Thyroiditis:​Evaluation and Treatment

Beatriz Martinez Quintero, MD, Virginia Commonwealth University School of Medicine, Richmond, Virginia
Cynthia Yazbeck, MD, and Lori B. Sweeney, MD, Central Virginia Veterans Affairs Health Care System, Richmond, Virginia

Thyroiditis is a general term for inflammation of the thyroid gland. The most common forms of thyroiditis encountered by
family physicians include Hashimoto, postpartum, and subacute. Most forms of thyroiditis result in a triphasic disease pat-
tern of thyroid dysfunction. Patients will have an initial phase of hyperthyroidism (thyrotoxicosis) attributed to the release
of preformed thyroid hormone from damaged thyroid cells. This is followed by hypothyroidism, when the thyroid stores are
depleted, and then eventual restoration of normal thyroid function. Some patients may develop permanent hypothyroidism.
Hashimoto thyroiditis is an autoimmune disorder that presents with or without signs or symptoms of hypothyroidism, often
with a painless goiter, and is associated with elevated thyroid peroxidase antibodies. Patients with Hashimoto thyroiditis and
overt hypothyroidism are generally treated with lifelong thyroid hormone therapy. Postpartum thyroiditis occurs within one
year of delivery, miscarriage, or medical abortion. Subacute thyroiditis is a self-limited inflammatory disease characterized
by anterior neck pain. Treatment of subacute thyroiditis should focus on symptoms. In the hyperthyroid phase, beta blockers
can treat adrenergic symptoms. In the hypothyroid phase, treatment is generally not necessary but may be used in patients
with signs and symptoms of hypothyroidism or permanent hypothyroidism. Nonsteroidal anti-inflammatory drugs and corti-
costeroids are indicated for the treatment of thyroid pain. Certain drugs may induce thyroiditis, such as amiodarone, immune
checkpoint inhibitors, interleukin-2, interferon-alfa, lithium, and tyrosine kinase inhibitors. In all cases of thyroiditis, surveil-
lance and clinical follow-up are recommended to monitor for changes in thyroid function. (Am Fam Physician. 2021;​104(6):​
609-617. Copyright © 2021 American Academy of Family Physicians.)

Thyroiditis is a general term for inflammation thyroid hormone from damaged thyroid follic-
of the thyroid gland, and it can be associated ular cells. This is followed by hypothyroidism,
with thyroid dysfunction. Thyroiditis is classi- when the thyroid stores are depleted, and then
fied according to clinical symptoms (painful or
painless), onset of symptoms (acute, subacute,
chronic), and underlying etiology (autoimmu- BEST PRACTICES IN ENDOCRINOLOGY
nity, infection, drugs, radiation). Painful types
of thyroiditis include subacute, suppurative, and Recommendations from the Choosing
radiation induced. Painless types include drug Wisely Campaign
induced, fibrous (Riedel thyroiditis), Hashimoto
thyroiditis (HT), postpartum, and silent. Recommendation Sponsoring organization
Most forms of thyroiditis result in a triphasic Avoid routinely performing thy- American Academy of
disease pattern of thyroid dysfunction. Patients roid ultrasonography in children Pediatrics – Section on
have an initial phase of hyperthyroidism (thyro- who have simple goiters or Endocrinology
autoimmune thyroiditis.
toxicosis) attributed to the release of preformed
Do not routinely perform thyroid Endocrine Society/
ultrasonography in patients with American Association of
CME This clinical content conforms to AAFP cri- abnormal thyroid function tests if Clinical Endocrinologists
teria for CME. See CME Quiz on page 562. there is no palpable abnormality
of the thyroid gland.
Author disclosure:​ No relevant financial
affiliations. Source:​For more information on the Choosing Wisely Campaign,
Patient information:​ A handout on this topic is see https://​w ww.choosing​wisely.org. For supporting citations and
available at https://​family​doctor.org/condition/ to search Choosing Wisely recommendations relevant to primary
thyroiditis. care, see https://​w ww.aafp.org/afp/recommendations/search.htm.

