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Painless thyroiditis

Painless thyroiditis
Author:
Kenneth D Burman, MD
Section Editor:
Douglas S Ross, MD
Deputy Editor:
Jean E Mulder, MD
Literature review current through: Jan 2024.
This topic last updated: Jun 05, 2023.

INTRODUCTION — Painless thyroiditis is characterized by transient hyperthyroidism, followed sometimes by hypothyroidism, and then recovery (figure 1). Synonyms for this disorder include silent thyroiditis, subacute lymphocytic thyroiditis, and lymphocytic thyroiditis with spontaneously resolving hyperthyroidism. Painless thyroiditis accounts for approximately 0.5 to 5 percent of cases of hyperthyroidism [1,2].

It has many similarities with postpartum thyroiditis but by definition excludes women who have a painless thyroiditis syndrome within one year after a delivery, abortion, or pregnancy loss. (See "Postpartum thyroiditis".)

The clinical features, diagnosis, and management of painless thyroiditis will be reviewed here. An overview of thyroiditis is discussed separately. (See "Overview of thyroiditis".)

PATHOGENESIS — Painless thyroiditis is considered a variant form of chronic autoimmune thyroiditis (Hashimoto's thyroiditis), suggesting that it is part of the spectrum of thyroid autoimmune disease [3]. The two disorders have some pathologic similarities (see 'Pathology' below), and many patients with painless thyroiditis have high serum concentrations of antithyroid peroxidase and antithyroglobulin (Tg) antibodies, many have a family history of thyroid autoimmune disease, and some develop overt chronic autoimmune thyroiditis several years later [4]. It affects women more often than men [3].

Painless thyroiditis is associated with specific human leukocyte antigen (HLA) haplotypes, most often HLA-DR3, findings that suggest an inherited susceptibility [5]. However, the association is considerably weaker than that between HLA-B35 and subacute thyroiditis. (See "Subacute thyroiditis".)

Factors postulated to initiate painless thyroiditis include excess iodine intake and various cytokines. A syndrome very similar to this disorder can occur in patients treated with interferon alfa, interleukin-2, lithium, tyrosine kinase inhibitors, as well as cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) and immune checkpoint inhibitors [6,7]. These observations raise the possibility that cytokines released in response to some (subclinical) injury or infection might initiate the disorder. (See "Overview of thyroiditis", section on 'Drug-induced thyroiditis' and "Drug interactions with thyroid hormones", section on 'Tyrosine kinase inhibitors' and "Toxicities associated with immune checkpoint inhibitors", section on 'Autoimmune thyroid disease'.)

Painless thyroiditis has occasionally occurred in clusters (eg, in nursery school workers) [8]. It has been reported to occur following cessation of glucocorticoids, after adrenalectomy in a patient with Cushing syndrome, following external radiation of the neck for Hodgkin lymphoma [9-11], and in association with lithium therapy [12]. Painless thyroiditis has also been associated with other disorders, including lymphocytic hypophysitis [13], systemic lupus erythematosus, and immune thrombocytopenia (ITP). However, it has not been proven that there is a causal association between any of these disorders and thyroiditis [14-16].

Whatever factors initiate painless thyroiditis, the resulting thyroid inflammation damages thyroid follicles and activates proteolysis of the thyroglobulin stored within the follicles. The result is unregulated release of large amounts of thyroxine (T4) and triiodothyronine (T3) into the circulation, resulting in clinical and biochemical hyperthyroidism. This state lasts only until the stores of thyroglobulin are exhausted, because new hormone synthesis ceases, not only because of damage to the thyroid follicular cells but also because of inhibition of thyroid-stimulating hormone (TSH) secretion by the high serum T4 and T3 concentrations. As the inflammation subsides, the undamaged or repaired thyroid follicles resume synthesis and secretion of thyroid hormone. There may be a transient period of hypothyroidism and increased TSH secretion before thyroid secretion becomes normal again. In a minority of patients, thyroid damage is sufficient to result in permanent hypothyroidism.

