Hashimoto's thyroiditis

Last updated

Hashimoto's thyroiditis
Other namesChronic lymphocytic thyroiditis, autoimmune thyroiditis, struma lymphomatosa, Hashimoto's disease
Hashimoto thyroiditis - alt -- very low mag.jpg
The thyroid of someone with Hashimoto's thyroiditis as seen with a microscope at low magnification
Specialty Endocrinology
SymptomsPainless goiter, weight gain, feeling tired, constipation, depression, dry skin, hair loss [1]
Complications Thyroid lymphoma. [2]
Usual onset30–50 years old [1] [3]
Causes Genetic and environmental factors. [4]
Risk factors Family history, another autoimmune disease [1]
Diagnostic method TSH, T4, anti-thyroid autoantibodies [1]
Differential diagnosis Graves’ disease, nontoxic nodular goiter [5]
Treatment Levothyroxine, surgery [1] [5]
Frequency5% at some point [4]

Hashimoto's thyroiditis, also known as chronic lymphocytic thyroiditis and Hashimoto's disease, is an autoimmune disease in which the thyroid gland is gradually destroyed. [1] [6] Early on, symptoms may not be noticed. [1] Over time, the thyroid may enlarge, forming a painless goiter. [1] Some people eventually develop hypothyroidism with accompanying weight gain, fatigue, constipation, depression, hair loss, and general pains. [1] After many years the thyroid typically shrinks in size. [1] Potential complications include thyroid lymphoma. [2]


Hashimoto's thyroiditis is thought to be due to a combination of genetic and environmental factors. [4] Risk factors include a family history of the condition and having another autoimmune disease. [1] Diagnosis is confirmed with blood tests for TSH, T4, and antithyroid autoantibodies. [1] Other conditions that can produce similar symptoms include Graves’ disease and nontoxic nodular goiter. [5]

Hashimoto's thyroiditis is typically treated with levothyroxine. [1] [7] If hypothyroidism is not present, some may recommend no treatment, while others may treat to try to reduce the size of the goiter. [1] [8] Those affected should avoid eating large amounts of iodine; however, sufficient iodine is required especially during pregnancy. [1] Surgery is rarely required to treat the goiter. [5]

Hashimoto's thyroiditis affects about 5% of Caucasians at some point in their lives. [4] It typically begins between the ages of 30 and 50 and is much more common in women than men. [1] [3] Rates of the disease appear to be increasing. [5] It was first described by the Japanese physician Hakaru Hashimoto in 1912. [9] In 1957 it was recognized as an autoimmune disorder. [10]

Signs and symptoms

Many symptoms are attributed to Hashimoto's thyroiditis. The most common symptoms include: fatigue, weight gain, pale or puffy face, feeling cold, joint and muscle pain, constipation, dry and thinning hair, heavy menstrual flow or irregular periods, depression, panic disorder, a slowed heart rate, and problems getting pregnant and maintaining pregnancy. [11]

Hashimoto’s disease is about seven times more common in women than in men. It can occur in teens and young women, but more commonly appears in middle age, particularly for men. People who develop Hashimoto’s disease often have family members who have thyroid or other autoimmune diseases, and sometimes have other autoimmune diseases themselves. [12]

The thyroid gland may become firm, large, and lobulated in Hashimoto's thyroiditis, but changes in the thyroid can also be nonpalpable. [13] Enlargement of the thyroid is due to lymphocytic infiltration and fibrosis, rather than tissue hypertrophy. While their role in the initial destruction of the follicles is unclear, antibodies against thyroid peroxidase or thyroglobulin are relevant, as they serve as markers for detecting the disease and its severity. [14] They are thought to be the secondary products of the T cell-mediated destruction of the gland. [15]

It is also characterized by invasion of the thyroid tissue by leukocytes, mainly T-lymphocytes. A rare but serious complication is thyroid lymphoma, generally the B-cell type, non-Hodgkin lymphoma. [16]

Risk factors

The strong genetic component is borne out in studies on monozygotic twins, with a concordance of 38–55%, with an even higher concordance of circulating thyroid antibodies not in relation to clinical presentation (up to 80% in monozygotic twins). Neither result was seen to a similar degree in dizygotic twins, offering strong favour for high genetic aetiology. [17]