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 THYROIDITIS
TABLE 1

Thyroiditis Subtypes
Type Etiology Clinical presentation Diagnosis

Chronic autoimmune Autoimmune Painless goiter;​euthyroidism, hypo- Presence of atrophic thyroid gland or
thyroiditis (Hashimoto thyroidism, subclinical hypothyroidism, nontender goiter with or without compres-
thyroiditis, chronic lym- and, rarely, transient hyperthyroidism sive symptoms (e.g., dysphagia);​thyroid
phocytic thyroiditis) (hashitoxicosis) function tests (differ with phase);​TPO* and
increase in thyroglobulin antibodies

Drug-induced thyroiditis See Table 2

Suppurative thyroiditis Multiple infectious Anterior neck pain, swelling, tender- Complete blood count with differential,
(infectious thyroiditis) organisms, most ness, odynophagia, fever, chills, and complete metabolic panel, blood cul-
commonly Staph- local lymphadenopathy tures;​computed tomography of the neck
ylococcus aureus, and chest with intravenous contrast;​
Streptococcus spp. thyroid function tests are usually normal
(hypo- or hyperthyroidism may occur);​
thyroid antibodies are often absent;​thyroid
ultrasonography and fine-needle aspiration
(diagnostic and therapeutic) if evidence of a
mass or fluid collection

Postpartum thyroiditis Autoimmune Hyperthyroidism alone, hyperthyroid- Presence of TPO antibodies and increase in
ism followed by transient or permanent thyroglobulin antibodies;​thyroid function
hypothyroidism, or hypothyroidism tests (differ with phase);​low radioactive
alone within 1 year of delivery, miscar- iodine uptake in the hyperthyroid phase†
riage, or medical abortion

Radiation-induced Radiation (radioio- Anterior neck pain, thyroid gland Clinical diagnosis made in the setting of
thyroiditis dine and external enlargement and tenderness;​transient recent radiation
radiation) hyperthyroidism;​occurs typically
within 2 weeks after radiation

Riedel thyroiditis (fibrous Unknown, auto- Destructive thyroiditis characterized Thyroid biopsy
thyroiditis) immunity may by dense fibrosis that can extend into
contribute to the adjacent tissues;​firm goiter;​com-
pathogenesis pressive symptoms (e.g., hoarseness,
dyspnea, dysphagia);​hypocalcemia
may occur due to fibrotic transforma-
tion of the parathyroid glands

Silent thyroiditis (silent Autoimmune Hyperthyroidism alone, hyperthyroid- Increase in TPO antibodies;​thyroid func-
sporadic thyroiditis, ism followed by hypothyroidism, or tion tests (differ with phase);​low radioactive
painless sporadic hypothyroidism alone iodine uptake in the hyperthyroid phase
thyroiditis, subacute
lymphocytic thyroiditis)

Subacute thyroiditis Post-viral Anterior neck pain, dysphagia, Thyroid function tests (differ with phase);​
(granulomatous thyroid- reported recent upper respiratory tract elevated erythrocyte sedimentation rate
itis, giant cell thyroiditis, infection;​hyperthyroidism followed by and C-reactive protein level;​increase in
de Quervain thyroiditis) transient hypothyroidism, and eventual TPO antibodies (up to 25% of patients have
restoration of thyroid function low titers);​low radioactive iodine uptake in
the hyperthyroid phase

NSAIDs = nonsteroidal anti-inflammatory drugs;​TPO = thyroid peroxidase.

*—Presence of elevated TPO antibody levels confers a risk of many types of thyroid dysfunction and is a general marker of thyroid autoimmunity.
Frankly elevated levels are more specific for Hashimoto thyroiditis.
†—Thyroid computed tomography with radioactive iodine uptake is contraindicated during pregnancy or breastfeeding.
Information from references 1-13.

