
Subacute thyroiditis (also termed De Quervain thyroiditis, granulomatous thyroiditis, or giant cell thyroiditis) is a self-limited inflammation of the thyroid characterized by a triphasic course of transient thyrotoxicosis, followed by hypothyroidism, followed by return to euthyroidism.[9] [10] The initial thyrotoxic phase is associated with thyroid pain, high serum thyroid hormone levels with a low radioiodine uptake, elevated erythrocyte sedimentation rate, elevated C-reactive protein, and a systemic illness similar to influenza, with fever, myalgia, and malaise.[11] [12] The etiology is presumed to be viral or autoimmune.[13] Strong risk factors include viral infection and the HLA-B*35 allele, which is seen in approximately 70% of patients with subacute thyroiditis.[14] The diagnosis of subacute thyroiditis is mainly based on clinical grounds, although imaging studies and laboratory investigation may sometimes be required to confirm the diagnosis. Not all patients require treatment, as symptoms may be mild and/or subsiding by the time the diagnosis is made.Summary
Hypothyroidism is a clinical state resulting from underproduction of T4 and T3. Patients with primary hypothyroidism usually present with nonspecific symptoms of weakness, lethargy, depression, and mild weight gain. TSH is the most sensitive and specific for diagnosing primary hypothyroidism; levels are elevated in primary hypothyroidism, although in subclinical disease levels may only be mildly elevated. Autoimmune thyroiditis (Hashimoto disease) is the most common cause of primary hypothyroidism in iodine-sufficient areas.[15] Key risk factors include female sex, middle age, family history of autoimmune thyroiditis, autoimmune disorders, treatment for thyroid disease, postpartum thyroiditis, Turner and Down syndromes, radiation therapy to head and neck, iodine deficiency, amiodarone use, and lithium use.Summary
The result of anterior pituitary or hypothalamic hypofunction. Central hypothyroidism is rare and accounts for less than 1% of hypothyroid cases.[15] Pituitary mass lesions, especially pituitary adenomas such as growth hormone- or adrenocorticotrophic hormone-secreting adenomas, are the most common cause.[16] Key risk factors include multiple endocrine neoplasia type I, head and neck irradiation, and traumatic brain injury. Diagnostic evaluation of central hypothyroidism includes serum TSH and free T4 concentrations. In central hypothyroidism, free T4 is low and TSH may be low, normal, or minimally elevated.Summary
Thyroid cancer most commonly presents as an asymptomatic thyroid nodule detected by palpation or ultrasound in women in their 30s or 40s. It is the most common endocrinologic malignancy.[17] Differentiated follicular cell-derived thyroid cancers (papillary, follicular, Hürthle cell) make up around 90% of cases. Genetic alterations underlie most thyroid cancers. The initial management decisions for patients with suspected thyroid cancer are guided by clinicopathologic features of the patient and the tumor contributing to perioperative (preoperative evaluations, intraoperative findings, and early postoperative testing) risk stratification.[18]Summary
A thyroid nodule is a discrete lesion distinct from the surrounding thyroid parenchyma. They can be found in 50% to 60% of healthy people.[19] Colloid nodules are the most common type of thyroid nodule.Most thyroid nodules are benign.[20] The risk of thyroid cancer in any patient presenting for nodule care is approximately 10% to 15%.[21] The clinical goal in the evaluation of the thyroid nodule is differentiating a benign from a malignant lesion. Ultrasonography is the initial test of choice for evaluating the structure and anatomic location of a neck mass.
Citations
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2. Alberta Medical Association. Investigation and management of primary thyroid dysfunction. Apr 2014 [internet publication].[Full Text]
3. Schneider C, Feller M, Bauer DC, et al. Initial evaluation of thyroid dysfunction - Are simultaneous TSH and fT4 tests necessary? PLoS One. 2018;13(4):e0196631.[Abstract][Full Text]
4. Haugen BR, Alexander EK, Bible KC, et al. 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer: The American Thyroid Association Guidelines Task Force on Thyroid Nodules and Differentiated Thyroid Cancer. Thyroid. 2016 Jan;26(1):1-133.[Abstract][Full Text]
5. Ross DS, Burch HB, Cooper DS, et al. 2016 American Thyroid Association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis. Thyroid. 2016;26:1343-421.[Abstract][Full Text]
6. Pearce EN. Diagnosis and management of thyrotoxicosis. BMJ. 2006 Jun 10;332(7554):1369-73.[Full Text]
7. Woolf PD. Transient painless thyroiditis with hyperthyroidism: a variant of lymphocytic thyroiditis? Endocr Rev. 1980 Fall;1(4):411-20.