Hashimoto's thyroiditis is associated with CTLA-4 (cytotoxic T-lymphocyte antigen-4) gene polymorphisms. CTLA-4 downregulates., i.e. transmits an inhibitory signal to T cells, so reduced functioning is associated with increased T-lymphocyte activity. [18] [19] A family history of thyroid disorders is common, with the HLA-DR5 gene most strongly implicated conferring a relative risk of 3 in the UK. [20]

Having other autoimmune diseases is a risk factor to develop Hashimoto’s thyroiditis, and the opposite is also true. [1] Autoimmune diseases most commonly associated to Hashimoto’s thyroiditis include celiac disease, type 1 diabetes, vitiligo, and alopecia. [21]

Preventable environmental factors, including high iodine intake, selenium deficiency, and infectious diseases and certain drugs, have been implicated in the development of autoimmune thyroid disease in genetically predisposed individuals. [22]

The genes implicated vary in different ethnic groups and the incidence is increased in people with chromosomal disorders, including Turner, Down, and Klinefelter syndromes usually associated with autoantibodies against thyroglobulin and thyroperoxidase. Progressive depletion of these cells as the cytotoxic immune response leads to higher degrees of primary hypothyroidism, presenting with low T3/T4 levels, and compensatory elevations of TSH.[ citation needed ]


Multiple mechanisms by which the pathology of Hashimoto's thyroiditis develops have been suggested.

Various autoantibodies may be present against thyroid peroxidase, thyroglobulin and TSH receptors, although a small percentage of people may have none of these antibodies present. As indicated in various twin studies, a percentage of the population may also have these antibodies without developing Hashimoto's thyroiditis. Nevertheless, antibody-dependent, cell-mediated cytotoxicity is a substantial factor behind the apoptotic fall-out of Hashimoto's thyroiditis. Activation of cytotoxic T-lymphocytes (CD8+ T-cells) in response to cell-mediated immune response affected by helper T-lymphocytes (CD4+ T-cells) is central to thyrocyte destruction. As is characteristic of type IV hypersensitivities, recruitment of macrophages is another effect of the helper T-lymphocyte activation, with Th1 axis lymphocytes producing inflammatory cytokines within thyroid tissue to further macrophage activation and migration into the thyroid gland for direct effect.[ citation needed ]

Gross morphological changes within the thyroid are seen in the general enlargement, which is far more locally nodular and irregular than more diffuse patterns (such as that of hyperthyroidism). While the capsule is intact and the gland itself is still distinct from surrounding tissue, microscopic examination can provide a more revealing indication of the level of damage. [23]

Histologically, the hypersensitivity is seen as diffuse parenchymal infiltration by lymphocytes, particularly plasma B-cells, which can often be seen as secondary lymphoid follicles (germinal centers, not to be confused with the normally present colloid-filled follicles that constitute the thyroid). Atrophy of the colloid bodies is lined by Hürthle cells, cells with intensely eosinophilic, granular cytoplasm, a metaplasia from the normal cuboidal cells that constitute the lining of the thyroid follicles. Severe thyroid atrophy presents often with denser fibrotic bands of collagen that remains within the confines of the thyroid capsule. [24]


Ultrasound imaging of the thyroid gland (right lobe longitudinal) in a person with Hashimoto thyroiditis Hashimoto-Thyreoiditis.JPG
Ultrasound imaging of the thyroid gland (right lobe longitudinal) in a person with Hashimoto thyroiditis

Diagnosis is usually made by detecting elevated levels of antithyroid peroxidase antibodies in the serum, but seronegative (without circulating autoantibodies) thyroiditis is also possible. [25]