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Complications Management

Hypothyroidism Levothyroxine
eventual restoration of normal thyroid function.
Some patients may develop permanent hypo-
thyroidism requiring thyroid hormone therapy
with levothyroxine. The three most common
forms of thyroiditis are HT, postpartum, and
subacute. Table 1 summarizes the etiology,
clinical presentation, diagnosis, complications,
Acute complications Hospitalization, airway monitor-
may include sepsis ing and stabilization, and empiric and management for different types of thyroid-
and airway compro- antibiotic therapy with penicillinase- itis, including less common types.1-13 Figure 1
mise;​in some patients, resistant penicillin and beta-lactamase is an algorithm for the diagnosis of suspected
destructive thyroiditis inhibitor (e.g., piperacillin/tazobactam
thyroiditis.14
may lead to permanent [Zosyn]), vancomycin if methicillin-
hypothyroidism resistant S. aureus is suspected;​
antibiotic therapy should be adjusted Hashimoto Thyroiditis (Chronic
to microbiology and antimicrobial Autoimmune Thyroiditis)
susceptibility data;​urgent transcu- EPIDEMIOLOGY
taneous or open-surgical abscess
drainage is recommended if airway is HT (i.e., chronic autoimmune thyroiditis or
compromised chronic lymphocytic thyroiditis) is the most
commonly encountered autoimmune disease
Up to 70% of patients Beta blockers for hyperthyroid symp-
develop recurrence toms;​levothyroxine for symptomatic worldwide.1,15 The estimated incidence of HT is
with subsequent hypothyroidism or patients who are 0.3 to 1.5 cases per 1,000 people per year.2 HT
pregnancies;​ perma- attempting pregnancy or breastfeed- may present with other autoimmune disorders,
nent hypothyroidism ing (in the hypothyroid phase), and
occurs in 15% to 50% of permanent hypothyroidism
such as type 1 diabetes mellitus, Addison dis-
women ease, rheumatoid arthritis, systemic lupus ery-
thematosus, Sjögren syndrome, autoimmune
Self-limited; hyper- Beta blockers for hyperthyroid
hepatitis, and vitiligo.1,16 HT occurs due to the
thyroidism generally symptoms;​NSAIDs usually provide
resolves within 1 month sufficient analgesia, and predni- formation of autoantibodies and direct injury to
sone (20 to 40 mg per day) is rarely the thyroid from an environmental trigger (e.g.,
required for thyroid pain infection, stress, iodine intake) in patients with
Most patients are No standardized treatment;​glu- genetic susceptibility. The degree of injury can
euthyroid, approxi- cocorticoids with mycophenolate differ among individuals but is often progressive
mately 30% develop mofetil (Cellcept) or tamoxifen have over time and can result in fibrotic transforma-
hypothyroidism been described in the literature,
tion of the gland.17
subtotal thyroidectomy is indicated to
relieve compressive symptoms
CLINICAL PRESENTATION
Patients with HT often present with a painless
10% to 20% of patients Beta blockers for hyperthyroid
develop permanent symptoms;​levothyroxine for goiter, with or without overt hypothyroidism.1
hypothyroidism;​5% to symptomatic hypothyroidism (in the In patients who are asymptomatic, HT is usu-
10% recurs hypothyroid phase) and permanent ally the incidental finding of the goiter that
hypothyroidism prompted an evaluation. Other patients may
Self-limited;​ most Beta blockers for hyperthyroid symp- report typical symptoms of hypothyroidism
patients are euthy- toms;​NSAIDs (e.g., ibuprofen, 1,200 such as fatigue, weight gain, cold intolerance,
roid within 12 months to 3,200 mg per day in divided doses) constipation, depression, myalgia, menorrhagia,
of onset;​5% to 15% and steroids (prednisone, 15 to 40 mg
of patients develop per day for 1 to 6 weeks, then taper)
and dry skin. Many of these symptoms overlap
permanent hypothy- for thyroid pain;​levothyroxine for with other disorders and may not always cor-
roidism;​1% to 4% recurs hypothyroidism relate with the degree of thyroid dysfunction.
In a 20-year follow-up study, clinical or bio-
chemical hypothyroidism developed in 55% of
the women who initially had positive thyroid
antibodies and an elevated thyroid-stimulating
hormone (TSH) level (greater than 6 mIU per L)
but a normal serum free thyroxine (T4) level.15

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 THYROIDITIS
TABLE 2

Drug-Induced Thyroiditis
Drug Clinical use Thyroid dysfunction Mechanism

Amiodarone Atrial fibrillation, ventricular arrhythmia Hypo- or hyperthyroidism Hypothyroidism:​direct toxic effect
on the thyroid gland
Hyperthyroidism:​2 types of
amiodarone-induced thyrotoxicosis
In type 1, there is increased syn-
thesis of thyroid hormone (usually
in patients with preexisting goiter);​
in type 2, there is excess release of
free thyroxine and free triiodothy-
ronine due to destructive thyroiditis

