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Subacute Thyroiditis

, M.D., FACP.

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Last Update: June 12, 2018.


Subacute thyroiditis (SAT) is an inflammatory condition of the thyroid with characteristic presentations and clinical course. Patients with the classic, painful (DeQuervain’s; Granulomatous) thyroiditis, (PFSAT) typically present with painful swelling of the thyroid. Transient vocal cord paresis may occur. At times, the pain begins and may be confined to the one lobe, but usually spreads rapidly to involve the rest of the gland ("creeping thyroiditis"). Pain may radiate to the jaw or the ears. Malaise, fatigue, myalgia and arthralgia are common. A mild to moderate fever is expected, and at times a high fever of 104°F (40.0°C) may occur. The disease process may reach its peak within 3 to 4 days and subside and disappear within a week, but more typically, onset extends over 1 to 2 weeks and continues with fluctuating intensity for 3 to 6 weeks. The thyroid gland is typically enlarged, smooth, firm and tender to palpation, sometimes exquisitely so. Approximately one-half of the patients present during the first weeks of the illness, with symptoms of thyrotoxicosis. Subsequently patients often experience hypothyroidism before returning to normal (see figure 1). This painful condition lasts for a week to a few months, usually demonstrates a very high erythrocyte sedimentation rate (ESR), elevated C- reactive protein (CRP) levels and has a tendency to recur.

Painless (silent, autoimmune) subacute thyroiditis (PLSAT) occurs spontaneously or following pregnancy when it is referred to as postpartum thyroiditis [PPT]). Autoimmune thyroiditis is histologically similar to Hashimoto's thyroiditis and occurs following 3.9-10% of pregnancies. The combination of thyroid enlargement usually without discomfort and, positive anti-thyroid antibodies, associated with typical thyroid function test abnormalities (see figure 1), over a 9-12 month course should alert the clinician to the presence of PLSAT.


A tendency for the painful form of the disease to follow upper respiratory tract infections or sore throats has suggested a viral infection. An autoimmune reaction is possible as patients with PFSAT often manifest HLA-Bw35 and those with PLSAT are frequently TPO or TG-ab positive. In both forms, clinical thyroid symptoms result from either the initial release of thyroid hormone from the inflamed tissue during the thyrotoxic phase or the lack of circulating thyroid hormones in the hypothyroid phase (See figure 1). Medications associated with SAT outlined in table 4.

Figure 1.

Figure 1.

Time Course of Subacute Thyroiditis


Subacute thyroiditis is a diagnosis made clinically. Anterior neck pain, preceded by an upper respiratory inflammation, alerts the clinician to the classic PFSAT. Differential diagnostic considerations include acute (suppurative, thyroid abscess) thyroiditis (see table 1), which is usually a painful nodular enlargement of the thyroid or unusual presentations of Graves’ or nodular thyroid disease (see table 2 below) with pain generated by capsular stretching.

Thyroid function tests (see table 3) during the painful (initial) phase of SAT often reveal a suppressed TSH and elevation of total T4 and T3 levels consistent with the thyrotoxic state. T3 (ng/dl) to T4 (ug/dl) ratio is less than 20 in all forms of SAT. ESR is almost always greater than 50, WBC counts and CRP levels are usually elevated in PFSAT. PLSAT (including PPT) is typically associated with the presence of anti-thyroid peroxidase (TPO-ab) and thyroglobulin (Tg-ab) antibodies, both of which are usually absent or present only in low titers in PFSAT. Thyrotropin receptor antibodies (TRAb) are usually positive in Graves' disease and absent or low level in patients with PFSAT as well as PPT.