Given the relatively nonspecific symptoms of initial hypothyroidism, Hashimoto's thyroiditis is often misdiagnosed as depression, cyclothymia, premenstrual syndrome, chronic fatigue syndrome, fibromyalgia, and less frequently, as erectile dysfunction or an anxiety disorder. On gross examination, a hard goiter that is not painful to the touch often presents; [23] other symptoms seen with hypothyroidism, such as periorbital myxedema, depend on the current state of progression of the response, especially given the usually gradual development of clinically relevant hypothyroidism. Testing for thyroid-stimulating hormone (TSH), free T3, free T4, and the antithyroglobulin antibodies (anti-Tg), antithyroid peroxidase antibodies (anti-TPO, or TPOAb) and antimicrosomal antibodies can help obtain an accurate diagnosis. [26] Earlier assessment of the person may present with elevated levels of thyroglobulin owing to transient thyrotoxicosis, as inflammation within the thyroid causes damage to the integrity of thyroid follicle storage of thyroglobulin; TSH secretion from the anterior pituitary increases in response to a decrease in negative feedback inhibition secondary to decreased serum thyroid hormones. Typically, T4 is the preferred thyroid hormone test for hypothyroidism. [27] This exposure of the body to substantial amounts of previously isolated thyroid enzymes is thought to contribute to the exacerbation of tolerance breakdown, giving rise to the more pronounced symptoms seen later in the disease. Lymphocytic infiltration of the thyrocyte-associated tissues often leads to the histologically significant finding of germinal center development within the thyroid gland.[ citation needed ]

Hashimoto's when presenting as mania is known as Prasad's syndrome after Ashok Prasad, the psychiatrist who first described it. [28]


Managing hormone levels

Hypothyroidism caused by Hashimoto's thyroiditis is treated with thyroid hormone replacement agents such as levothyroxine, triiodothyronine, or desiccated thyroid extract. A tablet taken once a day generally keeps the thyroid hormone levels normal. In most cases, the treatment needs to be taken for the rest of the person's life. If hypothyroidism is caused by Hashimoto's thyroiditis, the TSH levels may be recommended to be kept under 3.0 mIU/l. [29]


Overt, symptomatic thyroid dysfunction is the most common complication, with about 5% of people with subclinical hypothyroidism and chronic autoimmune thyroiditis progressing to thyroid failure every year. Transient periods of thyrotoxicosis (over-activity of the thyroid) sometimes occur, and rarely the illness may progress to full hyperthyroid Graves' disease with active orbitopathy (bulging, inflamed eyes). Rare cases of fibrous autoimmune thyroiditis present with severe shortness of breath and difficulty swallowing, resembling aggressive thyroid tumors, but such symptoms always improve with surgery or corticosteroid therapy. Primary thyroid B-cell lymphoma affects fewer than one in 1000 persons, and it is more likely to affect those with long-standing autoimmune thyroiditis. [30]


This disorder is thought to be the most common cause of primary hypothyroidism in North America; as a cause of nonendemic goiter, it is among the most common. [31] Hashimoto's thyroiditis affects about 5% of Caucasians at some point in their lives. [4] In the U.S., it affects fewer African-Americans, but is linked to greater mortality in the African-American population. [32] About 1.0 to 1.5 in 1000 people have this disease at any time. [31] It occurs between eight and 15 times more often in women than in men. Though it may occur at any age, including in children, it is most often observed in women between 30 and 60 years of age. [30] Some research suggests a connection to the role of the placenta as an explanation for the sex difference. [33]

It is more common in regions of high iodine dietary intake, and among people who are genetically susceptible. [30]


Also known as Hashimoto's disease, Hashimoto's thyroiditis is named after Japanese physician Hakaru Hashimoto (1881−1934) of the medical school at Kyushu University, [34] who first described the symptoms of persons with struma lymphomatosa, an intense infiltration of lymphocytes within the thyroid, in 1912 in a German publication. [35]

In 1957, it was recognized as an autoimmune disorder and was the first organ-specific autoimmune disorder identified. [10]


Pregnant women who are positive for Hashimoto's thyroiditis may have decreased thyroid function or the gland may fail entirely. [36] If a woman is TPOAb-positive, clinicians can inform her of the risks for themselves and their infants if they go untreated. "Thyroid peroxidase antibodies (TPOAb) are detected in 10% of pregnant women," which presents risks to those pregnancies. [36] Women who have low thyroid function that has not been stabilized are at greater risk of having an infant with: low birth weight, neonatal respiratory distress, hydrocephalus, hypospadias, miscarriage, and preterm delivery. [36] [37] The embryo transplantion rate and successful pregnancy outcomes are improved when Hashimoto's is treated. [37] Recommendations are to only treat pregnant women who are TPOAb-positive throughout the entirety of their pregnancies and to screen all pregnant women for thyroid levels. [36] Close cooperation between the endocrinologist and obstetrician benefits the woman and the infant. [36] [38] [39] The Endocrine Society recommends screening in pregnant women who are considered high-risk for thyroid autoimmune disease. [40]

Thyroid peroxides antibodies testing is recommended for women who have ever been pregnant regardless of pregnancy outcome. "...[P]revious pregnancy plays a major role in development of autoimmune overt hypothyroidism in premenopausal women, and the number of previous pregnancies should be taken into account when evaluating the risk of hypothyroidism in a young women [sic]." [41]

See also

Related Research Articles

Hyperthyroidism Thyroid gland disease that involves an overproduction of thyroid hormone.

