Subacute Painful Thyroiditis (de Quervain Thyroiditis)

How to Cite This Chapter: Braga M, Brito JP, Lewiński A, Płaczkiewicz-Jankowska E. Subacute Painful Thyroiditis (de Quervain Thyroiditis). McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. Accessed May 24, 2024.
Last Updated: January 17, 2021
Last Reviewed: January 17, 2021
Chapter Information

Definition, Etiology, PathogenesisTop

Subacute painful thyroiditis (de Quervain thyroiditis, granulocytic thyroiditis, subacute granulomatous thyroiditis, giant cell thyroiditis) is probably of viral origin and typically follows a 4-phase course. There is a strong correlation of subacute thyroiditis with the presence of human leukocyte antigen (HLA)-B35. The disease is usually preceded (2-8 weeks earlier) by an upper respiratory tract infection.

Clinical Features and Natural HistoryTop

The disease can be divided into 4 distinct phases (see Table 1). Initially the dominant features are painful swelling of the thyroid gland and fever; pain is referred to the ears, mandibular angle, throat, and upper chest, and it is accompanied by exquisite tenderness of the thyroid gland. Thyrotoxicosis (lasting 2-8 weeks) results from destruction of the glandular parenchyma and release of thyroid hormones. Fatigue, malaise, anorexia, and muscle pain are common. The pain and fever subside spontaneously and hormone levels normalize after 8 to 16 weeks. Phase 3 (hypothyroidism) is not always present. Permanent hypothyroidism is rare and recovery is almost always complete (phase 4). A rapidly growing nodule, requiring cytologic assessment to exclude malignancy, may actually be an inflammatory infiltrate in the course of subacute thyroiditis. In ~2% of patients the disease may recur after a long remission (up to 20 years).


Diagnostic Tests

1. Laboratory tests:

1) Extremely elevated erythrocyte sedimentation rate (ESR), usually >50 mm/h, and C-reactive protein (CRP) are common.

2) Thyroid-stimulating hormone (TSH) and thyroid hormones: see Table 1.

3) Antithyroid antibodies are uncommonly present; thyroglobulin (Tg) antibodies are more frequent than thyroperoxidase (TPO) antibodies.

2. Imaging studies: Thyroid ultrasonography reveals diffuse or focal hypoechogenicity of the thyroid gland and it is uncommonly needed for the diagnosis. Radionuclide thyroid imaging shows a very low iodine uptake, usually <1% to 3% (in the early phase of the disease).

3. Cytology (fine-needle aspiration biopsy): Rarely needed. The dominant cells are neutrophils, giant cells (characteristic polynuclear macrophages), and epithelioid cells (mononuclear macrophages).

Diagnostic Criteria

The key diagnostic criteria are a painful or tender goiter; elevated ESR, CRP, or both; transient thyrotoxicosis; and significantly decreased iodine uptake.

Differential Diagnosis

1. Acute infectious thyroiditis with abscess formation.

2. Other rare types of granulomatous thyroiditis: tuberculous thyroiditis, fungal thyroiditis (Aspergillus, Candida, Cryptococcus); Pneumocystis jiroveci thyroiditis in immunodeficient patients.

3. Traumatic thyroiditis.

4. Radiation thyroiditis.

5. Acute hemorrhagic nodule.

6. If pain is not a dominant feature, differential diagnosis should include painless (“silent”) thyroiditis and other forms of thyrotoxicosis (see Thyroiditis; see Thyrotoxicosis and Hyperthyroidism).


The hyperthyroid phase requires no antithyroid treatment, as it is not caused by excess thyroid hormone synthesis. Beta-blockers, such as propranolol, bisoprolol, or metoprolol, may be used in patients with bothersome symptoms of hyperthyroidism.

Administer acetylsalicylic acid 2 to 4 g/d or nonsteroidal anti-inflammatory drugs to control pain and inflammation if not contraindicated; if pain is severe, consider prednisone 40 to 60 mg/d for 1 to 2 weeks, then taper the dose down to discontinue treatment in ≤4 weeks. The use of glucocorticoids does not lower the probability of transient hypothyroidism, but it decreases and shortens discomfort.

In the hypothyroid phase consider levothyroxine (L-T4) replacement therapy in those with a TSH level >10 mIU/L, significant symptoms, or both; note that hypothyroidism is usually transient and therapy should not be continued indefinitely. Replacement therapy may be withheld after 6 to 8 weeks with a follow-up of thyroid function tests to be sure that hypothyroidism is not permanent. There is no indication for surgery, as the disease is self-limiting and does not cause permanent thyroid damage.


Table 6.7-3. Clinical phases of subacute thyroiditis (de Quervain thyroiditis)

Hormone levels

Iodine uptake

Clinical features

Phase 1

↑ FT4, ↑ FT3, ↓ TSH



Phase 2




Phase 3

↓ FT4, ↓ FT3, ↑ TSH



Phase 4




↑, increase; ↓, decrease; FT3, free triiodothyronine; FT4, free thyroxine; TSH, thyroid-stimulating hormone.

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