Silent thyroiditis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Silent thyroiditis, is also known as subacute lymphocytic thyroiditis. Silent thyroiditis is a type of resolving thyroiditis, which also includes postpartum thyroiditis. Silent thyroiditis was first described as the painless form of the subacute thyroiditis as the clinical course is same. It was differentiated from postpartum thyroiditis on the basis of thyroid involvement outside of the postpartum period. The exact pathogenesis of silent thyroiditis is not fully understood. It is thought that silent thyroiditis is the result of an autoimmune phenomenon. Activated matured T-cells (HLA-DR+CD3+), activated helper/inducer T-cells (HLA-DR+CD4+), activated suppressor, and cytotoxic T-cells (HLA-DR+CD8+) were higher in patients with silent thyroiditis as compared to the healthy controls. It indicates that the activation of T cells, especially of helper/inducer T cells, might have an important role in the pathogenesis of silent thyroiditis. Silent thyroiditis is associated with the HLA-DR3 and DR5 genes. Lymphocytic infiltration of the thyroid gland, the absence of Hurthle cells and germinal centers on histological analysis are the microscopic histopathological findings suggestive of silent thyroiditis. Silent thyroiditis may be caused by the activation of helper T cells and cytotoxic T cells, genetic factors, and autoimmune antibodies. Silent thyroiditis is a rare disease with the incidence of up to 23000 per 100,000 individuals with hyperthyroidism. The prevalence of silent thyroiditis is approximately 1000 per 100,000 individuals with thyrotoxicosis. Silent thyroiditis commonly affects patients in 30-40 years of age. Females are more commonly affected by silent thyroiditis than males. The female to male ratio is approximately 4 to 1. Silent thyroiditis is more common in areas of higher dietary iodine intake. Common risk factors in the development of silent thyroiditis include lithium, radiation therapy in Hodgkin’s lymphoma, cessation of corticosteroids in Cushing’s syndrome (post adrenalectomy), and certain autoimmune conditions. Silent thyroiditis presents with the symptoms of thyrotoxicosis. It further leads to a euthyroid phase and eventually hypothyroid phase before the complete resolution of the disease. Complications may include hypothyroidism. There are no established criteria for the diagnosis of silent thyroiditis. Decreased radioactive iodine uptake, elevated serum T3, and T4 are helpful in diagnosing silent thyroiditis. Histopathology is also important to differentiate silent thyroiditis from other forms of thyroiditis. Patients with silent thyroiditis usually appear fatigued and restless. Patients with silent thyroiditis may have the history of other autoimmune diseases such as SLE, immune thrombocytopenic purpura (ITP), and lymphocytic hypophysitis. The most common symptoms of silent thyroiditis are palpitations, tachycardia, nervousness, and tremors. Physical examination of patients with silent thyroiditis is usually remarkable for tachycardia and palpitations. In the recovery phase of silent thyroiditis, the patient may show signs of hypothyroidism. Laboratory findings consistent with the diagnosis of silent thyroiditis usually include increased free T3, free T4, decreased thyroid stimulating hormone in thyrotoxicosis and decreased free T3, free T4, increased thyroid stimulating hormone in hypothyroidism. Anti-thyroid peroxidase antibody is usually high. The most common EKG finding associated with the thyrotoxicosis in silent thyroiditis is sinus tachycardia. Rarely signs of myocardial damage, including ST segment elevation and arrhythmias, can also be seen in thyrotoxicosis. MRI is not used in the diagnosis of silent thyroiditis. However, diffusion-weighted MRI shows low apparent diffusion coefficient (ADC). 24-hour iodine-123 uptake is decreased in silent thyroiditis. The histological analysis in silent thyroiditis may show the infiltration of inflammatory cells, lymphoid follicles, and loss of the follicular integrity. Fine needle aspiration cytology helps to differentiate between the benign and malignant nodules. Pharmacologic medical therapies for silent thyroiditis include beta blockers for thyrotoxicosis symptoms and levothyroxine for the hypothyroidism if it follows the hyperthyroid state. Surgical intervention is not usually recommended for the management of silent thyroiditis.Thyroidectomy is considered only when there are repeated relapses despite appropriate treatment.