Hyperthyroidism is the condition that occurs due to excessive production of thyroid hormones by the thyroid gland. Thyrotoxicosis is the condition that occurs due to excessive thyroid hormone of any cause and therefore includes hyperthyroidism. Some, however, use the terms interchangeably. Signs and symptoms vary between people and may include irritability, muscle weakness, sleeping problems, a fast heartbeat, heat intolerance, diarrhea, enlargement of the thyroid, hand tremor, and weight loss. Symptoms are typically less severe in the elderly and during pregnancy. An uncommon complication is thyroid storm in which an event such as an infection results in worsening symptoms such as confusion and a high temperature and often results in death. The opposite is hypothyroidism, when the thyroid gland does not make enough thyroid hormone.

Thyroid Endocrine gland in the neck; secretes hormones that influence metabolism

The thyroid, or thyroid gland, is an endocrine gland in the neck consisting of two connected lobes. The lower two thirds of the lobes are connected by a thin band of tissue called the thyroid isthmus. The thyroid is located at the front of the neck, below the Adam's apple. Microscopically, the functional unit of the thyroid gland is the spherical thyroid follicle, lined with follicular cells (thyrocytes), and occasional parafollicular cells that surround a lumen containing colloid. The thyroid gland secretes three hormones: the two thyroid hormones – triiodothyronine (T3) and thyroxine (T4) – and a peptide hormone, calcitonin. The thyroid hormones influence the metabolic rate and protein synthesis, and in children, growth and development. Calcitonin plays a role in calcium homeostasis. Secretion of the two thyroid hormones is regulated by thyroid-stimulating hormone (TSH), which is secreted from the anterior pituitary gland. TSH is regulated by thyrotropin-releasing hormone (TRH), which is produced by the hypothalamus.

Graves disease Autoimmune endocrine disease

Graves disease, also known as toxic diffuse goiter, is an autoimmune disease that affects the thyroid. It frequently results in and is the most common cause of hyperthyroidism. It also often results in an enlarged thyroid. Signs and symptoms of hyperthyroidism may include irritability, muscle weakness, sleeping problems, a fast heartbeat, poor tolerance of heat, diarrhea and unintentional weight loss. Other symptoms may include thickening of the skin on the shins, known as pretibial myxedema, and eye bulging, a condition caused by Graves ophthalmopathy. About 25 to 80% of people with the condition develop eye problems.

Hypothyroidism Endocrine disease

Hypothyroidism, also called underactive thyroid or low thyroid, is a disorder of the endocrine system in which the thyroid gland does not produce enough thyroid hormone. It can cause a number of symptoms, such as poor ability to tolerate cold, a feeling of tiredness, constipation, slow heart rate, depression, and weight gain. Occasionally there may be swelling of the front part of the neck due to goiter. Untreated cases of hypothyroidism during pregnancy can lead to delays in growth and intellectual development in the baby or congenital iodine deficiency syndrome.

Thyroid-stimulating hormone (also known as thyrotropin, thyrotropic hormone, or abbreviated TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T4), and then triiodothyronine (T3) which stimulates the metabolism of almost every tissue in the body. It is a glycoprotein hormone produced by thyrotrope cells in the anterior pituitary gland, which regulates the endocrine function of the thyroid.


Myxedema is a term used synonymously with severe hypothyroidism. However, the term is also used to describe a dermatological change that can occur in hyperthyroidism and (rare) paradoxical cases of hypothyroidism. In this latter sense, myxedema refers to deposition of mucopolysaccharides in the dermis, which results in swelling of the affected area. One manifestation of myxedema occurring in the lower limb is pretibial myxedema, a hallmark of Graves disease, an autoimmune form of hyperthyroidism. Myxedema can also occur in Hashimoto thyroiditis and other long-standing forms of hypothyroidism.