Immune check- Treatment of diverse types of cancer Hypo- or hyperthyroidism Destructive thyroiditis mediated by
point inhibitors (e.g., melanoma, non–small cell lung cytotoxic T cells against the thyroid
cancer, small cell lung cancer, hepato- gland
cellular carcinoma, renal cell carcinoma,
triple-negative breast cancer)

Interferon-alfa Hairy cell leukemia, follicular lym- Hypo- or hyperthyroidism Autoimmune

phoma, melanoma, AIDS-related Kaposi Chronic autoimmune thyroiditis
sarcoma, chronic hepatitis B and C
Silent thyroiditis

Interleukin-2 Renal cell carcinoma, melanoma Hypo- more often than Autoimmune
hyperthyroidism

Lithium Depression, bipolar disorder Goiter Impaired iodine uptake;​inhibition

Hypo- more often than of thyroid hormone synthesis and
hyperthyroidism release;​increased thyroid autoim-
munity;​direct toxic effect on the
Chronic autoimmune thyroiditis thyroid gland

Tyrosine kinase Treatment of diverse types of can- Hypothyroidism Destructive thyroiditis;​impaired

inhibitors cer (e.g., non–small cell lung cancer, iodine uptake;​capillary regression
chronic myelogenous leukemia, renal induced by vascular endothelial
cell carcinoma, breast cancer, hepato- growth factor inhibition;​inhibition
cellular carcinoma, colorectal cancer) of thyroid peroxidase activity

Information from references 21 and 29-46.

DIAGNOSIS a small thyroid volume if underlying atrophy of

The diagnosis of HT can be established by a com- the thyroid gland has occurred.2 Patients with
bination of clinical features, thyroid function test goiter may have compressive symptoms such as
results consistent with subclinical hypothyroid- dysphonia, dyspnea, and dysphagia.1
ism (elevated serum TSH level, but normal serum
levels of T4 and free triiodothyronine [T3]) or overt TREATMENT
hypothyroidism (elevated TSH level with low T4 All patients with HT and hypothyroidism
and T3 serum levels), and elevated thyroglobulin require treatment, even if they are asymptom-
and thyroid peroxidase (TPO) antibodies.1,15 TPO atic. The goals of treatment include normalizing
antibodies are found in 95% of patients with HT, the TSH level and ameliorating symptoms of
whereas thyroglobulin antibodies are elevated in hypothyroidism. When deciding on the initial
60% to 80% of patients with HT.1 Some patients replacement dose of levothyroxine, the patient’s
may present with self-limited transient thyrotoxi- age and cardiac status should be considered. A
cosis or a hyperthyroid phase (i.e., hashitoxicosis) healthy, young patient without coexisting heart
caused by destructive inflammation attributed disease can be started on a full replacement dos-
to HT damaging the thyroid follicles, releasing age of levothyroxine (1.6 mcg per kg per day). A
excess thyroid hormone.18 The thyroid gland is lower dosage of levothyroxine (12.5 to 25 mcg
often diffusely enlarged and firm with an irregu- per day) is appropriate in older adults, patients
lar surface on examination.15 Some patients have with underlying coronary heart disease, and

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 THYROIDITIS
FIGURE 1

Thyroiditis suspected

Thyroid pain?

Yes No

Toxic appearing? Is the patient taking one of the drugs

commonly associated with thyroid
dysfunction (e.g., amiodarone, immune
Yes No checkpoint inhibitor, interferon-alfa,
interleukin-2, tyrosine kinase inhibitor)?
Infectious History of radia-
thyroiditis tion or trauma?
Yes No

Yes No Drug-induced Thyroid-stimulating

thyroiditis hormone level
Radiation- or Low thyroid-stimulating
trauma-induced hormone level, high
thyroiditis thyroglobulin level? Low High

Postpartum? Postpartum?
Yes No

Subacute thyroiditis Thyroid hemorrhage Yes No Yes No

Radioactive iodine uptake* Radioactive iodine uptake* Postpartum Hashimoto, silent,

or Hashimoto or subacute
thyroiditis (hypo- thyroiditis (hypo-
Low High Low High thyroid phase) thyroid phase)

Postpartum Graves Silent or subacute Graves

thyroiditis (hyper- disease thyroiditis (hyper- disease
thyroid phase) thyroid phase)

*—Radioactive iodine uptake and scan is contraindicated in patients who are pregnant and breastfeeding and is unreliable in patients with recent use
of radioiodine contrast or amiodarone therapy. Consider other imaging studies such as thyroid ultrasonography to evaluate thyroidal blood flow.

