• Thyroiditis is a term used to describe a diverse group of disorders associated with thyroid inflammation.
• Thyroiditis can be associated with a euthyroid state, thyrotoxicosis, or hypothyroidism.
• The clinical presentation of thyroiditis will direct the evaluation with useful testing to include measurement of thyroid hormone levels, thyroid antibody testing, white blood cell count, erythrocyte sedimentation rate, thyroid scintigraphy, and thyroid ultrasound.
• Abnormalities of thyroid hormone levels resulting from thyroiditis may be transient and require no or only short-term therapy.
• If symptomatic thyrotoxicosis is present, beta-blocker therapy should be initiated.
• Thyroiditis associated with persistent hypothyroidism is managed with synthetic thyroxine (T4, Levoxyl, Synthroid).
• Thyroid pain associated with subacute thyroiditis therapy is managed with a nonsteroidal antiinflammatory drug or, if ineffective, glucocorticoid therapy.
• Acute suppurative thyroiditis requires immediate parenteral antibiotic therapy as well as surgical drainage, if indicated.
Thyroiditis is a term used to describe a diverse group of disorders characterized by inflammation of the thyroid gland (Table 1). Presentation of thyroiditis is variable depending on the etiology. The most common thyroid disorder in the United States, Hashimoto’s thyroiditis, most often presents with hypothyroidism. Other forms of thyroiditis may present with thyrotoxicosis because of inflammation in the thyroid gland resulting in the release of stored hormone. Painful thyroiditis is seen with subacute, suppurative and radiation- induced thyroiditis, while other variants are most often painless.
Causes of Thyroiditis
Autoimmune thyroiditis: Hashimoto’s thyroiditis, postpartum thyroiditis, silent thyroiditis
Subacute thyroiditis, also known as de Quervain’s thyroiditis or subacute granulomatous thyroiditis Suppurative thyroiditis, also known as infectious thyroiditis or pyrogenic thyroiditis
Riedel’s thyroiditis, also known as fibrous thyroiditis Therapy induced thyroiditis: amiodarone (Cordarone), interferon-alpha, interleukin-2, lithium, tyrosine kinase inhibitors, radioactive iodine
The most common cause of hypothyroidism in iodine-sufficient areas of the world is Hashimoto’s thyroiditis, also known as chronic autoimmune thyroiditis. Elevated serum antithyroid peroxidase antibody concentrations are found in ~ 5% of adults and ~ 15% of older women; overt hypothyroidism is seen in up to 2% of the population. A variant of chronic autoimmune thyroiditis, postpartum thyroiditis, is a destructive thyroiditis induced by an autoimmune mechanism that occurs within 1 year of parturition. Postpartum thyroiditis occurs in up to 10% of women in the United States. Silent thyroiditis, is indistinguishable from postpartum thyroiditis, with the exception of lack of temporal relationship to pregnancy. Silent thyroiditis may account for about 1% of all cases of thyrotoxicosis.
Many medications are associated with an alteration in thyroid function testing; however, only a few are known to provoke an autoimmune or destructive inflammatory thyroiditis, including amiodarone (Cordarone), lithium, interferon alfa, interleukin-2, and tyrosine kinase inhibitors. Riedel’s thyroiditis is a progressive fibrosis of the thyroid gland with a prevalence of only 0.05% among patients with thyroid disease requiring surgery. Subacute thyroiditis is the most common cause of thyroid pain. It occurs in up to 5% of patients with clinical thyroid disease. Suppurative thyroiditis, most commonly caused by bacterial infection, is rare because of the thyroid gland’s encapsulation, high iodine content, rich blood supply, and extensive lymphatic drainage. Radiation-induced thyroiditis occurs in approximately 1% of patients who receive radioactive iodine therapy for hyperthyroidism.
Hashimoto’s thyroiditis is more common in women, particularly older women. Hashimoto’s thyroiditis is associated with several gene polymorphisms, suggesting a role for genetic susceptibility. Subacute thyroiditis frequently follows an upper respiratory tract infection, with its incidence highest in summer. Suppurative thyroiditis is most likely to occur in patients with preexisting thyroid disease, those with congenital anomalies such as pyriform sinus fistula, and those who are immunosuppressed.