Silent thyroiditis was identified as a separate form of thyroiditis a few decades ago. Silent thyroiditis was first described as the painless form of the subacute thyroiditis as the clinical course is same. It was differentiated from postpartum thyroiditis on the basis of thyroid involvement outside of the postpartum period.

Silent thyroiditis can be classified according to the development of symptoms into the hyperthyroid stage, euthyroid stage, and hypothyroid stage.

The exact pathogenesis of silent thyroiditis is not fully understood. It is thought that silent thyroiditis is the result of an autoimmune phenomenon. Activated matured T-cells (HLA-DR+CD3+), activated helper/inducer T-cells (HLA-DR+CD4+), activated suppressor, and cytotoxic T-cells (HLA-DR+CD8+) were higher in patients with silent thyroiditis as compared to the healthy controls. It indicates that the activation of T cells, especially of helper/inducer T cells, might have an important role in the pathogenesis of silent thyroiditis. Silent thyroiditis is associated with the HLA-DR3 and DR5 genes. Lymphocytic infiltration of the thyroid gland, the absence of Hurthle cells and germinal centers on histological analysis are the microscopic histopathological findings suggestive of silent thyroiditis.

Silent thyroiditis may be caused by the activation of helper T cells and cytotoxic T cells, genetic factors, and autoimmune antibodies.

Silent thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain’s thyroiditis, Hashimoto’s thyroiditis, Riedel’s thyroiditis, and suppurative thyroiditis. Silent thyroiditis must also be differentiated from other diseases which cause hypothyroidism. As silent thyroiditis may cause transient thyrotoxic symptoms, the diseases causing thyrotoxicosis must also be considered in the differential diagnosis.

Silent thyroiditis is a rare disease with the incidence of up to 23000 per 100,000 individuals with hyperthyroidism. The prevalence of silent thyroiditis is approximately 1000 per 100,000 individuals with thyrotoxicosis. Silent thyroiditis commonly affects patients in 30-40 years of age. Females are more commonly affected by silent thyroiditis than males. The female to male ratio is approximately 4 to 1. Silent thyroiditis is more common in areas of higher dietary iodine intake.

Common risk factors in the development of silent thyroiditis include lithium, radiation therapy in Hodgkin’s lymphoma, cessation of corticosteroids in Cushing’s syndrome (post adrenalectomy), and certain autoimmune conditions.

There is insufficient evidence to recommend routine screening for silent thyroiditis.

Silent thyroiditis presents with the symptoms of thyrotoxicosis. It further leads to a euthyroid phase and eventually hypothyroid phase before the complete resolution of the disease. Complications may include hypothyroidism.

There are no established criteria for the diagnosis of silent thyroiditis. Decreased radioactive iodine uptake, elevated serum T3, and T4 are helpful in diagnosing silent thyroiditis. Histopathology is also important to differentiate silent thyroiditis from other forms of thyroiditis.

Patients with silent thyroiditis may have the history of other autoimmune diseases such as SLE, immune thrombocytopenic purpura (ITP), and lymphocytic hypophysitis. The most common symptoms of silent thyroiditis are palpitations, tachycardia, nervousness, and tremors.

Patients with silent thyroiditis usually appear fatigued and restless. Physical examination of patients with silent thyroiditis is usually remarkable for tachycardia and palpitations. In the recovery phase of silent thyroiditis, the patient may show signs of hypothyroidism.

Laboratory findings consistent with the diagnosis of silent thyroiditis usually include increased free T3, free T4, decreased thyroid stimulating hormone in thyrotoxicosis and decreased free T3, free T4, increased thyroid stimulating hormone in hypothyroidism. Anti-thyroid peroxidase antibody is usually high.

The most common EKG finding associated with the thyrotoxicosis in silent thyroiditis is sinus tachycardia. Rarely signs of myocardial damage, including ST segment elevation and arrhythmias, can also be seen in thyrotoxicosis.

There are no x-ray findings associated with silent thyroiditis.

There are no echocardiograms associated with silent thyroiditis. Ultrasound findings associated with silent thyroiditis are hypoechoic areas, glandular irregularities, and nonhomogeneous echotexture.

There are no CT scan findings associated with silent thyroiditis.