Algorithm for the evaluation of people with suspected thyroiditis.

Adapted with permission from Sweeney LB, Stewart C, Gaitonde DY. Thyroiditis:​an integrated approach. Am Fam Physician. 2014;​90(6):​393.

those with tachyarrhythmias such as atrial fibril- per L or with symptoms, treatment with low-dose
lation. Treatment with T3 is not routinely rec- levothyroxine should be considered. An initial
ommended. The patient’s TSH level should be dosage of 25 to 50 mcg per day can be established
remeasured four to six weeks after initiation and and titrated in these patients similarly to patients
the dose of levothyroxine adjusted to achieve a who have overt hypothyroidism. If therapy with
value in the normal reference range (0.5 to 4.0 levothyroxine is not initiated, patients should be
mIU per L). Clinicians may try to achieve slightly monitored annually for the development of overt
higher TSH levels (4.0 to 6.0 mIU per L) in older hypothyroidism.15,19
patients. It is reasonable to make dosage adjust-
ments of 12.5 to 25 mcg of levothyroxine per day Postpartum Thyroiditis
at four- to six-week intervals until the intended EPIDEMIOLOGY
TSH level is reached. Postpartum thyroiditis is an autoimmune-
In patients with subclinical hypothyroid- mediated destructive thyroiditis that results in
ism and elevated TPO antibodies, especially transient or persistent thyroid dysfunction and
those with a serum TSH level of at least 10 mIU occurs within one year of delivery, miscarriage,

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 THYROIDITIS

or medical abortion. The lifetime incidence of destructive process, and antithyroid medications
postpartum thyroiditis is 5.4% in the general are not indicated.6,22 Treatment of the hypothy-
population and is increased in individuals with roid phase with levothyroxine is recommended,
other autoimmune diseases such as type 1 dia- especially if the patient is symptomatic, attempt-
betes or a personal or family history of thyroid ing pregnancy, or breastfeeding. Thyroid func-
disease.6,12 Recurrence rates approach 70% with tion testing should be performed every four to
each subsequent pregnancy.12 eight weeks. It is recommended to begin tapering
the levothyroxine dose around 12 months post-
CLINICAL PRESENTATION partum if the patient is not pregnant, attempting
Postpartum thyroiditis is a painless condition. to conceive, or breastfeeding, followed by peri-
A total of 40% of patients with postpartum thy- odic monitoring of thyroid function. The even-
roiditis present with isolated hypothyroidism, tual development of permanent hypothyroidism
whereas 25% to 40% experience a triphasic pattern has been described in 15% to 50% of patients with
of hyperthyroidism (thyrotoxicosis), followed by a history of postpartum thyroiditis.12 Those with
hypothyroidism and then euthyroidism. During a history of postpartum thyroiditis should have
the thyrotoxic phase, symptoms are usually mild an annual TSH test to evaluate for permanent
and begin two to six months postpartum. This hypothyroidism.22
phase typically lasts two to three months. The
hypothyroid phase occurs three to 12 months Subacute Thyroiditis
postpartum and is often symptomatic.12 EPIDEMIOLOGY
Subacute thyroiditis (i.e., subacute granuloma-
DIAGNOSIS tous thyroiditis or de Quervain thyroiditis) is a
The differential diagnosis in the thyrotoxic phase self-limited inflammatory disease of the thy-
includes Graves disease, which can also present roid gland. The incidence has been reported at
during the postpartum period.7 Measurement of 4.9 cases per 100,000 people per year.16 Women
thyroid antibodies can help distinguish between are more likely to be affected, with a peak inci-
postpartum thyroiditis and Graves disease. dence between 40 and 50 years of age.23,24 More
The presence of thyrotropin receptor antibod- cases are noted in the late summer and fall.23,24
ies usually indicates Graves disease. Elevated Subacute thyroiditis results from the inflamma-
TPO and thyroglobulin antibodies are often tory destruction of thyroid follicles;​the condition
found in patients with postpartum thyroiditis, often occurs after infection of the upper respira-
and mildly positive thyrotropin receptor anti- tory tract caused by Coxsackie virus, Epstein-
bodies have also been reported.12,20 In postpar- Barr virus, adenovirus, influenza viruses, and
tum thyroiditis, there is a release of preformed most recently SARS-CoV-2 virus.12,25 However,
thyroid hormone, and the T4:​T3 ratio is usually 25% of patients report symptoms of an upper
higher than in Graves disease. Physical examina- respiratory tract infection in the 30 days before
tion features specific to Graves disease, such as initial presentation.23,24
exophthalmos and thyroid bruit, are not found
in postpartum thyroiditis. Radioactive iodine CLINICAL PRESENTATION
uptake and scan will generally find a decreased Subacute thyroiditis is the most common cause
uptake in postpartum thyroiditis and increased of thyroid pain. Anterior neck pain is usually the
diffuse uptake in Graves disease. This imaging is presenting feature and prompts patients to seek
contraindicated in patients who are pregnant or medical attention. The neck pain can be unilat-
breastfeeding.7,12,21 eral or bilateral and may radiate to the jaw or
ear.23,24,26 Dysphagia may be present due to dif-
TREATMENT fuse thyroid gland enlargement (i.e., up to three
Treatment with beta blockers (e.g., propranolol, to four times its normal size). Patients may also
10 to 20 mg every eight hours), titrated to a dos- present with a prodrome of fatigue, myalgias,
age that provides symptomatic relief, is recom- low-grade fever, and pharyngitis. Most cases of
mended for patients who are symptomatic during subacute thyroiditis follow the triphasic pattern.
the thyrotoxic phase.21 Postpartum thyroiditis is a About 50% of patients present with the thyrotoxic

