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Am Fam Physician. 2021;104(6):609-617

Patient information: A handout on this topic is available at https://familydoctor.org/condition/thyroiditis.

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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 pattern 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 corticosteroids 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, surveillance and clinical follow-up are recommended to monitor for changes in thyroid function.

Thyroiditis is a general term for inflammation of the thyroid gland, and it can be associated with thyroid dysfunction. Thyroiditis is classified according to clinical symptoms (painful or painless), onset of symptoms (acute, subacute, chronic), and underlying etiology (autoimmunity, infection, drugs, radiation). Painful types of thyroiditis include subacute, suppurative, and radiation induced. Painless types include drug induced, fibrous (Riedel thyroiditis), Hashimoto thyroiditis (HT), postpartum, and silent.

Clinical recommendationEvidence ratingComments
In patients with Hashimoto thyroiditis (i.e., chronic autoimmune thyroiditis) and subclinical hypothyroidism, the thyroid-stimulating hormone level should be monitored annually.15,19 CExpert consensus and disease-oriented evidence
Radioactive iodine uptake and scan is contraindicated in patients who are pregnant or breastfeeding.7,12,21 CExpert consensus guideline
Beta blockers can treat thyrotoxic symptoms in patients with all forms of thyroiditis.21 BInconsistent or limited-quality patient-oriented evidence
Patients with a history of postpartum thyroiditis should have thyroid-stimulating hormone testing annually to evaluate for permanent hypothyroidism.22 CConsistent and good-quality patient-oriented evidence
If the etiology of thyrotoxicosis is not apparent based on initial evaluation, clinicians should test for thyrotropin receptor antibodies 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 CExpert consensus guideline
Patients with subacute thyroiditis should be started on high-dose 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 CExpert consensus
RecommendationSponsoring organization
Avoid routinely performing thyroid ultrasonography in children who have simple goiters or autoimmune thyroiditis.American Academy of Pediatrics – Section on Endocrinology
Do not routinely perform thyroid ultrasonography in patients with abnormal thyroid function tests if there is no palpable abnormality of the thyroid gland.Endocrine Society/American Association of Clinical Endocrinologists

Most forms of thyroiditis result in a triphasic disease pattern of thyroid dysfunction. Patients have an initial phase of hyperthyroidism (thyrotoxicosis) attributed to the release of preformed thyroid hormone from damaged thyroid follicular 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 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, and management for different types of thyroiditis, including less common types.113 Figure 1 is an algorithm for the diagnosis of suspected thyroiditis.14