Hashimoto’s thyroiditis, postpartum thyroiditis, and silent thyroiditis all have an autoimmune basis. The antithyroid immune response begins with activation of thyroid antigen-specific helper T cells. Once helper T cells are activated, they induce B cells to secrete thyroid antibodies; thyroid antibodies most frequently measured are those directed against thyroid peroxidase and against thyroglobulin. The mechanism for autoimmune destruction of the thyroid likely involves both cellular immunity and humoral immunity. Riedel’s thyroiditis is the local involvement of the thyroid in a systemic disease, multifocal fibrosclerosis; the etiology of Riedel’s thyroiditis is not known.
Although a viral cause of subacute thyroiditis has been proposed, clear evidence for this proposed etiology is lacking. Suppurative thyroiditis is most often associated with a bacterial pathogen; however, fungal, mycobacterial, or parasitic infections may also be the cause. Although rare, radiation-induced thyroiditis may occur following the treatment of hyperthyroidism with radioactive iodine because of radiation-induced injury and necrosis of thyroid follicular cells and associated inflammation.
A symmetrical, painless goiter is frequently the initial finding in Hashimoto’s thyroiditis. The usual course of Hashimoto’s thyroiditis is gradual loss of thyroid function. Among patients with this disorder who have subclinical hypothyroidism, overt hypothyroidism occurs at a rate of about 5% per year. The classic presentation of postpartum thyroiditis occurs in only approximately 30% of afflicted women, with the characteristic sequence of hyperthyroidism, followed by hypothyroidism, and then recovery. Persistent hypothyroidism is seen in up to 30% of women following an episode of postpartum thyroiditis. Silent thyroiditis is marked by a similar characteristic sequence of thyroid hormone dysfunction. However, it is not temporally associated with pregnancy; 20% will have residual hypothyroidism. Medication-induced thyroiditis is variable in its presentation. Amiodarone (Cordarone), rich in iodine, is associated with hypothyroidism and hyperthyroidism; type 2 amiodarone- induced thyrotoxicosis is due to a destructive thyroiditis process.
Lithium is more commonly associated with hypothyroidism. Interferon-alfa and interleukin-2 can cause both permanent and transient hypothyroidism likely related to the ability of these substances to induce or exacerbate thyroid autoimmune disease. Riedel’s thyroiditis presents with neck discomfort or tightness, dysphagia, hoarseness, and a diffuse goiter that is hard, fixed, and often not clearly separable from the adjacent tissues. Generally, patients are euthyroid, and their antithyroid antibody concentrations are often high. Subacute thyroiditis manifests with a prodrome of myalgias, pharyngitis, low-grade fever, and fatigue with subsequent fever and neck pain, and up to 50% of patients have symptoms of thyrotoxicosis. Patients with suppurative thyroiditis are usually acutely ill with fever, dysphagia, dysphonia, anterior neck pain with erythema, and a tender thyroid mass. Radiation-induced thyroiditis presents 5 to 10 days following radioactive iodine treatment with neck pain and tenderness. In addition, there can be a transient exacerbation of hyperthyroidism.
Diagnosis and Differential Diagnosis
The diagnostic approach to suspected thyroiditis can be focused based on an association with thyroid pain and circulating thyroid hormone status (Figure 1). Hashimoto’s thyroiditis is diagnosed when a goiter is found on examination with a subsequently noted elevation of thyroid antibodies or when subclinical or overt hypothyroidism is detected with associated elevated thyroid antibodies. Screening for postpartum thyroiditis with a measurement of TSH and free thyroxine should be undertaken in women presenting with symptoms of thyroid dysfunction in the postpartum period. If hyperthyroidism is present, thyroid scintigraphy (if not contraindicated, e.g., breastfeeding) or measurement of thyroid-stimulating immunoglobulins is helpful in the differentiation of postpartum thyroiditis from Graves’ disease. The diagnostic approach to silent thyroiditis is similar. The laboratory hallmark of subacute thyroiditis is a markedly elevated erythrocyte sedimentation rate; the leukocyte count is normal or slightly elevated. Thyrotoxicosis may be present; if so, thyroid scintigraphy will reveal a low iodine uptake state. Thyroid antibody testing is typically normal. Thyroid ultrasound reveals a hypoechogenic gland with low to normal vascularity. Suppurative thyroiditis is typically associated with normal thyroid function.
