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The broad category of thyroiditis includes the following inflammatory diseases of the thyroid gland:
(1) acute suppurative thyroiditis, which is due to bacterial infection;
(2) subacute thyroiditis, which results from a viral infection of the gland; and
(3) chronic thyroiditis, which is usually autoimmune in nature. In childhood, chronic thyroiditis is the most
common of these 3 types. The second form of thyroiditis, Riedel struma, is rare in children. Secondary
thyroiditis may be due to the administration of amiodarone to treat cardiac arrhythmias or the
administration of interferon-alpha to treat viral diseases.
Pathophysiology
Acute suppurative thyroiditis is rare in childhood because the thyroid is remarkably resistant to hematogenously spread
infection. Most cases of acute thyroiditis involve the left lobe of the thyroid and are associated with a developmental
abnormality of thyroid migration and the persistence of a pyriform sinus from the pharynx to the thyroid capsule.
The usual organisms responsible include Staphylococcus aureus,Streptococcus hemolyticus, and pneumococcus. Other
aerobic or anaerobic bacteria may also be involved.
Subacute thyroiditis is generally thought to be due to viral processes and usually follows a prodromal viral illness.
Various viral illnesses may precede the disease, including mumps, measles, influenza, infectious mononucleosis,
adenoviral or Coxsackievirus infections, myocarditis, or the common cold.
Because chronic thyroiditis in children is usually due to an autoimmune process, it is HLA-associated, similar to other
autoimmune endocrine diseases.
Sex
The pediatric male-to-female ratio for autoimmune thyroiditis ranges from 1:2 to 1:6. This is low when compared with the
90% female predominance in adults
Acute thyroiditis
A history of acute illness, including fever, chills, neck pain, sore throat, hoarseness, and dysphagia, is
common.
Neck pain is frequently unilateral and radiates to the mandible, ears, or occiput. Neck flexion reduces the
severity of the pain. The pain worsens with neck hyperextension.
Subacute thyroiditis
Physical
Acute thyroiditis
Subacute thyroiditis
The patient may have signs of systemic illness, such as low-grade fever and weakness.
Signs of hyperthyroidism, including increased pulse rate, widened pulse pressure, fidgeting, tremor,
nervousness, tongue fasciculations, brisk reflexes (possibly with clonus), weight loss, and warm moist skin,
may be present.
The thyroid gland may be enlarged and tender, with tenderness exacerbated by neck extension.
Initially, an enlarged, lumpy, bumpy, and nontender thyroid is often present. The gland may not
be enlarged, particularly in children who have profound hypothyroidism. Signs of hypothyroidism include
slow growth rate, weight gain, slow pulse, cold dry skin, coarse hair and facial features, edema, and delayed
relaxation of the deep tendon reflexes.
Signs of hyperthyroidism are occasionally present early in the disease.
Laboratory Studies
Acute thyroiditis
Subacute thyroiditis
The primary laboratory abnormalities are consistent with abnormal thyroid function. Initially, the thyroidstimulating hormone (TSH) level is suppressed, and the free thyroxine (T4) level is increased. As the disorder
progresses, transient or sometimes permanent hypothyroidism may develop.
The WBC count is usually within the reference range but may be mildly elevated. High-sensitivity Creactive protein levels are usually elevated in subacute thyroiditis.
Chronic thyroiditis
Imaging Studies
Radioactive iodine thyroid scanning
Radioactive iodine thyroid scanning is not necessary for acute suppurative thyroiditis because the
results are normal and do not aid in diagnosis. A scan may be helpful after diagnosis to identify a persistent
thyroglossal duct as a route for infection.
This test is also unnecessary for chronic thyroiditis because the results can be misleading and may
show increased uptake consistent with Graves disease, a multinodular goiter, or a hypofunctioning or
hyperfunctioning nodule.
Radioactive iodine thyroid scanning is helpful in patients with hyperthyroidism who are thought to have
subacute thyroiditis because the extremely low uptake is consistent with the thyrocellular destruction in
progress.