MRI is not used in the diagnosis of silent thyroiditis. However, diffusion-weighted MRI shows low apparent diffusion coefficient (ADC).

24-hour iodine-123 uptake is decreased in silent thyroiditis.

The histological analysis in silent thyroiditis may show the infiltration of inflammatory cells, lymphoid follicles, and loss of the follicular integrity. Fine needle aspiration cytology helps to differentiate between the benign and malignant nodules.

Pharmacologic medical therapies for silent thyroiditis include beta blockers for thyrotoxicosis symptoms and levothyroxine for the hypothyroidism if it follows the hyperthyroid state.

Surgical intervention is not usually recommended for the management of silent thyroiditis.Thyroidectomy is considered only when there are repeated relapses despite appropriate treatment.

There are no established measures for the primary prevention of silent thyroiditis.

There are no established measures for the secondary prevention of silent thyroiditis.

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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]

Silent thyroiditis was described as a separate form of thyroiditis a few decades ago. Silent thyroiditis was primarily known as the painless form of the subacute thyroiditis as clinical course is the same. It was differentiated from postpartum thyroiditis on the basis of thyroid involvement outside of the postpartum period.

Silent thyroiditis was primarily known as the painless form of the subacute thyroiditis as clinical course is the same. It was differentiated from postpartum thyroiditis on the basis of thyroid involvement outside of the postpartum period. In 1975, the detailed description of thyrotoxicosis caused by silent thyroiditis was published.^[1][2][3]

• In 1975, Papapetrou PD and Jackson IM first described the thyrotoxicosis caused by the silent thyroiditis.
• Postpartum thyroiditis is indistinguishable from silent thyroiditis. The sporadic nature of silent thyroiditis explains the involvement of thyroiditis outside of the postpartum period.
• Silent thyroiditis is also identical to the lymphocytic thyroiditis (Hashimoto’s thyroiditis) on biopsy but was differentiated on the basis of less extensive thyroid involvement.

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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]

Silent thyroiditis can be classified according to the development of symptoms into the hyperthyroid stage, euthyroid stage, and hypothyroid stage.

Silent thyroiditis can be classified according to the development of symptoms into the following stages:^[1][2]

• Hyperthyroid stage
  • It includes the symptoms of thyrotoxicosis.

• Euthyroid stage
  • Thyroid hormones are within the normal range and there are no specific symptoms.

• Hypothyroid stage
  • Thyroid hormones are decreased as a result of glandular damage.

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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]

The exact pathogenesis of silent thyroiditis is not fully understood. It is thought that silent thyroiditis is the result of an autoimmune phenomenon. Activated matured T-cells (HLA-DR+CD3+), activated helper/inducer T-cells (HLA-DR+CD4+), activated suppressor, and cytotoxic T-cells (HLA-DR+CD8+) were higher in patients with silent thyroiditis as compared to the healthy controls. It indicates that the activation of T cells, especially helper/inducer T cells, might have an important role in the pathogenesis of silent thyroiditis. Silent thyroiditis is associated with the HLA-DR3 and DR5 genes. Lymphocytic infiltration of the thyroid gland, the absence of Hurthle cells and germinal centers on histological analysis are the microscopic histopathological findings suggestive of silent thyroiditis.

The control, synthesis, and release of the thyroid hormone is usually controlled by hypothalamus and pituitary gland.[1][2] Thyroid hormones (T3 and T4) regulates the basal metabolic rate and influences oxygen consumption by tissues. They are crucial for normal development of the brain and growth of the body. Secretion of thyroid hormones follows upper control mechanisms from the hypothalamus and the pituitary. Thyroid releasing hormone (TRH) acts on thyrotropes releasing cells in the pituitary causing them to release thyroid stimulating hormone (TSH). TSH acts on thyroid gland by binding to specific membrane receptors and activating an intracellular pathway involving cAMP that ends in the formation and secretion of thyroid hormones. Iodine is essential for the synthesis of thyroid hormones. Iodide is taken up through a special Na/I transporter found in the membrane of thyroid follicular cell. After the iodide uptake, it goes through a series of organic reactions ending in the formation of the two forms of thyroid hormones: T3 and T4. T3 and T4 remain stored in the thyroglobulin within thyroid follicles and are released in response to further stimulation by TSH to the thyroid follicles. While T3 is 3 to 5 times more potent than T4, it represents only one-fourth of the total hormone secretion. T3 is thought to be the biologically active form of the hormone. Most of the circulating T3 is due to peripheral conversion of T4 in the liver and peripheral tissues while only a small percentage is secreted directly from the thyroid gland itself. T3 and T4 act on nuclear receptors (DNA binding proteins) and cause the regulate the transcription of many proteins to regulate the metabolic rate of the body. The higher regulation of thyroxine secretion follows the negative feedback role, meaning that high levels of T3 and T4 will suppress TRH and TSH secretion and vice versa (Low levels of thyroxine will stimulate TRH and TSH secretion). This is useful in diagnosing the cause of hyperthyroidism. TSH will be low in primary hyperthyroidism where the gland is the source of the excess hormones. In secondary hyperthyroidism, TSH will be high as the pituitary or the hypothalamus are the sources of the disease.

