Hashimoto's thyroiditis overview: Difference between revisions
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==Overview== | ==Overview== | ||
'''Hashimoto's thyroiditis''' or '''chronic lymphocytic thyroiditis''' is an [[autoimmune disease]] where the body's own [[antibody|antibodies]] attack the [[cell (biology)|cell]]s of the [[thyroid]].Hashimoto's thyroiditis was first described by [[Hashimoto Hakaru]] in 1912. He named it struma lymphomatosa which was renamed as Hashimoto's thyroiditis in 1931. [[Hashimoto's thyroiditis]] can be classified as primary or secondary types. Rarely, [[Hashimoto's thyroiditis]] can be categorized under the [[Polyglandular autoimmune syndrome|polyglandular syndromes]]. [[Hashimoto's thyroiditis]] (HT) is characterized by | '''Hashimoto's thyroiditis''' or '''chronic lymphocytic thyroiditis''' is an [[autoimmune disease]] where the body's own [[antibody|antibodies]] attack the [[cell (biology)|cell]]s of the [[thyroid]]. Hashimoto's thyroiditis was first described by [[Hashimoto Hakaru]] in 1912. He named it struma lymphomatosa which was renamed as Hashimoto's thyroiditis in 1931. [[Hashimoto's thyroiditis]] can be classified as primary or secondary types. Rarely, [[Hashimoto's thyroiditis]] can be categorized under the [[Polyglandular autoimmune syndrome|polyglandular syndromes]]. [[Hashimoto's thyroiditis]] (HT) is characterized by [[lymphocytic]] infiltration of the [[thyroid gland]] and production of [[antibodies]] that recognize thyroid-specific antigens. The pathogenesis is not yet completely understood. Thyroid cells undergo atrophy or transform into a type of [[follicular cell]] rich in [[mitochondria]] called Hurthle cell. It is currently thought that the disease is caused by abnormalities in [[Cellular immunity|cellular]] and [[humoral immunity]] which results in a localized [[cell-mediated immune response]] directed toward the thyroid parenchymal cells. This results in the decreased production of [[thyroid hormones]]. [[Hashimoto's thyroiditis]] is particularly common in middle aged women, Asians, and Whites. [[Hashimoto's thyroiditis]] usually begins slowly and may progress to [[hypothyroidism]]. Complications include [[heart failure]], [[lymphoma]], [[Myxedema|myxedem]]<nowiki/>a, and [[Tracheal compression|cervical compression]]. A positive history of [[autoimmune diseases]] and certain drug use are suggestive of Hashimoto's thyroiditis. The most common symptoms of Hashimoto's thyroiditis include [[fatigue]], [[constipation]], and cold intolerance. Laboratory findings consistent with the diagnosis of [[Hashimoto's thyroiditis]] usually include increased [[Thyroid-stimulating hormone|thyroid stimulating hormone]], decreased [[free T3]] and [[free T4]], and [[thyroid peroxidase|anti-thyroid peroxidase antibodies]]. [[Ultrasound]] findings associated with [[Hashimoto's thyroiditis]] are reduced [[echogenicity]], [[glandular]] irregularities, and [[nodules]]. 24-hour [[iodine-123]] uptake is decreased in [[Hashimoto's thyroiditis]]. The mainstay of therapy for [[Hashimoto's thyroiditis]] is [[Levothyroxine|synthetic levothyroxine]]. [[Corticosteroid]]<nowiki/>s and [[selenium]] can also be used in certain cases. [[Thyroidectomy]] is usually performed when the [[enlarged thyroid]] produces [[Tracheal compression|cervical compression]] symptoms and there is a high suspicion for [[malignancy]]. | ||
==Historical Perspective== | ==Historical Perspective== | ||
Hashimoto's thyroiditis was first described by [[Hashimoto Hakaru]] in 1912. He named it struma lymphomatosa which was renamed as Hashimoto's thyroiditis in 1931. | Hashimoto's thyroiditis was first described by [[Hashimoto Hakaru]] in 1912. He named it [[struma lymphomatosa]] which was renamed as Hashimoto's thyroiditis in 1931. | ||
==Classification== | ==Classification== | ||
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==Pathophysiology== | ==Pathophysiology== | ||