Thyroid ultrasonography
Procedures
Fine-needle thyroid aspiration
Subacute Thyroiditis
Subacute thyroiditis is a self-limited thyroid condition associated with a triphasic clinical course of
hyperthyroidism, hypothyroidism, and return to normal thyroid function.
Recognizing this condition is important; because it is self-limiting, no specific treatment, such as antithyroid or thyroid
hormone replacement therapy, is necessary in most patients.
In general, the following 3 forms of subacute thyroiditis are recognized:
Subacute granulomatous thyroiditis - Also known as subacute painful or de Quervain thyroiditis Subacute
lymphocytic thyroiditis - Also known as subacute painless thyroiditis
Subacute postpartum thyroiditis
Disease course
Although the etiology appears to be different for the 3 subtypes, the clinical courses are the same. High thyroid
hormone levels result from the destruction of the thyroid follicle and the release of preformed thyroid hormone into
the circulation, with thyrotoxicosis consequently developing. This phase lasts 4-10 weeks.
The disease undergoes remission in 2-4 months. At this time, the thyroid is depleted of colloid and is
now incapable of producing thyroid hormone, resulting in hypothyroidism. The hypothyroid phase may
last up to 2 months. Often, the hypothyroidism is mild, and no thyroid hormone therapy is required
unless the patient has signs or symptoms of hypothyroidism. As the follicles regenerate, the euthyroid
state is restored.
Pathophysiology
Destruction of follicular epithelium and loss of follicular integrity are the primary events in the pathophysiology of subacute
granulomatous thyroiditis. Thyroglobulin (TG), thyroid hormones, and other iodinated compounds are released into the
blood, often in quantities sufficient to elevate the serum thyroxine (T4) and triiodothyronine (T3) concentrations and suppress
thyroid-stimulating hormone (TSH) secretion. This state lasts until the stores of TG are exhausted or until healing occurs.
Thyroidal iodine uptake and new hormone synthesis temporarily ceases because of the low level of TSH.
As inflammation subsides, the thyroid follicles regenerate and thyroid hormone synthesis and secretion resume. In some
patients, several months are required for thyroid hormone synthesis to return to a normal rate; during that period, clinical
hypothyroidism may be evident.
Thyrotoxicosis
Excess thyroid hormone causes an increase in metabolic rate that is associated with increased total body heat production,
increased cardiovascular activity (eg, increased heart contractility, heart rate, vasodilation) to remove heat to the periphery
and remove metabolic wastes, and perspiration to cool the body.
The major symptoms of thyrotoxicosis include palpitations, nervousness, sweating, hyperdefecation, and heat intolerance.
Women often note a reduction in menstrual flow, or oligomenorrhea. Common signs of thyrotoxicosis include the following:
Etiology
The causes of subacute thyroiditis, other than those of subacute granulomatous thyroiditis, are not entirely clear.
Prognosis
The prognosis is excellent in 90-95% of patients who experience subacute thyroiditis. Approximately 5-10% of
patients have permanent thyroid dysfunction, usually hypothyroidism, after an episode of subacute thyroiditis.
Permanent goiter and thyroid dysfunction occur most frequently after postpartum thyroiditis.
History
Subacute granulomatous thyroiditis
Some patients experience a flulike prodromal episode 1-3 weeks prior to the onset of clinical disease. The natural
course of the disease can be divided into the following 4 phases, which usually unfold over a period of 3-6 months:
Acute phase - Lasts 3-6 weeks and presents primarily with pain; symptoms of hyperthyroidism also may
be present
Transient asymptomatic and euthyroid phase - Lasts 1-3 weeks
Hypothyroid phase - Lasts from weeks to months; it may become permanent in 5-15% of patients
Recovery phase - Characterized by normalization of thyroid structure and function
The diagnosis is made based on clinical findings. Prodromal flulike symptoms (fevers, myalgia, malaise) or known
infectious disease, such as pharyngitis, measles, mumps, Q fever, or typhoid fever, may occur. In young patients, de
Quervain thyroiditis may develop following an episode of Henoch-Schnlein purpura. However, a history of prodromal
symptoms often cannot be obtained.