CLINICAL FEATURES

Clinical manifestations — The thyroid gland is not painful or tender, but it is usually minimally, diffusely enlarged, and sometimes firm in texture. There may be nonspecific discomfort in the neck area but not specific thyroid pain. Approximately 5 to 20 percent of patients with painless thyroiditis have the characteristic sequence of hyperthyroidism, followed by hypothyroidism, and then recovery (figure 1) [17]. Hyperthyroid symptoms usually develop over one to two weeks and last from two to eight weeks before subsiding. The patient may have any of the common symptoms or signs of hyperthyroidism, such as weakness, fatigue, irritability, palpitations, stare and lid retraction, tachycardia, and tremor. However, the symptoms are usually mild.

The hyperthyroid phase may be followed by recovery or by hypothyroidism (usually clinically mild or even asymptomatic) for two to eight weeks, followed by recovery. Approximately 10 percent of patients may have additional episodes of painless thyroiditis, typically occurring years apart. Eventually, however, about 20 to 30 percent of patients develop chronic autoimmune thyroiditis with permanent hypothyroidism and perhaps 50 percent will have a goiter [2,4].

Some patients with painless thyroiditis present with symptoms of hypothyroidism (cold intolerance, constipation, fatigue), and the symptoms that are characteristic of the hyperthyroid phase are often only apparent retrospectively once the hypothyroid phase has been diagnosed. Others have no symptoms or signs. Painless thyroiditis is frequently incidentally detected by routine thyroid testing and the finding of an abnormal serum TSH.

Laboratory findings — Thyroid function tests vary during the course of painless thyroiditis, and changes in serum TSH typically lag behind changes in serum free T4 and T3. During the hyperthyroid phase, patients with painless thyroiditis have moderately elevated serum free T4, normal or slightly elevated T3, and low serum TSH concentrations, but some have only low serum TSH concentrations (subclinical hyperthyroidism). In patients with painless thyroiditis, the serum T3 concentrations are not disproportionately elevated as they are in patients with Graves' hyperthyroidism [18]. In thyroiditis, the hormones that appear in the blood from damaged follicles are in the same proportions as exist in the thyroid gland (T4>T3), while in Graves' disease thyroid deiodinase is activated, yielding a thyroidal secretory product containing relatively more T3.

In those patients who become hypothyroid, the serum T4 concentration may be low for several days to weeks before the serum TSH concentration becomes high, because of the preceding suppression of TSH secretion. Some patients have only elevation of serum TSH levels, indicative of subclinical hypothyroidism.

Serum antithyroid peroxidase concentrations are high in approximately 50 percent of patients at the time of diagnosis but not usually to the extent found in Hashimoto's thyroiditis [3,19]. The values may rise transiently in the following weeks and then decline, but they remain elevated after thyroid function returns to normal. Other thyroid antibodies, eg, anti-TSH receptor antibodies, may occasionally be detected during the illness or soon after it but do not appear to contribute to the thyroid dysfunction [20]. Serum thyroglobulin concentrations are high, and these elevations may persist after the recovery of thyroid function. The white blood cell count is usually normal, and the erythrocyte sedimentation rate and/or C-reactive protein are normal or slightly increased.

Thyroid scintigraphy — During the hyperthyroid phase of thyroiditis, values for thyroid radioiodine uptake are low, usually less than 1 percent, compared with high values in Graves' hyperthyroidism. Similarly, technetium scan shows an image with a very low radiotracer accumulation, whereas the image shows increased radiotracer accumulation in Graves' disease. These tests are extremely valuable in distinguishing painless thyroiditis from mild Graves' hyperthyroidism. (See 'Diagnosis' below.)

Patients who have been exposed to large amounts of iodine (eg, intravenous radiographic contrast, amiodarone, excess iodine supplements) may have a misleading low radioiodine uptake. In these cases, it may be beneficial to measure a random urinary iodine concentration to ensure that an elevated total body iodine content is not causing low thyroid radioiodine uptake, thus confusing the differentiation between painless thyroiditis and Graves' disease. (See "Iodine-induced thyroid dysfunction", section on 'Evaluation for underlying thyroid disease'.)