[[Hashimoto's thyroiditis]] (HT) is characterized by | [[Hashimoto's thyroiditis]] (HT) is characterized by lymphocytic infiltration of the [[thyroid gland]] and production of antibodies that recognize thyroid-specific antigens.The [[pathogenesis]] is not yet completely understood. [[Thyroid]] cells undergo atrophy or transform into a type of [[follicular cell]] rich in [[mitochondria]] called Hurthle cell. It is currently thought that the disease is caused by abnormalities in [[Cellular immunity|cellular]] and [[humoral immunity]] which results in a localized [[cell-mediated immune response]] directed toward the thyroid parenchymal cells. This results in the decreased production of [[thyroid hormones]]. | ||
==Causes== | ==Causes== | ||
Hashimoto's thyroiditis may be caused by [[T cell|T cells]] and [[B cell|B cells]] auto activation, genetic factors, and autoimmune antibodies against [[Thyrotropin receptor|thyrotropin receptors]]. | Hashimoto's thyroiditis may be caused by [[T cell|T cells]] and [[B cell|B cells]] auto activation, genetic factors, and [[autoimmune]] antibodies against [[Thyrotropin receptor|thyrotropin receptors]]. | ||
==Differentiating Hashimoto's Thyroiditis from other Diseases== | ==Differentiating Hashimoto's Thyroiditis from other Diseases== | ||
[[Hashimoto's thyroiditis]] must be differentiated from other causes of [[thyroiditis]], such as [[De Quervain's thyroiditis]], [[Riedel's thyroiditis]], and suppurative thyroiditis. | [[Hashimoto's thyroiditis]] must be differentiated from other causes of [[thyroiditis]], such as [[De Quervain's thyroiditis]], [[Riedel's thyroiditis]], and suppurative [[thyroiditis]]. | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
[[Hashimoto's thyroiditis]] is particularly common in middle aged women, Asians, and Whites. Annually, there are around 22 per 100,000 individuals worldwide. | [[Hashimoto's thyroiditis]] is particularly common in middle aged women, Asians, and Whites. Annually, there are around 22 per 100,000 individuals worldwide. | ||
==Risk Factors== | ==Risk Factors== | ||
Common risk factors in the development of [[Hashimoto's thyroiditis]] are family history, female gender, and other [[autoimmune diseases]]. | Common [[risk factors]] in the development of [[Hashimoto's thyroiditis]] are [[family history]], female gender, and other [[autoimmune diseases]]. | ||
==Screening== | ==Screening== | ||
There is insufficient evidence to recommend routine screening for [[Hashimoto's thyroiditis]]. | There is insufficient evidence to recommend routine screening for [[Hashimoto's thyroiditis]]. | ||
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===Echocardiography or Ultrasound=== | ===Echocardiography or Ultrasound=== | ||
Ultrasound findings associated with [[Hashimoto's thyroiditis]] are reduced [[echogenicity]], glandular irregularities, and nodules. | Ultrasound findings associated with [[Hashimoto's thyroiditis]] are reduced [[echogenicity]], [[glandular]] irregularities, and [[nodules]]. | ||
===Other Imaging Findings=== | ===Other Imaging Findings=== | ||
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===Other Diagnostic Studies=== | ===Other Diagnostic Studies=== | ||
The histological analysis in Hashimoto's thyroiditis may show inflammatory cell infiltration and hurthle cells. [[FNA|Fine needle aspiration cytology]] helps to differentiate between the benign and malignant nodules. <ref name="pmid24434360">{{cite journal |vauthors=Caturegli P, De Remigis A, Rose NR |title=Hashimoto thyroiditis: clinical and diagnostic criteria |journal=Autoimmun Rev |volume=13 |issue=4-5 |pages=391–7 |year=2014 |pmid=24434360 |doi=10.1016/j.autrev.2014.01.007 |url=}}</ref><ref name="urlThyroiditis — NEJM">{{cite web |url=http://www.nejm.org/doi/full/10.1056/NEJMra021194 |title=Thyroiditis — NEJM |format= |work= |accessdate=}}</ref> | The histological analysis in Hashimoto's thyroiditis may show [[inflammatory]] cell infiltration and hurthle cells. [[FNA|Fine needle aspiration cytology]] helps to differentiate between the [[benign]] and [[malignant]] [[nodules]]. <ref name="pmid24434360">{{cite journal |vauthors=Caturegli P, De Remigis A, Rose NR |title=Hashimoto thyroiditis: clinical and diagnostic criteria |journal=Autoimmun Rev |volume=13 |issue=4-5 |pages=391–7 |year=2014 |pmid=24434360 |doi=10.1016/j.autrev.2014.01.007 |url=}}</ref><ref name="urlThyroiditis — NEJM">{{cite web |url=http://www.nejm.org/doi/full/10.1056/NEJMra021194 |title=Thyroiditis — NEJM |format= |work= |accessdate=}}</ref> | ||