Local symptoms
Local symptoms can include the following:
Dysphagia
Hoarseness (uncommon)
Pain over the thyroid area that is gradual or of sudden onset
Pain is the presenting symptom in over 90% of cases. It usually involves both lobes of the thyroid; in 30% of cases, it
starts on one side and then migrates contralaterally within a few days. While the pain may be limited to the region of the
thyroid, it may also involve the upper neck, throat, jaw, or ears. Some patients may first consult an otolaryngologist.
The pain may be so severe that the patient cannot tolerate palpation of the neck. The pain is most commonly bilateral.
Occasionally, it may be unilateral, beginning in one lobe and spreading to the opposite side (creeping thyroiditis). Coughing,
swallowing, or even tightening a necktie aggravates pain.
Constitutional symptoms
Fever
Malaise
Anorexia
Fatigue
Muscle aches
Symptoms of hyperthyroidism
Hyperthyroidism is usually is mild, becoming severe only in rare cases. The symptoms are transient, typically lasting 3-6
weeks. Symptoms of hyperthyroidism occurring in the acute phase of subacute granulomatous thyroiditis include the
following:
Tachycardia
Tremulousness
Heat intolerance
Sweating
Nervousness
Warm skin
Frequent bowel movements
Symptoms of hypothyroidism
Symptoms of hypothyroidism occur in the late phase of the disease in up to 50% of cases. The hypothyroidism is most often
mild or moderate. It is also transient, lasting weeks to months in 90-95% of cases. Symptoms of hypothyroidism occurring
during the second phase of subacute granulomatous thyroiditis include the following:
Fatigue
Dry skin
Lethargy
Eyelid swelling
Cold intolerance
Constipation
Atypical symptoms
Atypical presentations of subacute granulomatous thyroiditisthat is, extremely rare symptoms that have been documented
as case reportscan include the following:
Physical Examination
All conditions described are associated with thyrotoxicosis and the signs and symptoms of hypermetabolism. None of the
forms of subacute thyroiditis is associated with the thyroid eye disease observed primarily with Graves hyperthyroidism. The
presence of bilateral proptosis and chemosis with high thyroid hormone levels and goiter is highly suggestive of Graves
disease.
Tachycardia
Tremulousness
Heat intolerance
Sweating
Nervousness
Warm skin
A rapid relaxation phase of tendon reflexes
Hashimoto Thyroiditis
Practice Essentials
Hashimoto thyroiditis is part of the spectrum of autoimmune thyroid diseases (AITDs) and is characterized by the
destruction of thyroid cells by various cell- and antibody-mediated immune processes. This condition is the most
common cause of hypothyroidism in the United States in individuals older than 6 years.
Fatigue
Constipation
Dry skin
Weight gain
More advanced/florid symptoms may include the following:
Cold intolerance
Voice hoarseness and pressure symptoms in the neck from thyroid enlargement
Slowed movement and loss of energy
Decreased sweating
Mild nerve deafness
Peripheral neuropathy
Galactorrhea
Depression, dementia, and other psychiatric disturbances
Memory loss
Joint pains and muscle cramps
Hair loss
Menstrual irregularities
Sleep apnea and daytime somnolence
Diagnosis
Physical findings are variable and depend on the extent of the hypothyroidism and other factors, such as age. Examination
findings may include the following:
Serum TSH levels: Sensitive test of thyroid function; levels are invariably raised in hypothyroidism due to
Hashimoto thyroiditis and in primary hypothyroidism from any cause
Free T4 levels: Needed to correctly interpret the TSH in some clinical settings; low total T4 or free T4 level in the
presence of an elevated TSH level further confirms diagnosis of primary hypothyroidism
T3 levels: Low T3 level and high reverse T3 level may aid in the diagnosis of nonthyroidal illness
Thyroid autoantibodies: Presence of typically anti-TPO (anti-thyroid peroxidase) and anti-Tg (anti-thyroglobulin)
antibodies delineates the cause of hypothyroidism as Hashimoto thyroiditis or its variant; however, 10-15% of patients with
Hashimoto thyroiditis may be antibody negative
The following tests are not necessary for the diagnosis of primary hypothyroidism but may be used to evaluate complications
of hypothyroidism in some patients, as indicated:
Management
Pharmacotherapy
The treatment of choice for Hashimoto thyroiditis (or hypothyroidism from any cause) is thyroid hormone
replacement. The drug of choice is individually tailored and titrated levothyroxine sodium administered orally,
usually for life.