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 THYROIDITIS

SORT:​KEY RECOMMENDATIONS FOR PRACTICE

Evidence
Clinical recommendation rating Comments

In patients with Hashimoto thyroiditis (i.e., chronic autoimmune C Expert consensus and
thyroiditis) and subclinical hypothyroidism, the thyroid- disease-oriented evidence
stimulating hormone level should be monitored annually.15,19

Radioactive iodine uptake and scan is contraindicated in patients C Expert consensus guideline
who are pregnant or breastfeeding.7,12,21

Beta blockers can treat thyrotoxic symptoms in patients with all B Inconsistent or limited-
forms of thyroiditis. 21 quality patient-oriented
evidence

Patients with a history of postpartum thyroiditis should have A Consistent and good-
thyroid-stimulating hormone testing annually to evaluate for quality patient-oriented
permanent hypothyroidism. 22 evidence

If the etiology of thyrotoxicosis is not apparent based on initial C Expert consensus guideline
evaluation, clinicians should test for thyrotropin receptor anti-
bodies to evaluate for Graves disease and order imaging studies
such as thyroid ultrasonography to evaluate thyroidal blood flow
and radioactive iodine uptake and scan to determine radioactive
iodine uptake.12,21

Patients with subacute thyroiditis should be started on high-dose C Expert consensus

acetylsalicylic acid or nonsteroidal anti-inflammatory drugs as
first-line therapy;​corticosteroid therapy should be initiated for
subacute thyroiditis in patients with severe neck pain or minimal
response to acetylsalicylic acid or nonsteroidal anti-inflammatory
drugs after four days.12,26

A = consistent, good-quality patient-oriented evidence;​ B = inconsistent or limited-quality patient-oriented evidence;​

C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the
SORT evidence rating system, go to https://​w ww.aafp.org/afpsort.

