Silent thyroiditis overview: Difference between revisions
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==Overview== | ==Overview== | ||
'''Silent thyroiditis''', more specifically and scientifically as '''subacute lymphocytic thyroiditis''', is a member of the group of thyroiditis conditions known as resolving thyroiditis, which includes a very similar condition to silent thyroiditis, '''postpartum thyroiditis'''. | '''Silent thyroiditis''', more specifically and scientifically as '''subacute lymphocytic thyroiditis''', is a member of the group of thyroiditis conditions known as resolving thyroiditis, which includes a very similar condition to silent thyroiditis, '''postpartum thyroiditis'''.Silent thyroiditis was first described as the painless form of the [[De Quervain's thyroiditis|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|HLA-DR+]]CD3+), activated [[Helper T cells|helper/inducer T-cells]] ([[HLA-DR|HLA-DR+]]CD4+), activated [[Suppressor T cells|suppressor]], and [[Cytotoxic T cell|cytotoxic T-cells]] ([[HLA-DR|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 T cells|helper/inducer T cells]], might have an important role in the pathogenesis of silent thyroiditis. Silent thyroiditis is associated with the [[HLA DR3-DQ2|HLA-DR3]] and [[HLA-DR5|DR5]] genes. [[Lymphocytic]] infiltration of the thyroid gland, the absence of Hurthle cells and [[Germinal center|germinal centers]] on histological analysis are the microscopic [[histopathological]] findings suggestive of silent thyroiditis. Silent thyroiditis may be caused by the activation of [[T helper cell|helper T cells]] and [[Cytotoxic T cell|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 [[Hypothyroidism|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]], [[Idiopathic thrombocytopenic purpura|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]]. | ||
==Historical Perspective== | ==Historical Perspective== | ||
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 [[De Quervain's thyroiditis|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 was identified as a separate form of thyroiditis a few decades ago. Silent thyroiditis was first described as the painless form of the [[De Quervain's thyroiditis|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. | ||
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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 [[hyperthyroid]] stage, [[euthyroid]] stage, and [[hypothyroid]] stage. | ||
==Pathophysiology== | ==Pathophysiology== | ||
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|HLA-DR+]]CD3+), activated [[Helper T cells|helper/inducer T-cells]] ([[HLA-DR|HLA-DR+]]CD4+), activated [[Suppressor T cells|suppressor]], and [[Cytotoxic T cell|cytotoxic T-cells]] ([[HLA-DR|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 T cells|helper/inducer T cells]], might have an important role in the pathogenesis of silent thyroiditis. Silent thyroiditis is associated with the [[HLA DR3-DQ2|HLA-DR3]] and [[HLA-DR5|DR5]] genes. [[Lymphocytic]] infiltration of the thyroid gland, the absence of Hurthle cells and [[Germinal center|germinal centers]] on histological analysis are the microscopic [[histopathological]] findings suggestive of silent thyroiditis. | 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|HLA-DR+]]CD3+), activated [[Helper T cells|helper/inducer T-cells]] ([[HLA-DR|HLA-DR+]]CD4+), activated [[Suppressor T cells|suppressor]], and [[Cytotoxic T cell|cytotoxic T-cells]] ([[HLA-DR|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 T cells|helper/inducer T cells]], might have an important role in the pathogenesis of silent thyroiditis. Silent thyroiditis is associated with the [[HLA DR3-DQ2|HLA-DR3]] and [[HLA-DR5|DR5]] genes. [[Lymphocytic]] infiltration of the thyroid gland, the absence of Hurthle cells and [[Germinal center|germinal centers]] on histological analysis are the microscopic [[histopathological]] findings suggestive of silent thyroiditis. Patients with silent thyroiditis may have the history of other autoimmune diseases such as [[SLE]], [[Idiopathic thrombocytopenic purpura|immune thrombocytopenic purpura]] (ITP), and [[lymphocytic hypophysitis]]. The most common symptoms of silent thyroiditis are [[palpitations]], [[tachycardia]], [[nervousness]], and [[tremors]]. | ||
==Causes== | ==Causes== | ||
Silent thyroiditis may be caused by the activation of [[T helper cell|helper T cells]] and [[Cytotoxic T cell|cytotoxic T cells]], [[genetic]] factors, and [[autoimmune]] antibodies. | Silent thyroiditis may be caused by the activation of [[T helper cell|helper T cells]] and [[Cytotoxic T cell|cytotoxic T cells]], [[genetic]] factors, and [[autoimmune]] antibodies. | ||
Revision as of 20:03, 22 September 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
Silent thyroiditis, more specifically and scientifically as subacute lymphocytic thyroiditis, is a member of the group of thyroiditis conditions known as resolving thyroiditis, which includes a very similar condition to silent thyroiditis, 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.
Historical Perspective
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.
Classification
Silent thyroiditis can be classified according to the development of symptoms into the hyperthyroid stage, euthyroid stage, and hypothyroid stage.
Pathophysiology
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. 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.
Causes
Silent thyroiditis may be caused by the activation of helper T cells and cytotoxic T cells, genetic factors, and autoimmune antibodies.
Differentiating ((Page name)) from Other Diseases
Epidemiology and Demographics
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.
Risk Factors
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.
Screening
There is insufficient evidence to recommend routine screening for silent thyroiditis.
Natural History, Complications, and Prognosis
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.
Diagnosis
Diagnostic Criteria
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.
History and Symptoms
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
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
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.
Electrocardiogram
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.
X-ray
There are no x-ray findings associated with silent thyroiditis.
Ultrasound
There are no echocardiograms associated with silent thyroiditis. Ultrasound findings associated with silent thyroiditis are hypoechoic areas, glandular irregularities, and nonhomogeneous echotexture.
CT scan
There are no CT scan findings associated with silent thyroiditis.
MRI
MRI is not used in the diagnosis of silent thyroiditis. However, diffusion-weighted MRI shows low apparent diffusion coefficient (ADC).
Other Imaging Findings
24-hour iodine-123 uptake is decreased in silent thyroiditis.
Other Diagnostic Studies
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.
Treatment
Medical Therapy
Pharmacologic medical therapies for silent thyroiditis include beta blockers for thyrotoxicosis symptoms and levothyroxine for the hypothyroidism if it follows the hyperthyroid state.
Surgery
Surgical intervention is not usually recommended for the management of silent thyroiditis.Thyroidectomy is considered only when there are repeated relapses despite appropriate treatment.
Primary Prevention
There are no established measures for the primary prevention of silent thyroiditis.
Secondary Prevention
There are no established measures for the secondary prevention of silent thyroiditis.