Surgery
Indications for surgery include the following:
A large goiter with obstructive symptoms, such as dysphagia, voice hoarseness, and stridor, caused by
extrinsic obstruction of airflow
Presence of a malignant nodule, as demonstrated by cytologic examination
Presence of a lymphoma diagnosed on fine-needle aspiration
Cosmetic reasons (eg, large, unsightly goiters)
See Treatment and Medication for more detail.
Background
Hashimoto thyroiditis (or Hashimotos thyroiditis) is characterized by the destruction of thyroid cells by various cell- and
antibody-mediated immune processes. It is the most common cause of hypothyroidism in the United States after age 6
years. Hashimoto thyroiditis is part of the spectrum of autoimmune thyroid diseases(AITDs). (See Etiology, Presentation,
and Workup.)
By strict criteria, Hashimoto thyroiditis is a histologic diagnosis first described by Hakaru Hashimoto, a Japanese surgeon
working in Berlin, Germany. His report, published in 1912, was based on the examination of 4 postoperative cases. He is
also credited with introducing the term struma lymphomatosa in reference to the syndrome.
Other variants of AITD include the following conditions:
Atrophic thyroiditis
Juvenile thyroiditis [2]
Postpartum thyroiditis
Silent thyroiditis
Focal thyroiditis
Etiology
The initiating process in Hashimoto thyroiditis is not well understood. [3, 4, 5, 6] The thyroid gland is typically goitrous but may be
atrophic or normal in size. Antibodies binding to and blocking the thyroid-stimulating hormone (TSH) receptor, thyrotropin
receptor blocking antibodies (TBII) have also been described and may contribute to impairment in thyroid function. The
result is inadequate thyroid hormone production and secretion, although initially, preformed thyroxine (T4) and
triiodothyronine (T3) may "leak" into the circulation from damaged cells.
Patients with Hashimoto thyroiditis have antibodies to various thyroid antigens, the most frequently detected of which include
anti-thyroid peroxidase (anti-TPO), antithyroglobulin (anti-Tg), and to a lesser extent, TSH receptor-blocking antibodies
(TBII). Nevertheless, a small percentage of patients with Hashimoto thyroiditis (approximately 10-15%) may be serum
antibody negative.
Other antithyroid antibodies found in AITD (including Hashimoto thyroiditis) include thyroid-stimulating antibody and cytotoxic
antibody.
Hashimoto thyroiditis has a markedly higher clustering of other autoimmunity diseases, including pernicious anemia, adrenal
insufficiency, cedliac disease and type 1 diabetes mellitus.[7, 8]
In a study of 830 patients with Hashimoto thyroiditis, Tagami et al reported slight, but significant, increases in TSH serum
levels and decreases in free T4 serum levels, with increasing patient age. In addition, TSH levels were positively correlated
with levels of total cholesterol, triglycerides, low-density lipoprotein (LDL), high-density lipoprotein (HDL), and non-HDL, as
well as with the ratio of LDL to HDL. Free T4 levels, on the other hand, were negatively correlated with these lipid
parameters.[9]
Epidemiology
Occurrence in the United States
Hashimoto thyroiditis is the most common cause of hypothyroidism in the United States after age 6 years, with the incidence
estimated to be 1.3% in a series of 5000 children aged 11-18 years. In adults, the incidence is estimated to be 3.5 per 1000
per year in women and 0.8 per 1000 per year in men. Incidence may be as high as 6% in the Appalachian region.