Levothyroxine, also known as L-thyroxine, is a manufactured form of the thyroid hormone thyroxine (T4). It is used to treat thyroid hormone deficiency, including the severe form known as myxedema coma. It may also be used to treat and prevent certain types of thyroid tumors. It is not indicated for weight loss. Levothyroxine is taken by mouth or given by injection into a vein. Maximum effect from a specific dose can take up to six weeks to occur.

Ord's thyroiditis is a common form of thyroiditis, an autoimmune disease where the body's own antibodies fight the cells of the thyroid.

Thyroid peroxidase enzyme

Thyroid peroxidase, also called thyroperoxidase (TPO) or iodide peroxidase, is an enzyme expressed mainly in the thyroid where it is secreted into colloid. Thyroid peroxidase oxidizes iodide ions to form iodine atoms for addition onto tyrosine residues on thyroglobulin for the production of thyroxine (T4) or triiodothyronine (T3), the thyroid hormones. In humans, thyroperoxidase is encoded by the TPO gene.

Thyroid disease type of endocrine disease

Thyroid disease is a medical condition that affects the function of the thyroid gland. The thyroid gland is located at the front of the neck and produces thyroid hormones that travel through the blood to help regulate many other organs, meaning that it is an endocrine organ. These hormones normally act in the body to regulate energy use, infant development, and childhood development.

Thyroiditis endocrine disease

Thyroiditis is the inflammation of the thyroid gland. The thyroid gland is located on the front of the neck below the laryngeal prominence, and makes hormones that control metabolism.

De Quervains thyroiditis Thyroid disease

De Quervain's thyroiditis, also known as subacute granulomatous thyroiditis or giant cell thyroiditis, is a member of the group of thyroiditis conditions known as resolving thyroiditis. People of all ages and genders may be affected.

Postpartum thyroiditis refers to thyroid dysfunction occurring in the first 12 months after pregnancy and may involve hyperthyroidism, hypothyroidism or the two sequentially. It affects about 5-10% of all women within a year after giving birth. The first phase is typically hyperthyroidism. Then, the thyroid either returns to normal or a woman develops hypothyroidism. Of those women who experience hypothyroidism associated with postpartum thyroiditis, one in five will develop permanent hypothyroidism requiring lifelong treatment.

Hashimotos encephalopathy Human disease (neurological condition)

Hashimoto's encephalopathy, also known as steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), is a neurological condition characterized by encephalopathy, thyroid autoimmunity, and good clinical response to corticosteroids. It is associated with Hashimoto's thyroiditis, and was first described in 1966. It is sometimes referred to as a neuroendocrine disorder, although the condition's relationship to the endocrine system is widely disputed. It is recognized as a rare disease by the NIH Genetic and Rare Diseases Information Center.

Autoimmune hypophysitis is defined as inflammation of the pituitary gland due to autoimmunity.

Autoimmune thyroiditis, is a chronic disease in which the body interprets the thyroid glands and its hormone products T3, T4 and TSH as threats, therefore producing special antibodies that target the thyroid's cells, thereby destroying it.

Thyroid disease in pregnancy can affect the health of the mother as well as the child before and after delivery. Thyroid disorders are prevalent in women of child-bearing age and for this reason commonly present as a pre-existing disease in pregnancy, or after childbirth. Uncorrected thyroid dysfunction in pregnancy has adverse effects on fetal and maternal well-being. The deleterious effects of thyroid dysfunction can also extend beyond pregnancy and delivery to affect neurointellectual development in the early life of the child. Due to an increase in thyroxine binding globulin, an increase in placental type 3 deioidinase and the placental transfer of maternal thyroxine to the fetus, the demand for thyroid hormones is increased during pregnancy. The necessary increase in thyroid hormone production is facilitated by high human chorionic gonadotropin (hCG) concentrations, which bind the TSH receptor and stimulate the maternal thyroid to increase maternal thyroid hormone concentrations by roughly 50%. If the necessary increase in thyroid function cannot be met, this may cause a previously unnoticed (mild) thyroid disorder to worsen and become evident as gestational thyroid disease. Currently, there is not enough evidence to suggest that screening for thyroid dysfunction is beneficial, especially since treatment thyroid hormone supplementation may come with a risk of overtreatment. After women give birth, about 5% develop postpartum thyroiditis which can occur up to nine months afterwards.This is characterized by a short period of hyperthyroidism followed by a period of hypothyroidism; 20–40% remain permanently hypothyroid.

