Subacute thyroiditis, in its narrow definition, refers to granulomatous thyroiditis (also known as de Quervain thyroiditis) or giant cell thyroiditis. It is the most common form of the disease, and the vast majority of cases are curable, with hypothyroidism (hypothyroid function) rarely becoming a long-term consequence.
Etiology
Subacute thyroiditis accounts for approximately 5% of thyroid diseases, with a male-to-female ratio of 1:(3–6). It is more commonly observed in women aged 40–50 years. Although it can occur throughout the year, it is more prevalent in the spring and autumn. The etiology is associated with viral infections, including influenza virus, coxsackievirus, adenovirus, and mumps virus.
In the early stages of the disease, thyroid follicular cells are destroyed, leading to the release of pre-synthesized T3 and T4 into the bloodstream and resulting in thyrotoxicosis with a reduced ¹³¹I uptake rate. In the later stages, most patients experience the restoration of thyroid follicular structure and function, with only a minority progressing to hypothyroidism.
Pathology
Lesions may have a diffuse or focal distribution. At the early stage, follicular destruction and neutrophilic infiltration are observed, followed by the formation of granulomas composed of histiocytes and multinucleated giant macrophages surrounding colloid. In the later stages of the disease, inflammation diminishes, with areas of varying degrees of fibrosis and follicular cell regeneration. These pathological changes often resolve completely as the disease improves.
Clinical Presentation
Many patients report a preceding history of upper respiratory tract infection. Typical cases progress through three phases: a thyrotoxic phase, a hypothyroid phase, and a recovery phase. The entire course of the disease lasts approximately 4–6 months, but in rare cases, it may fluctuate and persist for up to 2 years. The onset is often abrupt and characterized by anterior neck pain, frequently starting on one side, remaining limited to one side, or spreading contralaterally over time. The affected thyroid gland becomes enlarged and tender, with pain often radiating to the ears and worsening during swallowing.
Systemic symptoms may include fever, fatigue, weakness, heart palpitations, and diaphoresis. The thyroid gland is usually unilaterally or bilaterally enlarged to a mild or moderate degree, with a firm consistency and significant tenderness. In rare cases, cervical lymphadenopathy is present. During the hypothyroid phase, symptoms such as edema, cold intolerance, and constipation may appear.
Laboratory Examination
Findings vary depending on the clinical stage:
Thyrotoxic Phase
Elevated serum T3 and T4 levels are observed, along with a reduced 131I uptake rate, creating a "discordant phenomenon." During this phase, the erythrocyte sedimentation rate (ESR) is elevated, while leukocyte counts are mildly to moderately increased, with neutrophil numbers remaining normal or slightly elevated. Thyroid nuclear scans show areas of absent or low uptake, while thyroid ultrasound reveals hypoechoic patchy lesions with moth-eaten changes in the affected areas.
Hypothyroid Phase
TSH levels are elevated, T4 is normal or decreased, and the 131I uptake rate progressively returns to normal.
Recovery Phase
T3, T4, TSH, and 131I uptake rates return to normal levels.
Diagnosis and Differential Diagnosis
A clinical diagnosis can be made based on key features such as thyroid enlargement and tenderness, accompanied by systemic symptoms including fever, fatigue, heart palpitations, and cervical lymphadenopathy. Elevated ESR, elevated T3 and T4 levels, and reduced thyroid radioactive iodine uptake support the diagnosis.
Differential diagnoses should consider anterior neck mass and pain caused by other conditions, such as acute suppurative thyroiditis, thyroid cysts, tumors or nodules with acute hemorrhage, rapidly progressive thyroid carcinoma, infected thyroglossal duct cysts, infected branchial cleft cysts, or cervical cellulitis.
Treatment
Subacute thyroiditis is a self-limiting disease with a favorable prognosis. Mild cases may improve with the use of nonsteroidal anti-inflammatory drugs (NSAIDs). Patients with more pronounced systemic symptoms, significant fever, thyroid enlargement, and tenderness may also benefit from NSAIDs. Severe cases are treated with glucocorticoids, either alone or in combination with NSAIDs. Prednisone is commonly used at a daily dose of 20–40 mg, which can effectively alleviate thyroid pain. Dosage tapering is initiated 1–2 weeks after treatment onset, with a treatment duration of 2–3 months.
In rare cases of recurrence, retreatment with the same medications remains effective. For pronounced thyrotoxicosis symptoms, β-adrenergic blockers may be administered. Transient hypothyroidism may be treated with levothyroxine (L-T4) until thyroid function normalizes. Lifelong L-T4 replacement therapy is required for patients who develop permanent hypothyroidism.