In the Colorado Thyroid Disease Prevalence Study, involving 25,862 adults, the prevalence of elevated TSH in symptomatic
and asymptomatic adults was 9.5%, with a greater percentage of those involved being women. The prevalence of
hypothyroidism and of thyroid disease in general increases with age.
International occurrence
Worldwide, the most common cause of hypothyroidism is iodine deficiency. However, Hashimoto thyroiditis remains the
most common cause of spontaneous hypothyroidism in areas of adequate iodine intake. The annual incidence of Hashimoto
thyroiditis worldwide is estimated to be 0.3-1.5 cases per 1000 persons. [10, 11]
Prognosis
With early diagnosis, timely institution of levothyroxine replacement therapy, informed patient follow-up care, and
attention to other attendant complications, the prognosis in Hashimoto thyroiditis is excellent, with patients leading
a normal life. Untreated myxedema coma has a poor prognosis and a high mortality rate.
Morbidity related to Hashimoto thyroiditis typically results from failure to make the diagnosis of hypothyroidism or to institute
l-thyroxine replacement therapy in adequate doses, or from failure on the part of the patient to take the replacement
medication.
The increased prevalence of lipid disorders in association with untreated hypothyroidism has the potential to increase
morbidity from coronary artery disease.
The risk for papillary thyroid carcinoma is increased in patients with Hashimoto thyroiditis. [12] These cancers are not clearly
more aggressive than other papillary thyroid carcinomas.
Therapeutic complications
Complications of overreplacement with levothyroxine sodium Include the following:
Patient Education
Patients should know that thyroid replacement therapy in Hashimoto thyroiditis is, except in very rare cases, lifelong.
Patients must be informed about the importance of compliance with their replacement therapy and must be instructed to
report any symptoms suggestive of hyperthyroidism caused by overreplacement.
Patients must be instructed to separateby at least 4 hoursingestion of levothyroxine from ingestion of cholestyramine,
ferrous sulfate, sucralfate, calcium carbonate, aluminum hydroxide (and other antacids), and iron-containing multivitamins,
all of which impair the absorption of levothyroxine.
For patient education information, see the Thyroid and Metabolism Center, as well as Thyroid Problems.
Riedel Thyroiditis
Background
Riedel thyroiditis, or Riedel's thyroiditis (RT), is a rare, chronic inflammatory disease of the thyroid gland
characterized by a dense fibrosis that replaces normal thyroid parenchyma. The fibrotic process invades adjacent
structures of the neck and extends beyond the thyroid capsule.
Involvement in RT may be unilateral or bilobar. Thyroid function depends on the extent to which the normal thyroid
gland has been replaced by fibrotic tissue. Most patients are euthyroid, but hypothyroidism is noted in
approximately 30% of cases. Rarely, hyperthyroidism can occur, but this is probably secondary to a coexisting condition.
(See Prognosis, Presentation, and Workup.)
Some experts have traditionally believed that RT is not primarily a thyroid disease but rather that it is a
manifestation of the systemic disorder multifocal fibrosclerosis. Approximately one third of RT cases are associated
with clinical findings of multifocal fibrosclerosis at the time of diagnosis. (See Etiology.)
In 1883, Professor Bernhard Riedel first recognized the disease. He published a description of 2 cases in 1896 and of a third
case in 1897.[1] Riedel used the term eisenharte struma to describe the stone-hard consistency of the thyroid gland and its
fixation to adjacent structures. He noted the presence of chronic inflammation with fibrosis and the absence of malignancy
on microscopic examination. Simple wedge resection of the thyroid isthmus was used to alleviate tracheal obstruction and is
still the preferred surgical therapy for RT.
Complications
Because of the encroachment beyond the thyroid capsule, nonthyroid problems can be associated with RT.