TypeEtiologyClinical presentationDiagnosisComplicationsManagement
Chronic autoimmune thyroiditis (Hashimoto thyroiditis, chronic lymphocytic thyroiditis)AutoimmunePainless goiter; euthyroidism, hypothyroidism, subclinical hypothyroidism, and, rarely, transient hyperthyroidism (hashitoxicosis)Presence of atrophic thyroid gland or nontender goiter with or without compressive symptoms (e.g., dysphagia); thyroid function tests (differ with phase); TPO* and increase in thyroglobulin antibodiesHypothyroidismLevothyroxine
Drug-induced thyroiditisSee Table 2
Suppurative thyroiditis (infectious thyroiditis)Multiple infectious organisms, most commonly Staphylococcus aureus, Streptococcus spp.Anterior neck pain, swelling, tenderness, odynophagia, fever, chills, and local lymphadenopathyComplete blood count with differential, complete metabolic panel, blood cultures; computed tomography of the neck and chest with intravenous contrast; 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 collectionAcute complications may include sepsis and airway compromise; in some patients, destructive thyroiditis may lead to permanent hypothyroidismHospitalization, airway monitoring and stabilization, and empiric antibiotic therapy with penicillinase-resistant penicillin and beta-lactamase inhibitor (e.g., piperacillin/tazobactam [Zosyn]), vancomycin if methicillin-resistant S. aureus is suspected; antibiotic therapy should be adjusted to microbiology and antimicrobial susceptibility data; urgent transcutaneous or open-surgical abscess drainage is recommended if airway is compromised
Postpartum thyroiditisAutoimmuneHyperthyroidism alone, hyperthyroidism followed by transient or permanent hypothyroidism, or hypothyroidism alone within 1 year of delivery, miscarriage, or medical abortionPresence of TPO antibodies and increase in thyroglobulin antibodies; thyroid function tests (differ with phase); low radioactive iodine uptake in the hyperthyroid phaseUp to 70% of patients develop recurrence with subsequent pregnancies; permanent hypothyroidism occurs in 15% to 50% of womenBeta blockers for hyperthyroid symptoms; levothyroxine for symptomatic hypothyroidism or patients who are attempting pregnancy or breastfeeding (in the hypothyroid phase), and permanent hypothyroidism
Radiation-induced thyroiditisRadiation (radioiodine and external radiation)Anterior neck pain, thyroid gland enlargement and tenderness; transient hyperthyroidism; occurs typically within 2 weeks after radiationClinical diagnosis made in the setting of recent radiationSelf-limited; hyperthyroidism generally resolves within 1 monthBeta blockers for hyperthyroid symptoms; NSAIDs usually provide sufficient analgesia, and prednisone (20 to 40 mg per day) is rarely required for thyroid pain
Riedel thyroiditis (fibrous thyroiditis)Unknown, auto-immunity may contribute to the pathogenesisDestructive thyroiditis characterized by dense fibrosis that can extend into adjacent tissues; firm goiter; compressive symptoms (e.g., hoarseness, dyspnea, dysphagia); hypocalcemia may occur due to fibrotic transformation of the parathyroid glandsThyroid biopsyMost patients are euthyroid, approximately 30% develop hypothyroidismNo standardized treatment; glucocorticoids with mycophenolate mofetil (Cellcept) or tamoxifen have been described in the literature, subtotal thyroidectomy is indicated to relieve compressive symptoms
Silent thyroiditis (silent sporadic thyroiditis, painless sporadic thyroiditis, subacute lymphocytic thyroiditis)AutoimmuneHyperthyroidism alone, hyperthyroidism followed by hypothyroidism, or hypothyroidism aloneIncrease in TPO antibodies; thyroid function tests (differ with phase); low radioactive iodine uptake in the hyperthyroid phase10% to 20% of patients develop permanent hypothyroidism; 5% to 10% recursBeta blockers for hyperthyroid symptoms; levothyroxine for symptomatic hypothyroidism (in the hypothyroid phase) and permanent hypothyroidism
Subacute thyroiditis (granulomatous thyroiditis, giant cell thyroiditis, de Quervain thyroiditis)Post-viralAnterior neck pain, dysphagia, reported recent upper respiratory tract infection; hyperthyroidism followed by transient hypothyroidism, and eventual restoration of thyroid functionThyroid function tests (differ with phase); elevated erythrocyte sedimentation rate and C-reactive protein level; increase in TPO antibodies (up to 25% of patients have low titers); low radioactive iodine uptake in the hyperthyroid phaseSelf-limited; most patients are euthyroid within 12 months of onset; 5% to 15% of patients develop permanent hypothyroidism; 1% to 4% recursBeta blockers for hyperthyroid symptoms; NSAIDs (e.g., ibuprofen, 1,200 to 3,200 mg per day in divided doses) and steroids (prednisone, 15 to 40 mg per day for 1 to 6 weeks, then taper) for thyroid pain; levothyroxine for hypothyroidism

Hashimoto Thyroiditis (Chronic Autoimmune Thyroiditis)

EPIDEMIOLOGY

HT (i.e., chronic autoimmune thyroiditis or chronic lymphocytic thyroiditis) is the most commonly encountered autoimmune disease worldwide.1,15 The estimated incidence of HT is 0.3 to 1.5 cases per 1,000 people per year.2 HT may present with other autoimmune disorders, such as type 1 diabetes mellitus, Addison disease, rheumatoid arthritis, systemic lupus erythematosus, Sjögren syndrome, autoimmune hepatitis, and vitiligo.1,16 HT occurs due to the formation of autoantibodies and direct injury to the thyroid from an environmental trigger (e.g., infection, stress, iodine intake) in patients with genetic susceptibility. The degree of injury can differ among individuals but is often progressive over time and can result in fibrotic transformation of the gland.17

CLINICAL PRESENTATION

Patients with HT often present with a painless goiter, with or without overt hypothyroidism.1 In patients who are asymptomatic, HT is usually the incidental finding of the goiter that prompted an evaluation. Other patients may report typical symptoms of hypothyroidism such as fatigue, weight gain, cold intolerance, constipation, depression, myalgia, menorrhagia, and dry skin. Many of these symptoms overlap with other disorders and may not always correlate with the degree of thyroid dysfunction. In a 20-year follow-up study, clinical or biochemical 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

DIAGNOSIS

The diagnosis of HT can be established by a combination of clinical features, thyroid function test results consistent with subclinical hypothyroidism (elevated serum TSH level, but normal serum levels of T4 and free triiodothyronine [T3]) or overt hypothyroidism (elevated TSH level with low T4 and T3 serum levels), and elevated thyroglobulin and thyroid peroxidase (TPO) antibodies.1,15 TPO antibodies are found in 95% of patients with HT, whereas thyroglobulin antibodies are elevated in 60% to 80% of patients with HT.1 Some patients may present with self-limited transient thyrotoxicosis or a hyperthyroid phase (i.e., hashitoxicosis) caused by destructive inflammation attributed to HT damaging the thyroid follicles, releasing excess thyroid hormone.18 The thyroid gland is often diffusely enlarged and firm with an irregular surface on examination.15 Some patients have a small thyroid volume if underlying atrophy of the thyroid gland has occurred.2 Patients with goiter may have compressive symptoms such as dysphonia, dyspnea, and dysphagia.1

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