Leukocyte counts and erythrocyte sedimentation rates are elevated. Fine-needle aspiration with Gram stain and culture is the diagnostic test of choice. Radiation-induced thyroiditis should be considered if a temporal relationship to radioactive iodine treatment is present. If there is an exacerbation of hyperthyroidism immediately following radiation treatment for the same, consideration of radiation-induced thyroiditis due to the release of preformed thyroid hormone associated with destruction of follicular cells should be considered as an etiology of thyrotoxicosis in addition to the underlying disease process.
FIGURE 1 Clinical concern for thyroiditis—diagnostic algorithm. Abbreviations: RAIU = radioactive iodine uptake; TSI = thyroid- stimulating immunoglobulins.
Once overt hypothyroidism is present in the patient with Hashimoto’s thyroiditis, treatment with synthetic l-thyroxine (Levoxyl, Synthroid) therapy is indicated. The average replacement dose of thyroxine in adults is approximately 1.6 mcg/kg body weight per day. Adjustment of dosage is undertaken every 6 weeks until a euthyroid status is achieved. The majority of women with postpartum thyroiditis will not need treatment during either the hyperthyroid nor hypothyroid phase. If symptomatic hyperthyroidism is present, beta-blocker therapy can be used; antithyroid medications have no utility in the management of postpartum thyroiditis. Women with symptomatic hypothyroidism should be treated with synthetic thyroxine therapy; in asymptomatic women, initiation of thyroxine therapy should be considered if TSH is > 10 mU/L. Management of silent thyroiditis is the same as that for postpartum thyroiditis. Symptoms associated with Riedel’s thyroiditis may be relieved with prednisone; a small case series associated improvement and even resolution of the process with Tamoxifen therapy. Surgery is indicated in Riedel’s thyroiditis if compressive symptoms are present. The goal of therapy in subacute thyroiditis is to provide symptom relief. Nonsteroidal antiinflammatory medications are often adequate to control pain; if insufficient, glucocorticoid therapy should be initiated. Beta-blockade therapy can ameliorate symptoms of thyrotoxicosis if indicated.
Suppurative thyroiditis is managed with appropriate antibiotics and drainage of any abscess; the disease may prove fatal if diagnosis and treatment are delayed. Pain associated with radiation-induced thyroiditis can be managed with nonsteroidal antiinflammatory therapy, or, if ineffective, a short course of glucocorticoid therapy.
Radiation-induced thyroiditis is a self-limited process and will resolve spontaneously within days to weeks.
In the patient with Hashimoto’s thyroiditis with a euthyroid state, routine TSH testing should be undertaken give the risk of development of overt hypothyroidism at 5% per year. Any woman who has had postpartum thyroiditis should be monitored very closely for thyroid dysfunction with future pregnancies, as reoccurrence is likely. For women who have fully recovered from postpartum thyroiditis, yearly TSH measurements should be considered because of underlying chronic autoimmune thyroiditis and risk for overt hypothyroidism. Although overall recurrence rates for silent thyroiditis have not been well established, a similar monitoring plan is warranted for this variant of chronic autoimmune thyroiditis.
Subacute thyroiditis recurs in only about 2% of patients. Routine monitoring following resolution of process has not been defined.
1. Bogazzi F., Bartalena L., Martino E. Approach to the patient with amiodarone-induced thyrotoxicosis. J Clin Endocrinol Metab. 2010;95:2529–2535.
2. Cooper D.S., Ladenson P.W. The thyroid gland. In: Gardner D.G., Shoback D., eds. Greenspan’s Basic & Clinical Endocrinology. 9th ed. New York: McGraw-Hill; 2011. Available at http://accessmedicine.mhmedical.com/content.aspx? bookid=380&Sectionid=39744047 [accessed January 23, 2014].
3. De Groot L., Abalovich M., Alexander E.D., et al. Management of thyroid dysfunction during pregnancy and postpartum: An Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2012;97:2543–2565.
4. Pearce E.N., Farwell A.P., Braverman L.E. Thyroiditis. N Engl J Med. 2003;348:2646–2655.
5. Samuels M.H. Subacute, silent and postpartum thyroiditis. Med Clin North Am. 2012;96:223–233.