==Treatment== | ==Treatment== | ||
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The mainstay of therapy for [[Hashimoto's thyroiditis]] is [[Levothyroxine|synthetic levothyroxine]]. [[Corticosteroid]]<nowiki/>s and [[selenium]] can also be used in certain cases. | The mainstay of therapy for [[Hashimoto's thyroiditis]] is [[Levothyroxine|synthetic levothyroxine]]. [[Corticosteroid]]<nowiki/>s and [[selenium]] can also be used in certain cases. | ||
===Surgery=== | ===Surgery=== | ||
[[Thyroidectomy]] is usually performed when the enlarged thyroid produces [[Tracheal compression|cervical compression]] symptoms and there is a high suspicion for malignancy. | [[Thyroidectomy]] is usually performed when the enlarged thyroid produces [[Tracheal compression|cervical compression]] symptoms and there is a high suspicion for [[malignancy]]. | ||
===Primary Prevention=== | ===Primary Prevention=== | ||
There are no primary preventive measures available for [[Hashimoto's thyroiditis]]. | There are no primary preventive measures available for [[Hashimoto's thyroiditis]]. | ||
===Secondary Prevention=== | ===Secondary Prevention=== | ||
There are no secondary preventive measures available for [[Hashimoto's thyroiditis]]. | There are no secondary preventive measures available for [[Hashimoto's thyroiditis]]. | ||
==References== | ==References== | ||
Revision as of 15:27, 31 August 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]
Overview
Hashimoto's thyroiditis or chronic lymphocytic thyroiditis is an autoimmune disease where the body's own antibodies attack the cells of the thyroid. Hashimoto's thyroiditis was first described by Hashimoto Hakaru in 1912. He named it struma lymphomatosa which was renamed as Hashimoto's thyroiditis in 1931. Hashimoto's thyroiditis can be classified as primary or secondary types. Rarely, Hashimoto's thyroiditis can be categorized under the polyglandular syndromes. Hashimoto's thyroiditis (HT) is characterized by lymphocytic infiltration of the thyroid gland and production of antibodies that recognize thyroid-specific antigens. The pathogenesis is not yet completely understood. Thyroid cells undergo atrophy or transform into a type of follicular cell rich in mitochondria called Hurthle cell. It is currently thought that the disease is caused by abnormalities in cellular and humoral immunity which results in a localized cell-mediated immune response directed toward the thyroid parenchymal cells. This results in the decreased production of thyroid hormones. Hashimoto's thyroiditis is particularly common in middle aged women, Asians, and Whites. Hashimoto's thyroiditis usually begins slowly and may progress to hypothyroidism. Complications include heart failure, lymphoma, myxedema, and cervical compression. A positive history of autoimmune diseases and certain drug use are suggestive of Hashimoto's thyroiditis. The most common symptoms of Hashimoto's thyroiditis include fatigue, constipation, and cold intolerance. Laboratory findings consistent with the diagnosis of Hashimoto's thyroiditis usually include increased thyroid stimulating hormone, decreased free T3 and free T4, and anti-thyroid peroxidase antibodies. Ultrasound findings associated with Hashimoto's thyroiditis are reduced echogenicity, glandular irregularities, and nodules. 24-hour iodine-123 uptake is decreased in Hashimoto's thyroiditis. The mainstay of therapy for Hashimoto's thyroiditis is synthetic levothyroxine. Corticosteroids and selenium can also be used in certain cases. Thyroidectomy is usually performed when the enlarged thyroid produces cervical compression symptoms and there is a high suspicion for malignancy.
Historical Perspective
Hashimoto's thyroiditis was first described by Hashimoto Hakaru in 1912. He named it struma lymphomatosa which was renamed as Hashimoto's thyroiditis in 1931.