• The exact pathogenesis of silent thyroiditis is not fully understood. It is thought that silent thyroiditis is the result of an autoimmune phenomenon. The following features are suggestive of an autoimmune pathogenesis of silent thyroiditis:^[3][4][5][6]
  • Lymphocytic infiltration of the thyroid gland
  • Presence of antithyroid antibodies
  • Association with HLA-DR3 and DR5
  • Presence of anti-DNA antibodies

• Activated matured T-cells (HLA-DR+CD3+), activated helper/inducer T-cells (HLA-DR+CD4+), activated suppressor, and cytotoxic T-cells (HLA-DR+CD8+) were higher in patients with silent thyroiditis as compared to the healthy controls. It indicates that the activation of T-cells, especially of helper/inducer T cells, might have an important role in the pathogenesis of silent thyroiditis.^[7]

Silent thyroiditis is associated with the following HLA genes:^[5]

• HLA-DR3
• HLA-DR5

The following conditions are associated with silent thyroiditis:^{[8][9][10][11]}

• SLE
• Lymphocytic hypophysitis
• Immune thrombocytopenic purpura (ITP)
• Cushing’s syndrome (post adrenalectomy and steroid therapy cessation)
• Hodgkin’s lymphoma (post-irradiation)

Gross pathology findings in silent thyroiditis include:^[12]

• Diffuse goiter
• Slightly enlarged thyroid gland

• Microscopic histopathological findings in silent thyroiditis include:^[3][13]
  • Diffuse lymphocytic infiltrate
  • Lack of Hurthle cells (Askanazy cells) and germinal centers
  • Lack of fibrosis

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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]

Silent thyroiditis may be caused by the activation of helper T cells and cytotoxic T cells, genetic factors, and autoimmune antibodies.

Silent thyroiditis is usually caused by:^[1][2][3][4]

• Abnormalities in the regulatory T cells and cytotoxic T-cells
• HLA-DR3 and HLA-DR5 involvement
• Antithyroid antibodies

For the factors involved in the development of silent thyroiditis, please click here.

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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]

Silent thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain’s thyroiditis, Hashimoto’s thyroiditis, Riedel’s thyroiditis, and suppurative thyroiditis. Silent thyroiditis must also be differentiated from other diseases which cause hypothyroidism. As silent thyroiditis may cause transient thyrotoxic symptoms, the diseases causing thyrotoxicosis must also be considered in the differential diagnosis.

• Silent thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain’s thyroiditis, Hashimoto’s thyroiditis, Riedel’s thyroiditis, and suppurative thyroiditis.^[1]