8. Samuels MH. Subacute, silent, and postpartum thyroiditis. Med Clin North Am. 2012 Mar;96(2):223-33.[Abstract]
9. Nishihara E, Ohye H, Amino N, et al. Clinical characteristics of 852 patients with subacute thyroiditis before treatment. Intern Med. 2008;47(8):725-9.[Abstract][Full Text]
10. Fatourechi V, Aniszewski JP, Fatourechi GZ, et al. Clinical features and outcome of subacute thyroiditis in an incidence cohort: Olmsted county, Minnesota, study. J Clin Endocrinol Metab. 2003 May;88(5):2100-5.[Abstract][Full Text]
11. Pearce EN, Farwell AP, Braverman LE. Thyroiditis. N Engl J Med. 2003 Jun 26;348(26):2646-55.
12. Sweeney LB, Stewart C, Gaitonde DY. Thyroiditis: an integrated approach. Am Fam Physician. 2014 Sep 15;90(6):389-96.[Abstract][Full Text]
13. Zhang J, Ding G, Li J, et al. Risk factors for subacute thyroiditis recurrence: a systematic review and meta-analysis of cohort studies. Front Endocrinol (Lausanne). 2021 Dec 23;12:783439.[Abstract][Full Text]
14. Stasiak M, Tymoniuk B, Michalak R, et al. Subacute thyroiditis is associated with HLA-B*18:01, -DRB1*01 and -C*04:01-the significance of the new molecular background. J Clin Med. 2020 Feb 16;9(2):534.[Abstract][Full Text]
15. Chaker L, Bianco AC, Jonklaas J, et al. Hypothyroidism. Lancet. 2017 Sep 23;390(10101):1550-62.[Abstract][Full Text]
16. Bates AS, Van't Hoff W, Jones PJ, et al. The effect of hypopituitarism on life expectancy. J Clin Endocrinol Metab. 1996 Mar;81(3):1169-72.[Abstract]
17. Pizzato M, Li M, Vignat J, et al. The epidemiological landscape of thyroid cancer worldwide: GLOBOCAN estimates for incidence and mortality rates in 2020. Lancet Diabetes Endocrinol. 2022 Apr;10(4):264-72.[Abstract]
18. Gulec SA, Ahuja S, Avram AM, et al. A joint statement from the American Thyroid Association, the European Association of Nuclear Medicine, the European Thyroid Association, the Society of Nuclear Medicine and Molecular Imaging on current diagnostic and theranostic approaches in the management of thyroid cancer. Thyroid. 2021 Jul;31(7):1009-19.[Abstract][Full Text]
19. Gharib H, Papini E, Garber JR, et al. AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS, AMERICAN COLLEGE OF ENDOCRINOLOGY, AND ASSOCIAZIONE MEDICI ENDOCRINOLOGI MEDICAL GUIDELINES FOR CLINICAL PRACTICE FOR THE DIAGNOSIS AND MANAGEMENT OF THYROID NODULES--2016 UPDATE. Endocr Pract. 2016 May;22(5):622-39.[Abstract][Full Text]
20. Singh Ospina N, Iñiguez-Ariza NM, Castro MR. Thyroid nodules: diagnostic evaluation based on thyroid cancer risk assessment. BMJ. 2020 Jan 7;368:l6670.[Abstract]
21. Alexander EK, Cibas ES. Diagnosis of thyroid nodules. Lancet Diabetes Endocrinol. 2022 Jul;10(7):533-9.[Abstract]
Referenced Articles
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