phase, which typically lasts for three to six weeks. the thyrotoxic phase, TSH is usually suppressed
Symptoms are often mild and may include dia- with elevated or normal T4 and T3 levels. To dif-
phoresis, heat intolerance, tremors, palpitations, ferentiate from other causes of thyrotoxicosis,
and weight loss. Following the thyrotoxic phase, radioactive iodine uptake and scan should be
one-third of patients develop hypothyroidism, performed to demonstrate diffusely low iodine
which can last up to six months. There is no thy- uptake in the thyroid gland during the thyrotoxic
roid pain during this phase. Most patients return phase.12 The differential diagnosis of thyroid pain
to euthyroidism within 12 months of the onset of includes hemorrhage into a thyroid cyst and sup-
disease. Between 5% and 15% of patients develop purative thyroiditis caused by a bacterial infec-
permanent hypothyroidism.12 tion.27 Imaging is not usually necessary;​however,
thyroid ultrasonography could help distinguish
DIAGNOSIS between these entities. Thyroid ultrasonography
The diagnosis of subacute thyroiditis is mainly in subacute thyroiditis typically shows hetero-
clinical. During the initial thyrotoxic phase, the geneous hypoechoic parenchyma and decreased
patient presents with anterior neck pain, ten- vascularity, whereas acute thyroid hemorrhage
derness to palpation of the thyroid gland, and and suppurative thyroiditis show a focal cys-
signs and symptoms of thyrotoxicosis. Inflam- tic and/or solid mass in the area of the thyroid
matory markers such as erythrocyte sedimenta- pain.27,28 Patients with severe thyroid pain and
tion rate and C-reactive protein are elevated. In systemic symptoms (e.g., high fever, leukocytosis,

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 THYROIDITIS

cervical lymphadenopathy) should have fine- postpartum thyroiditis, silent thyroiditis, chronic
needle aspiration to rule out suppurative thy- lymphocytic thyroiditis, Hashimoto’s thyroiditis,
drug-induced thyroiditis, steroid therapy and thyroid-
roiditis.28 Otherwise, fine-needle aspiration is not itis, COVID-19 and thyroiditis, immune-checkpoint
routinely recommended. inhibitor therapy and thyroiditis, ICI-related thyroid-
itis. The search included meta-analyses, randomized
TREATMENT controlled trials, clinical trials, and reviews. Also
The goal of treatment is to ameliorate the pain searched were UpToDate and Essential Evidence
Plus. Search dates:​November 2020 through March
and thyrotoxicosis-related symptoms. Antibi- 2021, and July 2021.
otics have no role in the treatment of subacute
The views expressed in this article are those of the
thyroiditis.26 Because subacute thyroiditis is a authors and do not reflect the policy or position of
destructive process, the use of antithyroid drugs the U.S. Army Medical Department, Department
is not indicated. Treatment with beta blockers of the Army, Department of Defense, or the U.S.
for control of severe symptoms during the thyro- government.
toxic phase is recommended, although often no
treatment is needed if symptoms are mild.12 In The Authors
the thyrotoxic and painful phase, patients may be BEATRIZ MARTINEZ QUINTERO, MD, is a fellow
treated with high-dose acetylsalicylic acid, non- in the Department of Internal Medicine and the
steroidal anti-inflammatory drugs (NSAIDs), Division of Endocrinology, Diabetes and Metabo-
or corticosteroids.26 NSAIDs are considered lism at Virginia Commonwealth University School
the first-line treatment (e.g., ibuprofen, 1,200 to of Medicine, Richmond.
3,200 mg per day in divided doses). Glucocorti- CYNTHIA YAZBECK, MD, is an endocrinologist in
coids are used for severe cases or if acetylsalicylic the Division of Endocrinology at Central Virginia
acid or NSAIDs were not effective after four days Veterans Affairs Health Care System, Richmond.
of therapy.12,26 Pain resolution is faster with glu-
LORI B. SWEENEY, MD, is an associate professor of
cocorticoids than with NSAIDs.12 Prednisone in medicine in the Division of Endocrinology at Cen-
dosages of 15 to 40 mg per day has been proposed tral Virginia Veterans Affairs Health Care System.
for one to six weeks, followed by tapering dosages
of 5 mg every two weeks.12,13,23 During the tran- Address correspondence to Beatriz Martinez
Quintero, MD, Virginia Commonwealth University
sient hypothyroid phase, thyroid hormone sup-
School of Medicine, 1101 E. Marshall St., Rich-
plementation is used for patients with signs and mond, VA 23298 (email:​beamarquin@​gmail.com).
symptoms of hypothyroidism or in patients of Reprints are not available from the authors.
reproductive age who wish to become pregnant.
Levothyroxine should be used for 12 months and
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