Conditions	Causes	Age at onset	Pathological findings	Diagnostic approach
Silent thyroiditis	Autoimmune	All ages, peak at 30-40	Lymphocytic infiltration Lymphoid follicles	Increased TSH (hypothyroidism) and/or Decreased TSH (transient hypothyroidism) TPO antibodies present in high titer I-123 uptake usually decreased
Hashimoto’s thyroiditis	Autoimmune	All ages, peak at 30-50	Lymphocytic infiltration Germinal centers Fibrosis (in some variants)	Increased TSH (hypothyroidism) TPO antibodies present in high titer I-123 uptake usually decreased
Painful subacute (De Quervain’s) thyroiditis	Unknown	20-60	Giant cells Granulomas	Increased TSH (hypothyroidism) and/or Decreased TSH (Thyrotoxicosis) TPO antibodies absent or very low titer I-123 uptake decreased
Postpartum thyroiditis	Autoimmune	Childbearing age	Lymphocytic infiltration	Increased TSH (hypothyroidism) and/or Decreased TSH (transient hypothyroidism) TPO antibodies present in high titer I-123 uptake usually decreased
Riedel’s thyroiditis	Unknown	30-60	Dense fibrosis	Normal TSH (euthyroidism) TPO antibodies usually present I-123 uptake decreased or normal
Suppurative thyroiditis	Infection	Children, 20-40	Abscess formation	Normal TSH (euthyroidism) TPO antibodies absent I-123 uptake normal

• Silent thyroiditis must be differentiated from other causes of hypothyroidism on the basis of history and symptoms and laboratory findings:^{[2][3][1][4][5][6]}

Disease		History and symptoms		Laboratory findings							Additional findings
		Fever	Pain	TSH	Free T4	T3	T3RU†	Thyroglobin	TRH	TPOAb^
Transient hypothyroidism	Silent thyroiditis	–	–	↑/↓	↓/↑	Normal	↓	↑	Normal	Present (high titer)	May present primarily with hyperthyroidism
	Postpartum thyroiditis	+/-	+/-	↑/↓	↓/↑	Normal	↓	↑	Normal/↑	Present (high titer)	May present primarily with hyperthyroidism
	Subacute (de Quervain’s) thyroiditis	+/-	+/-	↑/↓	↓/↑	Normal	↓	↑	Normal	Low/absent	May present primarily with hyperthyroidism
Primary hypothyroidism	Autoimmune (Hashimoto’s thyroiditis)	–	–	↑*	↓	Normal/↓	Normal/↓	Normal/↑	Normal	Present (high titer)	May be accompanied by other autoimmune diseases
	Riedel’s thyroiditis	–	–	Normal/↑	Normal/↓	Normal/↓	Normal/↓	Normal	Normal	Usually present	Riedel’s thyroiditis usually presents with hard and fixed thyroid mass.
	Infectious thyroiditis	+	+	Normal	Normal	Normal	Normal	Normal	Normal	Absent	Infectious thyroiditis associated with neck pain
Others	Drug-induced	–	–	↑/↓	↓/↑	Normal	↓	Normal/↑	Normal	Absent**	History of hyperthyroidism History of trauma History of drug use, surgery, or radiation
	Radiation-induced
	Trauma induced
	Radioiodine induced
	Thyroidectomy
	Subclinical hypothyroidism	–	–	↑	Normal	Normal	Normal	Normal	Normal	Normal/↑	Asymptomatic

• Silent thyroiditis can initially present with thyrotoxicosis which must be differentiated from other causes of thyrotoxicosis.^{[2][3][1][4][5][6][7][8][9]}

Disease		History and symptoms		Laboratory findings								Additional findings
		Fever	Pain	TSH	Free T4	T3	T3RU†	Thyroglobin	TRH	TSH Receptor Antibody	TPOAb^
Thyroiditis	Silent thyroiditis	–	–	↑/↓	↓/↑	Normal	↓	↑	Normal	Absent	Present (high titer)	May present with hypothyroidism
	Hashimoto’s thyroiditis (Hashitoxicosis)	–	–	↑*	↓	Normal/↓	Normal/↓	Normal/↑	Normal	Absent	Present (high titer)	May be accompanied by other autoimmune diseases
	Subacute (de Quervain’s) thyroiditis	+/-	+/-	↑/↓	↓/↑	Normal	↓	↑	Normal	Absent	Low/absent	May present with hypothyroidism
	Postpartum thyroiditis	+/-	+/-	↑/↓	↓/↑	Normal	↓	↑	Normal/↑	Absent	Present (high titer)	May present with hypothyroidism
Primary hyperthyroidism	Grave’s disease	–	–	↓	↑	Normal/↑	↑	↑	Normal	Present	Absent	Patient may have opthalmopathy and dermopathy
	Toxic thyroid nodule	–	–	↓	↑	Normal/↑	↑(hot nodule)	Normal/↑	Normal	Absent	Absent	–
Secondary hyperthyroidism	Pituitary adenoma	–	–	↑	↑	Normal/↑	↑	Normal/↑	Normal	Absent	Absent	Inappropriately normal or increased TSH
Tertiary hyperthyroidism	Tertiary hyperthyroidism	–	–	↑	↑	↑	↑	Normal/↑	↑	Absent	Absent	Inappropriately normal or increased TSH
Drug induced	Amiodarone type 1	–	–	↓	↑	Normal/↑	↓	Normal/↑	Normal	Absent	Absent	High urinary iodine
	Amiodarone type 2	–	–	↓	↑	Normal/↑	Absent/↓	Normal/↑	Normal	Absent	Absent	High urinary iodine
Others	Factitious thyrotoxicosis	–	–	↓	↑	Normal/↑	↓	↓	Normal	Absent	Absent	Decreased thyroglobulin
	Trophoblastic disease	–	–	↓	↑	Normal/↑	↑	–	Normal	Absent	Absent	–
	Struma ovarii	–	–	↓	↑	Normal/↑	↓	–	Normal	Absent	Absent	–