Antithyroid autoantibodies (or simply antithyroid antibodies) are autoantibodies targeted against one or more components on the thyroid. The most clinically relevant anti-thyroid autoantibodies are anti-thyroid peroxidase antibodies (anti-TPO antibodies, TPOAb), thyrotropin receptor antibodies (TRAb) and thyroglobulin antibodies (TgAb). TRAb's are subdivided into activating, blocking and neutral antibodies, depending on their effect on the TSH receptor. Anti-sodium/Iodide (Anti–Na+/I) symporter antibodies are a more recent discovery and their clinical relevance is still unknown. Graves' disease and Hashimoto's thyroiditis are commonly associated with the presence of anti-thyroid autoantibodies. Although there is overlap, anti-TPO antibodies are most commonly associated with Hashimoto's thyroiditis and activating TRAb's are most commonly associated with Graves' disease. Thyroid microsomal antibodies were a group of anti-thyroid antibodies; they were renamed after the identification of their target antigen (TPO).

Thyroid's secretory capacity is the maximum stimulated amount of thyroxine that the thyroid can produce in a given time-unit.

Thyroid disease in women is an autoimmune disease that affects the thyroid in women. This condition can have a profound effect during pregnancy and on the child. It also is called Hashimoto's thyroiditis (theye-royd-EYET-uhss). During pregnancy, the infant may be seriously affected and have a variety of birth defects. Many women with Hashimoto's disease develop an underactive thyroid. They may have mild or no symptoms at first, but symptoms tend to worsen over time. If a woman is pregnant and has symptoms of Hashimoto's disease, the clinician will do an exam and order one or more tests.