Complications of Riedel thyroiditis can include the following:
Airway obstruction
Dysphonia
Hoarseness - Due to recurrent laryngeal involvement
Hypothyroidism
Hypoparathyroidism
Dysphagia
Stridor - Due to tracheal compression
Etiology
The etiology of Riedel thyroiditis (RT) is unknown, but it may be related to a relatively new group of rare disorders,
IgG4-related systemic disease (IgG4-RSD). One theory of pathogenesis postulates that RT results from an
autoimmune process. A second theory holds RT to be a primary fibrotic disorder. However, IgG4-RSD may unify these 2
seemingly disparate etiologies.
Autoimmune theory
The following evidence supports an autoimmune pathogenesis for RT:
The presence of antithyroid antibodies in a significant percentage of patients with RT (67% of 178 cases reviewed
in one study) [2]
The pathologic features of cellular infiltration, including lymphocytes, plasma cells, and histiocytes
The frequent presence of focal vasculitis on pathologic examination
The favorable response of a subset of patients with RT to treatment with systemic corticosteroids
However, the presence of normal lymphocyte subpopulations and normal serum complement levels weighs against an
autoimmune mechanism. Elevated levels of antithyroid antibodies may merely reflect the immune system's exposure to
sequestered antigens released by the destruction of thyroid parenchyma from a primary fibrotic disorder.
IgG4-RSD disorder
IgG4-RSD is a relatively new group of disorders that share similar presentations. These disorders have in common a
preponderance of excess IgG4. The disorders are characterized by lymphoplasmacytic infiltrates containing IgG4-positive
plasma cells.[4] These infiltrates ultimately lead to fibrosis and elevated serum levels of IgG4. [5, 6]
Epidemiology
United States
Riedel thyroiditis (RT) is a very rare condition. At the Mayo Clinic, 37 cases of RT were diagnosed in a series of 57,000
thyroidectomies performed between 1920 and 1984, for an incidence of 0.06%. The overall incidence among outpatients
was 1.6 cases per 100,000 population. Based on large databases in referral centers, it appears that over the previous
decades, the incidence of RT has been decreasing.
Prognosis
Riedel thyroiditis (RT) is generally a self-limited disease with a favorable prognosis. Death due to airway compromise
is very rare in treated patients. Occasionally, spontaneous remission has been reported. Patients can also relapse.
In RT, morbidity is most frequently related to local compressive symptoms, such as dysphagia, dyspnea, hoarseness, and
cough. Hypothyroidism is present in 30% of cases. Fibrotic invasion of adjacent anatomic structures may infrequently result
in symptoms related to recurrent laryngeal nerve paralysis or hypoparathyroidism.
One third of patients with RT ultimately develop at least 1 extracervical manifestation of multifocal fibrosclerosis (such as
retroperitoneal fibrosis, mediastinal fibrosis, or sclerosing cholangitis). [7] In such patients, the prognosis essentially becomes
that of extracervical fibrosclerosis. Therefore, when RT is diagnosed, it is essential to perform abdominal and chest imaging
studies to exclude concomitant, extracervical entities from multifocal fibrosclerosis. Fibrosclerosis of the surrounding tissue
by RT can lead to serious morbidity and death.
A retrospective institutional review of a rare form of invasive thyroiditis from the Mayo Clinic discussed the common
presenting symptoms and extrathyroidal involvement of the systemic fibrosclerosis. Treatments used in the 21 reported
patients included partial thyroidectomy, tamoxifen, and corticosteroid therapy. Other, less well validated studies include
mycophenolate mofetil[8] and rituximab.[9] Of note, no cause-specific mortality was noted, and the fibrotic process stabilized or
partially resolved in all patients.[3]
Retroperitoneal fibrosis
Mediastinal fibrosis
Orbital pseudotumor
Pulmonary fibrosis
Sclerosing cholangitis
Lacrimal gland fibrosis
Fibrosing parotitis