Ultrasound — Ultrasonography is not typically part of the evaluation of painless thyroiditis. If performed for the evaluation of suspected goiter or nodule, ultrasonography shows a heterogeneous, hypoechogenic, normal-sized or slightly enlarged thyroid gland. In addition, if a thyroid ultrasound is performed during the hyperthyroid phase of thyroiditis, there will be normal or decreased Doppler flow (as compared with increased in Graves' disease). (See "Overview of the clinical utility of ultrasonography in thyroid disease", section on 'Autoimmune thyroid disease'.)

Pathology — Fine-needle aspiration biopsy is not typically part of the evaluation of painless thyroiditis. If performed, fine-needle aspiration of the thyroid reveals lymphocytes and macrophages, normal thyroid epithelial cells, a few damaged thyroid follicles, and masses of colloid. During recovery, lymphocytic infiltration persists and there may be mild fibrosis, but the thyroid follicles are normal. These findings differ from those of chronic autoimmune thyroiditis in that there is more follicular disruption but fewer lymphocytes, fewer germinal centers, and less fibrosis in painless thyroiditis [19].

DIAGNOSIS — The diagnosis of painless thyroiditis is based upon clinical manifestations, laboratory findings, and, when needed, thyroid scintigraphy (eg, radioiodine uptake). Painless thyroiditis should be considered as the cause of hyperthyroidism in any woman (who is not postpartum) or man who has had symptoms for less than two months and has a small diffuse goiter or no thyroid enlargement. This diagnosis should be strongly considered in a hyperthyroid patient who has been receiving medication such as interferon alfa, interleukin-2, a tyrosine kinase inhibitor, as well as a cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) or immune checkpoint inhibitor. In addition, the presence of painless thyroiditis should be considered in patients with no symptoms who are found to have low serum TSH on routine testing.

For patients in whom the clinical suspicion of hyperthyroidism is high, we measure TSH, free T4, and total T3, rather than TSH alone. If a low TSH value is obtained during routine testing, serum free T4 and total T3 should automatically be measured on the same specimen or, if not possible, the patient should return for follow-up testing.

For nonpregnant patients with hyperthyroidism (low serum TSH, high free T4 and/or total T3) and without clinical manifestations of Graves' disease (eg, ophthalmopathy), a radioiodine uptake or technetium scan can differentiate painless thyroiditis from Graves' disease. Radionuclide imaging is contraindicated in pregnant women; hyperthyroidism during pregnancy is reviewed in detail separately. (See "Diagnosis of hyperthyroidism", section on 'Determining the etiology' and "Hyperthyroidism during pregnancy: Clinical manifestations, diagnosis, and causes", section on 'Establishing the cause'.)

During the hyperthyroid phase of painless thyroiditis, values for thyroid radioiodine uptake are very low, whereas they are at the upper end of normal or high in patients with Graves' disease. Technetium scan shows an image with a very low radiotracer accumulation, whereas the image shows increased radiotracer accumulation in Graves' disease. In most patients with a low radioiodine uptake or low radiotracer accumulation on technetium scan, re-evaluation of thyroid function tests in several weeks usually reveals more normal thyroid function, supporting the diagnosis.

In patients with mild hyperthyroidism and a serum free T4 that is higher relative to its upper limit of normal than is the serum total T3 elevation, a radioiodine uptake or technetium scan may be deferred and thyroid function monitored. If thyroid function normalizes within several weeks, the diagnosis of painless thyroiditis can be suspected, although mild Graves' disease can also occasionally follow this course.

DIFFERENTIAL DIAGNOSIS — During the hyperthyroid phase, painless thyroiditis must be distinguished from other causes of hyperthyroidism and diffuse goiter, such as Graves' disease, which is more common than painless thyroiditis, and TSH-induced hyperthyroidism (eg, TSH-secreting pituitary tumor), which is less common. Painless thyroiditis must also be distinguished from exogenous hyperthyroidism (ingesting T4, other thyroid hormone products, or even supplements that may contain thyroid hormone or its analogues), which may be associated with little or no thyroid enlargement.