  1. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 "Hashimoto's Disease". NIDDK. May 2014. Archived from the original on 22 August 2016. Retrieved 9 August 2016.
  2. 1 2 Noureldine, SI; Tufano, RP (January 2015). "Association of Hashimoto's thyroiditis and thyroid cancer". Current Opinion in Oncology. 27 (1): 21–5. doi:10.1097/cco.0000000000000150. PMID   25390557. S2CID   32109200.
  3. 1 2 Hiromatsu, Y; Satoh, H; Amino, N (2013). "Hashimoto's thyroiditis: history and future outlook". Hormones (Athens, Greece). 12 (1): 12–8. doi:10.1007/BF03401282. PMID   23624127. S2CID   38996783.
  4. 1 2 3 4 5 Pyzik, A; Grywalska, E; Matyjaszek-Matuszek, B; Roliński, J (2015). "Immune disorders in Hashimoto's thyroiditis: what do we know so far?". Journal of Immunology Research. 2015: 979167. doi:10.1155/2015/979167. PMC   4426893 . PMID   26000316.
  5. 1 2 3 4 5 Akamizu, T; Amino, N; DeGroot, LJ; De Groot, LJ; Beck-Peccoz, P; Chrousos, G; Dungan, K; Grossman, A; Hershman, JM; Koch, C; McLachlan, R; New, M; Rebar, R; Singer, F; Vinik, A; Weickert, MO (2000). "Hashimoto's Thyroiditis". PMID   25905412.Cite journal requires |journal= (help)
  6. "Hashimoto's disease". Office on Women’s Health, U.S. Department of Health and Human Services. 12 June 2017. Archived from the original on 28 July 2017. Retrieved 17 July 2017.PD-icon.svgThis article incorporates text from this source, which is in the public domain.
  7. "Hashimoto Thyroiditis – Endocrine and Metabolic Disorders". Merck Manuals Professional Edition. July 2016. Retrieved 30 December 2017.
  8. "Hashimoto Thyroiditis – Hormonal and Metabolic Disorders". Merck Manuals Consumer Version. Retrieved 30 December 2017.
  9. Shoenfeld, Yehuda; Cervera, Ricard; Gershwin, M. Eric (2010). Diagnostic Criteria in Autoimmune Diseases. Springer Science & Business Media. p. 216. ISBN   9781603272858.
  10. 1 2 Moore, Elaine A.; Wilkinson, Samantha (2009). The Promise of Low Dose Naltrexone Therapy: Potential Benefits in Cancer, Autoimmune, Neurological and Infectious Disorders. McFarland. p. 30. ISBN   9780786452583.
  11. "Hashimoto's disease – Symptoms and causes". Mayo Clinic. Retrieved 5 October 2018.
  12. "Hashimoto's disease fact sheet". Office on Women's Health, U.S. Department of Health and Human Services, womenshealth.gov (or girlshealth.gov). 16 July 2012. Archived from the original on 2 December 2014. Retrieved 23 November 2014.
  13. Page 56 in: Staecker, Hinrich; Thomas R. Van De Water; Van de Water, Thomas R. (2006). Otolaryngology: basic science and clinical review. Stuttgart: Thieme. ISBN   978-0-86577-901-3.
  14. "Pathogenesis of Hashimoto's thyroiditis (chronic autoimmune thyroiditis)". UpToDate.
  15. "Hashimoto Thyroiditis". NCBI StatPearls. 2019.
  16. Dayan CM, Daniels GH (1996). "Chronic autoimmune thyroiditis". American Family Physician. 61 (4): 335:99–107. doi:10.1056/NEJM199607113350206. PMID   8649497. Archived from the original on 13 April 2014. Retrieved 11 April 2014.
  17. Chistiakov, Dimitry A (2005). "Immunogenetics of Hashimoto's thyroiditis". Journal of Autoimmune Diseases. 2 (1): 1. doi:10.1186/1740-2557-2-1. PMC   555850 . PMID   15762980.
  18. Kavvoura, F. K.; Akamizu, T.; Awata, T.; Ban, Y.; Chistiakov, D. A.; Frydecka, I.; Ghaderi, A.; Gough, S. C.; Hiromatsu, Y. (2007). "Cytotoxic T-Lymphocyte Associated Antigen 4 Gene Polymorphisms and Autoimmune Thyroid Disease: A Meta-Analysis". Journal of Clinical Endocrinology & Metabolism. 92 (8): 3162–70. doi: 10.1210/jc.2007-0147 . PMID   17504905.
  19. Jacobson, Eric M.; Tomer, Yaron (2007). "The CD40, CTLA-4, thyroglobulin, TSH receptor, and PTPN22 gene quintet and its contribution to thyroid autoimmunity: Back to the future". Journal of Autoimmunity. 28 (2–3): 85–98. doi:10.1016/j.jaut.2007.02.006. PMC   2043086 . PMID   17369021.
  20. Tandon, N.; Zhang, L.; Weetman, A. P. (May 1991). "HLA associations with Hashimoto's thyroiditis". Clinical Endocrinology. 34 (5): 383–386. doi:10.1111/j.1365-2265.1991.tb00309.x. ISSN   0300-0664. PMID   1676351.
  21. Radetti G (2014). "Clinical aspects of Hashimoto's thyroiditis". Paediatric Thyroidology. Endocr Dev (Review). Endocrine Development. 26. pp. 158–70. doi:10.1159/000363162. ISBN   978-3-318-02720-4. PMID   25231451.