Radioactive iodine uptake and scan typically reveals a low RAIU and poor visualization of the thyroid in PFSAT and PLSAT whereas significant uptake is expected in Graves’ disease (GD) or toxic nodular goiters (TNG). PLSAT must be differentiated from other forms of low uptake thyrotoxicosis (see Table 2), iatrogenically (factitious [l-thyroxine (LT4), l-triiodothyronine (LT3) or T4/T3 combination (animal extract)] induced thyrotoxicosis results in a suppressed thyroglobulin (TG) level. Ectopic thyroid hormone production in a Struma Ovarii or functional metastatic thyroid cancer can be detected with total body scanning. Iodine contamination after a contrast enhanced CT, obliterates the RAIU and obscures the presence of the more frequently encountered Graves’ disease or a toxic multinodular goiter. A recent CT scan will frequently alert the clinician to this artifact. Urine iodine measurement can quantify the degree of iodine contamination present.

Thyroid ultrasound typically shows a heterogeneously hypoechoic pattern and has a suppressed vascular pattern in SAT while patients with Graves’ demonstrate hyper-vascularity. The presence of thyroid nodules supports the presence of a toxic nodular goiter. Localized PFSAT, can be suggestive of thyroid cancer. Usually the pain, elevated erythrocyte sedimentation rate and leukocytosis, and clinical remission or spread to other parts of the gland make clinical differentiation possible but may require a fine needle aspiration for definitive diagnosis.

Table 1.

Features Useful in Differentiating Acute Suppurative Thyroiditis (AST) and Subacute Thyroiditis (SAT)

Characteristic AST SAT
Prior URI88%17%
Symptoms of T-toxicosisUncommon47%
Sore throat90%36%
Painful thyroid swelling100%77%
Left side affected85%not specific
Migrating tendernessPossible27%
Erythema of skin83%not usually
Elevated WBC count57%25-50%
Elevated ESR100%85%
Abnormal TFTs5-10%60%
Alk-phos., AST/ALT Rarecommon
FNA Purulent, bacteria or fungi present~100%0
Lymphocytes, macrophages, PNMs, giant cells0~100%
123I uptake lowRarely~100%
Abnormal thyroid scan92%
Scan / US helpful in D/D75%
Gallium scan positive~100%~100%
Barium swallow = fistulaCommon0
CT scan usefulRarelynot useful
Clinical response to glucocorticoid treatmentTransient100%
Incision/drainage req.85%No
Recurrence following operative drainage16%No
Pyriform sinus fistula discovered96%No
URI= Upper Respiratory Infection, WBC= white blood cell count, ESR= Erythrocyte Sedimentation Rate, TFT’s= Thyroid function tests, Alk-Phos= Alkaline Phosphatase, AST= Aspartate Aminotransferase, ALT= Alanine Aminotransferase, FNA= Fine needle aspiration, US= Ultrasound examination, ↑= elevated

Table 2

Differential Diagnosis of Thyrotoxic Patients Based on Radioactive Iodine Uptake (RAIU)

Normal to ↑ 123-I RAIU Near absent 123-I RAIU
Graves’ diseasePainless (silent) thyroiditis
Toxic multinodular goiterAmiodarone-induced thyroiditis
Toxic solitary noduleSubacute (painful) thyroiditis
Trophoblastic (hCG mediated) diseaseIatrogenic or factitious thyrotoxicosis
TSH-producing pituitary tumorEctopic tissue (S. Ovarii, functional cancer)
Thyroid hormone resistanceAcute thyroiditis

Table 3

Differential Diagnostic Considerations in the Thyrotoxic Patient [Typical findings in each disease]

Element PFSAT PLSAT PPT Graves’
Neck Pain YesNoNoNo
Recent URI YesNoNoNo
Systemic symptoms YesNoNoNo
Recent Pregnancy NoNoYesNo
Thyroid symptoms YesYesYesYes
ESR ElevatedNormalNormalNormal
CRP ElevatedNormalNormalNormal
TSH ↑/ ↓/ Nl↑/ ↓/ Nl↑/ ↓/ NlSuppressed
FT4 ↑/ ↓/ Nl↑/ ↓/ Nl↑/ ↓/ NlNl/↑
TT3 ↑/ ↓/ Nl↑/ ↓/ Nl↑/ ↓/ NlNl/ ↑
T3/T4 < 20< 20< 20> 20
Thyroglobulin ElevatedElevatedElevatedElevated
TPO-ab Negative+/−, Pos+/−, Pos+/−, Pos
Tg-ab Negative+/−, Pos+/−, Pos+/−, Pos
TSHR-ab NegativeNegNegPos
RAIU/Scan Low/ Not visibleLow/ Not visibleLow/ Not visibleHigh/ diffuse
US Echo-genicity Hypo-
Vascularity DecreasedDecreasedDecreasedIncreased