Graves' disease – Painless thyroiditis can be distinguished from Graves' disease by its shorter duration, minimal thyroid enlargement, and a low thyroid radioiodine uptake (versus the high values in Graves' hyperthyroidism). When thyroid scintigraphy is contraindicated, painless thyroiditis and Graves' disease may also be distinguished by measuring serum thyroid stimulating immunoglobulins (TSH-receptor antibodies). Serum thyroid-stimulating immunoglobulins levels are typically elevated in Graves' hyperthyroidism but not in painless thyroiditis [21]. In addition, on ultrasound, thyroid Doppler flow is normal or decreased in the thyrotoxic phase of silent thyroiditis and increased in Graves' hyperthyroidism. (See "Disorders that cause hyperthyroidism", section on 'Graves' disease'.)

TSH-secreting pituitary tumor – Painless thyroiditis can be distinguished from TSH-induced hyperthyroidism by its shorter duration, minimal thyroid enlargement, and a low thyroid radioiodine uptake (versus the high values in excess TSH secretion). In addition, serum TSH concentrations are inappropriately normal or elevated in patients with TSH-induced hyperthyroidism but low in the hyperthyroid phase of painless thyroiditis. Ophthalmic findings, such as bitemporal hemianopsia, may be found in patients with a pituitary tumor secreting TSH.

Exogenous hyperthyroidism – Painless thyroiditis must also be distinguished from exogenous hyperthyroidism (ingesting T4 or thyroid hormone products), whether iatrogenic or factitious. Thyroid hormone or its active analogues have been found in various over-the-counter supplements and in meat products that contained thyroid gland fragments. Patients with these disorders have little or no thyroid enlargement (unless the thyroid hormone was given in hope of reducing a goiter), low thyroid radioiodine uptake values, and low serum thyroglobulin concentrations. In contrast, serum thyroglobulin levels are elevated in patients with painless thyroiditis. Careful history-taking should elicit information about thyroid hormone ingestion. (See "Exogenous hyperthyroidism", section on 'Causes'.)

During the hypothyroid phase, painless thyroiditis presents similarly to Hashimoto's thyroiditis. The diagnosis may be suspected if the patient recalls having had spontaneous resolving symptoms of hyperthyroidism weeks to a few months earlier. We do not routinely measure antithyroid peroxidase antibodies, since they are nonspecific and are frequently present in both diseases. If thyroid function normalizes within several weeks without thyroid hormone replacement, the diagnosis of painless thyroiditis is confirmed. (See "Disorders that cause hypothyroidism", section on 'Chronic autoimmune (Hashimoto's) thyroiditis'.)

TREATMENT — There are no studies assessing the optimal treatment of painless thyroiditis. Treatment is based upon observational data and clinical experience. Many patients with thyroiditis need no treatment during either the hyperthyroid or the hypothyroid phases, because thyroid dysfunction is rarely severe and it is transient.

Hyperthyroid phase – Patients who are symptomatic or who are at increased risk for atrial fibrillation should be treated with a beta-blocker during the hyperthyroid phase, unless there is a contraindication to their use. Options include propranolol (40 to 120 mg daily) or atenolol (25 to 50 mg daily) (see "Beta blockers in the treatment of hyperthyroidism"). Thyroid function should be monitored every four to eight weeks to confirm resolution of hyperthyroidism and to detect the development of hypothyroidism. Beta blockers should only be used during the hyperthyroid phase of painless thyroiditis.

In very rare cases of severely deranged thyroid function, glucocorticoid therapy has been used successfully [22]. There is no role for antithyroid drugs (ie, methimazole) or radioiodine therapy, because the hyperthyroidism is not caused by excess thyroid hormone synthesis and because uptake of radioiodine is very low.

Hypothyroid phase – An occasional patient may have sufficient symptoms of hypothyroidism to warrant thyroxine (levothyroxine, T4) therapy. In addition, we prefer to treat when the TSH exceeds 10 mU/L, even in the absence of symptoms.