(†)T3RU; Triiodothyronine Resin uptake. (^)TPOAb; Thyroid peroxidase antibodies.

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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]

Silent thyroiditis is a rare disease with the incidence of up to 23000 per 100,000 individuals with hyperthyroidism. The prevalence of silent thyroiditis is approximately 1000 per 100,000 individuals with thyrotoxicosis. Silent thyroiditis commonly affects patients in 30-40 years of age. Females are more commonly affected by silent thyroiditis than males. The female to male ratio is approximately 4 to 1. Silent thyroiditis is more common in areas of higher dietary iodine intake.

The incidence of silent thyroiditis is up to 23000 per 100,000 individuals with hyperthyroidism.^[1][2]

The prevalence of silent thyroiditis is approximately 1000 per 100,000 individuals with thyrotoxicosis.^[3][4]

Silent thyroiditis commonly affects patients in 30-40 years of age.^[5]

There is no racial predilection to silent thyroiditis.

Females are more commonly affected by silent thyroiditis than males. The female to male ratio is approximately 4 to 1.^[4]

Silent thyroiditis is more common in areas of higher dietary iodine intake. It is more common in the great lakes area of North America and Japan.^[5][6]

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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]

Common risk factors in the development of silent thyroiditis include lithium, radiation therapy in Hodgkin’s lymphoma, cessation of corticosteroids in Cushing’s syndrome (post adrenalectomy), and certain autoimmune conditions.

Common risk factors in the development of silent thyroiditis include lithium, radiation therapy in Hodgkin’s lymphoma, cessation of corticosteroids in Cushing’s syndrome (post adrenalectomy), and certain autoimmune conditions.^{[1][2][3][4][5]}

Common risk factors in the development of silent thyroiditis include:

• Lithium
• Radiation therapy in Hodgkin’s lymphoma
• Cessation of corticosteroids in Cushing’s syndrome (post adrenalectomy)

Less common risk factors in the development of silent thyroiditis include:

• SLE
• Immune thrombocytopenic purpura
• Lymphocytic hypophysitis

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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]

There is insufficient evidence to recommend routine screening for silent thyroiditis.

There is insufficient evidence to recommend routine screening for silent thyroiditis.

​

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Silent thyroiditis presents with the symptoms of thyrotoxicosis. It further leads to a euthyroid phase and eventually hypothyroid phase before the complete resolution of the disease. Complications may include hypothyroidism.

Silent thyroiditis presents as painless thyroid gland with symptoms of thyrotoxicosis. It further leads to an euthyroid phase and eventually hypothyroid phase before the complete resolution of the disease.^[1][2][3][4]

It follows the prodromal stage and includes the symptoms of thyrotoxicosis such as:

• Tachycardia and tremors
• Irritability and nervousness

Thyrotoxic stage is followed by a 1–3-week period of euthyroid phase.

The transient hypothyroid stage lasts for 6-12 months.

• Rarely, the hypothyroid stage may persist for a longer duration.

Complications that can develop as a result of silent thyroiditis include:^[1][5][4]

• Hypothyroidism
• Graves disease

Prognosis of silent thyroiditis is usually good.

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