Classification
On the basis of the etiology, Hashimoto's thyroiditis can be classified as primary or secondary types. Rarely, Hashimoto's thyroiditis can be categorized under the polyglandular syndromes.
Pathophysiology
Hashimoto's thyroiditis (HT) is characterized by lymphocytic infiltration of the thyroid gland and production of antibodies that recognize thyroid-specific antigens.The pathogenesis is not yet completely understood. Thyroid cells undergo atrophy or transform into a type of follicular cell rich in mitochondria called Hurthle cell. It is currently thought that the disease is caused by abnormalities in cellular and humoral immunity which results in a localized cell-mediated immune response directed toward the thyroid parenchymal cells. This results in the decreased production of thyroid hormones.
Causes
Hashimoto's thyroiditis may be caused by T cells and B cells auto activation, genetic factors, and autoimmune antibodies against thyrotropin receptors.
Differentiating Hashimoto's Thyroiditis from other Diseases
Hashimoto's thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain's thyroiditis, Riedel's thyroiditis, and suppurative thyroiditis.
Epidemiology and Demographics
Hashimoto's thyroiditis is particularly common in middle aged women, Asians, and Whites. Annually, there are around 22 per 100,000 individuals worldwide.
Risk Factors
Common risk factors in the development of Hashimoto's thyroiditis are family history, female gender, and other autoimmune diseases.
Screening
There is insufficient evidence to recommend routine screening for Hashimoto's thyroiditis.
Natural History, Complications and Prognosis
Hashimoto's thyroiditis usually begins slowly and may progress to hypothyroidism. Complications include heart failure, lymphoma, myxedema, and cervical compression.
Diagnosis
History and Symptoms
The hallmark of Hashimoto's thyroiditis is hypothyroidism. A positive history of autoimmune diseases and certain drug use are suggestive of Hashimoto's thyroiditis. The most common symptoms of Hashimoto's thyroiditis include fatigue, constipation, and cold intolerance.
Physical Examination
Patients with Hashimoto's thyroiditis usually appear fatigued and have myxedema. Physical examination of patients with Hashimoto's thyroiditis is usually remarkable for bradycardia, bradypnea and delayed reflexes.[1]
Laboratory Findings
Laboratory findings consistent with the diagnosis of Hashimoto's thyroiditis usually include increased thyroid stimulating hormone, decreased free T3 and free T4, and anti-thyroid peroxidase antibodies.
Electrocardiogram
The findings associated with ECG in Hashimoto's thyroiditis are bradycardia and decreased amplitude of cardiac waves.
Chest X Ray
The findings associated with Chest X ray in Hashimoto's thyroiditis are pleural effusion and cardiomegaly.
CT
Non-contrast CT may be used in Hashimoto's thyroiditis to assess the tracheal or esophageal compression.
MRI
There are no MRI findings associated with Hashimoto's thyroiditis.
Echocardiography or Ultrasound
Ultrasound findings associated with Hashimoto's thyroiditis are reduced echogenicity, glandular irregularities, and nodules.
Other Imaging Findings
24-hour iodine-123 uptake is decreased in Hashimoto's thyroiditis.
Other Diagnostic Studies
The histological analysis in Hashimoto's thyroiditis may show inflammatory cell infiltration and hurthle cells. Fine needle aspiration cytology helps to differentiate between the benign and malignant nodules. [1][2]
Treatment
Medical Therapy
The mainstay of therapy for Hashimoto's thyroiditis is synthetic levothyroxine. Corticosteroids and selenium can also be used in certain cases.
Surgery
Thyroidectomy is usually performed when the enlarged thyroid produces cervical compression symptoms and there is a high suspicion for malignancy.
Primary Prevention
There are no primary preventive measures available for Hashimoto's thyroiditis.
Secondary Prevention
There are no secondary preventive measures available for Hashimoto's thyroiditis.
References
- ↑ 1.0 1.1 Caturegli P, De Remigis A, Rose NR (2014). "Hashimoto thyroiditis: clinical and diagnostic criteria". Autoimmun Rev. 13 (4–5): 391–7. doi:10.1016/j.autrev.2014.01.007. PMID 24434360.
- ↑ "Thyroiditis — NEJM".