The usual dose of T4 is 50 to 100 mcg daily with periodic monitoring of serum free T4 and TSH. The exogenous T4 should be discontinued after three to six months. Initially, the dose can be halved and thyroid tests (TSH, free T4) re-evaluated four to six weeks later to insure normal thyroid gland function. If thyroid tests remain normal on half dose, thyroid hormone can be discontinued, with retesting of thyroid function in four to six weeks. If the TSH rises above normal on half dose, the previous dose of thyroid hormone should be resumed.

After recovery from thyroiditis, the patient should be told of the risk of chronic autoimmune thyroiditis, its symptoms described, and periodic follow-up advised. Although abnormalities in thyroid function resolve in most patients, 20 to 30 percent will develop permanent hypothyroidism [2,4]. Patients should also be informed about the possibility of recurrent episodes of thyroiditis, often many years in the future.

Rare patients with recurrent episodes of painless thyroiditis may choose to have their thyroid ablated with radioiodine between episodes when they are euthyroid and the radioiodine uptake has returned to normal. However, definitive therapy is rarely necessary [23]. Radioiodine therapy during the thyrotoxic phase is not effective, because the uptake of radioiodine by the thyroid is very low.

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Thyroiditis (The Basics)")

SUMMARY AND RECOMMENDATIONS

Clinical manifestations Painless thyroiditis is considered a variant form of chronic autoimmune thyroiditis (Hashimoto's thyroiditis), suggesting that it is part of the spectrum of thyroid autoimmune disease. The thyroid gland is not painful or tender, but is usually minimally, diffusely enlarged and sometimes firm in texture. The classic pattern of changes in thyroid function in patients with painless thyroiditis is transient hyperthyroidism, followed sometimes by hypothyroidism, and then recovery (figure 1). (See 'Pathogenesis' above and 'Clinical manifestations' above.)

Diagnosis – The diagnosis of painless thyroiditis is based upon clinical manifestations, laboratory findings, and, when needed, thyroid scintigraphy (eg, radioiodine uptake). For patients in whom the clinical suspicion of hyperthyroidism is high, we measure thyroid-stimulating hormone (TSH), free thyroxine (T4), and total triiodothyronine (T3). If a low TSH value is obtained during routine testing of an asymptomatic patient, serum free T4 and total T3 should automatically be measured on the same specimen or, if not possible, the patient should return for follow-up testing. In nonpregnant patients with hyperthyroidism and without clinical manifestations of Graves' disease (eg, ophthalmopathy), we measure 24-hour radioiodine uptake or perform a technetium scan while the patient is thyrotoxic to differentiate painless thyroiditis from Graves' disease. (See 'Diagnosis' above and "Diagnosis of hyperthyroidism", section on 'Determining the etiology'.)

Treatment

Mild thyroid dysfunction – Many patients with painless thyroiditis need no treatment during either the hyperthyroid or hypothyroid phases, because thyroid dysfunction is rarely severe and it is transient. Thyroid function tests should be monitored every four to eight weeks to confirm resolution of hyperthyroidism and to detect the development of hypothyroidism. (See 'Treatment' above.)

Symptomatic hyperthyroidism – Beta blockers are useful to relieve bothersome palpitations or tremulousness in symptomatic hyperthyroid patients. There is no role for antithyroid drugs or radioiodine in the treatment of the hyperthyroid phase of thyroiditis. (See 'Treatment' above.)

Symptomatic hypothyroidism or TSH >10 mU/L – Patients with symptomatic hypothyroidism require treatment with T4 (levothyroxine). For asymptomatic patients who have a serum TSH concentration >10 mU/L during the hypothyroid phase, we also suggest T4 replacement (Grade 2C). We typically treat with 50 to 100 mcg/day with periodic monitoring of serum TSH and free T4. We continue T4 for three to six months before attempting withdrawal. Thyroid tests (TSH, free T4) should be re-evaluated four to six weeks after withdrawal to ensure normal thyroid gland function. (See 'Treatment' above.)

Long-term prognosis – Approximately 10 percent of patients may have additional episodes of painless thyroiditis. Eventually, about 20 to 30 percent of patients develop permanent hypothyroidism. (See 'Treatment' above.)

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References

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