PFSAT= painful subacute thyroiditis; PLSAT= painless subacute thyroiditis;

PPT= postpartum thyroiditis

Table 4

Causes of Drug Associated Thyrotoxicosis

AmiodaroneIodine (AIT 1)months to yearsSupportive, ATDs, Perchlorate, Surgery
AmiodaroneThyroiditis (AIT 2)Often > 1 yearSupportive care, Surgery, Prednisone
LithiumThyroiditisOften > 1 yearATDs, Supportive
Interferon-αThyroiditis or Graves’MonthsSupportive, ATDs, and /or 131-I (Graves’ only)
Interleukin-2Thyroiditis or Graves’MonthsSupportive, ATDs, and /or 131-I (Graves’ only)
Contrast (I)Thyroid autonomyWeeks to monthsATDs
131-I AblationDestructive thyroiditis1-4 weeksSupportive, prednisone
131-I Rx of TMNGGraves’ disease3-6 months131-I, surgery, ATDs
ATD= Anti thyroid drugs, TMNG= Toxic Multinodular Goiter


In some patients, no treatment is required. For many, analgesic therapy for relief of pain can be achieved with non-steroidal anti-inflammatory agents. If this fails, prednisone administration should be employed with daily doses of 20-40 mg prednisone. After one to 2 weeks of this treatment, the osage is tapered over a period of 6 weeks. Most patients have no recrudescence of symptoms, but occasionally this does occur and the dose must be increased again. The recurrence rate of painful subacute thyroiditis after cessation of prednisolone therapy is about 20%. Beta blocking agents are usually administered for relief of thyrotoxic symptoms in the initial stage of SAT. Antithyroid drugs have no role in the management of established SAT as the excess thyroid hormone levels result from release of preformed thyroxine and triiodothyronine from inflamed tissue. Alternatively, oral cholecystographic agents may be used safely and effectively for the management of hyperthyroidism. Levothyroxine administration may be useful, at least transiently, if the patient enters a phase of hypothyroidism. Surgical intervention is not the primary treatment for subacute thyroiditis but is safe and with low morbidity if necessary because of the possibility of associated papillary cancer based on cytological examination.


In 90% or more of patients with classic painful subacute thyroiditis, there is a complete and spontaneous recovery and a return to normal thyroid function. However, the thyroid glands of patients with subacute thyroiditis may exhibit irregular scarring between islands of residual functioning parenchyma. Up to 10% of the patients may become hypothyroid and require permanent replacement with levothyroxine. Rates of permanent hypothyroidism after antibody positive PLSAT and especially PPT are significantly higher[3].


  1. Ross DS, Burch HB, Cooper DS, Greenlee MC, Laurberg P, Maia AL, Rivkees SA, Samuels M, Sosa JA, Stan MN, Waiter MA. American Thyroid Association Guidelines for Diagnosis and Manangement of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid. 2016;26(10):1343–1421. DOI. [PubMed: 27521067] [CrossRef]


  1. Shrestha RT and Hennessey, JV Acute and Subacute, and Riedel's Thyroiditis, In: De Groot LJ, Chrousos G, Dungan K, Feingold KR, Grossman A, Hershman JM, Koch C, Korbonits M, McLachlan R, New M, Purnell J, Rebar R, Singer F, Vinik A, editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-2018.
  2. Stagnaro-Green A, Schwartz A, Gismondi R, Tinelli A, Mangieri T, Negro R. High rate of persistent hypothyroidism in a large-scale prospective study of postpartum thyroiditis in southern Italy. J Clin Endocrinol Metab. 2011;96:652–657. http://www​.ncbi.nlm.nih​.gov/pubmed/21190974 [PubMed: 21190974]
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