  22. Saranac, L.; Zivanovic, S.; Bjelakovic, B.; Stamenkovic, H.; Novak, M.; Kamenov, B. (2011). "Why is the Thyroid So Prone to Autoimmune Disease". Hormone Research in Paediatrics. 75 (3): 157–65. doi: 10.1159/000324442 . PMID   21346360.
  23. 1 2 Kumar, Vinay (2010). "24: The Endocrine System". Robbins and Cotran Pathologic Mechanisms of Disease (8th ed.). Philadelphia, PA: Elsevier. p. 1113.
  24. Kumar, Vinay (2010). "24: The Endocrine System". Robbins and Cotran Pathologic Mechanisms of Disease (8th ed.). Philadelphia, PA: Elsevier. pp. 1112–1113.
  25. Grani, Giorgio; Carbotta, Giovanni; Nesca, Angela; D’Alessandri, Mimma; Vitale, Martina; Del Sordo, Marianna; Fumarola, Angela (4 October 2014). "A comprehensive score to diagnose Hashimoto's thyroiditis: a proposal". Endocrine. 49 (2): 361–5. doi:10.1007/s12020-014-0441-5. PMID   25280964. S2CID   23026213.
  26. Giannini, AJ (1986). The Biological Foundations of Clinical Psychiatry . New Hyde Park, NY: Medical Examination Publishing Company. pp.  193–198. ISBN   978-0-87488-449-4.
  27. "Hashimoto Thyroiditis Workup: Approach Considerations, Serum TSH Test and Other Studies, Ultrasonography". emedicine.medscape.com. Retrieved 4 December 2017.
  28. "Prasad's syndrome". Archived from the original on 9 June 2011.
  29. "Does Your Doctor Know About the New TSH Lab Standards?". Archived from the original on 4 December 2010.
  30. 1 2 3 Fabrizio Monaco (2012). Thyroid Diseases. Taylor and Francis. p. 78. ISBN   9781439868393.
  31. 1 2 Kumar, Vinay (2010). "24: The Endocrine System". Robbins and Cotran Pathologic Mechanisms of Disease (8th ed.). Philadelphia, PA: Elsevier. pp. 1111–205.
  32. Boyles, Med Page Today, May 23, 2013
  33. Wilson, Melissa A.; Trumble, Benjamin C.; Buetow, Kenneth H.; Garcia, Angela R.; Natri, Heini (1 July 2019). "The Pregnancy Pickle: Evolved Immune Compensation Due to Pregnancy Underlies Sex Differences in Human Diseases". Trends in Genetics. 35 (7): 478–488. doi:10.1016/j.tig.2019.04.008. ISSN   0168-9525. PMC   6611699 . PMID   31200807 . Retrieved 2 July 2019.
  34. Hakaru Hashimoto at Who Named It?
  35. Hashimoto, H. (1912). "Zur Kenntnis der lymphomatösen Veränderung der Schilddrüse (Struma lymphomatosa)". Archiv für Klinische Chirurgie (in German). 97: 219–248.
  36. 1 2 3 4 5 Lepoutre, Thibault; Debiève, Frederic; Gruson, Damien; Daumerie, Chantal (1 January 2012). "Reduction of Miscarriages through Universal Screening and Treatment of Thyroid Autoimmune Diseases". Gynecologic and Obstetric Investigation. 74 (4): 265–273. doi: 10.1159/000343759 . PMID   23147711.
  37. 1 2 Zaletel, Katja (2011). "Thyroid physiology and autoimmunity in pregnancy and after delivery". Expert Review of Clinical Immunology. 7 (5): 697–707. doi: 10.1586/eci.11.42 . PMID   21895480 . Retrieved 4 October 2015.
  38. Budenhofer, Brigitte K.; Ditsch, Nina; Jeschke, Udo; Gärtner, Roland; Toth, Bettina (27 October 2012). "Thyroid (dys-)function in normal and disturbed pregnancy". Archives of Gynecology and Obstetrics. 287 (1): 1–7. doi:10.1007/s00404-012-2592-z. ISSN   0932-0067. PMID   23104052. S2CID   24969196.
  39. Balucan, Francis S.; Morshed, Syed A.; Davies, Terry F. (1 January 2013). "Thyroid Autoantibodies in Pregnancy: Their Role, Regulation and Clinical Relevance". Journal of Thyroid Research. 2013: 182472. doi:10.1155/2013/182472. PMC   3652173 . PMID   23691429.
  40. "Endocrine Experts Support Screening for Thyroid Dysfunction in Pregnant Women". Endocrine Society. Endocrine Society. 26 March 2015. Archived from the original on 8 October 2015. Retrieved 4 October 2015.
  41. Carlé, Allan; Pedersen, Inge Bülow; Knudsen, Nils; Perrild, Hans; Ovesen, Lars; Rasmussen, Lone Banke; Laurberg, Peter (2 April 2014). "Development of Autoimmune Overt Hypothyroidism Is Highly Associated With Live Births and Induced Abortions but Only in Premenopausal Women". The Journal of Clinical Endocrinology & Metabolism. 99 (6): 2241–2249. doi: 10.1210/jc.2013-4474 . ISSN   0021-972X. PMID   24694338.
External resources